. Depa-rtment Of the Planet Earth 701 Street, SE- Suite 200, Washington, DC 20003 (301) 475-8366 - p1anetbarti1?erols.com; September 28, 2007 Dear Board Members, . Republican Party rule ls gradually winding down. Their general program in the past has been to sell off public lands and eliminate regulation before leaving of?ce, to raise money for future campaigns. 1. Deregulation of GMO Deregulation of genetically modi?ed organisms by the Department of Agrlculture is in progress. Here' IS a letter I sent to Senator Tom Harkin, Chair of the Senate Agriculture, Nutrition and Forestry Committee. Joe and Mae?Wan Ho have put together information packages, which Ijalso sent to Senator Harkin. These are enclosed. I I also received two responses from USEA, which contend that there are neither health or other' Issues with GMQ. Isn?t lit wonderful that they are perfectly safe. 2. Biofuels Do Not Reduce Global Warming. Nitrous oxide released from fertilizer uise' is a very potent greenhouse gas, and also depletes the stratospheric ozone layer. Crutzen points out that IS a greenhouse gas with a 100 year average global warming potential, 296 times greater than carbon dioxide. They ?nd that release of N20 from fertilizer usedlin production of biofuels like corn is 3 to 5 percent, or 3 to 5 times higher than assumed 1n current studies. The authors conclude: ?We conclude, however, that the relatively large emission of N20 exacerbates the already huge challenge of getting global warming under control.? Prairie grass or organic farming would likely offer vastly better results. 3. Global Warming. 1 .. The US Congress seems unlikely to pass legislation to control global warming this year. I am more than half-way on my presentation paper to Congress and should it have it done in a week. It?s a slow process. But, will be in time for the next session. So that?s the news. I haven?t heard back on my aluminum article, but - will self-publish if necessary. Best, Erik giv/ United States Department of Agriculture Animal and Plant Health InSpection Service 4700 River Road Riverdale. MD 20737 USDA SEP 11 2007 Mr. Erik Jansson President Department of the Planet Earth Suite 200, 701 Street, SE. Washington, DC. 20003 Dear Mr. ansson: Thank you for your letter of July 10, 2007, to SecretaryJohanns concerning a pending permit application for a proposed ?eld trial involving genetically engineered (GE) and wild strains of the bacterium Burkholderia glumae. We regret the delay in responding. We recognize your interest in this matter and appreciate the Opportunity to reSpond. Under the Coordinated Framework for Regulation of Biotechnology in the United States, our Agency works cooperatively with the US. Food and Drug Administration and the US. Environmental Protection Agency to ensure that the development, testing, and use of the products of biotechnology occur in a manner that is safe for plant and animal health, human health, and the environment. Our Agency?s Biotechnology Regulatory Services (BRS) program enforces the Plant Protection Act with respect to biotechnology, regulating the importation, interstate movement, and ?eld testing of GE organisms that may pose a risk to plant health. In April 2006, our Agency received a permit application from Louisiana State University for a proposed ?eld trial using four strains of the bacterium Burkholderz?a glumae. Two of these strains are found in the wild, and two are genetically engineered. Of the two wild-type strains, one causes a disease known as panicle blight, and the other is naturally nonpathogenic and endemic to the United States. The purpose of the proposed ?eld trial is to research the -.pathogenicity of Burkholderia glumae and assist in the development of control methods to reduce cr0p yield? loss caused by panicle blight. BRS of?cials prepared an environmental assessment (EA) to provide the public with documentation of our review and analysis of any potential. environmental impacts and plant pest risks associated with the proposed ?eld trial. On June 19, 2007, our Agency published a notice in the Federal Register (Docket No. APHIS-2007-0021) to- announce the availability of the EA and to seek public comments. The comment period closed on July 19, 2007. We carefully considered all comments received on or before that date, and on August 7, 2007, we issued the permit. Safeguarding American Agriculture APHIS is an agenty of Marketing and Regulatory Programs An Equal Opportunity Provider and Employer Mr. Erik Jansson Page 2 We would like to note that, in the EA, BliS carefully examined the environmental and human health issues of concern to you. 111egarding the transfer 9f antibiotic resistance genes, BRS concluded that, because these genes were originally derivedfrom naturally occurring soil?borne bacteria, the same genes are likely to already exist in soil bacteria found in Louisiana soils. Given that soilidwelling microorganisms likely already carry these antibiotic resistance genes, the presence of the genes in Burkholderia glumae is unlikely to cause an increase in the prevalence of antibiotic resistance genes in the' environment. In addition, based on current research, gene transfers from microorganisms to plants and animals 1n the envirOnment are unlikely to occur under the conditions of the ?eld test. In the EA, BRS also assessed the risk posed by the possible spread of the bacterial strains from the trial area to other rice crops. We would like to note that the wild-type strains, as well as the strains from which the transgenic strains were derived, are native to Louisiana and were collected from rice planted in that State. Because the wild-type, pathogenic bacterial strains are already present in Louisiana, the release of the wild- -.type strain does not constitute a release of novel bacteria. In fact, the amount of bacteria being released 1n the ?eld IS negligible compared to the amount of Burkholderra glumae currently resident 1n the surrounding area. In terms of human health, this means that the ?eld trial will not signi?cantly Increase the risk ofBurkholderz'a glumae to humans who may be susceptible to the pathogen. I We assure you that our Agency is committed to the safe ?eld testing of GE organisms, and we believe that the EA accurately described the risks involved 1n the Burkholderia glumae test. We encourage you to read the full EA, which you can ?nd on our Agency?s Web site at W. aphis. usda. gov/brs/aphisdocis/06_ 11101r_ ea. pdf. 1 1 We hope this informationis helpful. Sincerely, 0 Rebecca A. Bech Deputy Administrator I 1 Biotechnology Regulatory Services . . United States AUG 2 3 2007 Department of Agriculture Animal and? Plant Health Inspection Service 4700 River Road Mr. lErik 13-11530.? Riverdale. MD PreSIdent 20737 The Department of the Plant Earth Suite 200, 701 Street, Southeast Washington, DC. 20003 Dear Mr. ansson: Thank you for your letter of August 1, 2007, to Secretary Johanns concerning the regulation of plums genetically engineered for resistance to plum pox virus (PPV). We recognize your interest in this issue and appreciate the opportunity to reSpond. As you know, on July 13, 2007, our Agency published in the Federal Register a notice (Docket No. APHIS-2006-0084) advising'the public of our determination of nonregulated status of the plum (designated transformation event C5) genetically engineered to resist infection by. PPV. While we recognize that you disagree with our decision, we continue to believe that this plum line does not present a plant pest risk. Our decisions in this matter are based on sound science and were ?illy vetted through the regulatory process for the introduction of genetically'engineered organisms and products. This process included a 60-day public review and?comment period. .We assure you that our Agency fully considered the body of . . knowledge related to this plum variety before concluding that it does not pose a plant pest risk. We also reviewed and analyzed all comments received on the petition and draft environmental assessment (EA)?including those submitted by'p'arties opposed to the prOposal. A number of factors informed our ?nal decision, and we outlined these thoroughly in our response to the comments submitted. Our response and other related documents?including the ?nal EA and ?nding of no signi?cant impact?are available on our Agency?s Biotechnology Regulatory Services Web site. The address is A link to the documents is listed under the heading ?Petitions for Nonregulated Status Granted;? the petition number is 04-264-01 p. We hope this information is helpful. Sincerely, If 3 $5925 2p{ bf?? ?7 ?t?Rebecca A. Bech Acting D6puty Administrator Biotechnology Regulatory Services Safeguarding American Agriculture APHIS is an agency of USDA's Marketing and Regulatory Programs An Equal Opportunity Provider and Employer - . I Department of the Planet Earth 701 Street, SE - Suite.200, Washington, DC 20003 - . (301) 475-8366 - September 19, 2007 Senator Tom Harkin Chair Senate Agriculture, Nutrition and Forestry Committee SR 328A 4 Washington, DC 20510 0. Committee Re: USDA Proposes Regulation to Further Deregulate Hazardous Genetic Modi?ed Organisms: How Does This Further the Farm Economy? 1 Dear Chairman Harkin and Colleagues? As you can see, the Department of Agri?culture has proposed to further deregulate GMO plants and animals, despite evidence that many of these altered plants and animals pose severe health and environimental risks. A number of Judges have ruled against APHIS recently. As Dr Joseph Cummins and Dr. Mae-Wan Ho put it (Question #10 in the enclosed presentation): 3 criteria on regulation are so low that they cannot go any lower. One should be reminded that USDA has lost multiple lawsuits to civil society within the past year over its regulation of GM crops, which has been deemed inadequate.? Con?ict of Interest: The authors also point out the con?ict of interest of APHIS, seeking to deregulate patents they own and from which they will bene?t. The consequences of the lax program of APHIS can be severe: 1. For example, rats consuming genetically modi?ed Roundup Ready soybeans gave birth to severely stunted with over half of the litter dead by 3 weeks, and the remaining pups sterile. For a farmer, this would be economically disastrous. For the public, it would be a crime. 2. A recently approved GMO bacteria for rice could end up spreading virulent rice bacterial strains to the US commercial rice crop. Furthermore, the transgenic B. glumae proposed for release 13 also a serious human pathogen. 3. As always, multiple safer alternatives exist. Hasn?t the time come to ask the General Accounting Of?ce or other body to investigate the lax APHIS program? With best regards, Erik ansson, Pres". i ?i USDA Proposes Further De-regulation of GMOs The proposed changes make the regulatory regime even more permissive Prof? Joe Cummins and Dr. Mae-Wan Ho . This article was submitted to the USDA on behalf of ISIS. Please circulate widely to your policy-makers I . The United States Department of Agriculture (USDA) Animal and Plant Health Inspection Service (APHIS) has proposed changes to regulations on Introduction of Organisms and Products Altered or Produced Through Genetic Engineering, available for public comment before 11 September 2007 at: APHIS is seeking public comment on its draft environmental impact statement (DEIS) presenting alternatives in a series of qtiestions. The questions and our answers are given below. Question 1. Should APHIS continue to regulate GE [genetically engineered] organisms solely on the basis of potential risks as plant pests, or should they also be regulated based on other potential risks such as those for noxious iveeds and biological control organisms? Answer: APHIS should more realistically take into account the risk of transgenic contamination of crops and weedy relatives of the crops. The detrimental economic impact of transgenic contamination as well as the toxic potential, especially of pharmaceutical products or transgenic bi0polymers, must be evaluated. Crops modi?ed with genes to enhance energy production may genetically contaminate food crops. Finally, transgenic contamination should be treated as any other environmental pollution. APHIS should take into account the strong evidence that transgenic contamination is unavoidable (GM Contamination At 21 km and Farther. No (Zn-Existence Possible, 8135' 35) Question 2. Should a new system of risk-based permit categories be designed to deal with new products and new concerns? Answer: It is imperative that crops such as food crops modified to produce pharmaceutical I proteins or crops destined for energy production should be evaluated by criteria that are different from those of food crops in recognition that the transgenes pose unique dangers to 5 health. The same applies to transgenic/cloned ailimals or genetically engineered bacteria modi?ed for food/pharmaceutical purposes (G Food Animals (irons and Microbes for Health or Public Health Hazards? 32; Is FDA Promoting or Regulating Cloned Meat and Mi lk?P'SiS 33). In the case of transgenic and cloned animals, animal health and welfare must be included as part of the risk assessment. In the case of GM bacteria, the risks of horizontal gene transfer are the greatest. Question 3: Should APHIS continue to accommodate commercialization but in some cases . grant conditional approvals when additional information is needed about particular regulated - articles proposed for deregulation? Answer: De?nitely not. Conditional approval of transgenic crops is a terrible idea. The current system of ?eld test releases include veryllarge test areas, and even allows for commercial production of high value products such as pharmaceutical proteins produced on the test site (Finn-m Crop Products .1 n. US Market, SIS 23). This needs to be brought under stricter regulation rather than the relaxed scheme proposed. Question 4: Should APHIS modify its rules for regulating and con?ning plants producing pharmaceutical and industrial compounds? Answer: APHIS should st0p approving any open releases of such plants (Ban Plant-based Transgenic Plnu?maccut?icals, 23) as transgene contamination is unavoidable Question 5. Should APHIS regulate nonviable plant material derived from regulated plants? Answer: There is in a sense no nonviable plant material in the case of GE plants, as the GE DNA survives the plant and can be transferred horizontally to practically all species, in dust and debris from transgenic crops and the processed products of transgenic crops. Question 6: Should there be a new mechanism to provide oversight for pharmaceutical plants? Answer: Here to fore plants modi?ed to produce pharmaceutical proteins have not yet been approved for commercial production in NorthAmerica nor in Europe. Commercial production of crops such. as rice or saf?ower modi?ed to produce pharmaceutical proteins has been permitted in South America. These plants must not be released into the Open environment, but should be strictly contained in sealed greenhouses with pollen traps, to prevent transgene contamination of air, water and soil Question 7: Should low-level occurrence of a regulated article be exempted from regulation? Answer: De?nitely not. Low-level centamination with regulated articles should not be permitted, as unlike chemical contamination, transgene contamination has the potential to grow. The articles regulated must remain so at any detectable level. Question 8: Should low-risk organisms intended for importation for a nonpropagative use be exempted from regulatory review or be subject to expedited review? Answer: The presumption of ?low?risk? is highly questionable. Lethal pathogens have been created ?accidentally? on that presumption, and importation for contained use in research laboratories have a habit of leaking out (No 1-3 iosccuritv without Biosaibtv'SiS 26). What may be at issue here are genetically modi?ed crops imported from other countries for food, feed or processing. Japanese researchers found that modi?ed canola imported for oil extraction were Spilled along the transport corridors from dock to processing plant and took root in the soil of Japan They further found that the transport corridors from the production area to the dock in Canada were similarly polluted with modi?ed canola. The Japanese report should be taken seriously-and point out that imported transgenic material is bound to genetically pollute the country importing the crops. The low risk organisms fantasized by API-IIS simply do not exist. Question 9: Should interstate movement of GE Arabidopsis or other GE organisms be exempted from movement restrictions? Answer: No, they should not be exempted, for reasons given in answer to Question 8. Question 10: Should APHIS consider relieving other regulatory requirements when the environmental risk is low? Answer: criteria on regulation are so low that they cannot go any lower. One should be reminded that USDA has lost multiple lawsuits to civil society within the past year over its regulation of GM crops which has been deemed inadequate (Approval ol?Gi?vl Crops illegal. US Federal Courts Rule 34). Question 11: Should APHIS switch from prescriptive packaging-container requirements to performance-based ones? Answer: Packaging was discussed in the APHIS document but there was little speci?c information provided regarding the actual; packages. APHIS raises the spectre that packaging would be deregulated except for special cases, that proposal is premature and a threat to the environment. Additional Comment APHIS has not dealt with an important con?i?t of interest in their regulation of transgenic crops. That con?ict of interest ?ows from the fact that USDA both ?nancially bene?ts from its patents on modi?ed crops and promotes modi?ed crops. For example, APHIS granted the petition for deregulation of transgenic plums, even though an overwhelming majority of the public comments submitted went against the petition and there were outstanding safety concerns against deregulation [11] (Transgenic Plum Gets USi?m Non-regulated Status l-?iased on False Claimsof Safety. 35). This is the time for APHIS to put its house in order or hand the regulatory duty to an independent and unbiased agency, one incorporating representatives of the public including critics of transgenic crops as well as those creating and promoting them. Since 1999, ISIS has submitted close to 40 detailed objections to US regulatory agencies, mostly addressed to the We are extremely concerned over the regulatory regime on both sides of the Atlantic, where the precautionary principle is routinely ignored, science is manipulated and corrupted, and the law sidestepped in efforts to promote genetically modi?ed organisms (GMOs) in the face of massive public opposition and damning evidence piling up against the safety of GM food and feed. We have summarized these concerns in a recent scienti?c publication [12] GM Fried Nightmare Utilbldina in the Renulatorv Sham (Ho MW, Cummuns and Saunders PT, Microbial Ecology in Heaith and Disease 2007, 19, 66-77), which is enclosed with this submission. References 1. Ho MW. GM contamination at 21 km and farther, no co-existence possible. Science in 55, 30-31, 2007. 2. Cummins and Ho MW. GM food animals coming. Science in Society 33, 24-29, 2006. 3. Cummins and Ho MW. GM crops and microbes for health or public health hazards? Science in S't'icictv 32, 30-33, 2006. I 4. Ho MW and Cummins J. Is FDA promoting or regulating cloned met and milkbank?s 24-27, 2007. 5. Cummins J. Pharm crops in US market. iglL?liCLLl-?jlmich 7?5 28-29, 2004. 6. Cummins and Ho MW. Ban plant-based transgenic pharmaceuticals. Science in ?ociew 2:1, 29. 2004. . 7. Ho MW. No biosecurity without biosafety. Biodefence research endangers the public. Science in Societv 26. 44-47, 2005. 8. Yoshimura Y, Beckie HJ, Matsuo K. Transgenic oilseed rape along transportation routes and port of Vancouver in western Canada Environ Biosaf?ry Res. 2006 67-75. - 9. Saji H, Nakajima N, Aono M, Tamaoki M, Kubo A, Wakiyama S, Hatase Y, Nagatsu M. Monitoring the escape of transgenic oilseed rape around Japanese ports and roadsides Environ Biosa?aoz Res. 2005, 217-22. - 10. Cummins and Ho MW. Approval of GM crops illegal, US federal courts rule. 34. 24,. 2007. 11. Cummins and Ho MW. Transgenic plum gets USDA non-regulated status based on false claims of safety. Science in Societv 35, 35-36, 2007. 12. Ho MW, Cummins and Saunders PT. GM nightmare unfolding in the regulatory sham. Microbial Ecology in Health and Disease 2007, 19, 66-77. Microbial Ecology in Health and Disease 2007, 1?12, iFirst article REVIEW ARTICLE informa healthcare GM food' nightmare unfolding in the regulatory sham MAE-WAN H01, JOE owns/111x13"2 PETER of Sczence Soczety, London, UK, 2Department of Biology, University of Western Ontario, Canada and 3Deparzmem ofMazhematzcs, ng?s College, London, UK Abstract Our regulators are ignoring the precautionary principle, manipulating and corrupting science, sidestepping the law, and helping to promote genetically modi?ed organisms (GMOs) in the face of massive public opposition and damning evidence piling up against the safety of genetically modi?ed (GM) food and feed. GM nightmare unfolds Fem-ale rats whose diets were supplemented with genetically modi?ed (GM) Roundup Ready soy- beans gave birth to many severely stunted pups, i with over half of the litter dead by 3 weeks, and the surviving pups were sterile (1). This is the ?rst investigation into the effects of unprocessed GM feed on reproductive function and fetal and postnatal development, in an experiment lasting more than 90 days, a period set by the European Food Standards Authority (EFSA) (2), and the GM soya has been commercialized worldwide for food and feed since 1996. These ?ndings came from the laboratory of senior scientist Irina Ermakova at the Institute of Higher Nervous Activity and Neurophysiology of the Russian Academy of Sciences in Moscow. The results have been published in Russian 5), 1 and in several conference proceedings in English (6 9) These results are not an isolated case. They .top a growing stack of evidence from all over the world, indicating that GM food and feed may be inherently hazardous to health (see Table I) (10?24). Genetic modi?cation andlor the arti?cial transgenic DNA to blame? Many varieties of GM crops with different trans- genes, fed to rats, mice, cows, sheep, chickens, or human beings, resulted in illnesses and deaths. The obvious suspect is the GM process and/or the arti?cial transgenic DNA used. It is worth noting that transgenic DNAs are constructs that are entirely new to evolution. The. genes are considerably altered from their natural counterparts, combining c0pies of sequences from many different sources. For example, MON863 maize is described on the AGBIOS Database as follows (25): ?The introduced DNA contained the modi?ed cry3Bb1 gene from B. thun'ngz'ensz's subsp. kumamomensz's under the control of the promoter 358 promoter with 4 repeats of an activating sequence), plus the 5? untranslated leader sequence of the wheat Chloro- a/b binding protein (wt CAB leader) and the rice actin intron. The transcription termination sequence was provided from the 3? untranslated region of the wheat 17.3 kD heat shock protein (rahsp17). The modi?ed gene encodes a protein of 653 amino acids whose amino acid sequence differs from that of the wild-type protein by the addition of an alanine residue at position 2 and by seven amino acid changes.? The Coding sequence for was also modi?ed with numerous codon adjustments to compensate for codon bias 1n plants as opposed to bacteria. There are nine bits of DNA from different sources including the coding sequence, which has been substantially altered from the natural gene. The many homologies to different genomes including those of bacteria and viruses, the presence of recombination (fragmentation) hotspots such as the Correspondence: Mae-Wan Ho, Institute of Science in Society, 1?0 Box 51885, London NW2 QDH, UK. E-mail: (Received 13 March 2007; accepted 1' 6 March 2007) ISSN 0891-060X print/ISSN 1651-2235 onlinc 2007 Taylor 8: Francis D01: 10.1080l08910600701343781 Downloaded By: [informa internal users] At: 12:31 7 June 2007 2 Ho er al. Table I. .Accumulating evidence on the health hazards of GM food and feed. Table II. Potential hazards of genetically modi?ed organisms (GMOs). 1. Between 2005 and 2006, scientists at the'Russian Academy of Sciences reported that female rats fed GM soybeans produced excessive numbers of severely stunted pups and more than half of the litter dying within 3 weeks, while the surviving pups are completely sterile (main article). 2. Between 2004 and 2005, hundreds of farm workers and cotton handlers in Madhya Pradesh, India, suffered allergy from exposure to Rt cotton containing CryIAc or both CrylAc and CryIAb proteins (10). 3. BetWeen 2005 and 2006, thousands of sheep died after grazing on Bt cotton crop residues in four villages in the Warangal district of Andhra Pradesh in India (11). 4. In 2005, scientists at the Commonwealth Scienti?c and Industrial Research Organization in Canberra Australia teated a transgenic pea containing a normally harmless protein in bean (alpha-amylase inhibitor 1), and found it caused in?ammation in the lungs of mice and provoked sensitivities to other proteins in the diet (12,13). 5. From 2002 to 2005, scientists at the Universities of Urbino, Perugia and Pavia in Italy published reports indicating that GM-soya fed to young mice affected cells in the pancreas, liver and testes 6. In 2003, villagers in the south of the Philippines suffered mySterious illnesses whena- Monsanto Bt maiZe hybrid containing CrylAb protein came into ?ower; antibodies to the CryIAb protein were found in the villagers, there have been at least ?ve unexplained deaths and some remain ill to this day (19). 7. In 2004, Monsanto's secret research dossier showed that rats fed MON863 GM maize containing Cry3Bb protein devel- oped serious kidney and blood abnormalities (20) (see main text). 8. BetWeen 2001 and 2002, a dozen cows died in Hesse, Germany after eating Syngenta GM maiza Bt176 containing plus glufosinate-tolerance; and more in the herd had to be slaughtered from illnesses (21). 9. In 1998, Arpad Pusztai and colleagues formerly of the Rowett Institute in Scotland reported damage in every organ system of young rats fed GM potatoes containing snowdrop lectin, including a stomach lining twice as thick as controls (22). 10. Also in 1998, scientists in Egypt found similar effects in the gut of mice fed Bt pctato containing a CrylA protein (23). 11. The US Food and Drug Administration had data dating back to early 19905 showing that rats fed GM tomatoes with antisense gene to delay ripening had developed small holes in their stomach (22). 12. In 2002, Aventis company (later Bayer Cropscience) submitted data to UK regulators showing that chickens fed glufosinate-tolerant GM maize Chardon LL were twice as likely to die compared with controls (24). 358 promoter, and the general structural instability of transgenic DNA, are all factors that would greatly enhance horizontal gene transfer and recombination, the main route to creating new pathogens. We have spelt out the potential dangers of the GM process in numerous publications (see Table II) based on extensive reviews of the scienti?c literature, especially highlighting the hidden dangers arising from unintended horizontal transfer of transgenic DNA (26?35). a genes and gene products new to evolution could be toxic for humans and other animals or provoke serious immune reactions 0 The uncontrollable, imprecise process involved in making GMOs mutate and scramble genomes and can generate unintended toxic and immunogenic products; this is exacerbated by the instability of the transgenic DNA Endogenous viruses that cause diseases could be activated by the transgenic process a The genes in GMOs, including copies of genes from bacteria and viruses that cause disease as well as antibiotic resistance genes, may be transferred to other species via pollen, or by direct integration into other genomes in horizontal gene transfer 0 Disease-causing viruses and bacteria are created by horizontal transfer and recombination, and genetic modi?cation is nothing if not facilitated and greatly enhanced horizontal gene transfer and recombination oTransgenic DNA is designedto invade genomes, including those of animals and human beings, and its strong promorers may trigger cancer by activating cellular oncogenes a Herbicide-tolerant GM crops accumulate herbicide and herbicide residues that could be highly toxic to humans and animals as well as plants food is safe?? . Regulators have been assuring the public that food is safe? because people have been eating GM food since its ?rst release in 1994 and no one has been found to fall ill or die from it. However, there has been no labelling in countries like the United States where GM food and feed are most available, and many GM products are ?deregulated? and hence not knoWn or traceable as such. There has been no post-release monitoring, although research at the Centers for Disease Control suggested that food? related illnesses went up 2?10-fold in 1999 com- pared with a survey done just before GM food- was commercially released in 1994 (36,37). GM food and feed may be linked to chronic illnesses such as autoimmune disease from bacterial DNA or indeed any novel transgenic DNA (38?41), slow viruses or cancer (see Table II), which may be dif?cult to detect. Finally, animal feed accounts for up to half the world?s harvest (42), so most of the GM produce so far has probably gone in animal feed after being processed for seed oil, corn starch and syrup, and increasingly, ethanol and biodiesel (43,44). Proces~ sing will remove or destroy at least some of the toxic metabolites, proteins and transgenic DNA. Thus, GM produce is seldom eaten directly by either animals or human beings so far, except in Argentina, with dire consequences for health (45). In Argentina, GM soya has been promoted as a staple food, especially for the poor, which has no precedent in the world, and it is impossible to separate effects due OJ :5 runsoya per se, from those due to GM soya, and further, those due to the toxic herbicide Roundup (see later) sprayed from the air, dousing people and their homes. GM food is still being sent to Africa as ?food aid? after widespread rejection and protest (46), putting millions of the most hungry and vulnerable people at: risk from the health hazards of genetically modi?ed! organisms (GMOs), and threatening to contaminate: their food supply for years to come. Evidence ignored and dismissed by regulators for decades The list of evidence of GM hazards in Table I is by no means complete. In fact, evidence has been building up since the 19803 that should have halted the development or commercialization of many, if not all GM crops (10), if the precautionary principle had been applied. But our regulators were biased in favour of genetic modi?cation from the ?rst, and have systematically ignored and dismissed research ?ndings that might harm the fledgling biotech industry (47). We shall look at two examples the immunogenicity of Bt biopesticides and the hor? izontal transfer of transgenic DNA. Immunogem'cz?ty of Br toxins The Rt bacteria (Bacillus rhurz'engensz's) and Spores the source of Cry proteins involved in many of the cases of fatalities and illnesses in Table I - were linked to allergic reactions (48) before the Cry proteins were widely incorporated into GM crops 1 as ?biOpesticide?. Bt crops were introduced ?rst in the United States in 1996, and have expanded' substantially in global area with little research on the toxicity or immunogenicity of the Cry proteins. A research team in Cuba reported in 1999 that CrylAc is a powerful immunogen, and when fed to mice it induced antibody responses similar to those obtained with the cholera toxin (49). Contrary to the assumption that mammals do not have receptors for the protein, the team demonstrated that CryIAc binds to the inner surface of the mouse small intestine, especially to the brush border membranes, and induced a transient electrical hyperpolarization indicative of signi?cant biological effect (50). The transgenic Cry proteins may be worse than their natural counterparts. Green lacew- ings suffered signi?cantly reduced survival and delayed development when fed an insect pest (lepi- dopteran) that had eaten GM maize containing transgenic CrylAb, but not when fed the same pest treated with much higher levels of the natural toxin (51,52). All Cry proteins in Bt crops have GM food regulation 3 amino acid sequence similarities to known allergens (53?55), and are hence potential allergens until proven otherwise. Transgenic maize CrylAb was found to survive digestion in pigs (56,57), which would increase its immunogenic potential. The immunogenic potential of all transgenic proteins is Open to question since the demonstration that species-specific processing of proteins could turn a normally harmless bean protein into a pOWer? ful immunogenic when it was transferred to pea (12,13). And the tests carried out to detect such reactions are still not required by regulatory agencies anywhere in the world. Horizontal gene transfer happens We have raised the issue of unintended horizontal transfer of transgenic DNA with our regulators repeatedly since the late 19905 (26,58,59) when they denied vehemently that it could happen, and assumed mistakenly that DNA would be rapidly broken down in all environments. We presented an extensive review in 1998 (30), documenting evi- dence that DNA persists in all environments and pointed out that transgenic DNA enhances and facilitates horizontal gene transfer for reasons stated above (Table II). We called for a public enquiry, but to no avail. In 1999?2000, we alerted our regulators to the hazards of the 358 promoter, which is in practically every commercial transgenic variety com- mercialized, calling for the GM crops to be with- drawn. The 358 promoter has a recombination (fragmentation) hot spot, which would enhance horizontal transfer of transgenic DNA and make transgenic DNA and transgenic lines unstable (31,32). Furthermore, contrary to the then common assumption that the promoter was only active in plants and plant-like organisms, it is in fact active in species across the living world, animal and human cells included (33), with the potential for activating dormant viruses and triggering cancer. Recently, the 358 promoter was demon? strated to be active in human enterocyte?like cells (60). Evidence of transgenic instability has also emerged, with the 358 promoter representing a major breakpoint (see below). . By 1999, there was already evidence that 1101?- izontal transfer of transgenic DNA could occur, not only in the laboratory but also in the ?eld (61). Unfortunately, the researchers were far too cautious as scientists, and ended up denying the prime facz?e evidence that horizontal transfer of transgenic DNA had occurred (62), whereas a proper application of the precautionary principle would have made the researchers stress the possibility that it had occurred. Downloaded By: [informa internal users] At: 12:31 7 June 2007 4 H0 er al. Since then, evidence continued to accumulate (63). Transfer of transgenic maize DNA antibiotic resistance marker could occur before the DNA was completely broken down, even when the breakdown was rapid, as in the sheep rumen or in silage. DNA breakdown was extremely slow in saliva, and hence the oral cavity would be a very important site for horizontal gene transfer (64). High frequencies of horizontal transfer of trans- genic plant DNA were demonstrated for soil bac- teria, Pseudomonos stutzerz' and Acinetobacter sp. when the transgenic plant DNA contained sequence homologies to the bacteria (65). Again, the authors stressed that the transfer ?strictly depends on homo- logous sequences?, which could give the uninformed a false sense of assurance, forgetting that transgenic constructs contain homologies to many different Species of bacteria and viruses, and are therefore capable of engaging in high frequencies of horizontal gene transfer and recombination with all of them (63). We have drawn attention to further evidence of the enhanced horizontal transfer of transgenic DNA in our submissions (6 6,67) to the regulatory authorities in Hawaii objecting to an intended outdoor large- scale facility for transgenic strains of the alga, Chlomydomonas rez'nhardrz?z' producing a range of pharmaceutical proteins. We pointed that DNA not only persists in all environments, but also that transformation by direct uptake of DNA is a. major route of horizontal gene transfer among bacteria (68). The close similarities (homologies) between the transformed plastid in transgenic C. rez'nhardn'z' and bacterial genomes is expected to greatly increase the frequency of horizontal gene transfer, by up to a billion-fold and furthermore, the horizontal transfer of non-homologous DNA occurs at rela- tively high frequencies when a homologous DNA ?anchor sequence? is present, which can be as short as 99 bp. A review published in 2004 already listed at least 87 species of naturally transformable bacteria in the soil (70). . There is also evidence that transgenic DNA in food and feed may transfer into animal and human cells (71). Several studies have documented the survival of DNA in food/feed throughout the in- testinal tract in mice and pigs (56,72,73, and references therein), in the rumen of sheep (74), and in the rumen and duodenum of cattle (75), with varying degrees of sensitivities in PCR methods. In the only feeding trial in human volunteers (76), a single meal containing GM soya with about 3 1012 copies of the soya genome, the complete 2266 bp of the epsps transgene was recovered from the colost- omy bag in six of seven ileostomy subjects, although at highly variable levels, ranging from 1011 copies in one subject to 105 c0pies in another. This is a strong indication that DNA is not rapidly broken down in the gastrointestinal tract, con?rming earlier results from the same research group. In three of the seven ileostomy subjects, about 1 to 3 per million bacteria cultured from the contents of the colostomy bag were positive for the GM soya transgene, indicating that horizontal transfer of transgenic DNA had occurred, either before the single meal was taken, as claimed, or else as the result of the single GM soya meal, a possibility that cannot be ruled out (71). Interestingly, no bacteria were found to have taken up non-transgenic soya DNA, suggest- ing that transgenic DNA may be more successfully transferred for reasons given above. No transgenic DNA was found in the faeces of any of 12 healthy volunteers tested. Either the remaining DNA has completely broken down by then as claimed by the researchers, or else detectable frag- ments have all passed into the blood stream from the intestine (71). It is already known that food material can reach entering the intestinal wall directly, through Peyer?s patches. And fragments of plant DNA were detected in cow?s peripheral blood (77). From the blood, the DNA can be transported to and taken up by tissue cells, and this has been known from experiments since the late 19905. Transgenic DNA and viral DNA fed to mice ended up in cells of several tissues (78), and when fed to pregnant mice, the DNA crossed the placenta and entered the cells of the fetus and the newborn (79). DNA from ingested food plants were also taken up into tissue cells (80). Recent research has uncovered substantial amounts of DNA and RNA circulating in peripheral blood, which are actively secreted by living cells, and fully capable of transforming other cells (81,82). The nucleic acids appear to play a role in disease progression and metastasis of cancers. In plants too, foreign and endogenous nucleic acids circulate (83), apparently acting as intercellular messengers. There is a distinct possibility, therefore, that DNA from food could end up in peripheral blood and gain entry into cells (81). weigh: of evidence now undeniable but regulators helping to promote even more dangerous producrs By now, the evidence against the safety of GM food and feed has accumulated to such an extent that the regulators should be answering a charge of criminal negligence at the very least in continuing their campaign of denial and misrepresentation, while failing to impose a ban on further releases of all GM crops until and unless they have been proven safe by thorough independent investigations (19) Worse yet, the UK government has given the go-1 ahead for ?eld trials of GM potatoes that arj overwhelmingly rejected by consumers, all big foo companies, and the British Retail Consortium (84).l The GM potatoes contain transgenes conferring broad-spectrum potato blight resistance, Rpi?blbf' and They code for proteins with a nucleo- tide-binding site consisting of leucinevrich repeats, known to be immunogenic in mammals. BASF Plant Science GmbH, the German company that created the GM poratoes, had carried out no safety tests, andi was allowed to dismiss horizontal gene transfer by citing a single research paper long exposed to be fundamentally ?awed (28). Despite the misleading title of the publication (85) that horizontal gene transfer from the transgenic potato ?occurs, if at all, at an extremely low-frequency?, the actual results showed quite the opposite. A high transfer frequency of 5.8 ><10"2 per recipient bacterium was demon- strated under optimum conditions. But the authors then proceeded to calculate an extremely low theore? tical gene transfer frequency of 2.0 under extrapolated ?natural conditions?, assuming that dif- ferent factors acted independently. The natural condi- tions, however, were largely unknown and unpredictable, and even by the authors? own admis- sion, synergistic (multiplier) effects could not be ruled out. It is all the more important now for regulators to - take evidence seriously, as the biotech industry has been caught exaggerating the ?success? of GM crops in terms of the total area planted globally as opposition heightens worldwide (86), and GM cr0ps are also proving disastrous for agriculture, as Roundup Ready resistant superweeds have emerged (87) and BI cottons have failed disastrously in India, adding substantially to farmers? suicides (86), while Bt?resistant pests have evolved (88). But the industry is aggressively pushing new generations of even more dangerous products, with help from the regulators. Food crops are ?metabolically engineered? to over- produce single nutrients for ?health bene?ts?, pro- biotic bacteria are genetically modi?ed to serve the food industry and as vectors for gene therapy, and animals are genetically modi?ed for a variety of purposes of which GM meat and milk will be by- products. Many nutrients are known to be toxic in overdose (89), so food crops overproducing any single nu- trient could be a public health hazard, and geneti? cally modifying probiotic bacteria may turn them into pathogens pre?adapted to invade the gut, and should be strongly resisted if not banned (90,91). Foods derived from GM animals are likely to be GM food regulation 5 contaminated with potent vaccines, immune regula- tors and growth hormones, as well as nucleic acids, viruses and bacteria (92). Genetically modifying animals is questionable in terms of animal welfare and ethics; that applies eSpecially to cloned transgenic animals (93,94). But the United States Food and Drug Adminisrra- tion (FDA) and Department of Agriculture (USDA) have both presented cloned animals in a misleadingly positive light, implying that cloning by somatic cell nuclear transplant (SCNT) is no different from cloning by splitting embryos at the two- or four- cell stage. As is widely acknowledged (95), SCNT has an extremely low rate of success and causes massive suffering and death not just to cloned fetuses and calves, but also to the many surrogate mothers required. In short, crucial evidence has been systematically ignored or dismissed by our regulators. As we shall make clear below, there is little or no protection for the public and the environment under the current regulatory regime that has no regard for the precau- tionary principle. Scienti?c data are routinely ma- nipulated and science abused; regulators are colluding with industry to promote the products they are supposed, to regulate, even to the extent of breaking the law. Abusing science and the precautionary principle I726 precautionary pn'ncz'ple in Europe and the UK Regulators in Europe are bound by law to operate on the precautionary principle as stated in the interna- tional Cartegena Protocol on Biosafety for and the UK and the EurOpean Union have signed up to that, as have 137 other countries worldwide (96). It is ?taken into account? in the European Directive for deliberate release into the envir? onment of GMOs (97). The European Commission (EC) Communica- tion 'on the precautionary principle (98) made a strong statement: ?the Commission considers that the precautionary principle is a general one Iwhich should in particular be taken into consideration in the ?elds of environmental protection and human, animal and plant health.? It recognized that the precautionary principle has become ?a hill??edged and general principle of international law?, since it was written into the Framework Convention of Climate Change, Convention on Biological Diver~ sity, and in January 2000, Cartegena Protocol on Biosafety; it is also in the World Trade Organisation?s Agreement on Sanitary and Phytosanitary Measures and the Agreement on Technical Barriers to Trade. I Downloaded By: [informa internal users] At: 12:31 7 June 2007 6 MW Ho e: at. The watchdog, the Food Standards Agency is advised by the Advisory Committee on Novel Foods and Processes (ACNFP), which adver- tises itself as ?a nonstatutory independent body of scienti?c experts?, even though the majority of its members, including the chair, have vested biotech interests as shareholders of companies, paid con- sultants or recipients of research grants (99). The Food Standards Agency?s Approach to Risk (100) states: ?We will take a precautionary approach that is, we will not always wait until we have proof of a potential hazard to take action or issue advice. Such action will be taken on the best available evidence to protect public health. ?It will be reviewed if new evidence becomes available?. Manipulation of scientific evidence and abuse of science In practice, however, the manipulation of scienti?c evidence and abuse of science have prevented the precautionary principle being ever invoked, let alone applied at the national or international level. The regulators have been operating on the anti-precau- tionary principle (101). Not only do they require the public and genuinely independent scientists to prove there is hazard, they have persistently ignored all evidence of hazards submitted to them, and?instead, continue to misinform the public by citing highly flawed studies that claim to ?nd ?no e??ect?. Scientists have been drawn effectively into a closed loop of self-reinforcing ?advocacy science? (102) that excludes not just counter scientific evi? dence but evidence from the real world (see Table I), from the experience of the farmers and consumers the scientists are supposed toserve. Advocacy science has but one goal: to smooth the passage of GM produce into the market, without regard for safety or moral, ethical concerns. In the European Union (EU), scienti?c assess? ment on the safety of GM food products is done by the and a ?positive opinion? from the EFSA would invariably result in commercial approval for the producr. But positive opinions have been challenged on scienti?c grounds (103,104), and accusations of bias towards the biotech industry have come from both member states and civil society organizations. So much so that in April 2006, the EC decided to introduce improvements to ?scienti?c consistency and transparency of the deci- sions on (105). One particular study (106) cited by the ACNFP to dismiss Ermakova?s ?ndings (1) has been strongly challenged by scientists around the world (107). It used processed soya, made from batches of soya harvested in the middle of two certain ?elds in South Dakota, and formulated into rat chow by a com- mercial company, which were fed to small number of mice (not rats). These are other peculiarities in experimental design made the study not only sub- stantially different from that of Ermakova, but also completely unreplicable. The remarkable similarities in the composition of the GM and non-GM diet both supposed to contain 21.35% soya. meal Were beyond belief. There were no standard deviations to the ?gures provided; 59 of 78 Were identical to 2?3 signi?cant ?gures, and the rest differed so that they would have been within standard errors. Could it be that the researchers have been feeding both groups the same diet? There was no evidence that the two diets were different, no PCR on the food samples were performed to ascertain that one was transgenic and the other non?transgenic. Many other studies cited by the regulatory agen? cies that claim to show no effect are indeed highly misleading and/or seriously ?awed. We give only two further examples here. A paper claiming ?absence of toxicity? of Bt-pollen to the black swallowtail butter?y under ?eld condi- tions in the title (108) was faulted on experimental design, and actually demonstrated that Bt?pollen was highly toxic in laboratory experiments (109). A study commissioned by the UK FSA claiming ?no signi?cant difference? between cows fed GM and non-GM maize and soya diet, and failed to detect transgenic-DNA in milk (75) was exposed to be practically worthless in experimental design and methodology (110). Three cows were fed GM and three non-GM diets, on a peculiar ?single reversal design with 4-wk periods?, which meant that the groups of three cows alternated between GM and non-GM diets. The design should have generated nine data points each for the GM and non-GM diets, respectively, from a small number of cows; it also guaranteed to balance out the effects of GM versus non-GM diets and is hence useless for determining differences between the two. In addi- - tion, the researchers made a blunder. Two of the cows in the non-GM group were inadvertently fed on the GM-diet, so they ended up with 13 data points in the GM diet group and only 5 data points in the control non-GM diet group. Most serious of all, the PCR method for detecting transgenic DNA is so poor in sensitivity and the samples of milk they used were so small, that again, it would not have succeeded in detecting any transgenic DNA in milk. The issue of transgenic DNA in milk has resur- faced. An unpublished study from the Weihenste- phen Institute of Physiology and the Technical University of Munich showed that milk from coWs on transgenic feed did indeed show positive signals for transgenic DNA. Furthermore, the unpublished study was done on milk collected from dairy cows in r-9.. the farm in Hesse, Germany, where at least a dozen cows died after eating Syngenta?s GM maize Bt 176' (21) (see Table I). No autopsies were carried out on the cows, and this crucial study on transgenic DNA in milk dated 2000 remained under lock and key foi' more than 3 years before it was leaked to Green: peace (111). We can con?rm the presence of transgenic DNA in the milk samples, in our own review of the evidence (112). The review of the evidence on the safety of GM food and feed (2) is selective and biased, citing all studies claiming to ?nd no effect without com-' ment, while excluding most of the evidence of serious adverse effects, practically the entire list in' Table I, except for items 5, 9 and 10, which are dismissed with irrelevant unsubstantiated criticisms. It omitted to mention the large volume of literature on the potential hazards of transgenic DNA in horizontal gene transfer (Table II) and its successful detection in food and feed, and in tissues, cells and milk of animals fed GM produce (71,1 12), whenever the PCR detection methods were adequate to the task. Studies that claimed GM feed had no adverse effects came mainly from biotech companies (113); but these were often contested by independent scienti?c review (103,104). In Monsanto?s study on maize NK603 which claimed no effect, Seralini and colleagues (113) found ?more than 50 signi?cant differences between GM fed and control rats?. They further pointed out that sate-tolerant crops, which cover 87% of the global area of GM crops grown (114), are likely to be i contaminated with toxic levels of and Roundup (Monsanto?s formulation) herbicide and metabolites. Gyphosate is indeed highly toxic to human placental cells and embryonic cells, Roundup even more so (113,115,116), and the herbicide is lethal to frogs (117). Monsanto?s study on MON 863 maize turned up many adverse effects (20) that were dismissed by both Monsanto and EFSA as ?biologically insignif- icant?. Monsanto, supported by EFSA, kept the study from public scrutiny under a false claim of con?dential business information until a German court order a year later forced Monsanto to release the full report. Preliminary analysis by Seralini and colleagues (118) revealed serious ?aws in the study at every stage, from experimental design, to data collection, analysis and reporting. The GM-fed grOup was compared, not just to the group fed the non?GM isogenic line as it should have been, but also to ?ve more ?control? groups fed other non-GM varieties. This had the effect of increasing the range of variation and making the treatment group of animals too small, thereby considerably decreasing GM food regullan'on 7 the sensitivity of the test. The results were analysed with the wrong statistical tests, and despite having compared many variables, the correct standard statistical tools (multivariate and principal compo- nent analyses) were nor used. Instead, in comparing one variable at a time, the researchers failed to note signi?cant trends in body weight differences betWeen experimental and control animals. Statistically sig- ni?cant differences that nevertheless turned up Were then all dismissed as biologically insigni?cant; and the EFSA agreed, and gave MON 863 maize a ?positive opinion?. It is an absolute travesty that the health of people and planet is hanging on such gross distortion and corruption of science, aided and abetted by our regulators. Regulators that sidestep the law to protect the industry The UK FSA website contains the following descrip- tion of genetic modi?cation under food? (1 19): ?But whereas traditional methods involve mixing thousands of genes, genetic modi?cation allows just one individual gene, or a small number of genes, to be inserted into a plant, animal or micro-organism (such as bacteria), to change it in a pre-determined way. Through genetic modi?cation, genes can also be ?switched? on or off to change the way a plant or animal develops.? The description implies a level of precision and control in the process of genetic modi?cation that ?ies in the face of extensive evidence indicating that the very opposite is the case, especially for plants and animals. It is now generally accepted that the genetic modi?cation process is uncontrollable, unreliable and unpredictable, and far from precise. It damages the natural genetic material of the organism, result- ing in many unpredictable, unintended effects in the few ?successes?, including gross abnormalities that you can see, and metabolic changes that you can?t (26,27,35). A transgenic line is essentially derived from a single cell that has taken up and integrated the transgenic DNA into its genome, so the properties of the transgenic line will depend on where and in what form in the genome the insert(s) landed, and the collateral damages done to the genome, which will differ from one event to another. That is why the EU directive (97) requires event?speci?c characteriza- tion of the transgenic insert(s), which also provides a method for detecting transgenic contamination of non-GM produce, an increasingly frequent occur- rence, involving transgenic lines that have not even been approved for commercial release. Downloaded By: [informa internal users] At: 12:31 7 June 2007 8 H0 er at. And when that happens, as with the recent GM rice contamination, regulators came to the rescue on both sides of the Atlantic. The USDA proposed to deregulate the illegal rice to make it effectively legal, considering it as safe as a ?similar? variety that has been approved (120), making a mockery of event- speci?c characterization required by European law. The EFSA, while admitting that the available data were ?not suf?cient to allow the safety of LLRICE601 to be?assessed?, nevertheless considered that ?the consumption of imported long grain rice containing trace levels of LLRICE 601 is not likely to pose an imminent safety concern to humans or animal? (121). The FSA and ACNFP were even more obliging. Based on an incomplete dossier supplied by Bayer CropScience, they consulted two scientists, who also decided there was no ?imminent? safety concern (nore the quali?er ?imminent?). The FSA even told retailers in a memo later leaked to the press that there was no need to check whether any of the rice they were selling was tainted; which was against the law. It was only when Friends of the Earth threatened to take the FSA to court that the FSA backed down (121). There is yet another way in which our regulators have seriously sidestepped, if not broken the law. The EU Directive for deliberate release not only requires event-speci?c characterization of the trans- genic line, it also requires evidence of genetic stability of the insert(s) (97, p.30). For years, we had warned that the transgenic lines were unstable, not only in the silencing of the transgenes in later generations, but also in the structural instability of the GM inserts that tend to break, rearrange, delete or insert elsewhere in the genome. That would effectively transform the trans- genic line into something else that could be unsafe, and impossible to trace (122). It would also make the transgenic line illegal in European law. And yet, when it was discovered that the GM inserts of ?ve out of ?ve commercially approved transgenic varieties had rearranged since character- ized by the company (123), a clear sign of genetic instability (124), and the illegality was pointed out to the EFSA (125), neither the EFSA nor the Eur- opean Commission had seen ?t to withdraw com? mercial approval from those transgenic lines. The 35$ promoter was indeed identi?ed as a frequent break point (123), as we had predicted (31). We do not know how many other transgenic lines have proven unstable that continue to be given positive opinion and approval for the market. The lack of transparency and the increasing tendency to misuse business con?dentiality has kept information crucial for risk assessment and risk management out of the public domain. US courts rule GM crop ?eld tests and releases illegal There have been three recent court cases involving ?eld testing and approval of GM crops in the United States. In all three cases, the courts ruled against USDA for failing to carry out proper environmental impact assessment, making the original releases illegal. The ?rst case was on drug-producing GM crops. A federal district judge in Hawaii ruled in August 2006 that the USDA violated the Endangered Species Act as well as the National Environmental Policy Act in allowing drug-producing GM crops to be cultivated throughout Hawaii, and failing to conduct even preliminary investigations on environ- mental impact before the approval of planting. The case was heard in US District Court in Hawaii. The plaintiffs were the Center for Food Safety, KAHEA (The Hawaiian Environmental Alliance), Friends of the Earth, and the Pesticide Action Network, North America. The defendants were the US Secretary of Agriculture and administrators of the USDA. From 2001 to 2003, four companies ProdiGene, Monsanto, Hawaii Agriculture Research Center (HARC) and Garst Seed were allowed to plant corn and sugarcane genetically modi?ed to produce experimental pharmaceutical products such as vac- cines, hormones, cancer-?ghting agents and other proteins that are still under development and hence not yet approved. The plaintiffs argued that broke the law in issuing these permits. Because these crops produce pharmaceutical products that are still at the experimental stage of development, their effect on Hawaii?s ecosystem (eSpecially Hawaii?s 329 endan? gered and threatened species) is unclear. The experimental craps could cross-pollinate with exist- ing food crops, and contaminate the food supply. Animals feeding on the crops would also become unwitting carriers of experimental pharmaceutical products, causing even more widespread dissemina- tion of these experimental drugs. The court concluded that issuance of four permits was ?arbitrary and capricious? and ?an unequivocal violation of a clear congressional man- date? (126). The second ruling was even more signi?cant. A case was ?led in Federal Court Washington DC against the trials of GM creeping bentgrass by the Center for Food Safety, Klamath-Siskiyou Wildlan (18 Center, and other individuals and organizations in 2003. In February 2007, the court gave a decision d) 3 .5 r- 3.: CE Inthat broadly affects ?eld trials of all GM crops. Federal district 111d ge Harold Kennedy ruled that the USDA must halt approval of all new ?eld trials until more rigorous environmental reviews are conducted.I past approval of GM herbicide-tolerant creeping bent grass led to wideSpread dispersal of pollen from the GM grass, and approval of bent grass trials was ruled illegal (127). The third decision was on a case ?led' 1n Northern! California by the Center for Food Safety, environ- ment activists, seed producers and farmers. A Federal Court ruled (February 2007) that Monsan- to?s Roundup Ready alfalfa had been approved for commercial release illegally because there had been no Environment Impact Statement. (128). Accord- ing to the Center for Food Safety, the decision may prevent this season?s sales and planting of Monsan- to?s GM alfalfa and future submissions of other GM crops for commercial deregulation. In all three cases, USDA was found to have flouted the law and disregarded health and environmental concerns in their approvals of the GM crops. The failure to identify the locations and the exact nature of GM crops being tested must also be addressed along with the frivolous use of Con?dential Business Information designations to conceal crucial informa- tion for safety evaluation and the persistent regula- tory bias towards the uncritical acceptance of GM crops. At the recent Franco-British Council conference on Risk Management and Government Policy (129), David Gee, Project Manager of the European Environment Agency (EEA) talked about some of the case histories documented in the excellent EEA Report, Late Lessons from Early Whrm?ngs' (130) which covers ?sheries, radiation, benzene, asbestos, biphenyls (PCBs), halocarbons, (DES), antibiotics as growth pro- moters, sulphur dioxide, chemical contamination in the Great Lakes, tributyltin (T CB) antifoulants, hormones as growth promoters and BSE. We were struck at how GM food/feed looks so much like a replay of these cases in the ?misplaced science, and the wrong kind of science? dominating decision- making, with devastating consequences. Former UK Minister for the Environment Mi- chael Meacher told a public conference on Science, Medicine and the Law that we need independent science and scientists who take the precautionary principle seriously, and called for sweeping changes in science funding and scienti?c advice to the government (131). That applies all the more so to the regulatory agencies entrusted with the task of protecting the environment, human,. animal and plant health, in which they have singularly failed so far. References 1 . 2. 10food regulilz?on 9 - Ho MW. GM soya fed rats: stunted, dead or sterile. Science in Society 2007; 33 (in press). Safety and Nutritional Assessment of GM Plant derived Foodsl'Feed. The role of animal feeding trials. Draft report for public consultation. European Food Safety Authority, December 2006. . Ermakova IV. Genetically modi?ed soy leads to the decrease of weight and high mortality of rat pups of the ?rst generation. Preliminary studies. EcosInform (in Russian). . Ermakova IV. Mine-?eld of genetics. State Management of Resources 2006;2z44?52 (in Russian). . Ermakova IV, Barskov IV. In?uence of diet with the soy modi?ed by the gene CP4 EPSPS on physiological state of rats and their o?'spring. Agrarian Russia 2006 (in press). . Ermakova I.V. Genetically modi?ed organisms anil biologi- cal risks. Proceedings of- International Disaster Reduction Conference, Davos, Switzerland, August 27?September l, 2006: 168?71. . Ermakova IV. In?uence of genetically modi?ed soya on the birth-weight and survival of rat pups. Proceedings Epige- netics, Transgenic Plants and Risk ASSessment, 2006z4 1 . Ermakova IV. The effect of GM-soya on rats and their posterity. The ?rst International Forum on Patient Safety. 23?24 January 2006, p.30. . Ermakova IV. Diet with the food, modi?ed by gene EPSPS CP4, leads to the anxiety and aggression in rats. 14th European Congress of Nice, France, 4-8 March '2006. Ho MW. More illnesses linked to Bt crops. Science in Society. Ho MW. Mass deaths in sheep grazing on Bt cotton. Science in Society. Prescott VE, Campbell PM, Moore A, Mattes I, Rothenberg ME, Foster PS, et al. Transgenic expression of bean a- amylase inhibitor in peas results in altered structure and immunogenicity. Agric Food Chem. Ho MW. Transgenic pea that made mice ill. Science in Society. Malatesta M, Caperaloni C, Rossi L, Battistelli S, Rocchi MBL, Tonucci F, et al. Ultrastructural analysis of pancreatic acinar cells from mice fed on genetically modi?ed soybean. Anat. Malatesta M, Biggiogera M, Manuali E, Rochhi MBL, Baldelli B, Gazzanelli G. Fine structural analyses of pan- creatic acinar cell nuclei from mice fed on genetically modi?ed soybean. Eur] Histochem. Malatesta M, Caporaloni C, Gavaudan S, Rocchi MBL, Sera?ni S, Tiberi C, et al. Ultrastructural morphometrical and immunocytochemical analysis of hepatocyte nuclei from mice fed on genetically modi?ed soybean. Cell Struc't Funct. 2002, 27:175?80. Malatesta M, Tiberi C, Baldelli B, Battistelli S, Ma'nuali E, Biggiogera Reversibility of hepatocyte nuclear modi?ca? tions in mice fed on genetically modi?ed soybean. Eur] Histochem. Vecchio L, Cisterna B, Malatesta M, Martin TE, Biggiogera M. Ultrastructural analysis of testes from mice fed on genetically modi?ed soybean. Eur I Histochem. 2004548: 449-54. Ho MW. GM ban long overdue. Dozens ill at ?ve deaths in the Philippines. Science in Society. . French experts very disturbed by health effects of Monsanto GM corn. GMWatch, 23 April 2004. ww.gmwatch.org . I Downloaded By: [informa internal users] At: 12:31 7 June 2007 MW, Burcher S. Cows ate GM maize and died. Science in Society. Puszmi A, Bardocz S, Ewen SWB. Genetically modi?ed foods: potential human health effects. In: D?Mello JPF, editor. Food safety: contaminants and toxins. Scottish Agricultural College, Edinburgh: CAB International; 2003. Fares NH, El-Sayed AK. Fine structural changes in the ileum of mice fed on delta endotoxin-treated potatotes and transgenic potatoes. Nat Toxins. Novotny E. Animals avoid GM food, for good reasons. Science in Society. Agbios. http:Iiwmvagbioscomfmainphp Ho MW: Genetic engineering dream or nightmareP, 2nd edn. Bath: Gateway Books, Third World Network, 1998; Dublin: Gill and McMillan, Continuum, 1999; reprint with extended introduction, Third World Network, 2007. Ho MW. FAQs on genetic engineering. ISIS tutorial. httpa'! . l-Io MW. Horizontal gene transfer, the hidden hazards of genetic engineering. ISIS Report 2001. org.uk?iorizontal.php Ho MW. Special safety concerns of transgenic agriculture and related issues. ISIS Brie?ng for the Minister for the Environment, Rt Hon. Michael Meacher, April 1999. Ho MW, Traavik T, Olsvik R, Tappeser E, Howard V, von Weizsacker C, et al. Gene technology and gene ecology of infectious diseases. Microb Ecol Health Dis. 1998;10:33? 59. Ho MW, Ryan A, Cummins J. Cauli?ower mosaic viral promoter a recipe for Disaster? Microb Ecol Health Dis. Ho MW, Ryan A, Cummins J. Hazards of transgenic plants with the cauli?ower mosaic viral promoter. Microb Ecol Health Dis. Ho MW, Ryan A, Cummins J. promoter frag- mentation hotspot con?rmed and it is active in animals. Microb Ecol Health Dis. 2000;12:139. Ho MW. Horizontal gene transfer, book review. Heredity. Ho MW, Lim LC. The case for a GM-ftee ?rstainable world. Independent Science Panel Report. London: Institute of Science in Society and Third World Network, 2003; republished GM-free, exposing the hazards of biotechnology to ensure the integrity of our food supply. Ridge?eld, CT: Vitalltealth Publishing, 2004. Mead PS, Slutsker L, Dietz V, McCaig LF, Bresee JS, Shapiro C, et al. Food-related illness and death in the United States. Emerg Infect Dis. Ho MW. US foodborne illnesses up two to ten fold. ISIS Report 3 November 2001. also Science in Society 2002;13il4:23. Cummins J, Ho MW Bacterial gene's and autoimmune responses. ISIS News 20005: Heeg K, Zimmerann S. DNA as a Th1 Trigger. Int Arch Allergy Immunol. Ho MW. Gene therapy and naked DNA vaccines can trig- ger autoimmune reactions. ISIS News 1999;2: Suzuki K, Mori A, Ishii KJ, Singer DS, Dlinman DM, Drause PR, et al. Activation of target-tissue immune- recognition molecules by double-stranded polynucloetides. Proc Natl Acud Sci A. Genetically modi?ed animal feed. Brie?ng, Friends of the Earth, May 2006. grn_animal_feeds.pdf 43MW. Biofuels for oil addicts. Science in Society. 2006; 30:29 ?30. Ho MW. Biodiesel boom for Europe? Science in Society. Joensen L, Ho MW. Argentina?s GM woes. Science in Society. West African food aid contaminated with GM rice. Friends of the Earth Press Release, 24 November 2006. aid_cont_24112006.html Ho MW, Steinbrecher RA. Fatal ?aws in food safety assessment: critique of the joint FAOIWHO Biotechnology and Food Safety Report. Environmental 8t Nutritional Interactions. Bernstein IL, Bernstein JA, Miller M, Tierzieva S, Bernstein DI, Lumrnus Z, et al. Immune responses in farm Workers after exposure to Bacillus thuringiensis pesticides. Environ- mental Health PerSpectives line. org/members! 9 99I107p 5? 5-582bernsreinfbernstein? V?zquez-Padron RI, Moreno-Fierros L, Neri-Bazrin L, de la Riva G, Ldpez-Revilla R. Intragastrie and intraperitoneal administration of CrylAc protoxin from Bacillus thuringien- sis induce systemic and mucosal antibody responses in mice. Life Sci. V?zquez-Padron RI, Morreno-Fierros L, Neri-Bezan L, de la Riva GA, Lopez-Revilla R. CrylAc protoxin from Baci?us thn'ngienn?s sp. kurstaki HD73 binds to surface proteins in the mouse small intestine. Biochem Biophys Res Commun. Dutton A, Klein H, Romeis J, Bigler F. Uptake of Bt?toxin by herbivores feeding on transgenic maize and consequences for the predator cornea. Ecological Entomology. Romeis J, Dutton A, Bigler F. Bacillus thun'ngienris toxin (CrylAb) has no direct effect on larvae of the green lacewing cornea (Stephens) (Neuroptera: Journal of Insect Physiology. Kleter GA, Peijnenburg Ad ACM. Screening of transgenic proteins expressed in transgenic food crops for the presence of short amino acid sequences identical to potential, binding linear epitopes of allergens. BMC Structural Biology 200252:8. Fiers MWEJ, Kleter GA, H, Peiinenburg Ad ACM, Nap JP, van Ham RCHJ. Allermatchni, a webtool for the prediction of potential allergenicity according to current FAOIWHO Codex alirnentarius guidelines. BMC Bioinfor? matics 2004;5:133. 105.451l 133. Ho MW, Puszrai A, Bardocz S, Cummins J. Are transgenic proteins allergenic? Science in Society. Chowdhury EH, Kuribara I-I, Hino A, Sultana P, Mikarni O, Shimada N, et al. Detection of corn intrinsic and recombi- nant DNA fragments and CrylAb protein in the gastro- intestinal contents of pigs fed genetically modi?ed corn l. Anim Sci. 2003;81:2546w51. Ho MW. Transgenic DNA Bt toxin survive digestion. Science in Society. 2004;21:11. Ho MW. Are current transgenic technologies safe? Capacity building in biosafety urgently needed for developed coun- tries. In:_ Biosafety Capacity Building: Evaluation Criteria Workshop Proceedings. Stockholm Environment Institute, 1996. Ho MW, Tappescr B. Transgenic transgression of species integrity and species boundaries. In: Mulongoy K, ed. Proceedings of the W'orkshop on Transboundary Movement of Living Modi?ed Organisms Resulting from Modern 0.1 3 -.-In60. 61. 62. 63. 64. 65. 66. 67. 68. 69. 70. 71. 72. 73. 74. 75. 76. 77. Biotechnology: Issues and Opportunities for Policy-makers.- Aarhus, Denmark, Swiss Academy of the Environment, 1997. Myhre MR, Fenton KA, Eggert K, Nielsen KM, Traavik T. The 353 plant virus promoter is active in human enterocyte-like cells. Eur Food Res Technol 2005; DOI 10.10071y00217.005.0154.3 Gebhard F, Smalla K. Monitoring ?eld releases of geneti-z cally modi?ed sugar beets for persistence of transgenic plantI DNA and horizontal gene transfer. FEMS Microbiol Ecoli 1. Ho MW. Horizontal gene transfer happens. A practical: exercise in applying the precautionary principle. ISIS News' 20005. hori I Ho MW. Horizontal gene transfer happens II. ISIS Report, 4 May 2001. Duggans PS, Chambers PA, Heritage J, Forbes JM. Survivall of free DNA encoding antibiotic resistance from transgenic' maize and the transformation activity of DNA in ovine saliva, ovine rumen ?uid and silage e??luent. FEMS Micro- biol Lett. DeVries J, Meier P, Wackernagel W. The natural transfor? mation of the soil bacteria Pseudomonas stutzert? and Acme- mbacter sp. By transgenic plant DNA strictly depends on homologous sequences in the recipient cells. FEMS Micro? biol Lett. Ho MW, Cummins J. Molecular pharming by chloroplast transformation. Science in Society. Cummins J, Ho MW. GM pharmaceuticals from common green alga. Science in Society. de Vries J, Meier P, Wackernagel W. The natural transfor- mation of the soil bacteria Pseudomonas stoned and Acinetobacter sp. by transgenic plant DNA strictly depends on homologous sequences in the recipient cells. FEMS Microbiol Lett. I de Vries J, Herzfeld T, Wackernagel W. Transfer of plastid DNA from tobacco to the soil bacterium Acinetobacter sp. by natural transformation. Mol Microbiol. de Vries J, Meier P, Wackernagel W. Microbial horizontal gene transfer and the DNA release from transgenic crop plants. Plant and Soil. Ho MW. DNA in GM food 8: feed. Science in Society. 2004; 23:34?6. Chowdhury EH, Mikami O, Nakaiima Y, Hino A, Kuribara H, Suga K, et al. Detection of genetically modi?ed maize DNA ??agments in the gastrointestinal contents of pigs fed StarLink OBI-1351. Vet Hum Toxicol. 2003;45:95 Reuter T, Aulrich K. Investigations on genetically modi?ed maize (Ht-maize) in pig nutrition: fate of feed-ingested foreign DNA in pig bodies. Eur Food Res Technol. 2003; Duggan PS, Chambers PA, Heritage I, Forbes JM. Fate of genetically modi?ed maize DNA in the oral cavity and rumen of sheep. Nutr. 2003;89:159 ?66. Phipps RH, Deaville ER, Maddison BC. Detection of transgenic and endogenous plant DNA in rumen ?uid, duodenal digesta, milk, blood and feces of lactating dairy cows. Dairy Sci. Nethenvood T, Martin?Orue SM, O-Donnell AG, Gockling 8, Graham J, Mothers JC, et al. Assessing the survival of transgenic plant DNA in the human gastrointestinal tract. Nature Biotechnology. Espanier R, Klotz A, Draft J, Aulrich K, Pser R, Schwagele F, et al. The fate for forage plant DNA in farm animals: a collaborative case-study inVestigating cattle and chicken fed 78food regulation 11 recombinant plant material. Eur Food Res Technol. 2001; 212:129?34. . Schubbert R, Rentz D, Schmitz B, Doer?er W. Foreign (M13) DNA ingested by mice reaches peripheral leukocytes, spleen and liver via the intestinal wall mucosa and can be covalently linked to mouse DNA. Proc Natl Acad Sci A. Dtier?er W, Schubbert R. Uptake of foreign DNA from the environment: the gastrointestinal tract and the placenta as portals of entry. Wien Dlin Wochenstr. Hohlweg U, Doer?er W. 0n the fate of plant or other foreign genes upon the uptake in food or after intramuscular injection in mice. Mol Genet Genomics. Ho MW. Circulating DNA converts genomes? Latest exp os? on the ?uid genome. Science in Society. 2002;15:18. Samos J, Garcia-Olmo DC, Picazo MG, Rubio-Vitaller A, Garcia-Olmo D. Circulating nucleic acids in plasmal?serum and tumor progression. Are apoptotic bodies involved an experimental study in a rat cancer model. Ann YAcad Sci. Gahan PB. Circulating DNA. Intracellular and intraorgan messenger? Ann Acad Sci. Ho MW, Cummins J. Universal condemnation meets UK government?s green light for GM potato trials. Submission to UK Food Standards Agency, December 2006, also Science in Society 2007333 (in press). Schluter K, Futterer J, Potrykus I. Horizontal gene-transfer from a transgenic potato line to a bacterial pathogen occurs, if at all, at an extremely low- frequency. BiofTechology. Burcher 8. Global GM crops area exaggerated. Science in. Society 2007,33 (in press). Ho MW, Cummins J. Roundup ready sudden death, super- weeds, allergens to wipe GM crops the globe. Science in Society. Ho MW. Scientists con?rm failures of Bt crops. Science in Society. Cummins J, Ho MW. GM crops and microbes for health or public health hazards? ISIS submission to Codex Alimentar- ius, 2006; also Science in Society. Cummins J, Ho MW. Genetically modi?ed probiotics should be banned. Microb Ecol Health Dis. Cummins J, Ho MW. Reply to GM microbes for human health. Microb Ecol Health Dis. Cununins J, Ho MW. GM food animals coming ISIS submission to Codex Alimenarius, 2006; also Science in Society. Ho MW, Cummins J. Is FDA promoting or regulating cloned meat and milk? Science in Society. Ho MW, Cummins J. Cloned BSE-free cows, not safe not proper science. Science in Society. Wells DN. Animal cloning: problems and prospects. Rev Sci Tech. Cartagena Protocol on Biosafety (Montreal, 29 January 2000). =dt Directive 20017181130 of the European Parliament and of the Council of 12 March 2001 on the deliberate release into the environment of generically modi?ed organisms and repealing Council Directive Communication from the Commission on the Precautionary Principle, COM (2000) 1 ?nal. len01.pdf ACNFP Mcmbers' interests June 2006. Downloaded By: [informa internal users] At: 12:31 7 June 2007 12 100. 101. 102. 103. 104. _105. 106. 107. 108. 109. 110.- 111. 112. 113. 114. 114?11? Ho er al. The Food Standards Agency?s Approach to Risk, Food Standards Agency, 2001. Saunders PT. Use and abuse of the precautionary principle. ISIS submission to US Advisory Committee on Interna- tional Economic Policy Biotech. Working Group 13 July 2000. John B. Response from GM Free Cymru to the EFSA consultation on GMO feeding trials, 29 January 2007. httpa?! org/newsl?PresLNoticez February2006. Ho MW. Approval of maize endangers humans and livestock. Science in Society. Cummins oilseed rape GT73. Science in Society. MW. European Commission accuses its own food safety authority of GMO bias wide ranging changes introduced. Science in Society. 2006;30:16. Brake DG, Evenson DP. A generational study of tolerant soybeans on mouse fetal, postnatal, pubertal and adult testicular development. Food Chem Toxicol. 2004342: 29?36. John B. Email from Dr Brian John (GM Free Cymru) to Professor Mike Gasson (ACNFP Chairman) 21 January 2006 in Committee Paper for Discussion. Effect of GM Soya on Newborn Rats. http?mvwfood. 1_gmsoya.pdf Wraight CL, Zangeri AR, Carroll MH, Berenbaum MR. Absence of toxicity of Bacillus thun'ngiemis pollen to black swallowtails under ?eld conditions. Proc Natl Acad Sci. Ho MW. Swallowing the tale of the swallowtail. ISIS News 200035. #swal Ho MW. Exposed: more shoddy science in GM maize approval. Science in Society. Traces of genetic engineering detected in milk. Greenpeace, 22 June 2004. 47l.htm1 Ho MW. Cover-up over DNA in milk. Science in Society. Seralini G-E, Spiroux de Vendomois J, Cellier D. Criticisms and improvements of strategies for the safety assessment of GM plant derived foods or feed. An answer to EFSA Draft Report on Animal Feeding Trials with GMOs. January 2007. Heller L. Monsanto seeks approval for new GM soybean. Food Navigator, 14 February 2007. =741788tm 115. 116. 117. 118. 119. 120. 121. 122. 123. 124. 125. 126. .127. 128. 129. 130. 131. Richard S, Moslemi S, Sipahutar H, Benachour N, Seralini GE. Differential e??ects of and roundup human placental cells and aromatase. Environ Health Perspect. Ho MW, Cummins J. toxic Roundup Worse. Science in Society. 2005;26:12. Relyea RA. The impact of insecticides and herbicides on the biodiversity and productivity of aquatic communities. Eco- logical Applications. Preliminary report by Criigen on the ?First public investiga- tion of the crude data in Mon 863 toxicity tests on rats' 2005. GM food, Food Standards Agency. Cummins J, Ho MW. USDA poised to deregulate illegal GM rice. Science in Society. Saunders PT. GM rice contamination: how regulators tried to sidestep the law. Scrence in Society. Ho MW, Cummins J. GM food and feed not ?t for ?man or beast?. ISIS Report, ISP Brie?ng to UK Parliament, 7 May 2004. Collonier C, Berthier G, Boyer F, Duplan M-N, Fernandez S, Kebdani N, et a1. Characterization of commercial GMO inserts: a source of useful material to study genome ?uidity. Poster courtesy of Pr Gilles-Eric Seralini, President du Conseil Scienti?que du CRII-GEN. Ho MW. Transgenic lines prOVen unstable. Science in Society. 2003;20:35. Ho MW. Unstable transgenic lines illegal. Science in Society. 2004;21:23. Court rules federal government acted illegally in permitting ?eld trials of genetically engineered crops in Hawaii. Press Release Center for Food Safety, 14 August2006. Federal court orders for the ?rst time a halt to new ?eld trials of genetically engineered crops. Press Release, 6 February 2007. Federal court ?nds USDA erred in approving genetically engineered alfalfa without full environmental review. Press Release, Center for Food Safety, 8 February 2007. Gee D. Perceptions of the precautionary principle and the political consequences. Introducing the subject. Presenta? tion at Franco-British Council conference: Policy making and risk management. French and British viewpoints. 8 February, Paris, France, 2007. Harremos P, Gee D, McGarvin M, Stirling A, Keys Wynne B. Late lessons from early warnings: the precau? tionary principle 1896?2000. Environmental Issue Report No. 22. European Environmental Agency; 2002. Meacher M. Which science or scientists can you trust? Science in Society. (Abstract - N20 release frOm agro-biofuel production negates Page 1 of Volumes and Issues Contents of Issue 4 Atmos. Chem. Phys. Discuss., 7, 11191-11205, 2007 Author(s) 2007. This work is licensed under a Creative Commons License. N20 releasevfrom agro-biofuel production negates global warming reduction by replacing fossil fuels P. J. Crutzen1'2'3, A. R. Mosier?, K. A. Smiths, and W. Winiwarter3'6 1Max Planck Institute for Chemistry, Department of Atmospheric Chemistry, Mainz, Germany 2Scripps Institution of Oceanography, University of Califorlnia, La Jolla, 3InternatIOnal Institute for Applied Systems Analysis (IIASJIA), Laxenburg, Austria 4Mount Pleasant, SC, USA 5School of Geosclences, University of Edinburgh, Edinburgh, UK 6Austrian Research Centers ARC, Vienna, Austria Abstract. The relationship, on a global basis, between the amount of ?xed by chemical, biological or atmospheric processes entering the terrestrial and the total emission of nitrous oxide (N20), has been re-examined, using known global atmospheric removal rates and concentration growth of N20 as a proxy for overall emissions. The relationship, in both the pre-industrial period and in recent times, after taking into account the large?scale changes in fertiliser production and deforestation, is consistent, showing an overall conversion factor of This factor is covered only in part by the of ?direct" emissions from agricultural crop lands estimated by IPCC (2006), or the "indirect" emissions cited therein. This means that the extra N20 entering the atmosphere as a result of using to produce crops for biofuels will also be correspondingly greater than that estimated just on the basis of IPCC (2006). When the extra N20 emission from biofuel production is calculated in "COZ-equivalent" global warming terms, and compared with the quasi-cooling effect of "saving" emissions of fossil fuel derived C02, the outcome is that the production of commonly used biofuels, such as bibdiesel from rapeseed and bioethanol from corn (maize), can contribute as much or more to global warming by N20 emissions than cooling by fossil fuel savings. Crops with less demand, such as grasses and woody coppice species have more favourable climate impacts. This analysis only considers the conversion of biomass to biofuel. It does not take into account the use of fossil fuel on the farms and for ferblizer and pesticide production, but it also neglects the production of useful co?products. Both factors partially compensate each other. This needs to be analyzed in a full life cycle assessment. Discussion Paper (PDF, 382 KB) Interactive Discussibn (Open, 11 Comments) Citation: Crutzen, P. J., Mosier, A. R., Smith, K. A., and Winiwarter, W.: N20 release from agro?biofuel production negates global warming reduction by replacing fossil fuels, Atmos. Chem. Phys. Discuss, 7, 11191-11205, 2007. Bibtex EndNote Reference Manager Page 1 ot?l 1,531? i 1 . I Carol Van Strum I i I From: "Evan Manvel" i To: Sent: ,Friday, May 02, 2008 12:15 PM Subject: SalemWatch May 2 2008 OTC Considers Low-Herbicide Pilot Project Speak Up! The Oregon Department of Transportation (ODOT) routinely sprays roadsides with toxic herbicides throughout the spring and summer. Many of these chemicals are known or suspected carcinogens and endocrine disruptors. When you drive, bike or walk on these roads, you can be exposed to pesticides from soil contamination, eating sprayed .wild berries, and drifting or re-volatilizing vapors. Aquatic pla?,nts ?sh and other organisms are harmed sometimes by application near ditches or streams 1 The Oregon Transportation Commission, which governs ODOT, is considering a proposal to implement a pilot project along a stretch of Highway 101 in Lincoln County and' In all of Lane County. The pilot ?Last Resort? policy prohibits the routine and seasonal use of herbicides to kill unwanted vegetation along roadsides, and focuses on getting rid of weeds by regular assessment of road conditions, mechanical removal planting competing native species such as wildflowers, and scienti?cally determining if a need exists for chemicals before using herbicides. Please write to the Oregon Transportation Commislsion to ask them to support the pilot project and fund more ?no-spray" highways Direct letters to: Oregon Transportation Commission, clo Kim Jorda'n, OTC Secretary Kimberly Jordan@odot. state. or. us Phone: (503) 986-3450 A review: Aluminum as a causative co-factor for the ?dementia?; of Alzheimer?s disease. E.T. ansson Department of the Planet Earth, 7 01 Street, SE, Ste. 200, Washington, DC 20003 E?maii address: pianetearthd?erotscom. Tel: +1 301 475 8366, fax: 1 202 543 4791 . Additional supporting material is found at deptplanetearth. com Abstract This review explores an expert pr0posal made over a decade ago that aluminum is a . ?necessary but not sufficient? risk factor for the dementia of Alzheimer?s Disease (AD). More than twenty epidemiology studies repbrt a statistical relationship between exposure of the aging population to aluminum in food and drinking water and increased risk of elderly cognitive impairment and risk of dementia. An autopsy micr0500pic visualization of aluminum in brain cells of AD patients using the Walton stain reveals two basic types of pyramidal neuron death produced by accumulated brain aluminum. These are ?rst a cell death visually resembling necrosis and secondly brain cell death by mechanical enucleation from a persistent accumulation bf cellular neuro?brillary tangles (NFTs). The metal was found to be associated with the formation of all NF Ts, producing the characteristic protein folding. This autopsy finding supports a causative role of the metal in human AD dementia. Over a lifetime, aluminum bio-accumulates to relatively high concentrations in all human elderly brains. It is a reactive metal that readily complexes with basic br'ain biology and affects genes regulation. Abundant laboratory animal studies document mechanisms by which aluininum produces brain cell death and the erosion of white matter to reduce the connectivity of the brain. It is concluded from extensive literature that aluminum is a causative co-factor for the dementia of AD, which is a medical condition based on brain atrophy. Epidemiology studies identify an excellent public health Opportunity for largeuscale prevention of the dementia of AD through the reduction of dietary and drinking water aluminum contamination and the wider use of nutritional factors that chelate the metal. Keywords: Aluminum, Alzheimers, dementia, cognitive impairment 1. Introduction Chronic diseases of the aging process including Alzheimer?s Disease (AD) are generated by multiple causative factors. An abundance of epidemiology studies have identi?ed over twenty different approaches to effectively reduce AD risk by 50 percent or more, . after control of other factors These strategies include aluminum avoidance in the diet and water, and nutritional and lifestyle changes. Epidemiology also identify dietary and water exposure to aluminum as one of the largest and easily corrected risk factors AD is likely preventable in the 50 to 80 percent range which is a goal that can be achieved for the most part without drugs. In Icontrast, therapy for AD will always remain dif?cult due to severe brain atrophy in AD patients. Halting disease progression is the L) best h0pe. Therapy with aluminum chelation has shown promise in a human clinical trial. 9 Country comparisons indicate a large capacity for AD prevention. Age?adjusted AD rates in northern India are 73 percent less than those of Explanations include reduced dietary aluminum exposure and dietary factors that reduce absorption Many individuals are resistant to AD by virtue of genetics, lifestyle, environment and diet. Khatachurian et al mathematically projected from the Cache County Study that if all Americans lived to 100 years, about 28 percent of the population would avoid the disease 1. Alzheimer?s and AD with ?dementia? are different medical conditions. The dementia of AD is characterized by gross brain atrophy marked by uncontrolled and extensive brain cell death and a reduction of brain connectivity. Dementia is what sends pe0ple to the nursing home and not brain deposits. Human autopsy studies and more recently brain imaging studies in live patients have found only weak statistical correlation between senile plaque and neuro?brillary tangle (NFTs) deposits and elderly cognitive impairment or dementia. It is common for persons of normal cognition for their age to die with signi?cant densities of senile plaque and NFTs deposits Traditional brain deposits sequester aluminum to protect the brain from oxidation. Growing evidence indicates that the brain deposits characteristic of AD are initially protective of the brain in sequestering proteins and metals that cause oxidation and in?ammation. This con?icts with the viewPoints of the past. For the past twenty years, the primary focus of researchers studying AD has centered on beta-amyloid (AB), the presence of which is presently a mandatory de?nition of the disease. Yet a series of autopsy studies ?nd little statistical correlation between the brain deposits de?ning AD and cognitive impairment of the patients while they lived. Case Western Reserve University researchers and others have begun to assert an alternative vieWpoint that AB may not be an initiating factor, but rather ?secondary to other pathologic events?. They propose that AB may be a ?protective response to neuronal insult? The scientists question the validity of the oligomeric amyloid cascade hypothesis. Their new approach is beginning to gain traction because it ?ts the facts more adequately. Studies of thebiological interaction of aluminum and AB also suggest that the brain deposits that have de?ned AD over many years also protect the brain from oxidation generated by aluminum through sequestration of both aluminum and AB. Van Rensburg et al reported from an in vitro study that amyloid protein fragments bond with aluminum to quench the oxidative toxicity of both toxins AB are sticky proteins. The authors proposed that they and aluminum were ?meant to bond? which is not a stretch of imagination since amyloid precursor protein (APP) is a metal shuttle especially for c0pper. Senile plaques perform a similar sequestration function for a range of oxidating metals and AB. Likewise, the NF T?s protect the brain through aluminum sequestration. Walton?s recent - human autopsy study of AD patients using the Walton stain to visually locate aluminum within the cell discovered that human pyramidal brain cells could survive high densities of NFTs even to the point of death of the cell by mechanical enucleation The NFTs continuously chelated aluminum from the cytoplasm and incorporated the metal into the NFTs folded structure. This sequestration 'of aluminum reduced its toxicity to the neuron allowing a cell to survive longer. i 1..2 Aluminum induced brain cell death anld connectivity loss involves direct biological action. I Figure 1 summarizes the multiple ways that aluminum has been demonstrated to produ'ce brain atrophy and loss of connectivity in laboratory animals and humans. A supporting bibliography of over seventy published studies of brain atrophy produced by aluminum exposure and a description of a range of biblogical mechanisms involved IS available Aluminum is a substantial participant but is not the sole actor in producing severe brain atrophy and loss of brain connectivity in AD patients. The metal generates both oxidation or reactive oxygen species (ROS) and brain in?ammation in laboratory animal studies Lukiw et a1 ?nds that the ROS produced by aluminum, and aluminum combined with iron turned on and off a series of genes that are similarly affected in AD. A mixture of ?aluminum and iron has a synergistic adverse effect on brain cells. Continuous ROS expc:)sure also induces in?ammation and apoptosis genes, leading eventually to brain cell death [1 Lue et al, found that brain in?ammation distinguished between normal non-demented persons with heavy brain deposits of plaques and tangles and those with AD 1n an autopsy study 1.3. Aluminum also participates in generation of traditional AD brain deposits and markers. Aluminum not only generates brain atr0phy in a direct fashion, but also participates in generation of the traditional AD brain markers upon which the present rating systems of disease diagnosis are based. . I NFTs. Aluminum exposure is essential to the production of all NFTs by producing characteristic protein folding. Excessive generation of NF Ts leads toI brain cell death in humans by mechanical enucleation - Soluble Pratico et a1 the metal generates soluble AB and senile plaques in the brain of' transgelnic Tg2576 mice design to express human APP. Increased oxidation was seen as the trigger for this effect measured by brain isoprostane levels[l4]. Lukiw reports that toxins such as aluminum and non that generate ROS 1n the brain will trim on genes that encode for generation of Figure 1 (9) Some Mechanisms By Which Aluminum Exposure Kills Brain Cells In Vivo and Erode Brain White Matter and Connectivity Apoptosis Caspase induction, release of cytochrome c, and suppression of feedback mechanisms preventing programmed cell death such as Bel-2. Induction and suppression of genes involved in AD. Adverse effect on function of mitochondria and endoplasmic reticulum. Decrease of glutathion regeneration in mitochondria. Peri-nuclear clustering of mitochondria. Impairment of the ion pumps. Calcium homeostasis disruption. Oxidation of membranes and generation of soluble AB. Necrosis. In?ammation and oxidation. Induction of in?ammatory genes. Impairment of the ion pumps. Combination of apoptosis and necrosis. Glial cell death or impairment leading indirectly to neuron death. Enucleation by mechanical action of excessive accumulation of NFTs. Less explored cell death mechanisms. Nuclear translocation of alpha and promotion of anaerobiosis. Heme and red blood cell depletion. Interference with cerebral glucose metabolism. Slowing of cerebral blood ?ow due to damage to cerebral microvessels via amyloid angiopathy, in?ammation, adverse effect on blood vessel mitochondria and production of red blood cell membrane rigidity. Hyperammonemia. Induction and suppression of hypoxia genes involved in AD. 6. Death by loss of connectivity and lack of stimulation. Clogging of axons with neuro?brillary tangles. Damage to synapses directly, via reduction of axonal ?ow, or suppression of genes involved in synapsin. Dendritic pathology and reduction of dendritic connectivity. Interference with neurotransmitters. Oxidation of myelin and fatty acids. Disruption of the perforant path. Death of connective layers of brain. Isolation of hippocampus from the remainder of the brain. Source: Jansson ET, Presentation at the '7'h Keele Meeting on Aluminum, Uxinal, Mexico, 2007 Feb 27. Seventy supporting footnotes at: 18 AB Soluble AB has direct oxidative toxic pr0perties which can be signi?cantly quenched by sequestration in the senile plaques or by bonding with metals including aluminum In I onding with metals, AB and its parent compound APP perform as antioxidants. . Platelets, All and Aluminum in Early Onset AD: Platelets produce AB and have been used as a model for AD. It has been preposed that aluminum augments levels of AB in the human brain based on its generation of increased membrane ?uidity of blood platelets a condition which is speci?cally correlated with early onset AD A human clinical trial using modest zinc supplementation (twice the RDA) slowed AD disease progression by 7-9 months, but at the same time reversed the ?uidity of the blobd platelet membranes in persons with AD Zinc and aluminum are competitors in biology and likely dislodge each other from biological sites. A plausible mechanism is that membrane thinning will interfere with the proper functioning of oL-secretase, which cuts the amyloid precursor protein APP only at the surface of the membrane. Van Rensburg notes that the ?uidity of cell membranes generally decrease with age, especially in the endOplasmic reticulum [19] which is involved in brain cell death associated with either aluminum or AB exposures Senile Plaques How Much Aluminum Is Involved? Unlike NFTs which are clearly contaminated with and folded by aluminum, controversy continues about the role of aluminum in fonnation of senile plaques because detection of aluminum in the plaques has proven'dif?cult. Exley demonstrates that aluminum and iron added to AB in solution not; only precipitates it, but at the same time speci?cally produces the characteristic beta structures of senile plaques Copper and zinc do not produce thes:e beta structures. AI Bush et al in 1994 reported that zinc added to a glass beaker containing a solution of AB residues 1-4IO precipitated the AB It was also reported that the precipitation took place ?only? on surface of the glass containing aluminum silicate. The principal role of aluminum was con?rmed by adding kaolin to the solution, a hydrated aluminum silicate suspension, which also precipitated AB. The experimental result suggests thai it does not take very much aluminum to affect the solubility of AB in the presence of other metals - i.e. just the amount contained on the surface of glass or almost a catalytic effect which may be a reason that the measurement of aluminum in senile plaques has proven dif?cult. Another reason may be the obscuring of aluminum by the beta folding in the plaques, as was the case with measurement of aluminum in NF Ts Use of the autoclave by Murayama to unwind tile NFTs allowed the discovery-of aluminum that had been hidden from measuring equipment. Many years of autopsy studies of AD patients have found very little correlation between senile plaque densities and the measured cognition of the patients while they lived. We will return to this issue. The senile plaque de?nes AD, but not its dementia which is not mediated by the senile plaque. Aluminum does not exert toxic effect on the brain through the senile plaques. In sum, AD and AD with dementia are two different medical condition. 2. Aluminum is seen as a necessary but not suf?cient risk factor for AD. The Canadian pioneer DRC McLachlan and colleagues in 1991 pr0posed a limit on aluminum exposure: i.e. ?The evidence warrants a serious consideration of reducing human exposure to aluminum. We hypothesize that a public health effort to restrict human ingestion of aluminum would reduce the incidence of this chronic illness in the elderly McLachlan ventured additionally in 1993 to conclude that aluminum was a ?necessary but not suf?cient? risk factor for the development of AD based on the extensive scienti?c literature of the time A human clinical trial at the University of Toronto to chelate aluminum from the brain of AD patients slowed disease progression as measured by life skills by 50 percent over two years by removing one third of brain aluminum The conclusion that aluminum is a necessary but not suf?cient risk factor for AD is consistent with the genetic ?ndings of Lukiw et al [1 The team exposed untransformed human neural cells to 100 nano-molar aluminum sulfate using high density DNA microarrays that interrogate the expression of every human gene. Aluminum down-regulates some genes and up-regulates others, which can then be compared to gene expression in the brain tissue of AD patients. Of the most altered gene expression levels, 71 percent of aluminum-affected genes and 88 percent of aluminum induced genes exhibit expression patterns similar to those observed in AD. That leaves 13 to 28 percent of genesrto be affected by other environmental, nutritional or other factors including age itself before AD manifests itself. Alexandrov et al found aluminum and iron to be highly synergistic in up- or down- regulation of genes in a pattern similar to that of AD A further study by Lukiw and Pogue investigated the induction by aluminum and iron, both ROS producers, of speci?c micro RNA species in primary human brain cell cultures with similar biological outcomes The two metals have synergistic effects in up-regulation of Speci?c regulatory elements and pathologic genes that promote cell dysfunction and apOptotic cell death. Both aluminum and iron are present at elevated levels in the aging brain and both metals bioaccumulate during the aging process as noted below. McLachlan et al pr0posed that the goal for daily adult intake of aluminum from all sources should 3 mg or less, and that municipal drinking water concentrations should be maintained at less than 50 ug/liter based upon ?ndings of epidemiology Both programs remain practical, though regulatory action has stalled. The US Environmental Protection Agency has neither acted to reduce aluminum levels in drinking water nor prohibited the use of aluminum coagulants for water treatment. Aluminum food additives are still recognized by the US Folod and Drug Administration as ?generally recognized as safe? (GRAS). FDA was petitioned in 2005 to rescind this position Not all researchers venture as far as the Canadians. V.W. Gupta et a1 summarized a middle road: ?Finally, it is concluded based on extensive literature that the neurotoxic effects of aluminum are beyond any doubt,? and aluminum as a factor in AD cannot be discarded. However, whether aluminum is a sole factor in AD and whether it is a factor in all AD cases still needs to be understood? It is a more cautious approach. We should not forget that the Canadians over ten years ago had a large group of studies upon which to base their public health recommendations. Evidence is vastly better today. 3. Epidemiology links aluminum exposu to prevention of AD and elderly cognitive impairment. Twenty two drinking water epidemiology studies link aluminum to either higher risk of AD with dementia or to elderly cognitive impairment The later condition often converts to AD. In the United States where epidemiology forms the basis and backbone for governmental regulation of toxins, this number of studies historically represents a suf?ciently large body of evidence for a gotvemmental regulatory action. In different political times, public health regulation of the metal would be in progress. - . Aluminum Absorb'ed??om Drinking Water: 'The absorption of aluminum from drinking water is related to the other constituents of the water. Canadian studies ?nd that maintenance of a drinking water pH in the vicinity of 7.9 reduces the risk of both AD and elderly cognitive impairment by 50 percent [3 0-3 The ?nding indicates that skin, lung, nose, and perhaps mouth absorption (more alkaline surfaces than the stomach) may be important than stomach or gut absorption. A shower or bath in aluminum contaminated drinking water may pose a greater risk for AD than oral consumption of. the water. An additional 30 percent risk reduction was achieved in the Ontario studies by the presence of about 1 mg/liter of ?uoride in the water. iFluoride is an aluminum chelator [32] but is not recommended for prevention since it hasI other adverse health effects Soluble silicon or silicic acid in the drinking water is associated with a large reduction in AD and elderly cognitive impairment risk. Silicic acid reduces absorption and increases excretion of aluminum. The relationship of laluminum and silicon may involve threshold chemistry. French women who drank suf?cient bottled mineral water rich in soluble silicon to achieve a silicon intake greater than 12 mg/day experienced a 50 percent reduction in their risk of AD, but saw little bene?t at lower dosages Exley proposes mineral water to provide chelation therapy for AD It is also a capable preventative agent. Aluminum Absorbed From Food Additives: A study of dietary aluminum consumption from solid food over the previous ?ve year period by newly admitted residents to a geriatric center in Syracuse, New York linked aluminum statistically to AD [3 While a small sample size limited signi?cance for some categories of food, an enriched dietary I 1' aluminum consumption from food items constituted with aluminum based baking powder including biscuits, muf?ns, cornbread and corn tortillas over the 'previous ?ve years was associated with 100 percent risk for AD. None of the controls got the disease. Baking powder is inexpensively manufactured with calcium, a formulation without AD risk and already available on supermarket shelves for purchase. Other Non-Occupational Exposures: A 1990 retrospective case-control study of antacids and deodorants by Graves et a1 has often been cited by industry representatives as an argument that aluminum has no effect on AD disease It is a con?icted study: 0 The use of aluminum based deodorants increased the risk for developing AD by 60 percent. 0 The use of ?any? antacid, which might indicate stomach damage and enhanced metal absorption, was associated with a steep and statistically signi?cant dose- related AD- risk, with an overall OR of 11.7 comparing the highest third antacid use with the lowest third exposure level. 0 The use of speci?cally aluminum containing antacids reduced AD risk by 30 percent, which is consistent with other ?retrospective? studies. The ?ndings are consistent with the concept explored statistically in William Forbes? longitudinal study of men from age 45 to 75 that excessive aluminum exposure can shorten the lifespan of elderly persons. In a small sample, Forbes found evidence for a 41 percent increasedrisk of being deceased at age 73 for persons living in a water district where water aluminum exceeded 85 ug/liter Selective death of elderly persons such as from pneumonia, from the much higher dosage of antacids would bias the sampling pool of a ?retrospective? epidemiology study. Roberts compares the intestinal dosage of aluminum from antacids to be equivalent to the increased aluminum absorption in AD patients [3 It- is a high dose, particularly for those who are good absorbers of the metal as older peOple and AD patients tend to be. Persons who would have developed AD due to their aluminum exposure may already by . dead when the study commences and the participants selected. Longitudinal studies which monitor the mortality rates of the participants would be obligatory to ascertain the effect of aluminum based antacids on AD risk. 4. Aluminum interacts with other risk factorsincluding dietary factors. The interaction of aluminum with many other risk factors of AD adds plausibility to McLachlan?s proposal that the metal is a necessary but not suf?cient risk factor for AD. Many nutritional factors shown by epidemiology to be preventative of AD such as polyphenols from wine, ?avonoids and polyphenols from fruits and vegetable, and vitamins and .C are also aluminum chelators. A nutrient of special interest is folic acid which is preventative of AD Snowden?s matched control study from the Nun Study found that higher serum folic acid reduced the severity of atrophy of the brain?s neocortex [40] and that low folate was the only nutritional variable of 18 in this longitudinal study to show signi?cant correlation with brain atrophy. Bayder et al report that folic acid supplementation sharply reduced the level of alumimun in rat brain: i.e. it is a chelator Consumption of ?sh and the docosahexaenoic acid (DHA) from ?sh oil supplements or alternative sources interacts with aluminum through countervailing gene expression and through the maintenance of membrane integrity. Lukiw and Bazan characterized DHA as promoting ?survival A study from the Framingham Heart study concluded that the consumption of one daily ?sh oil pill would be suf?cient to reduce the risk of developing AD by almost 50 percent Lukiw et al demonstrate that DHA and one metabolite neuroprotectin D1 induces anti-apoptotic and neuroprotective gene expression Some of these same genesI are downregulated by aluminum and ABthe diet though not directly chelating aluminum tends to neutralize the adverse effects of aluminum generated oxidation on gene expression and membrane integrity. Likewise, cognitive and physical activity leads to brain secretion of chemicals that interact with aluminum. Yang ?nds that glial cell line-derived neurotrophic factor (GDNF) suppresses the adverse effect of aluminum in laboratory animals but brain derived neurotrophic factor (BDNF) may promote the deleterious effect of aluminum in laboratory animals Severe head trauma can be risk factor for AD, and has been shown to generate AB. Yet, aluminum is found approximately doubled in the brain of boxers suffering from Dementia Puglistica The mechanism of aluminum bioaccumulation in trauma is not known. In sum, there are many interactions and countervailing in?uences of the diet and environment on aluminum?s effect on the brain. 5. The brain substantially regulates aluminum. The brain does not recognize aluminum as safe, and possesses signi?cant chelation capacity to exclude and expel it. Natural brain defense mechanisms are insuf?cient to prevent a gradual bioaccumulation of the metal in the human brain over a lifetime. Gaoloyan et al described the effect of hypothalamic secreted proline-rich polypeptide in providing powerful control of brain aluminum Berg et al reported on dramatic reduction of brain aluminum in both Ts65Dn Down and control mice provided by the appetite satiating hormone Peptide YY This ?nding may provide a link between obesity and aluminum, since both are risk factors for AD. Spray in the nose or oral versions of PYY soon to be commercialized for appetite control should offer inexpensive therapeutic options for AD. Brain cell mitochondria also secrete aluminum chelation chemicals such as glutathione Another secreted anti-oxidant is alpha lipoic acid (ALA), which it likely an . aluminum chelator in that it restores glutathione levels in the mitochondria in brain cells [50] and moves vitamin C, another chelator, into cells. ALA is a competent brain iron chelator [50] and iron chelators are generallyI capable of chelating aluminum. Both antioxidants are available at drugstores and vitamin stores for purchase as dietary supplements and could provide inexpensive prevention and therapy programs. A small German human clinical trial found that ALA completely halted the progression of AD over an eleven month period 6. Aluminum is elevated in the blood of AD patients, and bio-accumulates in the brain in normal persons over a lifetime and at higher levels in AD patients. Average blood serum aluminum levels are higher in AD patients than in-controls, though with considerable individual variation. Smorgon et al reported from a sample of Italians . that high serum aluminum was a de?ning characteristic of persons with AD: i.e. a mean blood serum level of 0.745 mg/ml. Lesser aluminum blood levels were found in persons with cognitive impairment without dementia or with vascular dementia. Normal controls averaged 0.215 mg/ml in blood serum Aluminum absorption may increase with age. Taylor found that absorption of aluminum from a citrate?containing drink (290 mg Al, 4.8 citrate) in normal subjects increased exponentially with age after 65 paralleling the exponential increase in AD incidence, i.e. doubling every ?ve years. Aluminum absorption from the diet is increased in AD compared to younger persons, though again with considerable individual variation. Down?s patients have been shown to be more ef?cient absorbers of aluminum than the general population and most deve10p dementia by the age of ?fty. Aluminum bio-accumulates in the human brain-? in normal aging and in AD. Shimizu et al compared brain aluminum in non-demented elderly persons (aged 75-101) with younger non-demented adults (aged 32 to 46) using ?uorescent stain Hippocampus aluminum content averaged 28 times higher in the elderly and 19 times higher in the frontal lobe than in the younger normal persons. These higher alumintun levels roughly correlated with increased AD type of brain deposits. The study con?rms a bioaccumulation of brain aluminum during the human aging process. While the brain has powerful chelation capacity, it is insuf?cient to prevent gradual aluminum brain bioaccumulation which Edwardson et al estimated at 6ug per year of life The initiation of AD may involve only another doubling of brain aluminum beyond that experienced during normal aging, suggesting the possibility of thresholds Some brain compartments are better accumulators of the metal, and are involved early in the disease process. Andrasi et al found an approximately doubling of brain aluminum in four brain regions, but a seven fold increase in the entorhinal cortex, which is linked by white ?bers to the hippocampus and provides sensory information to the same Jagannatha compared the rate of change of brain aluminum against other metals including copper, zinc and iron As a mole percent of total metals, aluminum was 1.6 percent in the hippocampus of normal brains, 8.1 percent in moderate AD, and 48.4 percent in severe AD. Aluminum is present in all aging brains to participate in the biological changes of cognitive impairment and dementia. Bryant et al demonstrated that aluminum widely complexes with brain chemistry as the small size and the charge of aluminum allow it to enter a wide range of biology 7. Brain atrophy and loss of connectivity are key issues in the dementia of AD. Autopsy studies have consistently failed to ?nd signi?cant statistical relationship between AD diagnosed during life by cognitive testing and the density of brain deposits of senile plaques and NFTs upon death and brain autopsy. These brain deposits not the principal causes of the dementia of AD. In'stead, an abundant evidence indicate that brain atrophy especially the death of brain cells rind loss of brain connectivity are the principal sources of AD ?dementia?. i While aluminum exposure participates in the production of the traditional AD deposits; the key biological role of the metal consists.l of killing braincells and reducing brain connectivity. Here we brie?y summarize a rapidly growing scienti?c literature, ranging from autopsy studies to scans of the brains of living humans concerning the difference between AD and AD with dementia. Davis et al (1999) summarized the result of'their study of 59 elderly well educated subjects examined longitudinally for 8 years until death, when a brain autopsy was performed It was found that the brains of a large percentage of cognitively normal individuals contained numerous degenerative changes, many of which would classify the individuals as having AD under the Khatatu'rian, CERAD, and NIA-Reagan Institute guidelines. Only a small percentage of the normal group judged free of dementia during life was free of these brain changes: i.e. 17 percent. In short, the traditional brain deposits of AD had little statistical relationship to dementia. Edison et al (2007) compared brain amyloid loading in ?living? AD patients with cognition measured by glucose utilization, and found little correlation. The authors? conclusions are devastating to traditional viewpoints of the past twenty years concerning causation of AD dementia: ?The high frontal amyloid load detected by in AD in the face of spared glucose metabolism is of inteiest and suggests that amyloid plaque formation may not be directly resporisible for neuronal dysfunction in this words and faces and cortical uptake suggests that amyloid load contributes to cognitive impairment, the loss of this correlation on withdrawing the AD subjects with normal baseline [1 PET suggests that amyloid deposition alone is unlikely to explain memory dif?culties. ..It is conceivable that amyloid deposition occurs alongside :or before the intracellular processes that lead to cognitive dif?culties. This vieWpoint is reinforced by the stronger correlation . . . . . Though the correlation between 1mpa1red performance on recognltion tests for i 1,0 of recognition with temporal cortical hypometabolism which survived removal of an AD case with normal FDG uptake. . Decline in brain glucose metabolism, as measured by Edison, is a distinguishing preclinical factor separating persons with AD from persons with normal aging. Jagust et al used PET scans to conclude that decreased temporal and parietal glucose metabolism predicts a decline in global cognitive function, while medial temporal brain volume predicts memory decline in normal older persons Aluminum exposure is a participant in brain glucose deprivation in laboratory animals. Lai and Blass (1984) found that aluminum impairs brain glycolysis by inhibition of hexokinase activity in the cytoslic and mitochondria of rat brain In sum, while amyloid loading has little measured effect on glucose metabolism in living humans, there is evidence from animal studies that. aluminum adversely affects glucose metabolism. Goche et al (2002) reported from an autopsy of participants in the Nun Study that there two tracks to dementia. Religious sisters with high Braak stages (high density of traditional AD brain deposits) but with relatively intact hippocampal volume had MMSE scores very close to the normal range for their ages Brain volume determines who . becomes demented rather than density of senile plaques and NFTs. Brain atrophy in AD is con?rmed with MRI and with in vivo imaging programs as the causation of loss of cognition by AD patients: Brain imaging studies in living peOple, such as the study by Edison described above, have con?rmed that brain atrophy and loss of connectivity are the primary causation of the loss of cognition and memory in the elderly and in AD, rather than the traditional brain deposits of AD. Van der Pol demonstrates that brain atrophy occurs even in cognitively normal elderly persons aged 51 to 85, though brain volumes of normal 'persons remain considerably greater than those with AD The atrOphy and loss of connectivity of the AD brain is best seen in the perSpective of the ebb and ?ow of the normal brain into old age. McAuliffe summarizes that between the teen years and early adulthood, brain gray matter - shrinks and white matter or connectivity expands At age 60, white matter begins to decrease at an accelerated rate as myelin and the axons are eroded, while gray matter shrinkage continues. Persons with AD experience AD a greater level of atr0phy of both gray and white matter than cognitively normal persons. Some remedies can slow this process. Physical exercise can generate greater brain connectivity Peirera found that exercise can generate new neurons in the dentate gyrus in younger adults Exercise has minimal bene?t once AD has become established, and initiatives to slow brain atrOphy becomes difficult because the AD brain .. becomes increasingly poisonous. For example, the aluminum brain loading is high and accelerating and brain copper and zinc levels increase into moderate AD and then may decline - ll DeCarli et al found that atrophy of the medial temporal lobe that includes the hippocampus was a signi?cant predictor 0 which individuals with mild cognitive impairment (MCI) would progress to dementia within 3 to 5 years 190 individuals with MCI were classi?ed into ?ve categories of brain atrophy with a score of 0 being normal and 4 being markedly atrophied. MCI patients are known to have a higher risk of progression to dementia. For individuals with a brain atr0phy score of 1.0 or less, only 29.1 percent progressed to dementia within 3 years, compared to 75 percent for those with a rating greater than 2.0. Vitamin and donepezil had no effect on progression. Mungas et a1 surveyed the brains of 103 California residents with MRI scans. They had an average age at baseline of 74 years. It w'as found that hippocampal volume was the primary determination of memory decline, whereas decline in executive function was related to a mix of cerebral vascular disease and AD After control for these factors, white matter hyperintensity had little effect on cognitive impairment. Zarow et al found in comparing AD with ischemic vascular dementia that: ?Regardless?of causative diagnosis, the number of CA1 netirons correlates with magnetic resonance imaging-derived hippocampal volume. . .and memory score. . .We conclude that although CA1 neuron loss is more consistently observed in AD than ischemic vascular dementia, severity of loss shows the expected correlation with structure and function across causative subtype. Reduction in magnetic resonance imaging-derived hippocampal volume re?ect loss, rather than shrinkage of CA1 neurons. The brain imaging studies consistently concludes that brain atrophy is the key event in loss of memory and mental capacity in AD as Opposed to the brain deposits. 7.2. Isolation of the hippocampus by atrophy ofwlzite matter connections from entorhinal cortex is additionally important in memory loss. Stoub et al reported that atrophy of hippocampus was a statistically signi?cant predictor of declarative memory performance in comparing 40 individuals with amnestic mild cognitive impairment (MCI) against 50 healihy individuals. Both groups were approximately 78 years of age The entorhinal cortex also experienced statistically signi?cant increase in atrophy. This part of the brain receives sensory information that is relayed to the hippocampus through white matter ?bers. Loss of this connectivity through brain cell death 1n the entorhinal coritex or through loss of the white ?bers would isolate the hippocampus and thus extinguish memory. A signi?cant decrease 1n white matter volume 1n the brains amnestic MCI persons was I discovered, compared with age- -matched controls 1n the region of the parahypocampal gyrus that includes the perforant path. Regression analysis found that both hippocampal volume and parahippocampal white matter were statistically signi?cant predictors of memory performance. As the authors concluded: 12 ?These results suggest that, in addition to hippocampal atrophy, disruption of the parahippocampal white matter ?bers contributes to memory decline in elderly individuals with MCI by partially disconnecting the hippocampus from incoming sensory information? 8. Aluminum kills human brain pyramidal neurons in two ways and adversely affects brain connectivity. A human aut0psy study by Walton found that elevated cyt0plasmic aluminum was associated with all NFTs tangles in the AD brain Aluminum was measured using the recently deve10ped Walton stain that allows visualization within the cell of aluminum?s relationship to brain cell biology. The association of aluminum with all NFTs con?rms the ?ndings of Murayama using a different technique Walton reported that all human corticolimbic sections had neurons that stained for aluminum. There were two consistent tracks to pyramidal neuropathological processes in the human AD brain hippocampus related to the aluminum. Both processes could culminate in pyramidal neuron death. 0 Necrosis type of cell death: One track involved a progressive increase in nucleolus aluminum that was often associated with granulovacuolar degeneration with granules that stain for aluminum. The outcome visually resembles a necrosis type of cell death. 0 Enucleation type of cell death: The second track involved the formation of NFTs in regions of aluminum enriched cell cytoplasm. A continuing buildup of NFTs ultimately came to kill the neurons by displacing the cell nucleus outside the cell wall by mechanical enucleation. - Chelation of aluminum by NFT s: The evidence indicated that the continuing absorption of aluminum by the NFTs represented a type of natural in situ chelation that protects the neuron from an earlier death by a necrosis type of process 8.1. The basis for increased NFTs deposits due to aluminum exposure is explored in rats and species difference is noted with regard to senile plaques: Walton reports that aluminum inhibited activity in the rats, leading to hyperphosphorylated tau, which in humans will polymerizes to form NFTs. PP2A activity in the aluminum exposed rats was only 41 percent of the control rats Tau activity normally requires phosphate addition and then removal. The later function is performed by PPZAS. The resulting hyperphosphorylation of tau interferes with protein function, and neurons respond by. more protein leading to an accumulation in the neurons. In humans, the hyperphosphorylated tau is folded in the presence of aluminum to produce the NFTs which accumulate in the neuron. At high enough density, brain cell death occurs via enucleation. l3 Senile plaques are species Speci?c, and did not form in the genetically normal rats used in these experiments. Walton notes that the oxidation generated by an aluminum enriched diet in Tg2576 transgenic mice, engineered to contain a human gene to overexpress APP, will produce senile plaques more numerous and larger than in the mice fed the same diet without the aluminum supplementation 8.2. NFTs obstruct ?ow in the axons, leading to loss of brain connectivity. NFTs have a capacity to clog the axons and, inhibit the ?ow of tau, building material and signaling chemicals from glial cells along the axons which will eventually reduce brain connectivity. As Singer et a1 put the issue: ?The data suggest that as the size of the NFT in a cell increases there is less tau in the perikarya available to perform normal ?inctions such as microtubule polymerization and stabilization The authors propose that the aluminum-induced neuro?brillary tangle pathology shown in laborato?y rabbits may provide a model to study Alzheimer?s, diffuse Lewy body disease and Parkinson?s disease. I Slowing of axonal ?ow has been shown to occur early in the AD process Experiments by Shea et al in cell culture for'md that aluminum inhibited neuro?lament (NF) assembly, produced an accumulation df phOSphorylated NF in the perikarya and inhibited transport of the newly assembled NFs into axonal neuritis In a human aut0psy study, Apostolova et al found that ?subregional hippocampal atrophy spreads in a pattern that follows the known trajectory of neuro?brillary tangle dissemination The resulting loss of connectivity may starve the hippocampus of sensory information and leads to atrOphy. High aluminum levels found in the entorhinal cortex in AD patients, reported by Andrasi is relevant. Loss of neurons in that brain sector due to aluminum exposure will reduce the number of. axons connecting that :part of the brain to the hippocampus. Additionally, the clogging of the white matter ?bers linking the entorhinal cortex to the hippocampus with an overload of NFTs genlerated by aluminum will deprive the hippocampus to access to sensory information that is collected by the enthorhinal cortex. Once the hippocampus is isolated as Stoub and others have pr0posed memory ceases. 9. Aluminum causes atrophy of laboratody animal brain and loss of connectivity in multiple ways At the Seventh Keele Meeting on Aluminum held in Uxmal, Mexico in February 2007, Walton presented a video of the performance of elderly Wistar laboratory rats in a simple maze with chocolate bait. The video documents the published studies by Walton [77] The rats were exposed to aluminum in food and water similar to US human exposures from diet and water. At age of 28 months, tv'vo of the aluminum exposed rats began to behave like AD patients: i.e. become disoriented, groom excessively, and lose concentration. Their success in locating the chocolate bait fell to 30 percent compared to 90 percent for the unaffected rats. 14 The distribution of aluminum in brain cells in laboratory rats differs from that the human. Walton preposed that this intracellular distribution is a possible explanation why rats do not develop NFTs. The aluminum produced suf?cient brain dysfunction in some :of the elderly rats to mimic behavior seen in AD patients. 9.1. Apoptosis and necrosis are two basic mechanism of brain cell death. Figure 1 lists multiple mechanisms by which aluminum exposure has been demonstrated to kill brain cells in vivo in laboratory animals or to reduce brain connectivity. Here we can only brie?y describe some biological mechanisms from an abundant number of studies. bibilography of seventy Studies for ?gure 1 is available ApOptosis and necrosis are basic cell death mechanisms which are often speci?c to animal type. Laboratory rabbits tend towards an apoptosis mechanism in response to aluminum exposure whereas rodents tend towards a necrosis form of death Walton found a necrosis appearing cell death in human brain pyramid cells that had accumulated aluminum in the nucleolus. Most likely both apoptosis and necrosis mechanisms may be involved in human brain cell death as illustrated by a study by Johnson et a1 9.2. Aluminum adversely affects glial cells which substantially affects neurons. Glial cells outnumber neurons by 9 to 1 in the brain and are essential for neuronal function and the functioning of the axons Kashon et al found that cortical astrogliosis measured in aut0psy by levels glial ?brillary acidic protein (GF AP) had a correlation with the cognitive performance and dementia status of patients before death This was especially the case for GFAP measured in the temporal lobe and to a lesser extent the parietal lobes where AD brain injury is most prevalent. Glial cells absorb aluminum more readily than neurons. Evidence indicates that the death of neurons may be mediated by the adverse effect of aluminum on the viability and functioning of glial cells [83-84]. 9.3. Less explored mechanisms of brain cell death produced by aluminum. Less explored routes to brain cell death include the depletion of red blood cell and heme by aluminum?s effect directly on the bone marrow Florence et al reported that exposure of Wistar rats to aluminum citrate led to brain cell death that resembled necrosis This effect was only seen after 3 months and the authors proposed that the delay may represent the replacement time of red blood cells which have a lifetime of about 120 days in the rat. Pandav et al finds that the depletion of heme in aging humans is a risk factor for AD The brain is the largest user of glucose of any organ, with AD is associated with markedly impaired central glucose metabolism which can severely impair the viability of 15 brain cells. As previously noted, Lai and Blass ?nd that aluminum inhibits both the cytosolic and mitochondrial hexokinase activities in rat brain The aluminum exposure in these rats was similar to brain aluminum levels in AD and dialysis patients. Mallioux and Appana have recently explored the production of hypoxia and anaerobic metabolism in liver cells after the exposure to aluminum Whether this effect would affect brain cells directly or only indirectly through liver damage is not known. It could affect glucose metabolism indirectly. Hyperammonemia has been proposed as a mechanism by which aluminum kills brain cells by Deloncle et al [89] and by Berg et al Aluminum bonds to L-glutamate and inhibits metabolism of ammonia. Deloncle concluded that aluminum appears to produce accelerated aging. Little is known about the effect of aluminum on blood ?ow and oxygen levels in the . brain, though the metal causes hypertensiorir [90] and has been associated with amyloid' angiopathy of the cerebral microvessels Almninum rigidi?es the membranes of red blood cells [16] which might limit their ability to mechanically negotiate the small size of the microvessels. Mitochondrial and vascular lesions are seen in the brain blood vessels of AD patients, and aluminum 18 known to damage the viability of mitochondria Hypoxia which can be associated with blood vessel damage can up- and down- regulate genes in patterns that mimic AD I 9.4. Aluminum adversely a?cts brain connectivity. Already discussed has been the mechanical killing of neuron pyramid cells by the buildup of aluminum associated NFTs to eventually enucleate the cell. The NFTs can also clog up the axons to reduce ?ow, chemical communication by the glial cells, and brain connectivity. Aluminum also speci?cally oxidizes myelin which can reduce the ef?ciency of neurotransmission. It produces a retraction of the dendrites [95] and damages synapses 10. Summary Aluminum adversely affects the brain of aging humans and laboratory animals with a wide range of alterations of basic biology that leads to cell death and loss of brain connectivity. Additional research 1s needed on the alternative routes by which aluminum generates brain cell death. Other deleterious aluminum based mechanisms will likely be discovered. One might speculate an effect 01f the metal on arrested re- e?ntry of differentiated neurons into cell division that ultimately leads to neuron death 1n AD i Abundant evidence and the presence of relatively high dosages of the metal in all aging 1 brains support McLachlan?s proposal that aluminum is a ?necessary but not suf?cient? risk factor for AD for the most part. Whether this is the case in all individual circumstances needs further research. The eyidence is clearly suf?cient today to conclude that aluminum is a causative co-factor for the dementia of AD. Walton?s autopsy study visually demonstrates that alurininum participates directly in human brain 16 cell death. Gupta?s conclusion that the neurotoxicity of aluminum is beyond any doubt is ?illy supported by the evidence. Regulatory action for toxic metals like aluminum is based on a different standard of proof, with a greater emphasis on epidemiology and protection of the public health rather than absolute scienti?c certainty about biological mechanisms. Under the circumstances, governmental regulatory actions and parallel business act-ions to restrict exposure of the population in food and drinking water seem long overdue. Such initiatives would produce substantial health and economic bene?t to the population. Acknowledgement The Department of the Planet Earth is a non-pro?t citizen group with board member from the United States and Canada, which specializes in bringing medical information about toxins to the attention of governmental regulatory and research agencies. The organization, staff and board have not received ?nancial support for the preparation of this article. 17 Bibliography Jansson ET. Alzheimer disease is substantially preventable in the United States review of risk factors, therapy, and the prospects for an expert software system, Med Hypothesis Open literature at Jansson ET, Aluminum exposure and Alzheimer?s disease, Alzheimers Dis 2001 Open literature at wwdeptplanetearthcom Chandra V, Pandav R, Dodge, HH, Johnston, JM, Belle SH, DeKosky ST et a1. Incidence of Alzheimer?s disease in a rural community in India: the Indo-US study, Neurology 2001 985- 9. Khachaturian AS, Cororan CD, Mayer LS, Zandi PP, Breitner JCS for the Cache County Study Investigators. 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An extended bibliography for Figure 1 is available at: deptplanetearth. com [10] Campbell A, Becaria A, Lahiri DK, Sa arrnan K, Bondy SC. Chronic exposure to aluminum 1n drinking water increases in ammatory parameters selectively 1n the brain, Neurosci Res 2004 Feb 15 565-72. [11] Lukiw WJ, Percy ME, Kruck TP. Nanomolar aluminum induces pro-in?ammatory and pro-apOptotic gene expression in hiiman brain cells in primary culture, Inorg Biochem 2005 [12] Lue LF, Brachova L, Civin WH, Rogers J. In?ammation, A beta deposition and neuro?brillary tangle formation as correlates of Alzheimer?s disease neurodegeneration, Neuropathol Exp Neurol 1996 [l3] Murayama H, Shin RW, Higuchi J, Shibuya S, Muramoto T, Kitamoto T. Interaction of aluminum with PHF tau in Alzheimer?s disease neuro?brillary degeneration evidenced by desferrioxamine- assisted autoclave method, Am Pathol 1999 Sept, 155(3). 877- 85. 1 [l4] Pratico D, Uryu K, Sung S, Tang S, Trojanowski JQ, Lee VM. Aluminum modulates brain amyloidosis through oxidative stress in APP transgenic mice, FASEB 2002 Jul 1138-41. [15] Lukiw WJ, Pogue AI. Induction of speci?c micro RNA species by ROS- 19 generating metal sulfates in primary human brain cells, ?Inorganic Biochem 2007 June 13 [Epub ahead of print] . [16] van Rensburg SJ, Carstens ME, Potocnik FC, Aucamp AK, Taljaard JJ, Koch KR. Membrane ?uidity of platelets and in patients with Alzheimer?s disease and the effect of small amounts of aluminum on platelet and membranes, Neurochem Res 1992 Aug; 1 [17] Zubenko GS, Winwood E, Jacobs B, Teply I, Stif?er S, Hughes HB 3rd? et a1. PIOSpective study of risk factors for Alzheimer?s disease: results at 7.5 years, Am 1999 [18] Potocnik FC, van Rensburg SJ, Park C, Taljaard JJ, Emsley RA, Zinc and platelet membrane microviscosity in Alzheimer?s disease. The in vivo effect of zinc on platelet membranes and cognition, Afr Med 1997 Sept;87(9) 1116-9 [19] van Rensburg SJ, Daniels WM, van J, Potocnik FC, van der Walt BJ, Taljaard JJ, Lipid peroxidation and platelet membrane ?uidity- implications for Alzheimer?s disease, Neuroreport 1994 Nov 21 [20] Ghribi O, Hermann MM, DeWitt DA, Forbes MS, Savory J, Abeta 91-42) and aluminum induce stress in the endoplasmic reticulum in rabbit hippocampus, involving nuclear translocation of gad 153 and NF-kappaB, Brain Res Mol Brain Res 2001 Nov [21] Exley C, Aluminum and iron, but neither c0pper nor zinc, are key to the precipitation of beta-sheets of Abeta-42 in senile plaque cores in Alzheimer?s disease, Alzheimer?s Dis 2006 Review [22] Bush AI, Pettigell WH, Paradis MD, Tanzi RE, Modulation of A beta adhesiveness and secretase site cleavage by zinc, Biol Chem 1994 Apr [23] McLachlan DR, Kruck TP, Lukiw WJ, Krishnan SS. Would decreased aluminum ingestion reduce the incidence of Alzheimer?s disease? Can Med Assoc 1991 [24] McLachlan DRC in: Shovlin MG. Aluminum in drinking water and Alzheimer?s disease: a resource guide, American Water Works Association Research Foundation, Denver 1993. [25] McLachlan DR, Smith WL, Kruck TP. Desferrioxamine and Alzheimer?s disease: video home behavior assessment of clinical course and measures of brain aluminum, Therapeutic Drug Monitoring, 1993 [26] Alexandrov PN, Zhao Y, Pogue AI, Tarr MA, Kruck TP, Percy ME, et a1. Synergistic effects of iron and aluminum on stress-related gene expression in primary human neural cells, Alzheimers Dis 200 [27] Jansson ET, Review of evidence concerning the safety of aluminum based food additives in support of petition to FDA to rescind ?generally recognized as safe? status for these additives 2005, Sept 14. Available at: [28] Gupta,VB, Anitha S, Hegde ML, Zecca L, Garruto RM, Ravid R, et al, Aluminum in Alzheimer?s disease: are we still at a crossroad? Cell Mol Life Sci 2005 [29] A chartbopk of drinking water and food abstracts and charts available upon request and mailing address at: [30] Forbes WF, McLachlan DRC. Further thoughts on the aluminum-Alzheimer?s disease link, Epidemiol Commun Health 1996 20 [31] Forbes WF, McAiney CA, Hayward LM, Agwani N. Geochemical risk factors for mental functioning, based on the Ontario Longitudinal Study of Aging (LSA) II, the role of pH, Can on Aging 1994,13 :249l-67. [32] Chiba J, Kusumoto M, Shirai S, Ikawa K, Sakamoto- S. The in?uence of ?uoride ingestion on urinary aluminum excretion in humans, Tokoku Exp Med 2002 [33] Wang S-X, Wang Z-H, Cheng X-T, Li J, Sang Z-P, Zhang X-D, et a1. Arsenic and ?uoride exposure in drinking water: children?s IQ and growth in Shanyin County, Shanxi Province, China, Environ Health Perspectives 2007 Apr; 115(4): 643- 7 [34] Gillette? Guyonnet S, Andrieu S, Nourhashemi F, de la Gueronniere V, Grand] can H, Vellas B, Cognitive impairment and composition of- drinking water in women: ?ndings of the EPIDOS study, Am Clin Nutr 2005 Apr; 81(4): 897- 902. [35] Exley C, Korchazhkina 0, Job D, Strekopytov S, Polwart A, Crome P. Non? invasive therapy to reduce body burden of aluminum 1n Alzheimer?s disease, I Alzheimers Dis 2006 Sept, 10(1): 17-24. [36] Rogers MA, Simon DG. A preliminary study of dietary aluminum intake and risk of Alzheimer?s disease, Age and Ageing 1999 Open literature at PubMed. [37] Graves AB, White B, Koepsell TD, Rei?er BV, van Belle G, Larson EB. The association between aluminum-containing products and Alzheimer?s disease, Clinl Epidemiol 1990 35- 44. [38] Roberts NB, Clough A, Bellia JP, Kim Y. Increased absorption of aluminum from a normal dietary intake in dementia, Inorg Biochem 1998 [39] Luchsinger JA, Tang MX, Miller J, Green R, Mayeux R. Relation of higher folate intake to lower risk of Alzheimer disease in the elderly, Arch Neurol 2007 Jan 86- 92. [40] Snowdon DA, Tully CL, Smith CD, Riley KP, Markesbery WR. Serum folate and the severity of atrophy of the neoeortex in Alzheimer?s disease: ?ndings from the Nun Study, Am Clin Nutr 2000 Apr, 993? 8. [41] Baydar T, Nagymajtenyi L, Isimer A, Sahin G, Effect of folic acid supplementation on aluminum accumulation in rats, Nutrition 2005 Mar 21(3): 406- 510. [42] Lukiw WJ, Bazan NG, Survival signaling 1n Alzheimer?s disease, Biochem Soc Trans 2006 Dec ,34(Pt. 6): 1277- 82 [43] Johnson EJ, Schaefer Potential role of dietary n?3 fatty acids in the prevention of dementia and macular degeneration, Am Clin Nutr 2006' Jun ,83(6 Suppl): 1494S- 88. [44] Lukiw WJ, Cui JG, Marcheselli VL, Bodker M, Botkjaer A, Gotlinger K, et al. A role for docosahexaenoic acid- derived neuroprotectin D1 in neural cell survival and Alzheimer disease, Clin Investigation 2005 Oct 2774- 83. I [45] Yang SJ, Lee JE, Lee KH, Huh JW, Choi SY, Cho SW, Opposed regulation of 1 aluminum?induced apoptosis by glial cell line-neurotrophic factor and brain-derived neurotrophic factor 1n rat brains, Brain Res Mol Brain Res 2004 Aug 23 ,127(1- [46] Bouras C, Giannakopoulous P, Good PF, Hsu A, Hof PR, Perl DP, A laser microprobe mass analysis of brain aluminum and iron in Dementia pugilistica: Comparison with Alzheimer?s disease, Eur Neurol [47] Galoyan AA, Shakhlamov VA, Aghajanov MI, Vahradyan HG, Hypothalamic 21 proline-rich polypeptide protects brain neurons in aluminum neurotoxicosis, NeurochemRes 2004 [48] Berg BM, Croom J, Fernandez JM, Spears W, Eisen EJ, Taylor IL, et al, Peptide YY administration decreases brain aluminum in the Ts65Dn Down mouse model, Growth Dev Aging 2000 [49] P, Ahmad Shah Z, Kumar A, Islam F, Mishra KP, Role of combined administration of Tiron and glutathione against aluminum-induced oxidative stress in rat brain, Trace Elem Med Biol 2007 63- 70 Suh JH, Moreau R, Heath S-HD, Hagen TM, Dietary supplementation with alpha?lipoic acid reverses the age- -related accumulation of um and depletion of antioxidants in the rat cerebral cortex, Redox Report [51] Hager K, Marahrens A, Kenklies M, Riederer P, Munch G, Alpha?lipoic acid as a new treatment Option for Alzheimer type dementia, Arch Gerontol Geriatr 2001 [52] C. Smorgon C, Mari E, Atti AR, Dalla Nora E, Zamboni PF, Calzoni F, et al, Trace elements and cognitive impairment: an elderly cohort study, Arch Gerontol Geriatr Suppl, 2004, (9): 393- 402 [53] Taylor GA, Ferrier IN, McLoughlin II, a1rba1rn AF, McKeith IG, Lett D, et al, Gastrointestinal absorption of aluminum 1n Alzheimer? 3 disease, response to aluminum citrate, Age Ageing, 1992 [54] Moore PB, Edwardson JA, Ferrier IN, Taylor GA, Lett D, Tyler SP, et a1, Gastrointestinal absorption of aluminum is increased in Down?s Biol 1997 [55] Shimizu H, Mori T, Koyarna M, Sekiya M, Ooami H, A correlative study of the aluminum content and aging changes of the brain in non-demented elderly subjects, Nippon Ronen Igakkai Zasshi 1994 Japanese [56] Edwardson JA et al, Aluminum in Chemistry, Biology and Medicine, Raven Press, New York 1991235 [57] Andrasi E, Pali N, Molnar Z, Kosel S, Brain aluminum, magnesium and phosphorous contents of control and Alzheimer-diseased patients, Alzheimer?s Dis 2005 Aug, 273- 84 [58] Jagannatha RKS: Finding presented 1n Gupta VB, Anitha S, Hegde ML, Zecca L, Garruto RM, Ravid R, et a1, Aluminum 1n Alzheimer?s disease: are we still at a crossroad? Cell Mol Life Sci Footnote 19. [59] Bryant PL, Lukiw WJ, Gan Z, Hall RW, Butler LG, High-?eld 19.6T solid- state MAS NMR of in vitro aluminated brain tissue, Magnetic Resonance 2004 Oct; 1 70(2) :25 7-62 [60] Davis DG, Schmitt FA, Wekstein DR, Markesbery WR, Alzheimer neuropathologic alterations in aged cognitively normal subjects, Neuropathol Exp Neurol 1999 [61] Edison E, Archer HA, Hinz R, Hammers A, Pavese N, Tai YF, et a1, Amyloid hypometabolism and cognition in Alzheimer disease, An and PET study, Neurology 2007 [62] Jagust W, Gitcho A, Sun F, B, Mungas D, Haan M, Brain imaging evidence of preclinical Alzheimer?s disease in normal aging, Ann Neurol 2006 22 [63] Lai C, Blass JP, Inhibition of brain glycolysis by aluminum, Neurochem 1984 8-46. [64] Gosche KM, Mortimer JA, Smith CD, Markesbery WR Snowdon DA, Hippocampal volume as an index .of Alzheimer neuropathology: ?ndings from the Nun Study, Neurology 2002 [65] van de Pol LA, Hensel A, Barkhof F, Gertz HJ, Scheltens P, van der Flier WM, Hippocampal atrophy in Alzheimer disease: Age matters, Neurology 2006 Jan 236- 8 [66] McAuliffe K, Life of the brain, elderly: silver stars. The Brain, Discover 2007 Spring: 15- 17 [67] Pereira AC, Huddleston DE, Brickman AM, Sosunov AA, Hen R, McKhann GM, et al, An 1n vivo correlate of exercise-induced neurogenesis in the adult dentate gyrus, Proc Nat Acad Sci USA 2007 Mar 27'? ,1:04(13) 5638 -43 [68] DeCarli C, Frisoni GB, Clark CM, Harvey D, M. Grundman M, Petersen RC, et a1, and Scheltens for the Alzheimer? 3 Disease Cooperative Study Group, Qualitative estimates of medial temporal atrophy asla predictor of progression from mild cognitive impairment to dementia, Arch Neurol 2007 Jan; 64(1): 108-1 15 [69] Mungas D, Harvey D, Reed BR, Jagusit WJ, DeCarli C, Beckett L, et a1, Longitudinal volumetric MRI change and rate of cognitive decline, Neurology 2005 ,:65 565- 71 [70] Zarow C, Vinters HV, Ellis WG, Weiner MW, Mungas D, White L, et al, Correlates of h1ppocampal neuron numbers' 1n Alzheimer?s disease and ischemic vascular dementia, Ann Neurol 2005 June' 896- 903. Open literature NIH [71] Stoub TR, de Toledo-Morrell L, Stebbins GT, Leurgans S, Bennett DA, Shah RC, Hippocampal disconnection contributes to memory dysfunction in individuals at risk for Alzheimer?s disease, Proc Nat Acad Sci USA 2006 June 27 ,10:3(26) 10041 -5 [72] Walton JR, An aluminum-based rat model for Alzheimer? 5 disease exhibits oxidative damage, inhibition of PP2A activity, hyperphosphorylated tau, and granulovacuOIar degeneration, Inorg Biochem 2007 June 12 [Epub ahead of publication] Science Direct [73] Singer SM, Chambers CB, Newfry GA, Norlund GA, Muma NA, Tau' 1n aluminum- induced neuro?brillary tangles, Neurotokicology 1997 63- 7 [74] Stokin GB, LilIo C, Falzone TL, Bruseh RG, Rockenstein E, Mount SL, et a1, AxonOpathy and tran3port defects early in the pathogenesis of Alzheimer?s disease, Science 2005 Feb 1282- 8 [75] Shea TB, Wheeler E, Jung C, Aluminum inhibits neuro?lament assembly, cytoskeletal incorporation, and axonal transport. Dynamic nature of aluminum- induced perikaryal neurofilament accumulations as revealed by subunit turnover, Mol Chem Neuropathol 1997 Sept-Dec; 32(1 :17 39 [76] Apostolova LG, Dinov ID, Dutton RA, Hayashi KM, Toga AW, Cummings JL et i a1, 3D comparison of hippocampal atrOphy 1n amnestic mild cognitive impairment and Alzheimer?s disease, Brain 2006 Nov ,.129(Pt 11): 2867- 73 [77] Walton JR, A longitudinal study of rats chronically exposed to aluminum at human dietary levels, Neurosci Lett 2007 [78] Savory J, Rao JK, Huang Y, Letada PR, Herman MM, Age-related hippocampal 23 change in Bcl-2/Bax ratio,oxidative stress, redox?active iron and apoptosis associated with aluminum induced neurodegeneration: increased susceptibility with aging, Neurotoxicology 1999 [79] Miu AC, Andrees?cu CE, Vasiu R, Olteanu A1, A behavioral and histological study of the effects of long-term exposure of adult rats to. aluminum, Int Neurosci 2003 Sept, 113(9): 1197- 1211 [80] Johnson VJ, Kim SH, ShannaRP, Aluminum-maltolate induces ap0ptosis and necrosis in Neuro- 2A cells: potential role for p53 signaling. Toxicol Sci 2005 [81] Fields DR, The other half of the brain, Scienti?c American 2004 Apr:54-6l [82] Kashon ML, Ross Webster, O?Callaghan JP, Miller DB, Petrovitch H, Burch?el CM et a1, Associations of cortical astrogliosis with cognitive performance and dementia status, Alzheimer?s Dis [83] Aremu DA, Meshitsuka S, Some aspects of astroglial functions and aluminum implications for degeneration: review, Brain Res Brain Res Rev 2006 200 [84] Suarez-Fernandez MB, Soldado AB, Sanz? Medel A, Vega JA, Novelli A, Fernandez-Sanchez MT, Aluminum- induced degeneration of astrocytes occurs via apoptosis and results 1n neuronal death, Brain Res 1999 Jul 24, 835(2): 125- 36 [85] Garbossa G, Galvez GT, Castro ME, Nesse A, Oral aluminum administration to rats with normal renal function. 1. Impairment of Hum Exp Toxicol 1998 Jun; 1 12-7 [86] Florence AL, Gauthier A, Ponsar C, Van den Bosch de Agilar P, Crichton RR, An experimental animal model of aluminum overload, Neurodegeneration 1994 [87] Pandav RS, Chandra V, Dodge HH, DeKosky ST, Ganguli M, Hemoglobin levels and Alzheimer disease: an epidemiologic study 1n India, Am Geriatr 2004 Sept-Oct; 12(5): 523- 6 [88] Mailloux RJ, Appana VD, Aluminum toxicity triggers the nuclear translocation of HIF-lalpha and promotes anaerobiosis in hepatocytes, Toxicol In Vitro 2007 16-24 [89] Deloncle R, Huguet F, Fernandez B, Quellard N, Babin P, Guillard 0, Ultrastructural study of rat hippocampus after chronic-of aluminum L-glutamate: an acceleration of the aging process, Exp Gerontol 2001 [90] Granadillo VA, Tahan JE, Salgado O, Elejalde LE, Rodriguez-Iturbe B, Romero GB, et al, The in?uence of the blood levels of lead, aluminum and vanadium upon the arterial hypertension, Clin Chim Acta 1995 [91] Exley C, Esiri, MM, Severe cerebral congophilic angiopathy coincident with increased brain aluminum in a resident of Camelford, Cornwall, UK, Neurol Neurosurg 2006 [92] Ghribi O, DeWitt DA, Forbes MS, Herman MM, Savory J, Co-involvement of mitochondria and endoplasmic reticulum in regulation of apoptosis: changes in cytochrome c, Bel-2 and Bax in the hippocampus of aluminum-treated rabbits, Brain Res 2001 Jun [93] Bazan NG, Palacios-Pelaez R, Lukiw WJ, Hypoxia signaling to genes: signi?cance in Alzheimer?s disease, Mol Neurobiol 2002 24 [94] Verstaeten SV, Golub MS, Keen CL, Oteiza PI, Myelin is a preferential target of aluminum-mediated oxidative damage, Arch Biochem Biophys 1997 [95] Forbes MS, Ghribi O, Herman MM, Slavery J, Aluminum-induced dendritic pathology revisited: cytochemical and electron microscopic studies of rabbit cortical pyramidal neurons, Clin Lab Sci [96] Jing Y, Wang Z, Song Y, Quantitative study of aluminum-induced changes in synaptic ultrastructure in rats, Synapse 2004 [97] Zuh X, Lee HG, Perry G, Smith MA, Alzheimer disease: the two?hit hypothesis: an update, Biochim Biophys Acta 2007 25 rDepartment of the Planet Earth 701 Street, SE - Suite 200, Washington, DC 20003 (301) 47 5-8366 - planctbarth@cmls.60m; February 30, 2008 Hon. Bob Kerry and Hon. Newt Gingrich Co?Chairs, Biprtisan Alzheimer?s Study Group c/ 0 Alzheimer?s Study Group 1425 Street, NW, Suite 450 Washington, DC 20005 Re: Alzheimer?s is substantially preventable (in the 50 to 80 perent range) and partially treatable (stabilization). But, the role of aluminum as a "necessary but not sufficient" risk factor needs to be addressed for success. Dear Sirs, Over a decade ago, Dr. Donald McLachlan, Director of the Tanz institute of the University of Toronto, proposed that aluminum is a ?necessary but not sufficient? risk factor for Alzheimer?s. One has to make the same claim for aging itself. The two factors are related. 1 hope the enclosed summary studies are useful. The review, which is in press, summarizes some of the newest findings. 1. Gene Regulation: For example, very low levels of aluminum and iron similar to that in the aging human brain synergistically up- and down- regulate a large percentage of the genes in a similar fashion to what is experienced in AD, including genes for apoptosis, amyloid precursor protein, and down-regulation of the gene for synapsin. Enclosed are 3 studies by Walter Lukiw and others. 2. Aluminum and Neurotibrillary Tangles: Dr. Judie Walton has published several extraordinary studies using the Walton stain. Aluminum can be seen by microscope within the brain cell where it is associated with every NFT that was surveyed and with cell pathology. The metal prevents the breakdown of NFTs, where they accumulate in the cell to kill it by enucleation which can be seen in the autopsy tissue. Enclosed are 3 studies. At a dietary dosage of the metal similar to that of humans, some of Walton?s aging rats developed AD type of behavioral and memory changes which was recorded on video. 3. Epidemiology ls Persuasive: 0 Aluminum bioaccumulates in the brain of all persons in the a process - as much as 19 to 28 times between middle and old age. 0 AD may involve only another doubling of brain levels. 0 Twenty two drinking water studies and one food study link the metal to either AD or elderly cognitive impairment. 0 Blood levels of AD patients contain considerably higher aluminum levels, and the patients absorb the metal more readily from food. This is also the case of the elderly compared to younger persons. Enclosed is a chartbook describing the water and food studies, and secondly, a- presention I made at the Keele conference on aluminum in Mexico last year with charts. 4. Qge Prevention Opportunity As with all chronic diseases of the elderly, there is multiple causation of AD. For example, a recent report from the Framingham study concluded that the consumption of one fish pill per day could reduce AD risk by about 50 percent. This effect is probably not aluminum based, though fish oil may rescue the adverse gene regulation associated with alumium. Likewise, removal of lead from the environment may have beneficial effects on AD incidence again not aluminum based. Iron is also involved in a synergistic fashion with aluminum. On the other hand, a French study found that consumption of bottled water high in soluble silicon (Silicic acid) could reduce risk of AD by 50 percent in French women. Consumption of 12 mg/ day of silicon was required for this effect. Silicic acid is an aluminum chelator. A very large published scientific evidence supports Dr. McLachlan?s proposal that aluminum is a ?necessary but not sufficient? risk factor for AD for the most part. Remove the excessive human exposure to the metal, and 50 to 80 percent prevention appears to be possible based on the epidemiology. Indeed, many other prevention factors identified by epidemiology also chelate aluminum, Such as folic acid, ?avanoids and polyphenols from fruits and vegetables and wine and vitamins C. There are also powerful natural chelators in the human brain. Folic Acid: It seems likely that the supplementation of the food supply withxfolic acid, an issue we promoted some years ago, has likely already reduced age-adjusted incidence of AD .in the United States. Folic acid has several biological effects. In laboratory animals, folic acid is a competent brain aluminum chelator. (See last chart in Keele presentation.) 5. Biology Is Considerably Understood: A vast published literature: i.e. hundreds of studies, now exists concerning the biology of aluminum, which reduces the function of brain cell, kills them, and reduces brain connectivity. Walton presented photographs of aluminum associated with dead and dysfunctional brain cells in human autopsied brain. As noted, her rat studies using dosage similar to that of humans, found that some of the animals developed behavior resembling AD. 6. Best Therapy Also Partially Aluminum Based: Aluminum chelation' a University of Toronto study slowed the progression of AD by 50 percent. Likewise, the most? successful therapy was shown a small published German human clinical trial using alpha lipoic acid, which IS a good brain chelator of iron, but also of aluminum via enhancement of glutathione and vitamin C. ALA IS a potent anti-oxidant and rescues the health of the mitochondria which 15 Edamaged by oxidation. A new clinical trial 15 in progress using fish oil and ALA. One would speculate that this will stabilize the disease better than drugs on the market. 7. Remedies Are Very Inexpensive: We hope that the enclosed literature 13 helpful. There is great commercial opposition to consideration of the hundreds of published studies 0 the epidemiology and biology of aluminum' 1n AD. Other opposition comes from researchers trying to make a financial killing from drugs that break up beta-amyloid. (Aluminum exposure generates beta-amyloid by upregulating the gene through ROS) Remedies are very inexpensive: i.e. prevention of AD is cheap. For example, Roger and Simon?s study from Syracuse (enclosed) found that 1 ?every? person admitted to their geriatric center who had eaten food produced with aluminum containing baking powder got AD: i.e. 100 percent compared to zero incidence of AD among those who diet did not consume food such as pancakes, waf?es,,corn bread and other products. 0 Calcium based baking powder is inexpensive and already on the market: eg, Rumford and Fleichman. 0 Likewise, iron sulfate for drinking water is more effective in purification of water and similar in price to aluminum sulfate. - In September 2005, we petitioned the Food and Drug Administation?to rescind its ?generally recognized as safe? or GRAS characterization of aluminum based food additives; "The agency responded that they lacked enough staff to;read the petition even though the staff had already ?read it. One on side,?FDA was unable to reject-the petition on the facts. On the other side, the government did not wish to hear the issue, and had no enthusiasm for prevention of AD. We realize that study commissions for AD come and go. None in the past have looked at environmental causation like aluminum, which is like playing-cards without the kings and queens. You can?t succeed without a full deck. I?d be happy to discuss the rich evidence with your staff, or introduce you to people who really know the issue. We have been working on AD and aluminum since 1989. With best regards, Erik Iansson, Pres. planetearth@erols.com c. Commission members c. -_l?ril .ngp- Aqur {weak EH 452-1- . In. 1* g?xh 4 . w. ii" 551 at51"; 5? i539. I a: I Jag?!" 54W inf-n f. :5 an?? I at - 151- .. .- . 1?s- . -ir_ w- 3m.- . .154waf. 'a Necessary . but Insufficient State Renewable Polrtfolio Standards and Climate Change Policies By Benjamin K. Sovacool and Jack N. Barkenbus IN EUROPE this past February, then?British Prime Minister Tony Blair announced that the United Kingdom would support a 20 per- cent mandatory target for renewable power as a share of European generation capacity.? His announcement complements the policies of 17 other European Union countriIes that have also set some type of national. mandatory target for promoting renewable energy. And in terms of climate policy in Europe. the European Union Green- house Gas Emission Trading Scheme (EU ETS) calls for mandatory reductions in greenhouse gas emissions and allows countries to trade carbon credits. In the past five yearsI Brazil. China, Indonesia. Israel, Nicaragua, Norway", South KoreaI Sri Lanka. Switzerland. and Turkey have adopted mandatory renewable energy or climate change targets.2 These countries have frequently linked action On . :1 . -- "Eff fir" arm ?3 -- . waist-'4: rat- . ?-?xiiPk-?Ii . fifthrenewable energy and climate change together because they realize that the combustion of fossil fuels greatly contrib- utes to climate change, and they do not like fouling their own nests. Meanwhile, in the United States, the federal government has set no national target for renewable energy, established no national cap on greenhouse gas emis- sions, and refused to create a nationwide trading system for carbon credits. As a result of the administration?s unwill- ingness to take forceful actions com- and the Clean Water Act (PL 92-500) in 1972?to reorient the federal-state rela- tionship in environinental law. Its efforts were largely inspired by the unappealing prospect of having to live with 50 dif- ferent state air and water statutes. It was generally agreed that clean air and water necessitated federal preemption?that is, federal laws needed to trump state laws to provide regulatory clarity in addressing problems of national magnitude. Of course, the discussion of feder- al versus state governance dates back The United States remains unprepared to face the unprecedented energy and environmental challenges that loom in the future. mensurate with the nation's leadership and responsibilities, the country remains unprepared to face the unprecedented energy and environmental challenges that loom in the future. Prior to the 19705, the country faced a similar situation: U.S. regulation con- sisted of a medley of state laws, local ordinances, and common law nuisance protections that left signi?cant gaps in the scope and duration of environmental protection. However, it was generally believed that signi?cant inconsistencies were present in state regulation based on their relative differences in wealth, knowledge, and interest group pressure. A signi?cant disparity also occurred con- cerning the rate at which states adopted environmental regulation?a dispar- ity in?uenced by trends in population growth, the extent that environmental services were perceived to have a value in a state?s economy, and the revenue that individual states received from rec- reational activities such as hunting and fishing.3 Congress responded with an array of environmental statutes?most notably the Clean Air Act (PL 91-604) in 1970 22 ENVIRONMENT to the country's founding, and debates about federalism became especially pro- nounced during the era of the New Deal in the 19303. The Supreme Court has long fought to maintain a balancing act, towing the line to create ?dual federalism," where the federal government regulates issues of national import, and the states respond to issues of local import. This balance was believed to help achieve responsive governance, governmental competition, innovation, participatory democracy, and resistance to tyranny.4 Fast-forward to today, and such roles have oddly been reversed. In what Case Western Reserve University law professor Jonathan Adler termed a ?jurisdictional mismatch,? the state and federal govern- ments have seemingly subverted each other?s traditional roles.5 In a ?poaching of state and local government territory,? national policymakers have preempted state action concerning drinking water contamination, solid waste disposal, land restoration, and educational standards for teacher quali?cation and student per- formance.6 Congruously, in what Adler termed "letting ?fty ?owers bloom,? state and local govermnents have effec? tively shut down the national market on bromated ?ame retardants, adopted inter? national treaties on human rights, promot? ed smoking bans in bars and restaurants, and attempted to protect public health by regulating obesity and red meat.8 Free market advocates have occasion- ally derided the case for national action on renewable portfolio standards laws mandating that electricity suppliers use a certain percentage of renewable energy by a particular date. But propo- nents point out that these regulations are needed to correct three major market failures in the electric utility industry. First, they argue that electricity prices do not re?ect the social costs of generating power; second, that energy subsidies have created an unfair market advantage for fossil fuel and nuclear technologies; and third, that renewable energy generation is subject to a ?free rider" phenomenon.9 To gain the transparent and multiple bene?ts from renewable energy at a larger scale, bold federal action is essential. It is true that some states and regions of the nation are better positioned to exploit renew- able resources, but all regions can exploit some form of renewables, and RPS pro- posals have been crafted to allow for a large portfolio of choices at the electricity retail level. Most compelling, under the current state initiatives, renewables will still only account for 4 percent of national capacity by 2030. Climate change has been described as a "textbook example of an environmen- tal issue best addressed at the national and international levels.""' Greenhouse gas emissions are produced around the globe and accumulate in the atmosphere such that the impacts are not restricted to states, regions, or even countries. When problems are national or international in scale, the ?matching principle" in envi- ronmental law suggests that the level of jurisdictional authority should best match the geographic scale of that very. problem. In the case of climate change, this principle calls for national and VOLUME 49 NUMBER 6 -4 .n 93 ,a'rmr nv 5.- international action, not solely local or regional intervention.? In the last 10 years?from 1997 to 2006?federal bills promoting RPS were introduced in Congress 17 times.12 In addition, 102 legislative proposals deal- ing with climate change have been introduced from 1997 to 2004.13 All have been beaten back by Republican- dominated Congresses. Itis safe to say, therefore, that consider- able state action in both cases has arisen not because of some judgment that state- based action is optimal or preferable but rather because of the perceived policy vac- uum at the federal level. A federal-scale political philosophy of allowing market forces to determine energy and environ- mental policy dates back at least as far as the presidency of Ronald Reagan, and it has been reinforced by the political power of Washington, DC?based interest groups and trade associations who have a stake in maintaining the status quo. However, this philosophy and political structure is not mirrored throughout much of the country, and hence many states have become very active in the RPS and climate change arena. And, similarly, many other states that mirror the phiIOSOphy and approach of the federal level remain inactive. The piecemeal approach to renewables and climate change represented by state action, while laudable as an alternative to federal inaction and consistent with the way many issues are brought to the federal agenda (such as was the case for energy appliance standards and the JULYIAUGUST 2007 acid rain provisiops of the Clean Air Act Amendments of 1990), is ultimately an inadequate reSponse to the magnitude of the challenges the country faces in energy and climate change. A Brief Taxonomy of State Actions To be fair, state-based environmental regulation does bring with it some advan- tages. The states are generally believed to I I ?9 act as class1c laboratones of democracy, a concept Suprenie Court Justice Louis Brandeis promulgated in a dissenting opinion 75 years ago. 1? State policymak- ers have access to knowledge of local problems and coiliditions and are often more accountablel- to their constituents. Because they are closer to environmental problems and the regulated community, the states can devise more manageable and appropriate policies capable of catering to individual needs and exploiting opportu- nities peculiar to regions. State action can provide opportunities for experimenta- tion in designing policy, as the existence of many states acting at once promotes diversi?cation andiinnovation.15 There is no denying that the states have certainly takfen the lead in terms of experimenting Iwith RPS and climate change policies. In 1985, Iowa became the ?rst state to mandate utilities to purchase renewable a goal of 105 megawatts (MW) of installed renewable capacity by 1997). Minnesota followed in 1994.? Since then, no fewer than 2] states, plus the District of Columbia, have developed some form of These states have collectively launched hundreds of millions of dollars in renewable energy projects, the most aggressive being Cali- fornia (20 percent by 2010), New York (24 percent by 2013), and Nevada (20 percent by 2015)l8 (see Figure 1 on page 24). Similarly, the states have taken the initiative in addressing climate change, implementing comprehensive and cross- cutting programs to those narrowly focused on agriculture, transportation, education, and energy. Forty-one states have developed comprehensive green- house gas inventories, 28 have completed climate change action plans, and 14 have mandated greenhouse gas emissions tar? gets. The most aggressive is New York, aiming for 5 percent below 1990 carbon dioxide emissions levels by 2010, fol- lowed by Connecticut, Massachu? setts, Maine, New Hampshire, New ersey. Rhode Island, and Vermont (aiming for 1990 levels by 2010). California has set'ri target of returning to 1990 emission levels by 2020 and reaching levels 80 percent below that benchmark by 2050. Motivated to encompass a broader geographic area, eliminate duplication of work, and create more uniform regulatory eiivironments, many states have also established regional initiatives to fight climate change such as the Western Regional Climate Action Initiative (WGA) on the West Coast and the Regional Greenhouse Gas Initiative (RGGI) on the East Coast (see Figure 2 on page 25 and Table 1 on page 27). ENVIRONM ENT 23 Why State-Based Renewable Portfolio Standards Are Not Enough While the considerable state-based RPS activity, just described, can be laud- ed as better than no action at all, it is not necessarily superior to national legisla- tion. Important issues such as geographic scope, eligible technologies or indus- tries, inclusion of existing versus new technologies, and the speci?cs of credit trading have been decided differently in every state. Consequently, the resulting state-based market may create confusion, complexity, and inconsistency for policy- makers, investors, andbusinesses. Contrary to enabling a well?lubricated national renewable energy market, incon- sistencies between states?over what counts as renewable energy, when it has to come online, how large it has to be, where it must be delivered, and how it may be traded?clog the renewable ener~- gy market like coffee grounds in a drain. Implementing agencies and stakeholders must grapple with inconsistent state RPS goals, and investors must interpret com- peting and often arbitrary statutes.?9 To pick just a few prominent examples, Massachusetts set its target at 4 percent by 2011, while ?Rhode Island chose 15 percent by 2020. In Maine, fuel cells and high efficiency cogeneration units count as ?renewables,? while the standard in includes coal gasi?cation and small?scale fossil fuel power plants. Iowa, Minnesota, and Texas set their purchase requirements based on installed capacity, whereas other states set them relative to electricity sales. Maine, New Hampshire, Vermont, Connecticut, and Rhode Island trade renewable energy credits (RECs) under the New England Power Pool, whereas Texas has its own REC trading system. Minnesota and Iowa have voluntary standards with no penal- ties, whereas Massachusetts, Connecti- cut, Rhode Island, and all levy different noncompliance fees?? The 24 ENVIRONMENT result is a renewable energy market that deters investment, complicates compli- ance, discourages interstate cooperation, and encourages tedious and expensive litigation.21 The electricity utility industry is also transitioning away from a state-by-state energy market, making a state-by-state RPS approach anachronistic. The Energy Policy Act of 2005 removed the geo- graphic restrictions that limited public utility holding companies to single, inte- grated systems.? More utilities operate across state lines, and many have begun to merge and consolidate to maximize pro?ts and deal with the perceived chal- lenges of restructuring. Using individual Figure 1. State RPS policies (as-of March-2007) .. . Wrens . 6 SOURCE: Lawrence Berkeley National Laboratory, March 2007. Figure used courtesy of Ryan Wiser. .-. MN: 25409; by 2020-25 2013 IA- Ila: 105nm states as a crucible for innovations in electricity generation and marketing may have made sense when limits were placed on the size and geographic scope of util- ity holding companies, but it makes little sense now. Finally, state-based renewable port- folio standards risk challenges on legal grounds. Article 1, section 8 of the US. Constitution grants Congress the power ?to regulate commerce with foreign nations, and among the several states, and with Indian tribes?:4 In the many years since rati?cation of the Constitution, the U.S. Supreme Court has consistently used the converse of this part of the commerce clause (hence its description as the "der? .4- MA: w. by 2009 . .Rl:16% by 2019 - by 2010 -- NJ: 22.51". 2021 759. y01 tie-105'. by 2019 by 2022 PA. by 2020 in NOTE: Unlike other states, lowa measured its average megawatt hours of installed capacity, meeting it in 1997. Texas measures its goal in new megawatt (MW) capacity. Vermont (which mandates that all lead growth must be satisfiedby renewableenergy, applying only to new electric- ity demand) and Illinois (with a voluntarystandard of 8 percent by_2013) VOLUME 49 NUMBER mant commerce clause?) to strike down state legislation that it has determined might hinder or prohibit interstate trade. In 1986, the Court de?ned this to mean that a state cannot ?needlessly obstruct interstate trade or attempt to ?place itself in a position of economic The smooth functioning of the national market requires the federal government to prevent states from adopting protec- tionist or autarkic policies that would attribute a product?s market share to its geographic origins rather than to market mechanisms. Two potential con?icts exist between state RPS policies and the dormant corn- merce clause: geographic restrictions on eligible renewable resources and the dif- ferent ways states assign value to RECs. Illinois, Nevada, New Jersey, and Texas have all adopted restrictions that only count in-state renewable resources toward their respective RPS mandates. Some states that have implemented their own RPS mandates have adopted policies that devalue RECs from other states. Califor- nia?s RPS, for example, requires RECs to be bundled (thus disallowing unbundled RECs from other states). While no one has yet challenged the legality of these restrictions, several legal precedents sug- gest that a legal case against these restric- tions could prevail.? Taken together, state action on RPS is insuf?cient in significantly promot- ing national renewable energy capacity. Despite the progress made by state RPS, the deployment of renewable resources has stayed relatively the same. Almost 10 years ago, renewable energy technolo- gies constituted approximately 2 percent of the country?s electricity supply (When excluding large hydroelectric facilities).26 In 2006, the US. Energy Information Administration (EIA) estimated that non- hydroelectric renewables still provided about 2 percent of America's electric- ity supply. Even when all state RPS are included in projections, EIA esti- mates that the contribution of renewable JULWAUGUST 2007 resources is unlikely to exceed 3 percent of total electricity supply by 2017 or 4 percent by 2030.37 Why State-Based Action on Climate Change Is Not Enough Local and regional e??orts to combat climate change suffer from analogous dif?culties relating to design, complexity, and suf?ciency. Like RPS programs, state climate change policies lack consistency and harmony. Most attempt to promote research, ensure economic stability, and encourage F'gure Regional greenhouse gas Initiatives in the United States (as of March 2007) ?re?m. Western Regional Climate Action Initiative . i .. .i u. ?v the Plains public-private cooperation. However, they tend to place very little emphasis on mandatory standards and fail to create predictable regulatory environments. In other words, state policies ?provide lots of carrots but without any sticks.?28 Having a multitude of state greenhouse gas policies is also more costly than a single federal standard because it creates complexity for investors. State-by-state standards signi?cantly increase costs for those attempting to conduct business in multi-state jurisdictions.29 Statewide pro- grams also require separate inventory, monitoring, and implementation mecha- nisms to check progress against goals and provide feedback, adding to their costs?? .3, .. r- .. NEG-ECP I. NOTE: WGA is the Western Governor's Association Clean and Diversified Energy initiative, NEG- ECP is the New England Governor's Climate Change Action Plan, arid Is the Regional Greenhouse Gas Initiative. SOURCE: Pew Center on. Global Climate Change. State Action Maps, http: pewolimate. org/what_ b_eing_ done/in _the Hstatesfstate action _.maps cfm. I ENVIRONMENT 25 In addition, state programs provide incen- tives for local and regional actors to duplicate their research and development efforts on carbon-saving building tech- nologies and energy systems, compromis- ing a degree of efficiency." In- addition, as mentioned above, state? by-state action on climate change is prone to what is known as the ?free rider" phe? nomenon. For example, utilities operating - in a region that includes those states with mandatory emissions regulations and those without has an extra incentive to build new power plants only in those without. PacifiCorp, a utility serving customers in the Paci?c Northwest, has repeatedly attempted to build coal-?red power plants in Wyoming and Utah?state5 without mandatory greenhouse gas reduction tar- gets?but not in Oregon (which has man- dated a stabilization of greenhouse gas emissions by 2010) or Washington (which has mandated 1990 levels by 2020).32 The state-by-state patchwork of climate change policies, in other words,_allows stakeholders to manipulate the existing market to their advantage. Localized climate action also sends dis- torted price signals. By lowering demand for carbon-intense products, state stan- dards reduce the regional (and even glob- al) price for carbon-intense fuels. But in doing so, they provide further incentives for nearby states without climate regula- tion to do nothing because of lowered prices.33 Put another way, states acting on climate change depress the cost of fossil fuels and other carbon-intense commodi- ties by lowering demand for them and thus their price. Yet reduced prices encourage overconsumption in areas without carbon caps, decrease the incentive to enact ener- gy efficiency and conservation measures, and discourage the adoption of alter- native fuels for vehicles and renewable energy technologies. Finally, even the most aggressive cli- mate stalutes (aimed at cutting emissions by 2010) will make only a negligible contribution to offsetting greenhouse 26 ENVIRONMENT gas emissions. With the exception of New York and New Jersey (which rank ninth and seventeenth among states in greenhouse'gas emissions), the rest of all of the states with mandatory 2010 greenhouse gas reduction targets all rank relatively low in terms of their emissions. According to HA, by 2030, total energy- related carbon dioxide emissions will equal approximately 8.1 billion metric tons (equating to a 62 percent increase from 1990 levels with an average increase of 1.2 percent per year). Yet those states that have committed to achieving time- bounded, quantitative reduction targets for greenhouse gas emissions accounted for only around 20 percent of nationwide emissions in 2001.34 Even if all states with mandatory 2010 climate plans attained their targets, their policies would result in a reduction of approximately just 460 million metric tons of carbon dioxide by 2020?3 6.38 percent reduction compared to ElA?s ref- erence case. The other 36 states do not just offset these gains; the overall growth rate still increases at 1.06 percent every year. As a result, according to EIA, state- by-state reductions ?are nowhere near the magnitude of reductions needed to bring the U.S. into compliance with the Kyoto Protocol?s call for reductions of 5 percent below 1990 levels from 2008 to 2012??much less the reductions needed to avert dangerous interfer? ence with the climate system."35 The Right Kind of Federal Preemption For all of the reasons just cited; a strong case can be made for federal governance to preempt state initiatives that have pro- liferated on the RPS and climate change fronts. The concern, however, is that through the process of reaching federal consensus, some of the most aggressive and meaningful state programs will be preempted, leaving a watered-down, low- est?common denominator national stan- dard in their place. Such a concern is not merely academic. University of Arizona law professor Kirsten Engel has noted that in the 19.705, federal preemption was prompted by the desire to impose stronger federal programs than states themselves would impose. The 19905, however, saw a turnaround in which industry interest groups are advocating federal preemption to eliminate aggressive state standardsr?6 At least three of these efforts have surfaced in Congress during the past three years. In 2004, a proposal was advanced that would have overridden the states' ability to set more stringent zoning authority for the permitting of oil re?ner- ies and utilities. Another bill would have waived all forms of liability for industries involved in the production and sale of antifreeze coolants containing benzoate. And an amendment to a 2005 apprOpria- tions bill prohibited states from attempt- ing to duplicate Califomia?s efforts to cre- ate more protective automobile emissions standards.37 Thankfully, each of these efforts failed, but there has been talk that a federal RPS might include nuclear power and clean coal as ?renewable" options, a prospect that not only goes against com- VOLUME 49 NUMBER may: Aha??- my Manama-nM?um mon sense but strains credulity as well. The answer to this conundrum is to speci?cally allow for a multi?jurisdictional system of authority over RPS and climate change. University of Michigan profes- sor of public policy Barry Rabe and his colleagues have noted that the decision to pursue action at the federal or state level need not be perceived as an either/or prop- osition.38 In otiIer words, jurisdictional overlap is not only possible, but may even be preferable. This could be' accomplished by estab- lishing a federal "floor" without a ?ceil~ ing"; that is, a Irule that would impose requirements on ,each and every state but that would still allow states to exceed the federal minimum standards imposed. A federal RPS ?oor, for example, might be a requirement for retail electricity pro- viders to meet a 15 percent renewable target by 2020 or 2025. States, however, could be permitted to raise the require- ment to 20?25 percent within their own Table 1: Taxonomy of regional greenhouse gas initiatives in the United States (as of March 2007) . Regional effort Description of activities Participating states Year New England Attempts to achieve 1990 greenhouse gas Connecticut, Maine, Massachusetts, 2001 Governors' Climate emission levels by 2010 and 10 percent New Hampshire, Rhode Island' and Vermont Change Action Plan below 1990 levels by 2020 I (NEG-ECP) . Regional Greenhouse Phase I (2009?2015) will stabilize emis? Connecticut, Delaware, Maine, 2003 Gas Initiative (RGGI) sions at 121.3 million short tons of 002; Massachusetts (2007), Maryland (2007), Phase II (2015?2020) will reduce New Hampshire, New Jersey, New York, emissions by 10 percent below Phase I Rhode island (2007), and Vermont levels (roughly equivalent to 1990 levels) . . Powering the'Plains Brings together stakeholders to address Iowal MInnesota. North Dakota, 2003 Initiative climate issues surrounding energy :and South Dakota, and Wisconsin agriculture and reducing the risk of climate change I Western Governors' Participating states agreed to examline the Alaska, Arizona, California, Colorado, 2004 Association (WGA) feasibility of developing 30,000 megawatts HawaiiI Idaho, Kansas, Montana, Nebraska, Clean and Diversified of clean energy by 2015 and Increase Nevada, New Mexico, North Dakota, Energy Initiative energy ef?ciency 20 percent by 2020 Oregon, South Dakota, Texas, Utah' Washington, and Wyoming Western Regional Will set joint regional emissions target Arizona, California, New Mexico, Oregon. 2007 Climate Action and establish a cap-and-trade program for and Washington Initiative greenhouse gases by August 2008': NOTE: This table excludes the Midwest Greenhouse Gas R?gistry (Illinois, Indiana' Michigan, Minnesota' Ohio. and Wiscon- sin), which is still being formulated, and the Eastern Climate IRegistry, a mechanism for Northeastern and Mid-Atlantic states to report their emissions data. In addition to the states. a growing number of major companies have also taken action to set their own greenhouse gas reduction targets, improve energy efficiency, and participate in emissions trading For a summary of these actions, see Pew Center on Global Climate Change, ClImate Change ActI'th'es In the United States. 2004 ton, DC: Pew Center on Global Climate Change, 2004), 21? .50. Currently more than 650 local and city governments (such as Philadelphia, and Portland, Oregon) have implemented policies to achieve reductions In greenhouse gas emis- sions. For an excellent summary of these policies, see C. Carlarne, ?Climate Change Policies an Ocean Apart: EU US Cli- mate Change Policies Compared,? Penn State Enwronmentai Law Rewew 14, no. 3 (2006), 435- 82. SOURCE: Modified from Pew Center on Global Climate Change, State Action Maps, and US. Environmental Protection Agency, State and Regional Climate Actions Table, 2007 ENVIRONMENT 27 jurisdictions should they wish to do so. The federal floor might also consist of a standard set of renewables for inclusion. Once the minimum federal requirements are met through these renewables, states could add their own prefer- ences to meet state-based goals, whether they want to provide special incen- tives to promote solar pho- atovoltaics in the Southeast, small-scale hydroelectric in the Paci?c Northwest, or offshore wind along the East Coast. Similarly, greenhouse gas emission reduction targets could consist of a federal minimum as well as an additional state target. It may be that a federal ?oor will only set reduction targets out to .233 2020, while some states will want to go on record 3; - I as requiring emission cuts of at least 60 percent by 2050. A multiijurisdiction- al framework can accom- modate these differing goals and time frames, and it harkens back to a time in the 19605 and 19703 5:1: when federal preemption meant m?lm-Ting all states M. to meet a minimum level of requirements, rather than a more recent preoc- cupation with eliminating all the state regulations that overlap. The 1967 amendments to the Clean Air Act of 1963 is an example as it allowed California to establish vehicle air pollu- tion emission standards that were more stringent than those developed by the U.S. Environmental Protection Agency (EPA). In the Clean Air Act Amendments of 1977. all other states were given the opportunity to adopt California's stan- dards in the future or remain subject to the 28 ENVIRONMENT EPA standards. California has requested and been granted more than 40 excep- tions to EPA emission standards, and the system has not been overly burdensome to automakers}9 i 3'3: i? eases In areas outside of environmental regu- lation, the federal govemment has a long history of promoting minimum national standards that the states can exceed. The Fair Labor Standards Act, for instance, establishes a national minimum wage of $5.15 per hour and preempts Kansas?s rniserly rate of $2.65 but is surpassed by 38 other states that have set their own laws higher than the federal statute?with Connecticut offering $7.65 and Oregon $7.80.40 Other federal ?floors," ?savings clauses," and ?safety valves? have been established in the areas of health care insurance, civil rights, drug safety, and the sentencing of hate crimes.? Federal environmental law generally allows states to enact standards stricter than federal laws as re?ected in the Clean Water Act, .5, and more recently in the Toxic Substances Control Act, Resource Conserva- tion and Recovery Act, Federal Insecticide Fungi- cide and Rodenticide Act, and in the area of brown- ?elds regulation.?2 Such ?exibility in terms of a federal RPS or climate change statute would ensure that the states can continue to innovate while also mandating that all states move forward in promoting renewable energy and addressing climate change. Conclusion The RPS and green- house gas caps are excel? lent policy mechanisms: unlike other policy incen- tives such as tax credits and subsidies, these tools minimize government intervention and rely on the ef?ciency of the market?instead of continual monetary disbursements or political salience?to dictate how utilities, industries, and con- sumers promote renewable energy and ?ght climate change.? They also have the tendency to be self-expiring (or ?self- sunsetting?). When utilizing RECs and tradable permits, for example, the value of such commodities will automatically reach zero once the RPS and greenhouse gas target levels have been met. VOLUME 49 NUMBER 6 Ha -r-Aom? - The impressive growth in state-based RPS and climate change initiatives utiliz- ing these policy mechanisms is testimony, most of all, to woeful inaction at the federal level. Perhaps new Democratic control of Congress will overcome objec- tives at the federal level, but that remains to be seen.? A mold-jurisdictional approach to these issues would create a national system for the ?rst time requiring all states to par- ticipate in a harmonized system that would include the trading of RECS and nationally certi?ed carbon offsets. A consensus-based federal system would produce a meaning- ful and achievable regime eliminating the ?free rider? phenomenon that now exists. Under a mold?jurisdictional framework, however, states wanting to do more than what the federal program entails would be permitted to do so. Federal preemp- tion would not be permitted to snuff out these ?laboratories of democracy? that wish to go forward with bold. aggressive, and experimental programs. If these state programs are successful over time, one would expect to see their results gradually incorporated into the federal program. Ultimately, however, state experience will yield profuse results only if it inspires a national standard that motivates the country to truly promote renewable ener- gy and ?ght climate change. Benjamin K. Sovacool currently teaches in the Govem- ment and International Affairs Program at the Virginia Polytechnic Institute and State University in Blacksburg, Virginia He is a former Eugene P. Wigner Fellow at the Oalr Ridge National Laboratory in Oak Ridge. Ten- nessee. and a senior research fellow at the Network for New Energy Choices in New York. Sovaeool recently completed work on a grant from the National Science Foundation's Electric Power Networks El?ciency and Security Program investigating the social impediments to distributed and renewable energy systems. He also served as a senior research fellow for the Virginia Cen- ter for Coal and Energy Research, Where he assessed renewable energy issues for the state of Virginia. He may be contacted at sovacool?vt.edu. Jack N. Barkenbus is a senior research associate at the Vanderbilt Center for Environmental Management Studies in Nashville. He was formerly the executive director of the Energy. Environment and Resources Center at the University of Tennessee. Knoxville. has published widely in the areas of energy and environmental policy. as well as national defense, and is currently engaged in studies of sustainability and climate change. He may be contacted at jack.harkenbus@vanderbi lt.cdu. 2007 NOTES I I l. G. Parker, "Blair Backs EU Renewable Energy Targets." Financial Times. 28 February 2007. 3; also available at 2. REN21,Renewables Global Status Report: 2006 Update (Paris and Washington. DC: Secretariat and Worldwatch lnstitutis. 2006). 3. J. H. Adler. ?When [s ?No a Crowd? The Impact of Federal Action on Slate Environmental Regulation,? The Harvard Envimnrirentol law Review 31. no. 1 67?114. 4. K. H. Engel.? ?Harriessing the Bene?ts of Dynamic Federalism' in Environmental Law," Emory Law Journal 56, no. I (2006): 179. 5. l. H. Adler. ?Jurisdictional Mismatch in Environ- mental Federalism." New: York autumn? Environmental Law Journal 14, no. 1 (2005): 130-45. 6. lbid, page 167. 7. J. Adler. ?bet Fifty Flowers Bloom: Trans- forming the States into Laboratories of Environmental Policy," The Eederulisni Projecv?rlnrericott Enterprise institute. January 2002,- available at abstract=295424. 8. Engel, note 4 abovie. page 160. For more on what states are doing in terms of human rights and interna- tional treaties. see 8. L. Leaner. "Diffusion of Local Regulatory lnnovations:lThe San Francisco CEDAW Ordinance and the New York City Human Rights Initia- live." Columbia Law Review I04. no. 3 (2004): 763?70; G. Burroughs. ?Implementation of Human Rights by State and Local Governments.? New York University Reticw of law and Social Change 30. no 3 (2006): 4 1-22. For what states are doing in terms of health. see M. J. Horvick.? Examining the Underlying Purposes of Municipal and Statewide Smoking Bans." lttdirrno Law Journal 80, no. 3 (2005): 923?50; and B. Courtney. ?ls Obesity Really the Next Tobacco? Lessons Learned from Tobacco for Obesity Litigation.? Annals of Health Law 15, no. 1 (2006): 61?67. 9. For example, hidden costs (often referred to as ?negative externalities?), such as the need to secure for- eign imports of fuel. environmental damage from air and water emissions, medical expenses associated with air pollution and transportation accidents. and catastrophic global climate change. are not typically re?ected in the rates we pay for electricity. A majority of the federal budget for energy research and development over the past 50 years has also gone to conventional fossil fuel and nuclear industries and not toward renewable energy technologies. From 1948 to 1998, for instance. roughly 80 percent of U. S. Department of Energy appropriations for research and development have gone to nuclear and fossil fuel technologies. And since everyone bene?ts from the environmental advantages of renewable energy. private companies that invest millions of dollars in researching and developing clean energy technologies are often unable to recover the full pro?t of their invest- ments. lnevitably. the market allows some consumers to be?frce riders." bene?ting from the investments of others without paying for them. For more. see N. Nayak, Redi- recting America?s Energy: The Economic and Consumer Bene?ts of Clean Energy Policies (Washington. DC: Public Interest Research Group, 2005) 11: C. Levesque. "What Is the Percentage of Federal Subsidies Allottecl for Wind Power?? Renewable Energy Access. 10 April 200?, http: renewableenergyaccess. comlrealnewsl story?id=480?0; and B. Sovacool and C. Cooper, ?Big ls Beautiful: The Case for Federal Leadership on a National Portfolio Standard." Electricity Journal 20. no. 4 (May 2007): 48?61. 10. Engel. note 4 above, page 160. 11. K. H. Engel and S. R. Salcska, ?Subglobal Regu- lation of the Global Commons: The Case of Climate Change." Ecology Low Quarterly. 32. no. 2 (2005): 183?233. 12. Sovacool and Cooper. note 9 ab0ve. l3. Pew Center on Global Climate Change. Cli- mate Change Activities in the United States: 2001! Update (Washington. DC: Pew Center on Global Climate Change. 2004). 4. 14. Justice Brandeis stated. ?it is one of the happy incidents of the federal system that a single courageous State may. if its citizens choose. serve as a laboratory: and try novel social and economic experiments without risk to the rest of the country." (Dissenting opinion in New Store Ice Co. v. Uebntann. 235 US. 262. 52 S. CL 311. 76 747 (1932).) 15. For excellent summaries of these advantage: see T. D. Peterson and A. 2.. Rose, ?Reducing Con?icts Between Climate Policy and Energy Policy in the U.S.: The Important Role of the States.? Energy Policy?34. no. 5 (2006): 619?31: and K. Doran. "Can the US. Achieve a Sustainable Energy Economy from the Bot- tom- U?p? An Assessment of State Sustainable Energy Initiatives." Ivicar-intent Journal of Envimhtnentul Law 7. no.1 l6. In 1985. Iowa passed legislation to ?encourage the development of alternate energy production facilities and small hydro facilities In order to copserve our finite and expensive energy resources and to provide for their most cost effective use. 'The lavtr mandated that utilities enter into power purchase agreements with renewable energy producers and set the upper limit on aggregate purchases of renewable energy at l05 megawatts MW) In l994. Minnesota passed similar legislation. The ?rst state to actually use the RPS. however. was Cali- fornia, in legislation proposer] (hut ullimately defeated) in 1995. See J. W. Mueller. ?01' Credits and Quotas: ENVIRONMENT 29 Federal Tax Incentives for Renewable Resources. State Renewable Portfolio Standards. and the Evolution of Proposals for a Federal Renewable Portfolio Standard." Fordltatn Environmental law .loumal IS. no. I (2004): 91; and V. Lauber. and RPS: Options for a Hat- monised Community Framework.? Energy Policy 32. no. 12(2004}: 1405?14. . 17. This does not include Illinois. which set a volun- tary standard of 8 percent by 2013. or Vermont. which mandates that all load growth must be satis?ed by renew- able energy. Also excluded is New Hampshire. which passed an RPS on 26 April 2007. and Oregon. where a bill requiring 25 percent renewables by 2025 had passed both houses of the legislature as of the end of May 2007. Neither of these two bills had been signed into law at the time this article went to press. 18. See J. J. Fialka. ?States Power Renewable-Ener- gy Push." Wall Street Journal. 14 June 2006; T. Pctersik. State Renewable Ener Requirements and Goals: Sta- tus Through 2003 (Washington. DC: U.S. Department of Energy. 2004}. available at and US. Govemment ?Accountability Of?ce (GAO). Department of Energy: Key Challenges Remain for Developing and Deploying Advanced Energy Technologies to Meet Future Needs. GAO-07- 06 (Washington. DC. 2006). 61?62. 19. For an excellent overview of state renewable portfolio standards (RPS) programs. see Ftalka. ibid.: Petersilt. ibid.; B. G. Rabc. Race to the Top: The Expand- ing Role of U.S. State Renewable Portfolio Standards (Arlington. VA: Pew Center on Global Climate Change. 2006): National Renewable Energy Laboratory. Power Tedtnologies Energy Data Book. NREUTP-620-39728 (Golden. CO. 2006). available at analysislpower_databookl. 94-96; and R. ??ser. C. Narnovicz. M. Gieleeld. and R. Smith. ?The Experi- ence With Renewable Portfolio Standards in the United States." Electricity Journal 20. no. 4 (May 2007): 8~20. 20. See Massachusetts Division of Energy Resourc- es. Renewable Portfolio Standard: PolicyI Analysis. 16 December 2005. available at US. Department of Energy. "State Renewable Portfolio Standards and Purchase Requirements." Transportation Handbook. updated 2006. available at and National Renewable Energy Laboratory. Pau-?er Technologies Energy Data Book. 2006. available at 21. C. Flavin. J. L. Sawin. Podesla. A. U. Cohen. and B. Hendricks. American Energy: The Renewable Path to Energy Security (Washington. DC: Worldwatch lnsritute the Center [or American Progress. September 2006); and N. Rader and S. Hempling. Tire Renewable: Portfolio Standard: A Practical Guide (Washington. DC: National Association of Regulatory Utility Commission- ers, 2001). 22. D. A. Fine and D. N. Wang. "Private Equity and the Repeal of Electric light Power. November 2005. available at 23. Monte v. Taylor. 477 U.S. l31 {1986). 24. S. Hempling and N. Rader. State Implementation ofRenewables Portfolio Standards: A Review ofFedeml Law issues (Washington. DC: American Wind Energy Association. 1996). 6. 25. See K. H. Engel. ?The Dormant Commerce Clause Threat to Market-Based Environmental Regula- tion: The Case of Electricity Deregulation." Ecology Law Quarterly 26. no. 2 (1999): 243-449; and S. Fern rey. ?Renewable Orphans: Adopting Legal Renewable Standards at the State Level." Electricity Journal 19. no. 2 (2006): 52-61. . 26. N. A. Rader and W. P. Short ?Competitive Retail Markets: Tenuous Ground for Renewable Energy.? Electricity Journal 11. no. 3 (1998): 72. 27. US. Energy information Administration (EIA). Annual Energy Outlook 2006: Mt}: Projections to 2030 (Washington. DC: US. Department of Energy. 2006). 81. - 28. C. Carlarne. ?Climate Change Policies an Ocean Apart: EU US Climate Change Policies Compared." Penn State Environmental Law Review 14. no. 3 (2006): 472. 29. Duran. note 15 above. 30. T. D. Petersen. "The Evolution of State Climate Change Policy in the United States: Lessons Learned and New Directions." Widenerlaw Journal 14. no. 1 (2004): Environment. is now available online! 81?116. 31. Peterson and Rose. note 15 above. page 620. 32. "Doubts Cloud Coal~Plant Plan." Deseret News. 7 February 200?. 33. R. N. Stavins. ?Policy Instruments for Climate Change: How Can- National Governments Address at Global Problem?" The University of Chicago legal Forum ?997}: 293?323. 34. EIA. note 27 above. 35. EIA. note above. 36. Engel. note 4 above. page 185. 37. Engel. note 4 above. page 185. 38. B. G. Rabe. M. Roman. and A. G. Dobelis. "State Competition as a Source Driving Climate Change Mitigation." New York University Environmental Law Journal 14. no. 1 (2005): 45. 39. Engel. note 4 above. page 18?. 40. US. Department of labor. ?Minimum Wage Laws in the January 200?. available at .govlesa/minwage/arnericahon. 41. See W. W. Buzbee. ?Asymmetrical Regulation: Risk. Preemption. and the Floorl?Ceiling Distinction.? Emory University School aflaw Research Paper Series No. 07-10. available at http:llpapers.ssm.comisol3/ and A. Baker and E. A. Young. ?Federalism and the Double Standard of Judicial Review." Dulce low Journal 51. no. 1 (2001).: 158. 42. l'bid. 43. M. laccard. "Renewable Portfolio Standard.? in C. Cleveland. ed.. of Energy. Volume 5 (New York: Elsevier. 2004). 413?21. 44. Representative Tom Udall (D-NM) and Senator Jeff Bingaman have introduced RPS legislation in the current Congress. calling for renewable levels of 20 percent and 15 percent respectively by 2020. Five competing climate change bills have been introduced in the Senate. and the House of Representatives also has a number of competing bills and has created a Select Corn- mr'ttee on Energy Independence and Climate Change to inform House committees having oversight of the issue as to available policy options. click: 0%tlpi?heldref. melapre?SS. Com to register 30 ENVIRONMENT Questions? Contact "info@heldref.org' VOLUME 49 NUMBER 6 No Title . Page 1 of3 The Washington Post (pg. 131), November 4, 2007 TARGET IN THE WAR ON CANCER [Rathel's introduction: The war on cancer remains; focused on efforts to develop drugs and technologies that can find and treat the disease --to the tune of more than $100 billion a year in the US. alone. Meanwhile, the struggle basically ignores most of the things known to cause cancer, such 'as tobacco, radiation, sunlight, benzene, asbestos, solvents, and some drugs and hormones.] By Devra Davis [Devra Davis's most recent book is The Secret History of the War on Cancer.] We' ve been fighting the?vvar?on cancer for almost four decades now, since President Richard M. Nixon officially launched it in 1971. It's time to admit that our efforts have often targeted the wrong enemies and used the wrong weapons.? Throughout the, industrial world, the war on cancer remains focused on commercially fueled efforts to develop drugs and technologies that can ?nd and treat-the disease to the tune of more than $100 billion a year- in the United States alone. Meanwhile, the struggle basically ignores most of the things known to cause cancer, such as tobacco, radiation, sunlight, benzene, asbestos, solvents, and some drugs and hormones. Even now, modern cancer-causing agents such as gasoline exhaust, pesticides and other air pollutants are simply deemed the inevitable price of progress. They're not. Scientists understand that most- cancer is not born but made. Although identical twins start life with amazingly similar genetic material, as adults they do not develop the same cancers. As with most of us, where they live and work and the habits that they develop do more to determine their health than their genes do. Americans in their 205 today carry around in their bodies levels of some chemicals that can impair their ability to produce healthy children and increase the chances that those children will develop cancer. Consider the icon of American cancer, the cyclist Lance He's hardly alone as an inspiring younger survivor. Of the 10 million American cancer survivors who are alive five years after their diagnosis, about one in 10 is younger than 40. Could exposure to radiation and obesity- promoting chemicals help explain why, according to a study in the Journal of the National Cancer Institute, the rates of the testicular cancer that developed nearly doubled in most industrialized countries in the past three decades? Should we wait to find out? I'm calling for prudence and prevention, not panic! The Centers for Disease Control and Prevention and the Environmental Working Group have con?rmed that American children are being born with dozens of chemicals in their bodies that did not existjust two decades earlier, including toxic ?ame retardants from fabrics. A new study by Barbara and other scientists at the Public Health Institute in Berkeley, Calif, finds that girls exposed to elevated levels of the pesticide DDT before age. 14 are ?ve times more likely to develop breast cancer when they reach middle age. i Yes, the war has had some important successes: Cancer deaths in the United States are finally dropping, chiefly because of badly belated (and still poorly supported) efforts to curb smoking, reductions in the levels of some pollutants and signi?cant advances in the control of cancers[ of the breast, colon, prostate and cervix. But new cases Of cancer not linked to smoking or aging are on the rise, such as cancer in children and non-Hodgkin in people older than 55. And according to the CDC, cancer is the No. 2 cause of death for children and middle-age? people, second only to accidents. The longer view is troubling: The National Cancer Institute reports that from 1950 to 2001, the number of cancers of the bone marrow, the bladder and the liver doubled. Both public health and social justice demand that we focus more on the things that cause ca'ncer. 11/12/2007 1 No Title . . Page 3 of 3 Swiss and Chinese governments have set official exposure limits for cellphone microwave emissions that are 500 times lower than those the United States mandates. In Bangalore, India, it is illegal to sell a cellphone to a child younger than 16. As a basic precaution, people should use'the phones with earpieces or speakers, and young children should not use them at all -- consistent with warnings recently issued by the German and British governments. Because brain cancer can take 10 years or longer-to develop, nationalstatistics cannot be expected to show the health impact of today's skyrocketing cellphone use. But we shouldn't wait for the. cases to roll in before acting. - True, there are many uncertainties about environmental cancer hazards. But these doubts should not be confused with proof that environmental factors are harmless. The confusion arises for three different reasons. First, studying the ways that our surroundings affect our cancers is genuinely hard. Second, public and private funding levels for research and control of environmental cancer are scandalously low. Finally, those who profit from the continued use of some risky technologies have devised wellv?nanced efforts to sow doubt about many modern hazards, taking their cue from the machinations of the tobacco industry. The best crafted public relations campaigns masquerade as independent scienti?c information from unimpeachable authorities. No matter how much our efforts to treat cancer may advance, the best way to. reduce cancer?s toll is to keep people from getting it. We need to join the rest of the industrialized world by issuing a national ban on asbestos and forbidding smoking in the workplace and other public spaces. We mustreduce the hazards faced by those working to build our homes, transport our goods and make the products .we consume. We should restrict CT scans of children to medical emergencies, limit the use of diagnostic radiation in general, ban young children from using cellphones and keep. the rest of us from using tanning beds. And we must recognize that pollutants do not need passports. Controlling cancer, like controlling global warming, can take place only on an international scale. We can and must -- do better. - Devra Davis, a professor at the University of Pittsburgh's Graduate School of Public Health, directs the Center for Environmental Oncology. Her most recent book is "The Secret History of the War on Cancer.? - 104.htm 1 1/12/2007 No Title . Page 2 or 5 For example, blacks and other minorities still die of many forms of cancer more often than do whites. Could this be tied to the fact that so many African Americans hold blue- collar jobs, which may bring them into contact with carcinogens? Or because poor blacks are more likely to live in polluted neighborhoods, or eat diets higher In cancer-causing fats? We can't say, and we're not even trying to find out. The vast cancer??ghting enterprise has decidedly different priorities. Even our triumphs in battling Cancer can leave us with tragic shortcomings. Consider one irony of oncology: Many of the agents that can so effectively rout cancer early in life, such as chemotherapy and radiation, can also increase the risks of falling prey to-other forms of the disease later on. According to a study in the Journal of the Royal Society of Medicine, one out of every three girls treated with radiation before age 16 to arrest Hodgkin's disease -- a cancer of the system that often occurs in young people will develop breast cancer by age 40. Of course, many cancers in children and young adults might have been avoided in the first place without earlier exposure to cancer-causing agentsE . We also need to weigh the downsides of the way we use radiation today to find problems in the healthy public, especially the young. A consensus statement from the American College of Radiology notes that "the current annual collective dose estimate from medical exposure in the United States has been calculated as roughly equivalent to the total worldwide collective dose generated by the nuclear catastrophe at Chernobyl. Most parents (and many emergency? medicine physicians) don't know that a single CT scan of a child' 5 head can deliver the same radioactive doseEas that in 200 to 6, 000 chest X- -.rays Some pediatric experts recommend that CT scans of children be restricted to medical emergencies and kept at doses as low as reasonably possible. Even Eso, according to the American College of Radiology, the use of CT scans has jumped tenfold in the past decade -- a change that stems from the pro?tability and growth of "defensive medicine, and one that has not resulted in any improvement in our overall health that I can discern. The Food and Drug Administration, the Consumer Product Safety Commission and the Environmental Protection Agency often lack the authority and resources to monitor and control tobacco smoke, asbestos, tanning salons and the cancer-causing agents in food, water and the everyday products we use on our bodies and in our homes. Under antiquated laws, chemical and radiation hazards are examined one at a time, if at all. Of- the nearly 80,000 chemicals regularly bought and sold today, according to the National Academy of Sciences, fewer than 10 percent have been tested for their capacity to cause cancer or do other damage. As a result of these policy failures, the United States often stands alone and not in a good way. Unlike Italy, Ireland, France, Albania, Argentina, Uruguay and many other coUntries, the United States has failed to ban smoking in public spaces nationwide. Unlike European children, American kids are exposed to small levels of known carcinogens in their food, air, shampoos, bubble baths and skin creams such as the clear, colorless liquid known as 4-dioxane," a common contaminant that causes cancer in animals and has been banned from cosmetics by the European Union. In fact, our growing dependence on many unstudied modern conveniences makes us the subjects of vast, uncontrolled experiments to which none of us ever consents. Consider cellphones, whose long- -term health consequences could prove disastrous. Experimental ?ndings show that cellphone radiation damages living cells and can penetrate the skull. Widely publicized research on cellphone use in the early 19905 indicates that the phones are safe, but those studies did not include any children and excluded all business users. While exposure levels are much lower on newer phones, the effects of gadgets that have increasingly become part of our children's lives remain unstudied. That's unwise. Recent reports from Sweden and France, published in the journal Occupational and Environmental Medicine, reveal that adults who have used cellphones for 10 years or more have twice as much brain cancer on the side of their heads most frequently exposed to the phone. The 104.htm . 1 1/ 1 2/2007 AlterNet: Lobby to Hide Cancer Dangers Has Government's Hand Page 1 or .1 Alteriiat . .. The HT: is the gimme-1 Lobby to Hide Cancer Dangers I-Ias Government's Helping Hand By Michelle Chen, In These Times Posted on November 19, 2007, Printed on November 19, 2007 http: 11 Industry special interests are burying information on cancer-causing chemicals and, according to watchdog groups, the government is helping them do it in the name of "data quality." . In a study of the National Institutes of Health's National Toxicology Program, 0MB Watch, a DC?based policy-research group,ireports that industry is frustrating the {work of government researchers with petitions that are light on science but heavy with accusations of anti-business "bias." 1 Public interest advocates warn that corporations are co- opting the federal Data Quality Act to paralyze scientists with frivolous allegations of maccuracy, driving a stealth assault on public?health research In 2000, Congress passed the Data Quality Act under the guidance of Jim Tozzi, a former administrator with the Of?ce of Management and Budget under Reagan who now heads the industry-backed Center for Regulatory Effectiveness (CRE). The two-paragraph statute broadlyimandates that agencies uphold "the quality, objectivity, utility and integrity of information" they disseminate. That's a laudable principle, critics say, but the corporate?friendly Bush administration is promoting exploitation of the law. "It's provided a mechanism for industry associations to take another bite of the apple, says OMB Watch analyst Clay Noithouse, "to raise another challenge against a regulation coming into effect and affecting their business practices." In ?scal years 2003 and 2004, the Environinental Protection Agency (EPA), Health and Human Services and other federal bodies ?elded 80 "substantive" Data Quality Act requests for corrections, more than half of which came from industry, according to the Government Accountability Of?ce. The resulting bureaucratic review process could take as long as two years. 1 1 0MB Watch focused on the National Toxicology Program' 5 biennial "Report on I Carcinogens, which describes 1, 700 substances linked to genetic mutations or cancer. Rigorously reviewed by toxicology experts, the research IS used by health professionals, community groups and environmental regulators. The upcoming edition has been delayed by more than a year while Health and Human Services . mulls 10 data-quality complaints from industIies. . .. 11/19/2007 AlterNet::Lobby to Hide Cance'r Dangers Has Government's Helping Hand 1? - Page 3 of 3 Michelle Chen has written for the South China Moming Post, Glamor, 1N COM and her own zine, cain. @2007 Independent Media Institute. All rights reserved. View this story online at11/19/2007 AlterNet: Lobby to Hide Cancer Dangers Has Government?s Helping Hand Page 2 of 3 i "In 2004, To'zzi's CRE ?led petitions seeki . formal review of the toxicology program's research and peer-review procedures Speci?cally those concerning a widely used pesticide called Atrazine. Joining CRE were the Kansas Com Growers Association and other trade groups. The Natural Resources Defense Council, an environmental action group, has pushed the EPA (with little success) to more regulate Atrazine. The organization says the complaints are not about ensuring: the quality of information but about blocking 1t from public view. "The petition was aimed at preventing Atrazine from getting listed in the 'Report on Carcinogens' by preventing the entire report from getting issued, says Jen Sass, a senior scientist with the Natural Resources Defense Council. Tozzi, whose group openly receives funding from industry co-petitioners, acknowledges the stake in challenging government research. Because the data is used to create costly regulations, he contends, "of course the is used by industry, because industry pays the bill.?l I The American Chemistry Council, a trade association representing chemical manufacturers, tried to capitalize on the Data Quality Act in 2004 by protesting that a document used by the National Toxicology Program's scienti?c reviewers "wrongly characterize[d] the canoer potentia of the industrial chemical naphthalene. This could lead to "product liability claims, diminished sales.. and related commercial damage," the association claimed. After a year and a half of review, Health and Human Services denied the petition. OMB Watch says that because there are other, more-reasonable safeguards for vetting information, like public comments,: the government should place limits on data-quality petitions so that corporations have one less avenue to in?uence policies and science that protect the public. Yet some watchdogs have wielded the Data Quality Act to beat industry at it's own game. In 2004, Public Employees for Environmental Responsibility (PEER), a nonprofit group, success?slly used the Act to challenge invalid scienti?c analyses that enabled the U. S. Fish and Wildlife Service to in?ate population assessments of endangered Florida Panthers. Public interest groups, says PEER Executixie Director Jeff Ruch, have "far more opportunities to expose industry manipulation of the science in the regulatory agencies than the industry has to expose anti-industry bias." Nonetheless, 'Rena Steinzor, an environmental law expert with the Center for Progressive Reform, says that even if some' challenges are legitimate, the Data Quality Act ultimately bleeds an already embattled regulatory system. just think it's counterproductive," says Steinzor. "These health and safety agencies which have suffered a lot already from attacks from the Bush administration don't need to be any more demoralized and harassed." 64 1 1/11 9/2007 Department of the Planet Earth 701 Street, SE - Suite 200, Washington, DC 20003 (301) 475-8366 - planetbarth @erols.com; June 2, 2007 Dear Board Members, Had an interesting trip to Oberlin College, where I gave a 20 minute presentation on global warming. Because of the Oberlin Environmental Alumni work and enthusiastic student efforts, Oberlin has decided to become a carbon dioxide neutral campus. The College of the Atlantic and two junior colleges from southern California have also moved in this direction. Jay is holding the Beyond Pesticides annual conference in Chicago, with a featured Rodale speaker talking about how organic farming can store carbon in the soil. This conclusion is based upon the analysis of many years of records from the experimental farm in Kutztown, It is likely that the no-till farming methods don?t perform very well in this regard, as the carbon is at the surface of the soil where it can be oxidized. Elizabeth has recently been written up in the Economist about her smart deal with the Liberal Party in trying to win a seat for the Green Party. (See attached.) 1. ticall difi ani I called RObin Pam of Rep. Henry -Waxman?s staff concerning a possible investigation of the disasterous programs of USDA and other agencies in regulating the safety of GMO. She agreed that the program was a mess, but thought that Waxman?s House committee, Oversight and Government Reform, is not the proper investigating agency, since they are more interested in FDA. Enclosed is Joe?s comments on the GM Eucalyptus environmental assessment done by USDA, which is incompetent and illegal as usual. The Bush administration has now issues a series of rules on federal regulation which makes regulation on any subject impossible unless a company is making a campaign contribution. (See article.) As a result, getting anything done before the election is unlikely unless we are willing to come forward with substantial campaign money. What I would propose is an educational package to each member of Congress on the issue of GMO, perhaps featuring three different problems and the need for 9 liar deal Mr Dion made with Elizabeth 1 .iorlcu i president. Hugo Chavez. however. Mr Jrrea has not hesitated to make moves .nat could discomfort his oil-laden neigh- bour. Earlier this month, he signed a deal with Brazil to co-operate in the production of ethanol. Meanwhile, Petroecuador. the Ecuadorian state oil company. has signed a memorandum of understanding with Petrobras. Brazil's state oil company. to ex- ploit in. an oil?eld representing around a quarter of Ecuador?s tot? But more than his pi other populist policies. strength of the preside: that is giving cause for a. ousting. with his blessin members of Congress.f the president in at the referendum, is part: Though the congressmi by alternates they themselves had picked. the new deputies have shown themselves loyal to Mr Correa rather than to their own political parties. This can be explained in part by the president's undeniable charisma. In the town of Pingue. shortly before reaching Bafios. Mr Correa attended a gathering of refugees made homeless by the eruption of the Thngurahua volcano a year ago. A build of a rugby player. on the ground to watch Jerform a play. He then :le girl in his arms and r. She looked delighted. Bar'ios. he announced. to ise. the end of the coun~ night of neoliberalism". ~depending on what ar~ I Canada A Winter of Liberal discontent OTTAWA The Liberals' new leader fails to boost the HEN St?phane Dion won the leader- ship of Canada?s Liberals last De- cember. the party faithful knew he had his faults: a poor command of English. a repu~ tation for being inflexible and no real ap~ petite for the cut and thrust of political bat- tle. But with the opinion polls at that time showing the party within striking distance of Stephen Harper's minority Conserva- tive government. liberals were con?dent that even an imperfect leader could topple the Tories and restore them to their rightful place in charge of Canada. which they had run for more than a dozen years until 2006. Almost ?ve months after choosing their new leader. that con?dence has evap- orated. and many Liberals are questioning whether they picked the right man. The ex. pected boost in voter support has not come about. Indeed. the most recent poll shows that 42% of voters deem Mr Harper the best national leader and a mere 17% back Mr Dion. The Liberals' only consola- tion is that the Conservatives? comfortable lead is not yet big enough to assure them a parliamentary majority in the event of a new election. But that is thin comfort. The unhappiness inside Liberal ranks burst into the open last weekend when a former prime-ministerial spokesman. Ray Heard. told the Toronto Star. Canada?s bestselling newspaper. that he supported a move to dump Mr Dion ?before it?s too late". That outburst was triggered by a pecu- I May. the leader of the Green Party. He promised not to run a Liberal candidate '8 ?agging fortunes gainst her in the Nova Scotia constitu- ency where she would otherwise stand only an outside chance of winning the Greens their ?rst seat. In return. Ms May promised not to run a Green candidate against the Liberal leader in his safe Mon- treal constituency. Mr Dion. a former envi- ronment minister. portrayed the deal as a non-partisan gesture designed to give the increasingly popular green agenda more prominence. But. as bewildered Liberals pointed out. their own party gained noth- ing. and Mr Dion had made it look as though only a fringe party was entitled to care about the environment. The deal was The Economist iapril Zist 2007 all the stranger given Mr Dion?s own repu- tation as an ardent green. albeit in a party that did little for the environment during almost 13 years in power. A few days earlier. the Liberals had lost one of their most glamorous politicians. Belinda Stronach. whose wealth. looks and romances made her the closest thing the party had to a celebrity. declared that she was leaving politics to return to Magna International. a car-parts company con- trolled by her father. Though derided by many as an opportunist~she left the Con- servatives two years ago after unsuccess- fully contesting the party leadership?Ms Stronach attracted attention. money and votes to a party in need of all three. The Liberals' malaise seems to go deeper than one miscalculation by Mr Dion over green politics and the loss of a high-pro?le MP. A ?irther 14 of the 103 Lib- erals who won parliamentary seats in the January 2006 federal election have like- wise decided not to stand again. This comes on top of three defections: two to the Conservatives and a third who has chosen to sit as an independent. A chang- ing of the guard is no bad thing in a pol'tj? cal party. but when quite so many 0* MP5 decide to abandon national polit suggests they do not expect imminent re- election and ajob in government. It is too early to write Mr Dion off. Jean Chr?tien went through a similar rough patch when he became Liberal leader in 1990. but went on to win three successive general elections. starting with the slaugh~ ter of 1993 in which the Conservatives were down to two seats. Mr Dion could still turn opinion by exploiting a reputation for integrity and intelligence. This. however. will take time that he may not have. Mr Harper is eager to convert his minority government into a majority. If his poll numbers edge higher. it will not be long before he calls a new election? whether the Liberals are ready or not. I Exit Stronach. one of many leaving the listing ship comprehensive legislative programs. The idea would be to warm up the issue for progress after the election. So, I will put together a package. 2. Aluminum and Alzheimer?s. I withdrew the proposed article in the Journal of Inorganic Biochemistry for the second time, because one reviewer insisted that proof requires the exposure of human subjects to aluminum and then measuring brain cell death. This idea does not seem lawful, if it was even feasible. Out of the blue came an e-mail from Gjumrakch Aliev proposing that we submit a chapter to their new review book on Alzheimer?s. I sent him an abstract, and this looks like a possible. The other authors are home run hitters in the field. We will see Whether a Masters in City Planning can compete with the A just published study in Neurology, using modern brain imaging equipment (PET and MRI) finds little correlation between brain function and the density of senile plaques in living elderly persons. This corroborates the findings from autopsy studies that senile plaques do not cause Alzheimer?s. The whole thing has been a fraud. I send Robin Pam of Waxman?s staff some information on the FDA petition on aluminum, but I doubt that anything will happen. 3. global Warming. Bad news and good news. A just published report in the Proceedings of the National Academy of Science finds that global C02 emissions have been increasing by a 3.1 percent/ year rate from 2000 to 2004, compared to a 1.1 percent/ year rate in the 1990?s. This means that the 10 year limit proposed by Dr. James Hansen for leveling off C02 to prevent massive ice melt may have to be accomplished in 9 years. Wow. Furthermore, the waters of the Southern Ocean have stopped absorbing CO2 being apparently being saturated. On the good side, the technology - particularly solar - is really moving along. Suntech believes that they can produce solar modules equal in cost to production of electricity by coal in just five years. Their present PV efficiency is about 20 percent Boeing?s subsidiary, Spectrolab, has just produced a ?41 percent? efficient PV cell. Using solar power to heat every residential water heater in North America would be equivalent to reducing the total annual C02 emissions from all the cars and light trucks in North America. That is because electric power generation is only 30 percent efficient - wasting the rest of the fuel up the stack and from the transmission lines. Solar hot water heating is already cost equivalent to electric water heating. Thirty percent of residential hot water in Florida was produced with solar heat in the 1930?s. With plug in hybrids, a global ban of the traditional lightbulb in favor of compact fluorescents (Austrialia has just banned the lightbulb), it seems quite possible that James Hansen?s goal can be reached even within 9 years. Finally, the last time energy prices were as high as today, US C02 emissions leveled off for 15 years as a result of in?ationary recession. (US emissions of C02 leveled off in 2006, unless the figures were falsified. The US is likely in the early stages of recession.) I will try to put together a simple presentation of these ideas, and send them around to the Congress in the next few weeks. Best regards, 22/ Erik Washington Watch ?are? ya. we, set. .. .3 (if in.? .. . J., Transforming the Rules on Federal Regulations NOREEN PARKS - I i I mid-January, as national attention focilsed on congressional reorganiza- tion and the never-ending controversies surrounding the Iraq war, the White House rewrote key chapters of the book on federal regulations. In one fell swoop, Executive Order 13422 made economic criteria the primary basis for regulation, placed fresh restrictions on agencies, ampli?ed the role of the White House Of?ce of Management and Budget (OMB), and extended the already protracted process of rule- making. US Chamber of Commerce spokesman William Kovacs hailed the moves as the ??rst truly signi?cant hold federal bureaucrats to account and insist they act with discre- tion when imposing new and expensive burdens on businesses and consumers.? But government watchdogs contend that the new order further politicizes the regulatory system, subverts agen- cies? abilities to ful?ll their legal man- dates, and erodes Congress's role in setting regulatory standards. In brief, four important changes were enacted, affecting the federal agencies responsible for public health, safety, and environmental regulation. First, agencies must, justify proposed new regulations to Of?ce of Information and Regulatory Affairs (OIRA) by identifying and assessing the speci?c ?market failure? or other prob? lem that needs ?xing. Second, within each agency, a presidential appointee will serve as regulatory policy of?cer, with broad control over rulemaking. Third, agencies must estimate the cu- mulative annual costs of compliance for rules they expect to publish over a budget year. And fourth, OIRA now will review not only formal rules but also ?signi?cant? guidance documents, agency missives that clarify regulations. The House Science and Technology Committee held oversight hearings on the executive order in February. Among those testifying was Sally Katzen, OIRA 322 BioScience - April 2007 Vol. 57 No. 4 administrator under former President Clinton. Katzen argued that the admin- istration had offered no explanation of the problems that prompted the new order. Furthermore, the order follows other recent controversial White House directives concerning information quality, peer review standards for regu- latory science, risk assessments, and guidance practices. 'Together, Katzen asserted, these measures represent ?a steady and unwavering effort to consol- idate authority 1n OMB and further re- strict agency autonomy and discretion.? The most recenf executive order states that ?no rulemaking shall com- mence nor be included? for considera- tion without the 1approval of an agency?s regulatory policy of?cer, unless speci?cally authorizied by the agency head. This means that presidential ap- pointees could quash efforts such as new US Food and Drug Administration rules for the use of nanotechnology 1n medical devices, for example, or FCC (Federal Communications Commis- sion) requirements that lights at feder- ally licensed communications towers be changed to make the :towers less deadly to migratory birds?ibefore the public even learns that such regulations are being considered. ?At any point in the process, the regulatory policy of?cer will be able to intervene,? said Rick Mel- berth of OMB Watch, _a Washington, DC?based nonpro?t organization. David Vladeck, of Georgetown Uni- versity School of Law and a member of the OMB Watch board of directors, de- cried the apparent sea?chan'ge in regula- tory philosophy signaled by the market failure ?super-mandate.? It ?appears nowhere in statute,? he testi?ed, ?and it cannot be reconciled with the domi- nant thrust of the health and. safety statutes, which are designed to prevent deaths and injuries by avoiding market failure, rather than waiting until it is too late and market failure is evident.? In his comments to the committee, the Chamber of Commerce?s?lKovacs stated that agencies issue some 4000 new regulations annually, as well as thousands of guidance documents. More than 110,000 regulations cur- rently exist, he said, with compliance costs estimated to be as high as $1.13 trillion (a ?gure disputed by Katzen). Kovacs lauded the expansion?of White House scrutiny of guidance documents, which have been used to accomplish ?backdoor regulation," he said. ?There?s a grain of truth to this,? Melberth conceded, as agencies are looking for faster ways of doing their job. But Congress speci?cally exempted guidance documents from the external appraisals required for formal rules, he said, adding that saddling the system with additional layers of review? including scienti?c and technical re- view?that substitute OMB for agency expertise only delays actions required bylaw. Likewise, Vladeck and others ex- pressed wariness over the new require- ment that agencies aggregate the annual compliance costs of new rules, saying that doing so would open the door for OIRA to cap the compliance costs agen? cies may impose. ?Nothing in the statutes Congress has enacted gives OIRA the right to ration through regulation,? Vladeck testi?ed. A Congressional Research Service re- port published 5 February character- ized the executive order as a ?clear expansion of presidential authority over rulemaking? that meshes With the administration?s view of the? unitary executive. ?It concluded that the ulti- mate impacts will depend on how the changes are implemented. Noreen Parks (e-nmil: nmparks@pixi.com) is a ??eeinnce science and environmental writer based in Hawaii. doi:10.1641f8570405 Include this information when citing this material. 1 1 . . ?mus?qua.) ?Jam GM Eucalyptus Environmental Assessment Irregular USDA ?s environmental assessment uses con?dential business information liberally and ?'ivolously and violates its own regulation if not federal law Prof Joe Cummins and Dr. Mae- Wan Ho Irregularities at USDA . has prepared an environmental assessment in response to a permit application (APHIS Number 06-325-111r) ?'om ArborGen LLC (ArborGen) to ?continue? a ?eld test of genetically engineered"(transgenic) Eucalyptus trees during which the trees may ?ower. These plants are clones codenamed EH1 derived from a hybrid of Eucalyptus grandis Eucalyptus and have been genetically engineered with three different constructs. The primary purpose of the test is to examine the ef?cacy two of the constructs intended to confer cold tolerance, and a gene designed to reduce ?ower development. There are serious irregularities with the USDAJAPHIS environmental risk assessment First, the genes in all three constructs are claimed as con?dential business information I (CBI). In addition, the selectable marker gene that accompanies the constructs is also claimed as CBI. Second, according to APHIS, the ?eld test was originally planted under APHIS Noti?cation (05-256-03r) but that permit was for a different organism - Eucalyptus grandis - not the hybrid in the current application 06-325-111r. Third, ArborGen was charged with non-compliance on 17 July 2006 for failing to maintain the identity of trees in their test plots and the infraction was resolved by the removal of the offending trees from the test location Because APH-IS has allowed the transgenes to be designated CBI, the environmental assessment can have no credence because there is no way that an independent investigator can judge the assurances given in the APHIS report. The report stated ?The gene used as a selectable marker is claimed as CBI. In a-number of instances, plants transformed with this gene have been deregulated by APHIS. Consequently, APHIS has determined the presence of this gene will have no signi?cant environmental impacts.? If the marker is a deregulated item, allowing it to be designated CBI seems both frivolous and irregular. The fact that is now giving approval for a previous charge of non- compliance is a clear violation of its own regulation, if not federal law. Potential misrepresentation The environmental assessment claims that the GM hybrids did not contain genes for toxins. However, a patent application by ArborGen for regulation of reproduction in Angiosperms and Gymnospenn plants does employ the potent cell toxin barnase for cell ablation The well known toxicity of barnase to mammals as used in cell ablation to control ?owering has been discussed 6] (".Ferminator Trees, 26; Chronicle ofAn Ecological Disaster .Foretold 18). The use of that toxin gene may have been covered up .by the CBI designation. ArborGen has a number of patent for modi?cation of gene? expression all of which pose a signi?cant threat to the. environment which has not previously been subject to regulatory scrutiny. but CBI designation provided by APHIS will prevent independent scrutiny and assessment. The various known complication resulting, from the use of transgenes similar to those available for use by ArborGen were recently reviewed [13, 14] (View from MADS House, 26); GM Food Nightmare Unfolding in the Regulatorv Sham, ISIS scienti?c publication). Federal Courts in the US have ruled against the Department of Agriculture (USDA) in three successive cases for failing to carry out proper environment impact assessment, making the original approvals of GM crops illegal. In all three cases, USDA was found to have ?outed the law and disregarded health and environmental concerns in their approvals of the GM.crops As we pointed out, the failure to identify the locations and the exact nature of GM crops being tested must also be addressed along with the frivolous use of Con?dential Business Information designations to conceal crucial information for safety evaluation and the persistent regulatory bias towards the uncritical acceptance of GM crops. The current application for GM eucalyptus trees must be rejected. Furthermore, a ban on further spread of GM forest trees should be implosed References 1 1. Environmental Assessment In response. to permit application (06-325- I 1 1 It) received from ArborGen LLC for a ?eld-test of genetically engineered Eucalyptus grandis Eucalyptus US. Department of Agriculture Animal and Plant Health Inspection Service Biotechnology Regulatory Services 2007, 2. Information Systems for Biotechnology Eucalyptus grandis 09/29/05 ArborGen http: 11biap. vt. edu/cfdocs/?eldtests3. c?n 3. USDA- APHIS- -Biotechnology Noncoimpliance History Company/Institution: ArborGen, LLC July 17,2006 1- 4. Rottman W, Norris-Caneda and Zhang C. ArborGen Reproductive ablation constructs United States Patent Application 20060085867 5. Cummins and Ho MW. Terminator trees Science in Societv 26 7, 2005. 6. Ho MW and Cummins J. Chronicle of all ecological disaster foretold. Science in Society 18, 26-27, 2003. 7. Perera R, Rice S, Woods M, Eagleton and Visser L. Compositions and methods for the modi?cation of gene expression. ArborGen-Rubicon United States Patent 2007 I 7,211,713. 8. Chang S, Connet M, Emerson S, Forster R, Gause K, Havukkala I, Higgins and R. Cell signalling genes and related methods United States Patent Application 20070039071. 9. Bloksberg N, Bryant C, Connett'M, Emerson S, Frost M, Forster R, Llewellyn R, Murray G, Higgins C, Lasham A, Lund S, Troy S, Magusin A, Phillips J, Puthigae S, Veerakone S, Westwood C, Gause K, Wood M, Havukkala I, Rottmann W. ArborGen Transcription Factors United States Patent Application 20070039070. 10. Forster R, Connett M, Emerson S, Grigor M, Higgins C, Lund Magusin A and 11. 12. 13. 14. 15. .16. B. Cell cycle genes and related methods United States Patent Application 20060010516. Rajan P, Rice S, Eagleton C, Wood and Visser E. Arborgen Composition and methods for the modi?cation of gene expression States Patent Application 20050244968. Phillips J, Puthigae S,Yao J, Flinn B, Forster and Ealeton ArboreGen Vascular- preferred promoters States Patent Application 20040163146. Cummuns J. View from MADS house. Science in Secietv 26, 2005. Ho MW, Cummins J. and Saunders P. GM food nightmare unfolding in the regulatory sham Microbial Ecology in Health and Disease 2007 (in press). Cummins and Ho MW. Approval of GM crops illegal, US Federal Courts rule. Science in Society 34 (in press). Cummins and Ho Moratorium on all GM trees and ban on GM forest trees. ISIS Report 2007, on all GM Treesohn 21 May 2007 Prof. Joe Cummins Reply to comments from an academic One academic commenter made the following accusations: "Some opponents claim that one of the traits utilized by ArborGen is being kept confidential. Although the Federal Register Notice described one trait as con?dential, this was not the case for the EA itself, where all the traits are described. This objection leads me to believe that these commenters did not actually read the EA. The intent of publishing the EA is to engage the public during the review process. Commenters are encouraged to avail themselves of this opportunity.? Reply to the comment: The normal definition of trait In genetics, a trait refers to any genetically determined characteristic The com'menter somehow seems unaware that the characteristics such as cold tolerance which are mentioned in the APHIS environmental assessment do not really go into whether or not the characteristics are indeed, genetic traits Genetic traits should have been identified by their genetic characteristics and certainly their transgenic origin. Gosh, academics do seem to get arrogant! ?Many opponents called for full disclosure of the genes utilized by ArborGen. While disclosure of genes should be encouraged, this must be balanced against the need to protect intellectual property (IP). The development of biotechnology- derived products is an expensive endeavor (in part due to the need to meet rigorous regulatory requirements). As such, it is of utmost importance that be protected in order to ensure and encourage continued investment in the technology? Reply to the comment; Intellectual property is normally protected by patents and patent applications and ArborGen has previously disclosed their genes in their patent and patent applications. Patent applications and Patents must be public in order for the system to work. APHIS seems silly in colluding with corporations to hide information that is publicly available in patent applications, patents or publications. At any rate, many if not most undergraduate laboratories and certainly corporate laboratories can easily read the crops genetic code to uncover the genetic modification. Indeed, the traceability of the transgenes in the environment is aborted by the careless use of the CBI designation. The CBI designations seem to be political tools and pretences to avoid public scrutiny. Opponents also called for disclosure of the field-trial location. There are many examples of tests that have been vandalized, resulting in the loss of years of hard work and valuable data. Hence, site security is an important consideration, and is justified.? The public deserves to know locations in their neighbourhood where things that may hurt them are located. Corporations should deal with any possible vandalism by providing on site security on their test plots. Site secrecy is not for vandalism, I believe, but to protect corporations from lawsuits from injured neighbours. In a couple of comments, Barnase is described as a toxin. There is no information in the EA that indicates whether or not barnase is one of the genes being studied. Even if Barnase is-in the-ArborGen trees, it has been included in other products that have been deregulated by APHIS, as well as being reviewed by the Food and Drug Administration on numerous occasions (for use in corn, oilseed rape, and chicory)." Reply to the comment; Barnase does appear in one patent application by ArborGen for control of flowering in Eucalyptus, as indicated in my earlier comment. Any claim by APHIS, or for that matter, from FDA that barnase is not toxic to human cells fails to acknowledge a large body of publications where, for example, barnase is used in the targeted-ablation of human cancer cells. The point of my original comment was to point out the danger to the public in failing to acknowledge to the public that toxins were being employed or, even worse, to deny that the toxins were being used. Unfortunately, APHIS corporations and much of science academia seem to regard the human public as being convenient white mice for their experiments. Holding back the truth is essential to maintaining a docile herd. Page 1 of 1 Main Identity From: "Erik Jansson" To: Sent: Tuesday. May 22. 2007 9:43 PM Subject: Petition to FDA on aluminum food additives Dear Robin. just sent you a site to download our FDA petition of September 14. 2005: Docket No. We asked FDA to rescind the "generally recognized as safe" GRAS designation for aluminum based food additives including many brands of baking powder. food dyes. etc. A substantial literature on epidemiology indicates that this program has the potential to reduce Alzheimer?s disease and elderly cognitive impairment short of AD rates by 50 to 80 percent. The costs are very low. Calcium based baking powder has been available in the supermarket for many years. and costs of reducing aluminum levels in the food supply are trivial. Secondly. such a has the potential to reduce the shortfall of the medical trust funds by 23 to 42 percent over the next 50 years. FDA's management was not impressed. On March 13,!2006. Laura Tarantino. Director of the Of?ce of Food Additive Safety, Center for Food Safety and Applied Nutrition wrote: I "Dear Mr. Jansson. This letter is in response to the citizen petition that you submitted on Septemer 14. 2005. the Food and Drug Administration rescind the Generally Recognized as Safe (GRAS) status of aluminum-based substances listed in 21 CFR Part 182. You also ask FDA to investigate the affect other food ingredients have on the absorption of aluminum. The purpose of this response is to advise you. in accordance with 21 CRF that we have not reached a decision on your petiton within the 180 days of the ?ling of the petitiOn because of the limited availability of resources and other agency priorities." Sincerely yours. Laura M. Tarantino This is open-ended and will continue. of course. until we have a new President. Lack of interest in preventing Alzheimer's in view of other agency priorities is a big health issue which will go a good ways in sinking the medical system of the nation. . We have submitted many other supplements to the original petition since 2005, as new medical literature on aluminum is published. Dr. DRC McLachlan. former director of the Tanz Institute of the University of Toronto. proposed over a decade ago that aluminum was "a necessary but not suf?cient" risk factor for Alzheimer's based on the extensive literature of that time. In 35 years of non-pro?t work on'toxins. have never seen a supporting literature as extensive as this. including 22 drinking water epidemiolrogy studies and one food study. Best regards. Erik Jansson planetearth@erols.com (301) 475-8366 Page 1 Main Identity From: "Gjumrakch Aliev" To: "Erik Jansson" Cc: "George Perry" "Justin Shenk" Sent: Wednesday, May 30, 2007 8:27 PM Subject: RE: A review: If you are interested, we have prepared an article. Our particular interest is aluminum, and our speciality of 35 years is regulation of toxins. Alzheimer's is substantially a preventable disease. Best regards, Erik Jansson, Exec. Dir. Dear Dr Jansson, Great Could you please prepare your review in the style of J. Neurological Sciences? I look forward to receiving your contribution. Best regards, Sincerely G. Aliev - . .. -. mu. m. ..H- ?a - . . c-ur: From: Erik Jansson [mailtoz planetearth@erols. com] Sent: Wed 5/30/2007 6: 54 PM To: Gjumrakch Aliev Subject: A review: If you are interested we have prepared an article. Our particular interest is aluminum and our speciality of 35 years is regulation of toxins. Alzheimer's is substantially a preventable disease. Best regards, Erik Jansson, Exec. Dir. A review: Aluminum as a causative co-factor for the ?dementia? of Alzheimer?s disease. E.T. Jansson Department of the Planet Earth, 701 Street, SE, Ste. 200, Washington, DC 20003 E?mail address: planetearth@erols.com, Tel: +1 301 475 8366, fax: 1 202 543 4791 Additional supporting material is found at deptplanetearth. com Abstract This review explores an expert proposal made over a decade ago that aluminum is a ?necessary but not suf?cient? risk factor for the dementia of Alzheimer?s Disease (AD). More than twenty epidemiology . studies report a statistical relationship between exposure of the aging population to aluminum in food and drinking water and increased risk of elderly cognitive impairment and risk of dementia. An autopsy microscopic visualization of aluminum in brain cells of AD patients using the Walton stain reveals two basic types of pyramidal neuron death produced by accumulated brain aluminum. These are ?rst a cell death visually resembling necrosis and secondly brain cell death by mechanical enucleation from a persistent accumulation of cellular neuro?brillary tangles (NFTs). The metal was found to be associated with the formation of all NFTs, producing the characteristic protein folding. This autopsy ?nding supports a causative role of the metal in human AD dementia. Over a lifetime, aluminum bio- accumulates to relatively high concentrations in all human elderly brains. It is a reactive metal that readily complexes with basic brain biology and affects genes regulation. Abundant laboratory animal studies document mechanisms by which aluminum produces brain cell death and the erosion of white matter which reduces the connectivity of the brain. It is concluded from extensive literature that aluminum is a causative co-factor for the dementia of AD, which is a medical condition based on brain atr0phy. Epidemiology studies support an excellent public health Opportunity for large reductions 'of the 5/3 0/2007 - Burmese! - Ho'y 31 - June 6. 2001 Slash Greenhouse Gases Solar Power solar water heater will do the Earth and your wallet good I heard that using a solar powered water heater in my home would reduce my [02 emissions signi?cantly. Is this true? And what are the costs?- - ?hnoI16tsn,ano.iw 11 average four?per- son household with an electric water eater needs about. 6,400 kilowatt-hours of electricity per year to heat its water, according to mechanical engineers at the Uniyersi- ty of Wisconsin?s Solar Energy Labora- tory. Assuming the electricity is gener- ated by a typical power plant with an ef?ciency of around 30 percent, it means that the average electric water heater is responsible for about eight tons of carbon dioxide annually, which is. almost double that emitted by a typ- ical modern automobile. The same family of four using either a natural gas or oil-?red water heater will contribute about two tons of carbon dioxide emissions annually in heating their water. I with i .. I Surprising' as it may seem; ana- believe that the annual total car- bon dioxide produced by residential water heaters throughout North Amer: ice is roughly equal to that produced by all of the cars and light trucks driving around the continent. Another way of looking at it: half of all households . 11 used solar water I heaters, the hon dioxide emis- sions wbuld be the same?as dou- aues?ons aAnswers bliilg? the fuel- Abaur?ur Environment ef?ciency: of all That might not be such a tall order. According to the Environmeiital and Energy Study Institute, 1. 5 Imillion solar water heaters are already in use in U.S. homes and businesses. Systems can work in any climate. The Institute esti- mates that 40 percent of all U. 8. homes have suf?cient access to sunlight such that 29 million additional solar heaters could be installeld right now. Another great reason to make the switch is a ?nancial one. Residential_ solar water heating systems cost between $1,500l'and $3,500 compared to $150 to $450 for electric and gas heaters, according'to the Environmen- tal and Energy Study Institute. But 1 reduction in car- with savings in electricity or natural gas, solar water heaters pay for them- . selves within four to eight years. They last between 15 and 40 years the same as conventional systems so after that initial payback period is up, 'zero energy cost essentially means having. free hot water for years to come. What?s more, in 2005 the U.S. began offering homeowners tax credits of up to 30 percent (capped at $2,000) of the cost of installing a solar water heater. The credit is not available for swimming pool or hot tub heaters, and the system must be certi?ed by the Solar Rating and Certi?cation Corporation. Zoning and building codes relating to the installation of solar water heaters usually reside at the local level, the US. Department of Energy?s Consumer?s Guide to Renewable Ener- gy and Energy Ef?ciency reports, so consumers should research the stan- dards for their own communities and - hire a-certi?ed installer familiar with local requirements. Homeowners beware: Most municipalities require a building permit for the installation of a solar hot water heater onto an existing house.? For more information: U.S. Department of Energy: Got an environmental question? Send it to: Earth'I?alk, do Er?I'he Environmental Magazine, P.0. Box 5098, Westport, CT 06881: submit it at. memagazine. comfearthtalk/thisweek: or e-mail earthtaleemagazinexom. Read past columns at:, I Print the story taxi ixE?J SCIENCE PHYSICS TECH NEWS 40% ef?cient solar cells to be used for solar electricity Scientists from Spectrolab, Inc., a subsidiary of Boeing, have recently published their research on the fabrication of solar cells that surpass the 40% ef?ciency milestone?the highest ef?ciency achieved for any photovoltaic device. Their results appear in a recent edition of Applied Physics Letters. Most conventional solar cells used in today?s applications, such as for supplemental power for homes and buildings, are one?sun, single-junction - silicon cells that use only the light intensity that the sun produces naturally, and have optimal ef?ciency for a relatively narrow range of photon energies. The Spectrolab group experimented with concentrator multijunction solar cells that use high intensities of sunlight, the equivalent of 1005 of suns, concentrated by lenses or mirrors. Signi?cantly, the multijunction cells can also use the broad range of in sunlight much more efficiently than single-junction cells. "These results are particularly encouraging since they were achieved using a new class of metamorphic semiconductor materials, allowing much greater freedom in multijunction cell design for optimal conversion of the solar spectrum," Dr. Richard R. King, principal investigator of the high ef?ciency solar cell research and development effort, told PhysOrg.com. "The excellent performance of these materials hints at still higher ef?ciency in ?iture solar cells." In the design, multijunction cells divide the broad solar spectrum into three smaller sections by using three subcell band gaps. Each of the subcells can capture a different wavelength range of light, enabling each subcell to ef?ciently convert that light into electricity. With their conversion ef?ciency 6/1/2007 Print the story Page 2 of 2 measured at 40.7%, the metamorphic multijunction concentrator cells surpass the theoretical limit of 37% bf single-junction cells at 1000 suns, due to their multijunction structure. While Spectrolab's primary business is supplying PV cells and panels to the aerOSpace industry (many of their solar cells are used on satellites currently in orbit), the company envisions thatl this breakthrough will also have applications in commercial terrestrial solar electricity generation. The research that led to the discovery of the high ef?ciency concentrator solar cell was funded partly by the Department of Energy?s National Renewable Energy Laboratory, and will play a signi?cant role in the government?s Solar America Initiative, which aims to make solar energy cost-competitive with conventional electricity generation by 2015. The company has said that these solar cells could help concentrator system manufacturers produce electricity at a cost that is competitive with electricity generated by conventional methods today. The Spectrolab scientists also predict that with theoretical ef?ciencies of 58% in cells with more than three jurictions using improved materials and designs, concentrator solar cells could achieve ef?ciencies of more than 45% or even 50% in the future. Citation: King, R. R., Law, D. C., Edmondson, K. M., Fetzer, C. M., Kinsey, G. 8., Yoon, H., Sherif, R. A., and Karam, N. H. ?40% ef?cient metamorphic multijunction solar cells.? Applied Physics Letters 90, 183516 (2007). Capyright 2007 PhysOrg. com. All rights reserved. This materia! may not be published, broadcast, rewritten or redistributed in whole or part without the express written permission of Org. com. i This news is brought i?o you by PhysOrg. com 87 . 6/1/2007 Global and regional drivers of accelerating C02 emissions Michael R. Raupach?", Gregg Marland?, Philippe Ciai55, Corinne Le Qu?r?'ml, losep G. Canadell', Gernot Klepper?. and Christopher B. Field? 'Global Carbon Project, Commonwealth Scientific and Industrial Research Organisation, Marine and Atmospheric Research, Canberra. ACT 2601, Australia; *Carbon Dioxide Information Analysis Center, Oak Ridge National Laboratory, Oak Ridge, TN 37831: ?Commissariat a I?Energie Atomique, Laboratorie des Sciences do Climat et de I?Environnement, 91191 Gif sur Yvette, France; ?School of Environment ScienCes, University of East Anglia, Norwich NR4 7T1 United Kingdom; iBritish Antarctic Survey, Cambridge. CBS OET. United Kingdom: ?Kiel Institute for the World Economy, 0- 24105 Kiel, Germany; and "Carnegie Institution of Washington, Department of Global Ecology, Stanford. CA 94305 Edited by William C. Clark, Harvard University, Cambridge, MA, and approved April 17, 2007 (received for review January 23, 2007) C02 emissions from fossil-fuel burning and industrial processes have been accelerating at a global scale, with their growth rate increasing from 1.1% y-1 for 1990-1999 to y" for 2000- 2004. The emissions growth rate since 2000 was greater than for the most fossil-fuel intensive of the Intergovernmental Panel on Climate Change emissions scenarios developed in the late 19905. Global emissions growth since 2000 was driven by a cessation or reversal of earlier declining trends in the energy intensity of gross domestic product (GDP) and the carbon intensity of energy (emissionsrenergy). coupled with continuing increases in population and per-capita GDP. Nearly constant or increas- ing trends in the carbon intensity of energy have been recently observed in both developed and developing regions. No region is decarbonizing its energy supply. The growth rate in emissions is strongest in rapidly developing economies. particularly China. Together, the developing and least-developed economies (forming 80% of the world's population) accounted for 73% of global emissions growth in 2004 but only 41% of global emissions and only 23% of global cumulative emissions since the mid-18th cen- tury. The results have implications for global equity. carbon intensity of economy carbon intensity of energy emissions scenarios fossilfuels Kaya identity Atmospheric C03 presently contributes m63% of the gaseous radiative forcing responsible for anthropogenic climate change (I). The mean global atmospheric concentration has increased from 280 in the 1700s to 380 in 2005, at a progressively faster rate each decade (2, This growth is governed by the global budget of atmospheric CO: (4), which includes two major anthropogenic forcing fluxes: emis- sions from fossil-fuel combustion and industrial processes and (if) the flux from land?use change. mainly land clearing. A survey of trends in the atmospheric budget (3) shows these two fluxes wcrc. respectively, 7.9 gigatonnes of carbon y" and in 2005 with the former growing rapidly over recent years, and the latter remaining nearly steady. This paper is focused on emissions from fossil-fuel combustion and industrial processes. the dominant anthropo- genic forcing flux. We undertake a regionalizcd analysis of trends in emissions and their demographic, economic, and technological drivers, using the Kaya identity (defined below) and annual time-series data on national emissions. population, energy consumption, and gross domestic product (GDP). Un- derstanding the observed magnitudes and patterns of the factors influencing global C02 emissions is a prerequisite for the prediction of future climate and earth system changes and for human governance of climate change and the earth system. Although the needs for both understanding and governance have been emerging for decades (as demonstrated by the United Nations Framework Convention on Climate Change in 1992 and the Kyoto Protocol in 1997}, it is now becoming widely perceived that climate change is an urgent challenge requiring globally concerted action, that a broad portfolio of mitigation measures is required (5. 6), and that mitigation is not only feasible but highly desirable on economic as well as social and ecological grounds (7). The global emission flux from fossil fuel combustion and industrial processes (F includes contributions from seven sources: national-level combustion of solid. liquid, and gaseous fuels; flaring of gas from wells and industrial processes; cement production; oxidation of nonfuel hydrocarbons; and fuel from "international bunkers" used for shipping and air transport (separated because it is often not included in national invento- ries). Hence FSulid 4 FLittuitl F?as FFlarc ??35 "36?ir FCementt+ I ~39; v: where the fractional contribution of each source to the total for 2000?2004 is indicated. The Kaya identity-?5 (8, 9) expresses the global as a product of four driving factors: Metatarsal where is global population. is world GDP or gross world product, is global primary energy cunsumption, is the pcr-capita world GDP, 6 is the energy intensity of world GDP. and FIE is the carbon intensity of energy. Upper? and lowercase symbols distinguish extensive and intensive variables. Authorcontributions: M.R.R.. P.C.. C.L.Q., J.G.C.. and C.B.F. designedresearch; M.R.R.. G.M.. P.C.. and J.G.C. perfumed research; M.it.R.. G.M.. P.C.. and G.K analyzed data; and M.H.R., G.M., GK. and C.B.F. wrote the paper. The authors declare no conflict of interest._ This article Is a PNAS Direct Submission. Freely available online through the PNAS open access option. Abbreviations: GDP. gross domestic product: MER. market exchange rate; purchasing power parity; IPCC. Intergovernmental Panel on Climate Change; EU. European Union; FSU. Former Soviet Union; D1. developed countries: 02. developing countries: 03, least- developed countries: CDIAC, U.S. Department of Energy Carbon Dioxide Information and Analysis Center; EIA. US Department of Energy Energy Information Administration. 'To whom correspondence should be addressed. Email: micluelxaupach?csiro on. data are available at ?Yamajl, K., Matsuhashi, R., Nagata, Y., Kaye. Y., An integrated System for CO,-rfnergyl? GNPAnalysis: Case Studies on Economic Measures for 0: Reduction in Japan. Workshop on C0: Reduction and Removal: Measures for the Next Century, March 19. 1991. International Institute for Applied Systems Analysis, Lavenburg, Austria. This article contains supporting inlonnatlon online at gnaw-33: ascetic." 2007 by The National Academy of Sciences of the USA PNAS Early Edition 0' . 1 Based on climate model studies and the history of the Earth the authors Print the story Page 1 of 2 f? ?1171?? SCIENCE: PHYSICS: TECH 1 Research ?nds that Earth's climate is approaching 'dangerous' point NASA and Columbia University Earth Institute research ?nds that human-made greenhouse gases have brought the Earth?s climate close to critical tipping points, with potentially dangerous consequences for the planet. From a combination of climate models, satellite data, and paleoclimate records the scientists conclude that the West Antarctic ice sheet, Arctic ice cover, and regions providing fresh water sources and species habitat are under threat from continued global warming. The research appears in the current issue of Atmospheric Chemistry and Physics. Tipping points can occur during climate change when the climate reaches a state such that strong amplifying feedbacks are activated by only moderate additional warming. This study ?nds that global warming of 0. 1n the past 30 years has been driven mainly 'by Increasing greenhouse gases, and only moderate additional climate forcing 1s likely to set in motion disintegration of the West Antarctic iCe sheet and Arctic sea ice. Amplifying feedbacks include increased absorptidn of sunlight as melting exposes darker surfaces and speedup of iceberg discharge as the warming ocean melts ice shelves that otherwise inhibit ice-?ow. The researchers used data on earlier vyarm periods in Earth?s history to estimate climate impacts as a function of global'temperature, climate models to simulate global warming, and satellite data to verify ongoing changes. Lead author James Hansen, NASA Goddard Institute for Space Studies, New York, concludes: ?If global emissions of carbon dioxide continue to rise at the rate of the past decade, this! research shows that there will be disastrous effects, including increasingly rapid sea level rise, increased frequency of droughts and ?oods, and increased stress on wildlife and plants due to rapidly shifting climate zones}; The researchers also investigate what;would be needed to avert large climate change, thus helping de?ne practical implications of the United Nations Framework Convention on Climate Change. That treaty, signed in 1992 by the United States and almost all natiohs of the world, has the goal to stabilize atmospheric greenhouse gases ?at a level that prevents dangerous human- made interference with- the climate system.? conclude that additional global warming of about or more, above global temperature in 2000, is likely to be dangerous. In turn, the temperature limit has implications for atmospheric carbon dioxide (C02), which has already increased from the pre-industrial 'level of 280 parts per million (ppm) to 383 today and is rising by about 2 per year. According to study co?author Makiko Sato of Columbia?s Earth Institute, I . 1/2007 Print the story ?the temperature limit implies that CO2 exceeding 450 is almost surely dangerous, and the ceiling may be even lower.? The study also shows that the reguction of non?carbon dioxide forcings such as methane and black soot can 0 fset some C02 increase, but only to a limited extent. Hansen notes that ?we probably need a full court press on both C02 emission rates and non-C02 forcings, to avoid tipping points and save Arctic sea ice and the West Antarctic ice sheet.? A computer model developed by the Goddard Institute was used to simulate climate from 1880 through today. The model included a more comprehensive set of natural and human-made climate forcings than previous studies, including changes in solar radiation, volcanic particles, human-made greenhouse gases, ?ne particles such as soot, the effect of the particles on clouds and land use. Extensive evaluation of the model?s ability to simulate climate change is contained in a companion paper to be published in Climate Dynamics. The authors use the model for climate simulations of the let century using both ?business-as?usual? growth of greenhouse gas emissions and an ?altemative scenario? in which emissions decrease slowly in the next few decades andithen rapidly to achieve stabilization of atmospheric C02 amount by the end of the century. Climate changes are so large with ?business-as-usual?, with additional global warming of that Hansen concludes ??business-as-usual? would be a guarantee of global and regional disasters.? However, the study ?nds much less severe climate change one-quarter to one?third that of the "business-as-usual" scenario when greenhouse gas emissions follow the alternative scenario. ?Climate effects may still be substantial in the 'altemative scenario?, but there is a better chance to adapt to the changes and ?nd other waysto further reduce the climate change,? said Sato. While the researchers say it is still possible to achieve the ?alternative scenario,? they note that signi?cant actions will be required to do so. Emissions must begin to slow soon. ?With another decade of ?business?as? usual? it becomes impractical to achieve the ?alternative scenario? because of the energy infrastructure that would be in place? says Hansen. Source: NASA/Goddard Space Flight Center This news is brought to you by PhysOrg.cam 5/31/2007 ENN: Environmental News Network . Page 1 of 1 Study Shows Southern Ocean Saturated with Carbon Dioxide May 18, 2007 By Deborah Zabarenko, Reuters I WASHINGTON - The Southern Ocean around Antarctica is so loaded with carbon dioxide that it can barely absorb any more, so more of the gas will stay in the atmosphere to warm up the planet, scientists reported Thursday. Human activity is the main culprit, said researcher Corinne Le Quere. who called the ?nding very alarming.? The phenomenon wasn't expected to be apparent for decades, Le Quere said in a telephone interview from the University of East Anglia in Britain. 1 i "We thought we would be able to detect these only the fsecond half of this century. say 2050 or so," she said. But data from 1981 through 2004 show the sink is already full of carbon dioxide. "80 I ?nd this really quite alarming." The Southern Ocean is one of the world' 5 biggest reservoirs of carbon known as a carbon sink. When carbon is in a sink -- whether it's an ocean or a forest both of which can lock up carbon dioxide -- it stays out of the atmosphere and does not contribute to global warming. The new research, published in the latest edition of the journal Science, indicates that the Southern Ocean has been saturated with carbon dioxide at least since the 1980s. This is signi?cant because the Southern Ocean accountsifor 15 percent of the global carbon sink, Le Quere said. GLOBAL WARMING SPURS WINDS 1 Increased winds over the last half-century are to blame for the change Le Quere said. These winds blend the carbon dioxide throughout the Southern Ocean mixing the naturally occurring carbon that usually stays deep down with the human- caused carbon. When natural carbon is brought up to the surface by the winds it is harder for the Southern Ocean to accommodate more human- generated carbon which comes from factories coal- ?red power plants and petroleum- powered motor vehicle exhaust. The winds themselves are caused by two separate human factors. First, the human-spawned ozone depletion in the uppei' atmosphere over the Southern Ocean has created large changes in?temperature throughout the atmosphere, Le Quere said Second the uneven nature of global warming has produced higher temperatures in the northern parts of the world than' In the south which has also made the winds accelerate In the Southern Ocean. "Since the beginning of the industrial revolution the world's oceans have absorbed about a quarter .of the 500 gigatons (500 billion tons) of carbon emitted into the atmosphere by humans Chris Rapley of the British Antarctic Survey said' In a statement. "The pdssibility that' In a warmer world the Southern Ocean -- the strongest ocean sink -- is weakening is a cause for concern, Rapley said. 3 Another sign of warming in the Antarctic was reported Tuesday by NASA, which found vast areas of snow melted on the southern continent in 2005 in a process that may accelerate invisible melting deep beneath the surface} I I Source: Reuters . Contact Info: . Website I 5/18/2007 Fif/ fef+? F. eter Reader Page 1 A Wee/(iv Analysis QfEucrgy Sroc'ks (rising {he May- 15. 2007 Peak Oil Test Looming Summary and Recommendation Gradually rising prices are accompanying a gradual peaking of oil production and pointing to investment opportunity in buy-recommended oil and gas producers including ConocoPhillips (COP), XTO Energy (XTO) and Occidental Petroleum (OXY). World oil production may have already peaked at about 85 million barrels daily (mmbd) where it has been stuck for the past year (see chart Global Oil Production). With current demand near 86 mmbd, the difference has been made up by declining inventory. Gasoline stored in the U.S. is especially low (see chart from the BIA, U.S. Gasoline Stocks). The apparent peak may be tested later this year as both the IEA and the EIA, the well-known consuming country government energy forecasters, expect oil production to break out to a new high of 87 mmbd. Regardless, maintaining current production is enough of a challenge, we think, to propel a continuation in the recently renewed uptrend in long-term oil price now quoted at $68 a barrel (see table Six-Year and One-Year Natural Gas and Oil Futures). Kurt H. Wulff, CFA Global Oil Production, 2006-2007 International Energy Agency (IEA) ~13? . U.S. Energy Information Administration (E IA) - EIA May 2006 Forecast Million Barrels Daily on A. I i 0601 0602 0603 0604 0702E 0703E 0704E Historical independent energy investment analysis by Kurt Wulff doing business as McDep Associates is representation is made as to their accuracy or completeness. Mr. Wulff is not paid by covered companies. Neither he nor his spouse trade a subject stock within a week before or after a change in rating. Print the story ?age I- of 2 17? 9E: mm PHYSICS: TECH: mmo news Soils offer new hope as carbon sink Trials of agrichar using pyrolysis The huge potential of agricultural soils to reduce greenhouse gases and increase production at the same time has been reinforced by new research ?ndings at NSW Department of Primary Industries' (DPI) Wollongbar Agricultural Institute. 1 Trials of agrichar - a product hailed as a saviour of Australia's carbon- depleted soils and the environment have doubled and, in one case, tripled crop growth when applied at the rate of 10 tonnes per hectare. Agrichar is a black carbon byproduct of a process called pyrolysis, which involves heating green waste or other biomass Without oxygen to generate renewable energy. Tim Flannery, Australian of the Year and renowned scientist, conservationist, writer and explorer, is a major advocate of agrichar and pyrolysis. In The Bulletin magazine, Flannery recently ranked "fostering pyrolysis?based technologies" fourth among his ?ve steps for saving the planet, because they convert crop waste into fuel and agrichar which can be used to enhance soil fertility and store carbon long-term. I NSW DPI senior research scientist Dr Lukas Van Zwieten said soils naturally emit? about 10 times more greenhouse gas on a global scale than the burning of fossil fuels. "So it is not surprising there is so much interest in a technology to ?Create clean energy that also looks up carbon in the soil for the long term and lifts agricultural production, he said. The trials at Wollongbar have focused on the bene?ts of agrichar to agricultural productivity. "When applied at 10t/ha, the biomass of wheat was tripled and of soybeans was more than doubled," said Dr Van Zwieten. "This percentage increase remained the same when applications of nitrogen fertiliser were added'to both the agrichar and the control plots. "For the wheat, agrichar alone was about as bene?cial for yields as using nitrogen fertiliser only. "And that is without considering the other bene?ts of agrichar." Regarding soil chemistry, Dr Van Zvirieten said agrichar raised soil pH at about one-third the rate of lime, lifted calcium levels and reduced aluminium toxicity on the red ferrosol soils of the trial. "Soil biology improved, the need for added fertiliser reduced and water holding capacity was raised," he said; The trials also measured gases given off from the soils and found signi?cantly lower emissions of carbon dioxide and nitrous. oxide (a greenhouse gas more than 300 times as potent as carbon dioxide). 1 NSW DPI environmental scientist Steve Kimber said an added bene?t for both the farmer who applies agrichar and the environment is that the carbon in agrichar remains locked up in the soil for many years longer than, for . 6/1/2007 ?Print the story example, carbon applied as compost, mulch or crop residue. "We broadly categorise carbon in the soil as being labile (liable to change quickly) or stable depending on how quickly they break down and convert into carbon diOXide," he said. "Labile carbon like crop residue, mulch and compost is likely to last two or three years, while stable carbon like agrichar will last up to hundreds of years. "This is signi?cant for farmer costs because one application of agrichar may be the equivalent of compost applications of the same weight every year for decades. "For the environment, it means soil carbon emissions can be reduced because rapidly decomposing carbon forms are being replaced by stable ones in the form of agrichar." Unfortunately, agrichar is not widely available. BEST Energies Australia, a company involved with NSW DPI in the trials, has a pilot plant at Gosford which is producing minimal amounts for research purposes. "We are hoping the technology will take hold and pyrolysis plants will be built where there is a steady stream of green or other biomass waste providing clean energy that is carbon negative," Dr Van Zwieten said. "But until pyrolysis plants are up and running, the availability of agrichar for farmers will be scarce." Source: New South Wales Department of Primary Industries This news is brought to you by PhysOrg.com 6/ 1/2007 ENN: Environmental News Network Page 1 of 2 G8 Greenhouse Gas Emissions Rise; U.S. Not Worst May 31. 2007 By Alister Doyle. Reuters OSLO -- Greenhouse gas emissions by leading industrialised nations have accelerated since 2000 and several countries are performing worse than the United States Which opposes a UN. pact for curbing global warming. U.N. data shows. Leaders of the Group of Eight rich nations meet in Germany next week with President George W. Bush resisting pressure by German Chancellor Angela Merkelto agree to cap emissions. mainly from burning fossil fuels. But Bush is not alone in presiding over rising emissions. i "Growth rates of emissions in the U.S. are slowing." 'said Michael Raupach. of the Earth Observatio'n Centre in Canberra. Australia. of overall greenhouse gas trends. "European emissions are creeping up in the post-2000 years." National data submitted to the U. 3 Climate Change Secretariat show that overall emissions by G8 nations rose 2.0 percent from 2000 to 14. 3 billion tonnes in 2005 and were up 0.7 percent since 1990. the base year for the U. N. Kyoto Protocol. Among G8 nations. Russia. ltaly and Canada have all had bigger rises than the 1.6 percent U.S. gain since 2000. when Bush won election to the White House. The revival of the Russian economy after the collapse of the Soviet Union is a main spur. Only Britain. Germany and France have cut back since 2000. Since 1990. however. the United States has had a 16.3 percent rise. second Worst behind Canada. All G8 nations back Kyoto except the United States. the biggest world emitter. And Kyoto nations expect falls in emissions in coming years when investments. for instance in energy efficiency or wind or hydro power. will take effect. G8 comparisons for 2005 are possible after Canada and Japan gave data this week. KYOTO I "The main driver for emissions has not been the Kyoto Protocol but how economies have been developing," said Keywan Riahi. a senior researcher at the International Institute for Applied Systems Analysis in Austria. Economic growth and rising populations tend to spur emissions from factories. power plants and cars but energy ef?ciency. partly inspired by Kyoto. and a shift away from heavy industry towards services are among brakes for GB na?ons. 1 Among big shifts, Russian emissions are up 7.3 percent since 2000. mainly driven by an economic rebound after the collapse Of the Soviet Union and its smokestack industries. But Russia is still 28.7 percent below 1990 levels. Bush said in 2001 that Kyoto would threaten U.S. jobs and wrongly excluded developing nations from ?rst targets of a 5 percent cut by 2008-12. He prefers voluntary agreements and investments in new technologies, such as hydrogen or clean coal. "My personal view is that the importance of Kyoto was not for the actual emissions reductions it may achieve -- which are tiny compared with what is needed -- but rather that Kyoto was a ?rst attempt to build a global consensus and commitment." Raupach said. . "in that. it has been less than fully successful." he said. Merkel wants Bush to agree to Kyoto-style caps, with extra urgency after U.N. climate reports this year have said world emissions will need to be cut to help avert more huriger. water shortages. heatwaves and rising seas. The White House said last week that preliminary data 'showed that U. 8. emissions of carbon dioxide. the main greenhouse gas. fell by 1. 3 percent in 2006. "We are effectively confronting the important challenge of global climate change. Bush said. Raupach said. however, that a warm winter contributed to out US. heating demand and a less than scorching 2005 i 15/31/2007 .ENN: Environmental News Network summer had also curbed use of air conditioning. Source: Reuters Contact'lnfo: Website 5/31/2007 I Department of the Planet Earth 701 Street, SE - Suite 200, Washington, DC 20003 (301) 475-8366 - July 11, 2007 Dear Board Members, Joe has just submitted objections to a program proposing almost a biological warfare program on American rice crops and humans. See the enclosed brief which I sent to the Secretary of Agriculture. We need a new President soon. First Southern State: There is good news on the state response to global warming. Governor Charlie Crist of Florida will issue an executive order on Friday to not only control automobile greenhouse gas pollution, but also to match the California program: i.e. lower Florida?s contribution of C02 to 1990 levels by 2025 and 80 percent lowr by 2050, despite an expected doubling of population. 80, this would be the first southern state to commit to a Kyoto Protocol type of program. Utah?s governor has also committed. So, our state program which I began in 1996, has picked up momentum. Now we need a new President. I have been attempting to put together a new paper on what can be done in 10 years to curtail the US contribution to global warming, considering Dr. James Hansen?s proposal that we only have ten years or ice melt cannot be prevented. He also proposes a 16 foot rise in water levels by the end of this century, and an 82 foot eventual rise. (See enclosed testimony to Congress.) Unfortunately, I have encountered a slight writers block since the issue is so complicated, and I need to make the presentation simple. For example, with carbon dioxide emissions now rising at a 3.2 percent per year rate, compared to 1.1 percent of the 1990 to 1999 period, timing of adverse effects are now moved up by 2/ 3rds. It has been proposed that 1000 of carbon dioxide would be achieved in the atmosphere with business as usual by 2200. This would cause ?extinction? of higher animal life including humans, probably as hydrogen sulfide bubbles out of the oceans to poison the atmosphere. Now we are only talking about 65 years to the initiation of extinction. Wow. One good thing is that the soils of organic farming may be an excellent carbon dioxide sink, based on the records of the Rodale Institute experimental farm in Kutztown. Perhaps we can qualify organic farming to receive C02 abatement subsidies - Le. a good project for legislation? Best, Erik to sign strict emissions orders - 07/10/2007 - MiamiHerald.com Page 1 of 3 MiamiHerald.com 3 Posted on Tue, Jul. 10, 2007 Crist to sign strict emissions orders BY MARY ELLEN KLAS Florida will adopt California's car-pollution standards the toughest in the nation -- and become the ?rst state in the Southeast to enact targets for reducing greenhouse gases, under executive orders Gov. Charlie Crist plans to sign Friday in Miami. Drafts of the orders released Tuesday would require the state secretary of environmental protection to immediately ad0pt rules to limit pollution-causing emissions for cars, diesel engines and electric companies. The orders also impose tough new energy conservation goals for state agencies, demand better fuel ef?ciency from state-owned vehicles and require state cars to ?use ethanol and biodiesel fuels when locally available." But the most optimistic step in Crist's green agerida is the requirement to lower the amount of carbon dioxide in the air to 1990 levels by 2025, and 80 .percent lower by 2050, in spite of what is expected to be a near doubling of the state's population. "Florida is the second fastest-growing state in the union with respect to the annual increase of new greenhouse gas emissions," the governor's draft order states, adding ?immediate actions are available and required to reduce emissions of greenhouse gases in Florida." Crist will sign the orders at a two-day climate change summit he is hosting in Miami beginning Thursday. The summit will feature speeches by California Gov. Arnold Schwarzenegger and environmental activists Robert Kennedy Jr. and Theodore Roosevelt IV. The governor's orders say the new rules can be enacted without approval from the Legislature because they are based on existing state environmental laws. STRICT CONTROLS The orders would bring Florida's pollution controls up to par with at least two dozen other states on the East and West coasts but would be the strictest in the Southeast. Former Gov. Jeb Bush rejected appeals from environmentalists to support similar pollution control standards, although he quietly drafted a carbon-reductions policy in the ?nal months of his term. Crist, who was elected in November, has vowed to make reducing greenhouse gases in Florida a priority. One of the orders he will sign says the state's vulnerability to rising ocean levels and violent weather makes global climate change one of the most important issues facing the state of Florida this century." Under the California emissions standards, automakers that sell cars in Florida beginning with the 2009 model year would have to reduce greenhouse gas pollutants, such as carbon dioxide, by 25 percent for cars and 18 percent for sport utility vehicles. 7/1 1/2007 . i Crist to sign strict emissions orders - 07/10/2007 - MiamiHerald.com Page At least 12 other states have adopted California's standards, including New York, New Jersey and Automakers are challenging the standards in court and, for two years, the federal Environmental Protection Agency has refused to allow the new law to take effect. Environmentalists hailed the proposals, and utility executives said they were cautious but encouraged. "They're very signi?cant and very comprehensive," said Susan Glickman, a consultant for the National Resources Defense Council and other environmental groups. ?It's clear from these executive orders that he is dead serious about reducing [carbon dioxide] emissions. The governor's goals now provide the starting point for the Legislature to enact them." RENEWABLE SOURCES The governor's orders also require electric companies to reduce greenhouse emissions to 2000 levels by 2017 and to 1990 levels by 2025. They also ask the Public Service Commssion, the state agency that regulates utilities, to impose rules this year that require electric companies to produce 20 percent of their electricity from renewable sources, "with a strong focus on solar and wind energy." Regulators would set the deadlines. Florida Power Light President Armando Olivera said he hadn't seen the proposed executive order but the company, the largest producer of solar?power and wind-power energy in the nation, generally supports increasing the state's reliance on renewable energy. "It depends on what the rules are and how those rules are developed," he said. ?But we are obviously very supportive of renewables and we think it should beta huge element of our energy policy." Crist's orders include several elements of an energy bill passed by legislators that he vetoed last month because it didn't go far enough. Among them: State agencies must buy cars with the highest fuel ef?ciency, maintain vehicles to maximize gas mileage and use biofuels when possible instead of gasoline. Rental car contracts must put a priority on ?iel ef?ciency. The state will also give agencies a preferred products list and require that meetings and conferences take place in hotels or centers that have been given a "green lodging" certi?cation from the Department of Environmental Protection. Sen. Lee Constantine, an Altamonte Springs Republican who supported the bill Crist vetoed and authored a bill last year that authorized a state energy plan, said he was encouraged by the governor's proposals but considers it the ?rst step. ?The goal here is to move forward fast," he said. ?I'm h0peful the executive order does that, but we still have to do legislation." - 2007 Miami Herald Media Company. All Rights Reserved. 8/v-print/story/ 166659.html 7/1 1/2007 Department of the Il?lanet Earth 701 Street, SE - Suite.200, Washington, DC 20003 (301) 475-8366 - planetbarth?crols.com; 3 July 10, 2007 Honorable Mike channs Secretary . Department of Agriculture I 1400 Independence Ave. SW Washington, DC 20250 Re: Another Dangerous Series of Eield Tests for GMO Bacteria for Rice; Dear Secretary ohanns, Enclosed is a description of a series of proposed ?eld tests for non-pathogenic and pathogenic bacteria in rice. Every aspect of this proposed program carries 'risk not only to the general public, but for the US rice crop itself. 1) The non-pathogenic tests as seems customary at USDA carry antiobiotic resistance markers for the antibiotics kanamycin and ampicillin. These genes can be transferred to soil bacteria as is acknowledged by but presumed to be an insigni?cant problem. Why? The pathogenic wild strain ?open ?eld tests? proposed are astonishing and dangerous as you can see. I - could end up spreading virulent rice bacterial strains to the US commercial rice crop. - Secondly, the transgenic B.. glumae proposed for release is also a serious pathogen for humans. A case of an infant infected with this bacteria is described. 3) There are good alternatives for these issues including quorum sensing. Hasn?t the time come for the Secretary of Agriculture to step in and provide someI leadership on these issues, and promote the alternative programs that provide safety for America?s rice crops and for people? APHIS seems to need some leadership infusion on these issues. Hope this is helpful. With best ards, Erik anss Pres. Page 1 of 4 Main Identity 1 From: "jcummins" To: "Erik Jansson" Sent: Tuesday, July 10. 2007 9:09 AM Subject: dangerous bacterium released Dangerous Field Test of Non-pathogenic GM Bacteria The non-pathogenic GM bacteria not only carry antibiotic resistance marker genes, but the proposed ?eld tests will also involve the release of the wild-type bacterium that is pathogenic to rice and may cause disease in human beings Prof. Joe Cummins and Dr. Mae-Wan H0 I . This report has been submitted to the USDA on behalf of ISIS, please circulate widely. Bacterium causing rice panicle blight The United States Department of Agriculture Animal and Plant Health Inspection Service carried out an Environmental Assessment 1n response to a permit application (06-111-01r) received from Dr. Milton Rush of Louisiana State University for a ?eld test of two non-pathogenic, genetically engineered strains of Burkholderia glumae, and IS available for public comment by 19 July 2007 at: http: regulations. Burkholderia glumae Kurita et Tabei IS a bacterial plant pathogen that causes bacterial panicle blight 1n rice, and IS transmitted by infected seed. This bacterium was ?rst described in Japan as the cause of grain rotting. and seedling blight and is considered one of the most important rice pathogens 1n Japan. Epidemics of panicle blight occurred 1n the southern rice producing area of the United States during the 1995 and 1998 growing seasons, with yield losses 1n some ?elds estimated to be as high as 40 percent. Currently, there is no control method for panicle blight in the US, where most commercially grown frice varieties are susceptible to the disease. Field-testing non-pathogenic, transgenic strains of B. glumae is supposed to provide information on bacterial panicle blight infection of rice, and indicate potential routes for control of the pathogen. Non-pathogenic transgenic bacteria contain two antibiotic resistance markers B. glumae has been modi?ed by disrupting the disease-causing gene, resulting in avirulent or non-pathogenic transgenic; strains. One virulence factor 1n B. glumae 18 the compound toxo?avin, a yellowish substance that results 1n signi?cant damage to rice in the infected plants. Toxo?avin IS produced In Burkholderia by an operon (group of genes with a de?ned function) consisting of the tox gene cluster controlled by the toxR gene that is activated when the bacterium invades the rice plant. Disruption of the toxA gene results in mutants that do not produce toxo?avin. The cloning vector also contains two selectable markers, the gene :7/10/2007 Page 2 of 4 (nptII) for neomycin phOSphotransferase from Streptomyces kanamyceticus and the gene (bla) for beta-lactamase from Escherichia coli, providing resistance to kanamycin and ampicillin, respectively. The promoter each of the genes is the Bacteriophage T7 promoteir, and the terminator a TAA codon sequence. The donor DNA sequences are stably and irreversibly integrated into the bacterial genome, where they are maintained and inherited as any other genes of the bacteria cell The avirulent non-pathogenic strain therefore also can'ies stable resistance to the antibiotics kanamycin and ampicllin. The potential for horizontal gene transfer of the antibiotic resistance markers to soil bacteria 15 acknowledged 1n the assessment, but IS presumed to have insigni?cant consequences. This presumption is not borne out by a wealth of evidence we have presented repeatedly to our regulators, the most recent in June 2007 (GM Food Nightmare Unfolding in the Regulatory Sham ISIS scienti?c publication) Pathogenic wild- -type bacteria will be released 1n ?eld-tests of non-pathogenic strains Two experiments will be conducted; the ?rst evaluates toxo?avin as a disease causing agent by challenging the rice plants with wild- -type B. glumae, the second involves inoculating the rice with the transgenic avirulent bacterium followed by challenge with the virulent strain to see whether or not the presence of the avirulent strain will protect rice from B. glumae infection. These are obviously dangerous experiments to be carried out in the open ?elds; as the wild-type pathogen could easily spread from the experimental ?elds to other rice crops. The risks are unjusti?able, especially when there are other safer strategies. An alternative approach to controlling B. glumae is via ?quorum sensing?, a regulatory network in?uencing virulence based on the local density of bacteria that intercommunicate with one; another. Quorum sensing can occur within a single bacterial species as well as between I diSparate Species, and can regulate a host of different processes, essentially serving as a simple communication network. The bacteria signal to one another via special molecules. For example, toxo?avin is regulated by a quorum sensing mechanism that uses N?acyl homoserine lactones as signal molecules. A Burkholderia endophyte (a bacterium that lives inside the plant) was selected from rice and feund to be non-pathogenic to rice and to inhibit pathogenic fungi. The endophyte, modi?ed with a gene from Bacillus thuringiensis specifying N-acyl homoserine lactones, was found to prevent toxo?aVin and virulence of B. glumae Genetic modi?cation involving quorum sensing provides an alternative, also avoids use of the antibiotic resistance genes described above because toxo?avi-n can be detected by its ?uorescence and its absence is readily detected.? Another danger from the transgenic B. glumae. proposed for release is that the genus contains serious pathogens for humans: B. cepacia is a potent pathogen (Bio? remediation Without Caution, 230; B. thailandensis caused pneumonia and septicemia B. dolosa 1s pathogenic for people with cystic ?brosis B. gladioli caused ocular keratitis in an individual with diabetes, and is also found in other diseases and a number of other Burkholderia species are inc/2007 Page 3 of4 associated with human infections. It is not at all surprising, therefore. that a B. glumae infection was observed 'n an infant with chronic granulomatous disease Further investigation of the clinically isolated strain of B. glumae showed that ihe bacterium caused severe disease in rice, and a quorum sensing regulated secreted lipase was implicated in the pathogenesis of the clinical strain The USDAXAPI-IIS assessment did not consider human infection by B. glumae a serious matter based on the single human case, nor did it recommend precaution for those working with the pathogen, who will most likely take the pathogen to their homes, families and neighbours. The dangers of the transgenic B. glumae itself as a potential pathogen armed with two antibiotic resistance marker genes that could further transfer horizontally to other known Burkholderia pathogens appear to have completely escaped the notice of Both and the scientists involved should be held responsible for any harm caused to people and crops, should they allow this ?eld release to go ahead. References 1. US. Department of Agriculture Animal and Plant Health Inspection 1 Service Biotechnology Regulatory Services USDA APHIS Envirorunental Assessment In response to a permit application (06-1 1 1-01r) received from Dr. Milton Rush of Louisiana State University for a ?eld test of two non-pathogenic, genetically engineered strains of Burkholderia glumae. http: regulations. gov 2. Ho MW, Cummins and Saunders P. GM food nightmare unfolding in the regulatory sham. Microbial Ecology in Health and Disease 2007,19, 2, 66 77. 3. Cho HS, Park SYand Park SH. Interference of quorum sensing and virulence of the rice pathogen Burkholderia glumae by an engineered end0phytic bacterium FEMS Microbiol Ecol. 2007 4. Cummins and Ho MW. Bio-remediation without caution Science in Society 23, 40, 2004 5. Glass MB, Gee JE, Steigerwalt AG, Cavuoti D, Barton T, Hardy RD, Godoy D, Spratt BG, Clark TA and Wilkins PP. Pneumonia and septicemia caused by Burkholderia thailandensis in the United States. Clin Microbiol. 2006, 44(12), :4601-4. 6. Caraher E, Duff C, Mullen T, Mc Keon S, Murphy P, Callaghan and McClean Invasion and bio?lm formation of Burkholderia dolosa is comparable with Burkholderia cenocepacia and Burkholderia multivorans. Fibros. 2007, 7. Ritterband D, Shah M, Cohen K, Lawrence and Seedor J. Burkholderia gladioli keratitis associated with consecutive recurrent endophthalmitis. Cornea 2002, 21(6). 602-3. 8. Weinberg JB. Alexander BD. Majure JM, Williams LW, Kim JY. Vandamme and LiPuma JJ. Burkholderia glumae infection in an infant with chronic granulomatous disease. Clin Microbiol. 2007. 45(2). 662-5. 9. Devescovi G. Bigirimana J. Degrassi G. Cabrio L. Lipuma JJ. Kim J. llwang and Venturi V. A clinical isolate ofBurkholderia glumae causes severe disease in rice; involvement ofa quorum sensing regulated secreted lipase. Appl Environ Microbiol 2007 Jun 8; [Epub ahead of print] doi:10.l . I Dangerous Human-Made Interference with Climate Testimony of I I James E. Hansen 4273 Durham Road, Kintnersville, PA 1 Ito Select Committee on Energy Independence and Global Warming United States House of Representatives 26 April 2007 1. Summary scienti?c data and analysis reveal that the Earth is close to dangerous climate change, to tipping points of the system with the potential for irreversible deleterious effects. The information derives in part from paleoclimate data, the record of how climate changed in the past, as well as from measurements being made now by satellites and in the ?eld. The Earth?s history shows that climate is remarkably sensitive to global forcings. Positive feedbacks predominate. This has allowed the entire planet to be whipsawed between climate states. Huge natural climate changes, from glacial to interglacial states, have been driven by very weak, very slow forcings, and positive feedbacks. Now humans are applying a much stronger, much faster forcing as we put back into the atmosphere, in a geologic heartbeat, fossil fuels that accumulated over millions of years. Positive feedbacks are beginning to occur, on a range of time scales. The climate system has inertia. Nearly ?Jll response to a climate forcing requires decades to centuries. But that inertia is not our friend. It means that there is additional climate change in the pipeline that will occur in coming decades even without additional greenhouse gases. The upshot is that very little additional forcing is needed to cause dramatic effects. To cause the loss of all summer Arctic ice with devastating effects on wildlife and indigenous people. To cause an intensi?cation of subtrOpical conditions that would greatly exacerbate water shortages in the American West and many other parts of the world, and likely render the semi- arid states from west and central Texas through Oklahoma, Kansas, Nebraska and the Dakotas increasingly drought prone and unsuitable for agriculture. To cause the extermination of a large fraction of plant and animal species, an indictment of humanity?s failure to preserve creation. For humanity itself, the greatest threat is the likely demise of the West Antarctic ice sheet as it is attacked from below by a warming ocean and above by increased surface melt. There is increasing realization that sea level rise this century may be measured in meters if we follow business-as-usual fossil fuel emissions. There is a bright side to this planetary emergency. We can successfully address the emergency only by stabilizing climate close to its present state; there is no viable option. Adaptation to a continually rising sea level is not possible. Therefore, if we address the problem, there will be no need to adapt to the highly deleterious regional climate changes mentioned above. In the process we can preserve creation and restore acleaner, healthier atmosphere. The dangerous level of C02 is at most 450 ppm, and it is probably less. The low limit on CO2 forces us to move to the next phase of the industrial revolution. Changing light bulbs and making ethanol from corn will not solve the problem, although the former act is useful. Science provides a clear outline for what must be done, a four point strategy: First, we must phase out the use of coal and unconventional fossil fuels except where the C02 is captured and sequestered. There should be a moratorium on construction of old- technology coal-?red power plants. Second, there must be a rising price (tax) on carbon emissions, as well as effective energy ef?ciency standards, and removal of barriers to ef?ciency. These actions are needed to spur innovation in energy ef?ciency and renewable energies, and thus to stretch oil and gas supplies to cover the need for mobile fuels during the transition to the next phase of the industrial revolution ?beyond petroleum?. Third, there should be focused efforts to reduce non-C02 human-made climate forcings, especially methane, ozone and black carbon. Fourth, steps must be taken to ?draw down? atmospheric C02 via improved farming and forestry practices, including burning of biofuels in power plants with C02 sequestration. 3 Note that I do not specify an exact fraction by which C02 emissions must be reduced by 2050 or any other date. Indeed, science is not able to specify an exact requirement now, but we can say that emissions must be reduced to a fraction of their current values. Given the fact that readily available oil will surely be employed for mobile sources, and given the magnitudes of the different fossil the] reservoirs, it seems best to frame the problem as I have in this four-point strategy, and adjust Speci?c targets and policies as knowledge improves. Responsibility of the United States for global climate change exceeds that of any other nation by more than a factor of three, even thongh China' 15 passing the United States 1n current emissions. The United States will continue to be primarily responsible for climate change for decades to come. The above conclusions follow from the science. In part because of resistance that the scienti?c conclusions have met among special interests, and because of misinformation about the science that has been spread, I believe that it is not inappropriate for me to discuss my opinions about implications of this research for citizens in our democratic system. My opinions carry no more weight than those of any other citizen, but conceivably my experience in presenting this research in different circles allows some insight. In any case, I have as much right to express my opinion as do the special interests. In my opinion, the' United States should recognize openly its leading role in causing human-made climate change and take a leadership role in addressing the matter. We have a moral responsibility to do 50. Moreover, it is in our interest to take actions now. We can bene?t economically from extensive technology development, with many. good high-tech high-pay jobs. Of course, moving to the next phase of the industrial revolution will require changes, dislocations, sacri?ces and hard work. But these provide' no reason for inaction. - We cannot let the pleadings and misinformation of special interests determine our actions, special interests driven by motives of short-term pro?t. And we cannot shrink from our personal responsibilities. We are now, through our government, standing alongside the polluters, of?cially as a hulking ?friend of the court?, arguing against limitations on emissions. . Is this the picture of our generation we will leave for our children, a picture of ignorance and greed? We live in a democracy. Policies represent our collective will. We cannot blame others. If we allow the planet to pass tipping points, to set in motion irreversible changes to the detriment of nature and humanity, it will be hard to explain our role to our children and grandchildren. We cannot claim, with legitimacy, that ?we did not know?. In my Opinion, it is time for the public to demand, from government and industry, priority for actions needed to preserve the planet for future generations. 2. Basis for Testimony My testimony is derived primarily from the six publications listed below. It is based on a much broader body of knowledge of the scienti?c community, which is not practical to document 1n the brief hours available to prepare this testimony. The ?rst three publications below are now ?in press? and will appear in coming weeks. These three papers are in regular peer-reviewed scienti?c journals, each having been reviewed by either two or three scienti?c peers. The fourth publication also has been reviewed and recommended for publication by both anonymous referees; I will make some slight edits to that paper before returning it to thejournal within the next few weeks. The ?fth article is my attempt to describe conclusions from this research in a language intended for a broader audience. The 4 sixth article is the draft of an article, available as a referenceable preprint in the physics electronic ArXiv, which we will soon be submitting to a regular printjoumal. A. Dangerous human-made interference with climate: a (3188 modelE study (Hansen, J, and 46 co-authors, Aromas. Chem. Phys, in press, 2007, available at etal 3.html B. Climate change and trace gases (in press: Phil. Trans. Royal Soc.) etal 2.html C. Climate simulations for 1880-2003 with GISS modelE (in press: Climate Dynamics) 15 D. Scienti?c reticence and sea level rise (accepted for publication: Environ. Res. Lett.) E. State of the Wild: Perspective of a Climatologist (accepted, to be edited) Opdf F. Implications of ?peak oil? for atmospheric C02 and climate (?rst draft available in ArXiv) 3. Science In the past few years it has become clear that the Earth is close to dangerous climate change, to tipping points of the system with the potential for irreversible deleterious effects. Paleoclimate data show that climate is remarkably sensitive to global forcings. Positive feedbacks have caused the entire planet to be whipsawed between climate states, driven by very weak climate forcings. - The time scale for full glacial-to-interglacial climate changes is millennia. However, this millennial time scale re?ects the time scale of the slow weak climate forcing due to_Earth orbital changes, not an inherent climate response time. Indeed, the response time of the climate system to rapid forcings, such as human-made greenhouse gases, will be decades to centuries, a ?mction of ocean mixing time and climate feedbacks. This decade-century climate response time is unfortunate for humanity. It is long enough to prevent pe0ple from seeing immediate consequences of human-made climate forcings, as much of the climate change is still ?in the pipeline?. Yet it is short enough for large climate impacts to occur this century. The concept of additional global warming ?in the pipeline? is not new, but it has become more ominous through the realization that several nominally ?slow? climate feedbacks are likely to have signi?cant effect on decadal time scales. These include poleward movement of vegetation, darkening and disintegration of ice sheets, and greenhouse gas feedbacks. These ?slow? feedbacks, which are not included in their entirety in standard IPCC simulations, are positive and thus they amplify expected anthropogenic climate change. The implication of the scienti?c understanding is that the planet is on the verge of dramatic climate change. It is still possible to avoid the most deleterious effects, but only if prompt actions are taken to stabilize global temperature close to its present value. Because of the profound implications, it is appropriate to clarify the basis of these conclusions. We ?rst discuss fundamental aspects of the climate system: climate forcings, feedbacks and response times. We then make note of how the Earth?s climate responded to forcings in the past few million years. Finally, we summarize the basis for the conclusion that present climate is on the verge of critical tipping points. A. Climate System Climate 1s an average of weather over some period, including the variability and extremes within that period. Because day-to-day weather ?uctuations are so large, it is not easy to notice small changes of the average weather or climate. However, moderate changes of climate can have signi?cant effects, for example, on the ability of plants and animals to survive in a given region and on the stability of large lce masses and thus sea level. Climate varies a lot without any help from humans. In part the variations are simply chaotic ?uctuations of a complex dynamical system, as the atmosphere and ocean are always sloshing about. The climate also responds to natural forcings, such as changes of the brightness of the sun or eruptions of large volcanoes, which discharge small particles into the upper atmosphere where they re?ect sunlight and cool the Earth. Climate forcing. A climate forcing is alperturbation of the Earth?s energy balance that tends to alter the Earth?s temperature. For example, if the brightness of the sun increases 2% that is a positive forcing of about 4.5 W/m2 (watts per square meter), because it results in an increase of that amount in the energy absorbed by the Earth. Such a forcing would upset the normal . balance that exists between the amount of solar energy absorbed by the Earth and the amount of heat radiation emitted to space by the Earth. So the Earth responds to this forcing by warming up until its thermal radiation to space equals the energy absorbed from the sun. Doubling the amount of carbon dioxide (CO2) in the atmosphere causes a global climate forcing similar in magnitude to that for a 2% increase of solar irradiance. The C02 forcing works by making the atmosphere more opaque to in?'ared radiation, the of the Earth?s heat radiation. As a result of this increased opacity the heat radiation to space arises from greater heights in the atmosphere. Because the temperature falls off with height in the lower atmosphere, energy radiated to Space with doubled 18 reduzced by an amount that IS readily calculated from radiation physics to be approximately 4 W/mz. So the planet?s energy imbalance 15 about the same as for a 2% 1ncrease of solar irradiance. In either case, the Earth: responds by warming up enough to restore energy balance. Climate models show that, as might be expected, two forcings of similar magnitude yield similar global temperature change, although variations in the? ??ef?cacy of speci?c forcings of the order of 20% are not uncommon, and a few more extreme cases have been found. Variations in ef?cacy are primarily a result of the differences in the physical locations (latitude or altitude) of the forcings, which affects the degree to which the forcings can bring climate feedbacks into play, as discussed below. Climate sensitivity and climate feedbacks. Global climate sensitivity is usually de?ned as the global temperature change that occurs at ?equilibrium i. after the climate system has; had a long time to adjust, in response to a speci?ed forcing. The speci?ed forcing lS commonly taken to be doubled CO2, thus a forcing of about 4 W/mz. Climate sensitivity can be evaluated either theoretically, with the help of climate models, or empirically, from the Earth's climate history. :In either case, it must be recognized that the climate sensitivity so inferred depends upon what climate variables are ?xed as Opposed to being allowed to change in response to the climate forcing. The now famous 1979 National Academy of Sciences study of climate sensitivity chaired by Jules Charney focused on a case in which atmospheric water vapor, clouds and sea ice are allowed to vary with the climate,-but other factors such as ice sheets and the global distribution of vegetation are kept ?xed as unchanging boundary conditions. Also long-lived greenhouse 6 . I . gases (GHGs), such as carbon dioxide (C02), methane (CH4) and nitrous oxide (N20) are taken as speci?ed boundary conditions or forcings. In reality all of these boundary conditions can change in reSponse to climate change, in which case they become climate feedbacks that can be either positive feedbacks (magnifying the climate change) or negative feedbacks (diminishing the climate change). The choice of feedbacks that were allowed to operate in the Charney study (water vapor, clouds, sea ice) was in part based on realization that these variables change rapidly, they are ?fast feedbacks?. Thus if one is interested in climate change on the time scale of decades or longer, these feedbacks must be allowed to operate. Ice sheets and forest cover, on the other hand, might be considered ?slow feedbacks?, not expected to change much on decadal time scales. In addition, climate models were not yet capable of modeling these slower processes. The Charney study suggested that equilibrium climate sensitivity was for doubled C02, with uncertainty at least 50% Improving climate models continue to yield global climate sensitivity for doubled C02, but uncertainty remains because of the dif?culty of accurately simulating clouds. A more de?nitive evaluation of climate sensitivity is provided by the Earth?s history. With the same choices for the variables speci?ed as forcings, empirical data for climate change over the past 700,000 years yield a climate sensitivity of for each W/m2 of forcing, or- for a 4 W/m2 forcing. (see Figure 2 of Reference B). This empirical evaluation of climate sensitivity eliminates the concern with climate models, that they may inadvertently exclude important processes. The real world climate change included any cloud feedbacks that exist. Climate response time. A practical dif?culty with climate change arises from the fact that the climate system does not respond immediately to climate forcings. Figure 1 shows the climate response to a forcing introduced at time 0. It requires about 30 years for 50% of the eventual (equilibrium) global warming to be achieved, about 250 years for 75% of the reSponse, and perhaps a millennium for 90% of the surface response. The exact shape of this reSponse function depends upon the rate of mixing in the ocean, thus upon the realism of the ocean model that is used for its calculation. The response time also depends upOn climate sensitivity, the response being slower for higher sensitivity. The reason for this is that climate feedbacks come into play in response to climate change, not in response to the forcing per se, and thus with stronger feedbacks and higher climate sensitivity the response time is longer. The curve in Figure 1 was calculated for sensitivity for doubled C02. This long response time means that even when GHGs stop increasing, there will be additional warming ?in the pipeline?. Thus we have not yet felt the climate impact of the gases that have already been added to the atmosphere. This lag effect makes mitigation strategies more arduous. i I I so - linear scale -- 7.: Er"- 105: state 2-0 lit-{I 20:: 2?03 100-315-110 year Figure 1. Climate reSponse function (percent of equilibrium response) based on global surface air warming of GISS modelE coupled toRussell ocean model (Reference B). 7 SIow climate feedbacks. The ?Charney?, or fast feedback, climate sensitivity is intended to be relevant to decadal time scales. But it is . ecoming clear that other feedbacks, omitted because they are ?slow? and dif?cult to deal with, may also be important. One ?slow? feedback is the poleward niovement of forests with global warming. If evergreen forests replace tundra and scrubland vegetation, it makes the surface much darker. Trees are ?designed? to capture ef?ciently, and thus they can provide a strong positive climate feedback. Forest cover is a powerful ,positive feedback 'at Northern Hemisphere high latitudes, and signi?cant changes are already beginning. Another ?slow? feedback is associated with ice sheets. An ice sheet does not need to disappear for signi?cant feedback to occur: just the change of ice surface albedo (re?ectivity) that occurs with increased area and melt season duration contributes a large local climate feedback. This feedback occurs in a region where warming is especially important, because of the effect of warming on ice sheet disintegraticsm and sea level rise. Increased areas of surface melt, and lengthening melt season, are observed on both Greenland and West Antarctica. Still another "slow feedback 18 the effect of warming on emissions of long-lived GHGs from the land or ocean. Melting of tundra in North America and Eurasia is observed to be causing increased ebullition of methane from methane hydrates. It 15 apparent that these ?slow feedbacks, which are primary causes of the extremely high climate sensitivity on paleoclimate time scales, as discussed below, are beginning to operate already in response to the clear global warming trend of the past three decades. B. Earth?s History Civilization developed during'the present interglacial'period, the Holocene, a period of relatively stable climate, now almost 12, 000 years in duration. In this period the Earth has been warm enough to prevent formation of ice sheeis 1n North America or Eurasia, but cool enough to keep Ice sheets on Greenland and Antarctica. :Sea level rose by more than 100 meters between the peak of the last we age, 20, 000 years ago and the Holocene. After sea level ?nally stabilized, about 7,000 years ago, the ?rst urban centers developed at many points around the globe, perhaps because of the increase in coastal margin productivity that occurred with sea level stabilization and thus the increased availability of high quality food necessary for urban development (Day et al., Emergence of complex societies after sea level stabilized, EOS Trans. Amer. Geophys. Union 88, 10 {a?i West-rm Equatorial Pacrfic 1 p5 \{Hhon Years (13) Indian Ocean SET . I l- -: 1.111 {-3111 I - - ?l 1 mas-1 1 - '1 IS CZQEB?1neanh ?5315-it?d 50 13?5? 205}?- zit-3' 5-3 23-35 01c} i Dare 1:313? Figure 2. Western Equatorial Paci?c (Medina-[Elizade and Lea, The mid-:Pleistocene transition in the tropical Paci?c, Science 310, 1009-1012, 2005. I "t 1 135'} 13': How much warmer does the Earth need to be to destabilize ice sheets and initiate eventual sea level rise of several meters or more? Figures 2 and 3 provide useful indications. 8 With the warming of the past 30 years, key tropical regions are now within or less of the x/ warmest interglacial periods of the past million years (Figure 2). In the warmest of these interglacial periods, when global mean temperature was not more than about warmer than today, sea level is estimated to have been 4 :h 2 higher than today (speci?cally during the previous interglacial period, about 130,000 years ago). It is important to note that the large global climate changes illustrated in Figure 2 are entirely accounted for by two mechanisms: changes in the surface albedo of the planet (due to ice sheet area, vegetation distribution, and exposure of continental shelves) and changes in the amount of long-lived greenhouse gases (C02, CH4, N20) in the atmosphere. Both the albedo and GHG changes occurred as feedbacks on these long time scales, the principal instigator of the climate changes being changes of the Earth?s orbital elements (the tilt of the Earth?s spin axis to the orbital plane, the eccentricity of the orbit, and the season of Earth?s closest approach to the sun) due to gravitational pull of Jupiter, Saturn and Venus on Earth. As feedbacks, the albedo and GHG changes tended to lag the climate change by several hundred years. It is probably not coincidental that the lag time is comparable to the ~500 year time scale for ocean turnover. It is important to note that the response time for the ?slow? feedbacks is much faster than the time scale of the orbital forcing changes. The principal orbital forcing is change of the tilt of the Earth?s Spin axis, which varies from about to 241/2" at a ?'equency of about 41,000 years (41 kyr). When the tilt is large it exposes both poles (at 6 month intervals) to increased summer insolation that tends to melt ice sheets, while small tilt allows polar ice sheets to grow. This is the most important orbital forcing, because it has the same sign in the two hemispheres. And this forcing is always present, independent of the eccentricity of the Earth?s orbit. The eccentricity (non-circularity) of the Earth?s orbit varies irregularly from about zero (circular orbit) to about 0.06. The time scale of the changes, as the Earth is tugged by several planets, is not so regular as for tilt, but the largest changes are on ~100 time scales. When the eccentricity is signi?cantly different than zero the third orbital parameter comes into play: the season when the Earth is closest to the sun, or, stated differently, the precession of the equinoxes. This precession is the most rapid of the orbital forcings, going through a complete cycle in about 23 kyr. Eccentricity and precession, working together, cause climate change on ~23 and ~100 periodicities, but the forcing has opposite sign in the two hemispheres, so the net global effect tends to be small, except in special cases as noted below. The eccentricity/precession forcing functions via its effect on seasonal insolation. Today, f0r example, the Earth is closest to the sun in January and furthest away in July. This situation favors growth of ice sheets at high latitudes in the Northern Hemisphere, as the relatively warm winters increase atmospheric moisture and snowfall, while the cool summers allow a budding ice sheet to survive. Thus the natural tendency today, absent humans, would be toward the next ice age, albeit . the tendency would not be very strong because the eccentricity of the Earth?s orbit is rather small However, another ice age will never occur, unless humans go extinct. Although orbital changes are the ?pacemaker? of the ice ages, the two mechanisms by which the Earth becomes colder in an ice age are reduction of the long-lived GHGs and increase of ice sheet area. But these natural mechanisms are now overwhelmed by human-made emissions, so GHGs are skyrocketing and ice is melting all over the planet. Humans are now in control of global climate, for better or worse. An ice age will never be allowed to occur if humans exist, because it can be prevented by even a ?thimbleful? of CFCs (chloro?uorocarbons), which are easily produced. 3150' Global Sea Let e1 Tempe: arm-e Pic-xv WWMM 1111111111111 I 1.11:: 1 113g 4,5 - 31113113111113qu 351:: 3-13: 15-12 2-1-11 . 2531:: 513-1 Figure 3. Proxy record of Plio Pleistocene (3. 5 million years) temperature and ice volume. Based on oxygen isotope preserved 1n shells of benthic (deep ocean dwelling) foraminifera. (Lisieki and Raymo, A Pliocene-Pleistocene stack of 57 globally distributed benthic 5130 records, Paleoceanogr. 20, PA1003, doi: But back to the natural world: why did the principal periodicity of ice ages change about one million years ago from 41 3r to 100 kyr? Figure 3 illustrates this change. H20 molecules that contain the oxygen isotope 30 are heavier and thus move more slowly than H20 molecules containing the more abundant 160. Therefore H20 molecules with 180 evaporate ?'om the ocean less readily. As a result, ice sheets are depleted 1n 80, and as ice sheets grow the proportion of 8'0 in ocean water increases. These changes aIre recorded 1n the '80 of shells of microscopic marine animals preserved now in oceans sediments. Figure 3 shows a record of 8'0 1n ocean Sediments around the world (from Lisieki and Raymo, A Pliocene-Pleistocene, stack of 57 globally distributed benthic 6180 records, Paleoceanogr. 20, PA1003, 5?30 (5 means the change of? relative to a standard case)? 1n Figure 3 shows the 41 frequency of global temperature that existed up until about one million years ago when it changed to a frequency of about 100 kyr. Before noting the explanation for this transition, which may be very simple, I need to ?rst note that there are two factors that in?uence 5180 signi?cantly: one, already mentioned, is the amount of we locked 1n ice sheets sea level), and the other 15 the ocean temperature at the location where the microscopic creatures (benthic, deep ocean dwelling, foraminifera, whose shells carry the 5180 record) lived. The long-tenn trend' 1n Figure 3 is a consequence of both the ocean becoming colder over that period and more (isotopically light) water being locked 1n ice sheets on the continents. At the beginning of this period (3.5 million years ago, the middle of the Pliocene epoch) the world was warmer than today and sea level was 25 :t 10 In (80 30 feet) higher. Figure 3 also shows that the amplitude {of the glacial-interglacial climate ?uctuations increased as the world became colder. This is because the ice/snow albedo feedback becomes larger as the planet becomes colder and has larger area of Ice and snow. The period of the glacial- interglacial swings was ~41 up until one million years ago, because the areas of' Ice and snow in the two hemispheres were comparable, and thus the effects of eccentricity and precession, oppositedn the two hemiSpheres, tended to largely offset each' other In global effect. However, by one million years ago the Earth had become cold enough for a huge ice sheet (called the Laurentide ice sheet) to cover most of Canada, reaching into parts of the United States. A comparable area of ice/snow could not form in the Southern Hemisphere, because at those latitudes there is no land in the Southern Hemisphere, but rather roaring east-west ocean currents. This huge asymmetry between the hemispheres allowed the 10 eccentricity/ precession effects to become important, so thereafter the global temperature contains signature of all of the ~23, ~41 and ~100 periodicities. The astute reader is probably asking: why was the Earth gradually getting colder, ice area growing, and sea level falling, overall, during the past several million years. The reason, almost surely, was the strong orogeny (mountain building) during the past 10-20 million years. The South American continent has been hitting a rough spot, pushing up the Andes rapidly. It is hard to determine the exact rate, but available evidence indicates, for example, that between 11 and 7 BP (before present) the Andes were rising at a rate of about 1 mm per year, 1 km per million years (Ghosh et al., Rapid uplift of the Altiplano revealed through [30180 bonds in paleosol carbonates, Science, 311, 511-515, 2006). The Himalayas have also been rising rapidly during the past 40 million years (Raymo and Ruddiman, Tectonic forcing of the late Cenozoic climate, Nature, 359, 117-122, 1992), as the Indian plate is crashing into Asia. Rising mountains increase the rate of weathering of the rocks, and thus the deposition of carbonates on the ocean ?oor, thus drawing down atmospheric C02 amount. The precise ice core records of atmospheric CO2 amount go back only about 700,000 years, so we must use much more crude estimates of the atmospheric C02 content, for example, the stomata of leaves change as atmOSpheric C02 changes. From such evidence, it is estimated that the C02 amount 31/2 million years ago was probably in the range 350-450 ppm. It is apparent that the Earth?s history has much to tell us about what degree of atmospheric change will constitute ?danger?. I have described some of the empirical information about climate sensitivity and climate feedbacks. There is another vital piece of information in the paleoclimate data that warrants Special attention, because it is relevant to what may be the greatest danger that humanity faces with climate change: sea level rise. One thing that the paleoclimate record shows us is that ice sheet disintegration and sea level rise are usually much more rapid than the Opposite process of ice sheet growth and sea level fall. This is reasonable because ice sheet disintegration is a wet process with many positive feedbacks, so it can proceed more rapidly than ice sheet growth, which is limited by the snowfall rate in cold, usually dry, places. At the end of the last ice age sea level rose more than 100 in less than 10,000 years, thus more than 1 per century on average. At times during this deglaciation, sea level rose as fast as 4-5 per century. If we follow ?business-as-usual? GHG emissions, yielding global warming this century of a few degrees Celsius, how long will it take for West Antarctica and Greenland to begin to disintegrate? In the past, an answer to this question has been given based on ice sheet models that were built to try to match paleoclimate records of sea level change. These models tend to require millennia for ice sheets to change by large amounts. It is now reasonably clear that those models were based on a false premise and incomplete physics. The large sea level changes between glacial and interglacial times typically require several thousand years. However, this correSponds to the time scale of the changing forcing, not an inherent response time of the ice sheets. 0n the contrary, there is no evidence of any substantial lag between the forcing and the ice sheet reSponse (references and above). The most rapidly changing paleoclimate forcing has a time scale of 11-12 ky from minimum forcing to maximum forcing, and the changes of sea level are practically coincident with the changes of forcing, suggesting that ice sheets can respond to forcings within centuries. C. Current Situation People arejust beginning to notice that climate is changing. Global warming, in the past 30 years, is much smaller than day to day weather ?uctuations or even mean local temperature anomalies. However, the warming is larger over land than over ocean, and the 11 astute observer can note changes that have occurred over the past several decades. A typical . isotherm (line of a given average temperature) is now moving poleward, in typical land areas, by about 50 km per decade. As this warming continues, or accelerates with ?business-as-usual? GHG emissions, it will begin to have dramatic effects, as discussed in the next section. To understand the urgency of addressing the global warming problem, it is necessary to recognize a critical distinction that exists among pollution problems arising in the fossil-fuel- driven industrial revolution. When the industrial revolution began in Britain it was powered ?rst by coal, the most abundant of the fossil ?Jels. Later discoveries of oil and gas, which are more mobile and convenient fossil fuels, provided energy sources that helped power the developed world to ever greater productivity and living standards. We did not face up to the dark side of the industrial revolution until it was thrust in our face. London choked on smog. A river in the United States burned. Forests were damaged by acid rain. Fish died in many lakes. These problems were traced to pollutants from fossil ?Jels. We have solved or are solving those pollution problems, at least in developed countries. But we did not address them until they hit us with full force. That approach, to wait and see and ?x the problems post facto, unfortunately, will not work in the case of global climate change. On the contrary, because of the inertia of the climate system, the fact that much of the climate change due to gases already' in the air is still? in the pipeline, and the time required for economically-sensible phase-out of existing teizhnologies, 1gnoring the climate problem at this time, for even another decade, would serve to [lock 1n future catastrophic climatic change and impacts that will unfold during the remainder of this century and beyond (references A and B). But there IS no reason for gloom and doom. On the contrary, there are many bright sides to the conclusion that the ?dangerous? level of C02 15 no more than 450 ppm, and likely much less than that. It means that we, humanity, are forced to ?nd a way to limit atm05pheric C02 more stringently than has generally been assumed. In so doing, many consequences of high C02 that were considered inevitable can be avoided. We will be able to avoid acidi?cation of the ocean with its destruction of coral reefs and other ocean life, retain Arctic' Ice, prevent the West from become intolerably hot with deserti?cation of presently semi- -arid regions, and the other undesirable consequences of large global warming. It 15 becoming clear that we must make: a choice. We can resolve to move rapidly to the next phase of the industrial revolution, and' 1n so doing help restore wonders of the natural world, of creation, while maintaining and expanding bene?ts of advanced technology. Or we can continue to ignore the problem, creating a different planet, with eventual chaos for much of humanity as well as the other creatures on the planet. 4. Metrics for Dangerous Climate Change I have argued elsewhere (Hansen, New York Review of Books, no. 12, July 13, 2006) that ice sheet disintegration and extermination of species deserve high priority as metrics for dangerous climate change, because, for all practical purposes, these consequences are irreversible. Regional climate change also has great impacts on humanity. A. Sea Level Rise The sharpest criterion for de?ning dangerous climate change 18 probably maintenance of long-term sea level close to the present level (reference A), as about one billion people live within 25 elevation of today?s sea level. These areas (Figure 4) include many East Coast U.S. cities, almost all of Bangladesh, and areas occupied by more than 250 million pe0ple in China. 12 The Earth?s history suggests that a C02 level exceeding 450 is almost surely dangerous, in the sense of risking sea level rise of several meters or more. Indeed, the Earth?s history suggests that the C02 limit may be signi?cantly lower than-that. Reduction of non-C02 forcings provides some, but only moderate, ?exibility in the C02 ceiling. U.S. Area Under Water Europe Area Under Water . ., . ?'l-Tm 1] (i 35. 35 :10? I090 3515 0 Ii 35 3.5 :5 300 ml!) 4:05. Central Asia: Area under Water Far East: Area under Water - .. 2-31 15 3?5 .?sno um (.500 r. 15 3.5 :5 Jon anon 533: Figure 4. Areas under water for speci?ed sea level increases. Blue regions would be expected to eventually be under water with global warming as great as that of the middle Pliocene Sea level change has received less attention in the past than it warrants, because of a common presumption that ice sheets had an inertia preventing substantial changes on time scales shorter than millennia. Closer inspection of paleoclimate data calls that assumption into question, and increasingly rapid changes on West Antarctica and Greenland, observed by satellite and in the ?eld during the past few years, are truly alarming. West Antarctica is of particular concern, because, as a marine based ice sheet, global warming attacks it from both below and above. Sea level is already raising at a rate of 3.5 cm per decade (more than one foot per century) and the rate is accelerating. It is impossible to say at exactly what level of global warming cold accelerate to meters per century, because ice sheet disintegration is a very non- a" linear process in which changes can occur suddenly. But paleoclimate data suggests that we are not far from such a level of global warming. B. Extermination of Species Climate change is emerging while the state of the wild is stressed by other forces. Pressures include destruction of habitat, hunting and resource use, pollution, and introduction of exotic competing species. Climate effects are magni?ed by these stresses, including human- caused fragmentation of ecosystems. As a result, continued business-as-usual greenhouse gas emissions threaten many ecosystems and their species, which together form the fabric of life on Earth and provide a wide range of services to humanity. 13 Animals and plants migrate as climate changes, but their potential escape routes may be limited by geography or human-made obstacles. Polar species can be pushed off the planet, as they have no place else to go. In Antarctica, A!delie and emperor penguins are in decline, as shrinking sea ice has reduced the abundance of krill, the penguins shrimp-like food source (Gross, As the Antarctic ice pack recedes, a fragile ecosystem hangs in the balance, Biol. Arctic polar bears are also feeling the pressure of melting sea ice. Polar bears hunt seals on the sea ice and fast in the summer, when the ice retreats from shore. As ice is receding earlier, populations of bears in Canada have declined about 20%, with the weight of females and the number of surviving cubs decreasing a similar amount?All . .2 . . unassumsgraas Figure 5. Polar bear numbers are in decline. populations?the weight of females and the number of cubs have decreased about 20 perceht. (Image Credit: Paul Burke, First People) The apparent good news is that the US. Fish and Wildlife Service is considering whether it will protect polar bears under the Endangered Species Act (Pennisi, U.S. weighs protection for polar bears, Science 315, 25, 2007). I say apparent, because the announcement was made only after the Fish and Wildlife Service was taken to court for failure to act. And connection of polar bear plight to greenhouse gas emissions has beien drawn only by those bringing suit, not by the government. Life in alpine regions, including the biqlogically diverse slopes leading to the mountains, is similarly in danger of being pushed off the planet. As a given temperature range moves up the mountain the area with those climatic conditions becomes smaller and rockier, and the air thinner. The resulting struggle for life is already becoming apparent in the southwest United States, where the effects are hastened by intensifying drought and ?re. The Mount Graham red squirrel survives now on a single Arizona mountain, one of the ?islands in the sky? in the American Southwest. These ?islands? are green regions scattered on mountains in the desert. Stresses on this species include introduction of a grey squirrel that raids the food middens built by the red squirrel. Classi?ed as endangered, the Graham red squirrel' population rebounded to over 500 by 1999 (Jordan, Computers may help save Mount Graham red squirrel, Um'v. Arizona News, April 27, 2006), but has since declined to between 100 andi200 (Egan, Heat invades cool heights over Arizona desert, New York imes, 27 March 2007). Loss of the red squirrel will alter the forest, as its middens are a source of food and habitat for chipmunks, voles and mice. 14 Sim?: rt. I -. :31' ;r a '1 II .- "17- -. I 3.315.355it?? {frag} -. - tci?z?? - Li - J?c . Flgure 6. Mount Graham Red Squirrel survrves on a smgle mountain in Arizona, one of dozens of ?islands in the sky?, green regions surrounded by desert. Green islands and squirrels are pushed higher as temperature rises and will be pushed off the planet if global warming continues. (Credits: PHOTOSMITH, 2004, Claire Zugmeyer and Bruce Walsh, University of Arizona.) The new stress driving down Graham red squirrel numbers, perhaps toward extinction, is climatic: increased heat, drought and ?res. Heat-stressed forests are vulnerable to prolonged beetle infestation and catastrophic ?res. Rainfall still occurs, and when it does it can be substantial because warmer air holds more water. But dry periods are more intense and resulting forest ?res burn hotter, thus leaving an almost?lifeless ?scorched earth? so devastated that lower reaches of the forest cannot recover, becoming part of the desert below. Might the Graham red squirrel be ?saved? by transplantation to a higher mountain, where it could compete for a niche? One dif?culty would be the ?tangled bank? of interactions that has evolved among species (Montoya et al., Ecological networks and their fragility, Nature 442, 259- 264, 2006). What is the prospect that humans can understand, let alone reproduce, all the complex interactions that create ecological stability? ?Assisted migration? thus poses threats to other species (Zimmer, A radical step to preserve a Species: assisted migration, New York Times, 23 January 2007), as well as uncertain prospects for those that are transported. The underlying cause of the climatic threat to the Graham Red Squirrel, and millions of other species, is continued ?business-as-usual? increase of fossil fuel use. The best chance for all species, including humans, is a conscious choice by the latter species to pursue an alternative energy scenario, one leading to stabilization of climate. C. Regional Climate Change Regional climate changes due to global warming may have the greatest impact on humans in the near-term. Changes of the hydrologic cycle are of special concern. An expansion and intensi?cation of subtropical dry conditions occurs consistently in climate model simulations of global warming. Practical impacts include increased drought and forest ?res in regions such as the Western United States, Mediterranean, Australia, and parts of Africa. Paleoclimate data provide ?thher evidence of increased drought in the Western United States accompanying warmer climate. It is dif?cult to specify a precise threshold for ?dangerous? based on regional effects, but there is already evidence that some of these impacts are beginning to be detectable. Thus regional climate change, as well as sea level and species, would be protected by stabilizing global warming near its current level. 15 5. Four-Point Strategy to Stabilize Climate The evidence we have presented is no reason for gloom and doom. Instead, we must resolve to move rapidly to the next phase of the industrial revolution. In doing so, we can help restore wonders of the natural world, of creation, while maintaining and expanding bene?ts of advanced technology. Actions that are needed become apparent upon review of basic fossil fuel facts. Figure 7a shows estimated amounts of C02 in each fossil fuel reservoir: oil, gas, coal and unconventional fossil fuels (tar sands, tar shale, heavy oil, methane hydrates). A signi?cant fraction of oil and gas has already been used (dark portion of bar graph). Proven and anticipated reserves are based on Energy Information Administration estimates. Other experts estimate higher or lower reserves, but the uncertainties do not alter our conclusions. {Gt} Fossil Fuel Resen'oirs co. I'ijn) (bf: Cumulative Emissions 13v Region WeReserve Growth so "j 3: {7:53. 1000 - El Prom: Rescr-ts Methane . {game .-.- E1 Emissions mas-10:25} Hrm?atJim.- 60 ?if" ,h Iva-jib as? ha. a .3 9.. 0? up: 51.4. .. . .. wo? 311-3 3. 4o 2 oz :urcpe t- - - . . 400' Gemmw 20 . .. 1 - - lime knackIn: k'ia. .7 jag-5"; . . .. rain-If." $311.Oil (3:15 Can! Other I 1850 1900 1550 'Ciunulam'e 1311113310115 to 2003 std) Per I. spit: :ossil Fuel Rate {101:3 1. arbon year person} a Rest of Europe Emma: Awamlm '5 Aims: S. line: 1:213" [era-re Inn Canada Gummy ?agd-z?m Japan Decreaamg Total Ezmssicus Figure 7. Carbon dioxide contained in fossil fUBl reservoirs, the dark areas being the portion already used, c) Cumulative fossil fuel CO2 emissions by different countries as a percent of global total, Per capita emissions for the ten largest emitters of fossil fuel C02 (Marland, A Compendium of Data on Global Change, Oak Ridge Natl. Lab., 2006). - Data on fossil fuel reservoirs must be combined with knowledge about the ?carbon cycle?. The ocean quickly takes up a fraction of fossil'?Jel CO2 emissions, but uptake slows as C02 - added to the ocean exerts a ?back pressure? on the atmosphere. Further uptake then depends upon mixing of C02 into the deep ocean and ultimately upon removal of C02 from the ocean via formation of carbonate sediments. As a result, one?third of fossil fuel C02 emission remains in the air after 100 years and one-quarter still remains after 500 years. 16 One conclusion from these fossil fuel facts is that readily available oil and gas resources alone will take atmospheric C02 to the neighborhood of 450 ppm. Coal and unconventional fossil fuels could take atmospheric C02 to far greater levels. These carbon reservoirs are an important boundary condition in framing solutions to the climate crisis. A second boundary condition is the Earth?s energy imbalance, which de?nes the ?momentum? of the climate system. Creation of ?a different planet?, with an ice-free Arctic and eventual disintegration of ice sheets, can be averted only if planetary energy balance is restored at an acceptable global temperature, one that avoids these catastrOphic changes. Estimates of permissible additional warming must be re?ned as knowledge advances and technology improves, but the upshot of science is that the ?safe? global temperature level is, at most, about greater than year 2000 temperature. It may be less, indeed, I suspect that it is less, but that does not alter our conclusions. A limit on added global warming implies a C02 ceiling of about 450 (reference A). There is some ?play? in the CO2 ceiling due to other human-made climate forcings that cause warming, especially methane, nitrous oxide, and ?black soot?. The ?altemative scenario? (Hanse et al., Proc. Natl. Acad. Sci., 97, 9875-9880, 2000), designed to keep additional warming under has C02 peaking at 475 via an assumed large reduction of CH4. However, human- made sulfate aerosols, which have a cooling effect, are likely to decrease and tend to offset reductions of positive non-CO2 forcings. Therefore 450 is a good first estimate of the maximum allowable CO2. Indeed, if recent mass loss in Antarctica is the beginning of a growing trend, it is likely that even 450 is excessive and dangerous. The low limit on allowable carbon dioxide has a bright side. Such a limit requires changes to our energy systems that would do more than solve the sea level problem. They would leave ice in the Arctic and avoid dramatic climate changes in other parts of the world. Air pollutants produced by fossil fuels, especially soot and low level ozone, also would be reduced, thus restoring a more pristine, healthy planet. Most species on the planet could survive. An outline of the strategy that humanity must follow to avoid dangerous climate change emerges from the above boundary conditions. It is a four-point strategy (following tables). Outline 0f Solution Methods to Reduce CO2 Emissions 1. Goa! only in Powerniarns Sequestration 1. Energy Efficiency Conservation Phase?out old techz-iology. Timeta ble TBD More Efficient Technoiogy 2. Stretch Cenventio?nal Oil Gas Life Style Changes Via Incentives {Carbon tax] 8. Standards 2. Renewable 8. COz-Free Energy Avoid Unconventional Fossil Fuels Hydro 3. Reduce non-CO: Climate Geothermal Methane. Black Soot. Nitrous Oxide 4. Draw Down Atmospheric CO, liriproved Agricuitnrai 8. Forestry Practices '9 WM Perhaps BiofueI-Powered Power-Plants '5 Three are Essential 3. Capture 8. Seouestration A. Coal and Unconventional Fossil Fuels First, coal and unconventional fossil fuels must be used only with carbon capture and sequestration. Existing coal-?red power plants must be phased out over the next few decades. This is the primary requirement for avoiding ?a different planet?. It is probably impractical to prevent use of most of the easily extractable oil and its use in small mobile sources. This makes it essential to use the huge coal resource in a way cuach that the C02 can be captured, and, indeed, the logical use of coal is in power plants. It is important to 17 recognize that a substantial fraction of the C02 emitted, if it is not captured, will remain in the air for an eternity. Thus the most critical action for saving the planet at this time, I believe, is to prevent construction of additional coal-?red power plants without C02 capture capability. As governments around the world, not only in the United States, China and India, fail to appreciate this situation, it is important that citizens draw attention to the issue. B. Stretching Oil and Gas with a Carbon Tax 1 Oil and gas must be ?stretched? so as toicover needs for mobile fuels during the transition period to the next phase of the industrial era ?beyond petroleum?. This ?stretching?, almost surely, can only be achieved if there is a continually rising price on carbon emissions. Innovations will be unleashed if industry realizes that this rising price is certain. Ef?ciency standards, for vehicles, buildings, appliances, and lighting are needed, as well as a carbon price. The carbon tax will also avert the threat of emissions from unconventional fossil ?iels, such as tar shale. C. Drawing Down AtmOSpheric C02 Because CO2 is already near the dangerous level, steps must be taken to ?draw down? atmospheric C02. Farming and forestry practices that enhance carbon retention and storage in the soil and biosphere should be supported. In addition, burning biofuels 1n power plants with carbon capture and sequestration could draw down atmospheric CO2 (Hansen, Political interference with government climate change science, 19 March 2007 testimony to Committee on Oversight and Government kReform of the U.S. House of Representatives, in effect putting anthropogenic C02 back underground where it came from. C02 sequestered beneath ocean sediments is inherently stable (House et al., Permanent carbon dioxide storage in deep-sea sediments, Proc. Natl. Acad. Sci, 103, 12291-12295), and other safe geologic sites may also be available. I This use of biofuels in a power plant, which would draw down atmospheric C02, should be contrasted with use of corn-based ethanol to power vehicles. The latter process still results in large increases of atmOSpheric C02, increases food prices worldwide, and results in deforestation and poor agricultural practices as greater land area is pressed into- service. In the use of bio?Jels for power plants, mentioned above, we would envisage use of cellulosic ?bers and native grasses harvested with non-till practices. Limited land: availability may make it difficult for biofuels to be the long-term solution for vehicle propulsion. D. Non-C02 Climate Forcings A reduction of non-C02 forcings can be a significant help in achieving the climate forcings needed to keep climate change within given bounds. Reduction of non- -C02 forcings has bene?ts for human health and agriculture [West et al., 2005; Air Pollution Workshop, giss. nasa. as well as for climate. Reduction of non-C02 . forcings 1s especially effective 1n limiting Arctic climate change (reference A). I 18 Research 1 Arsenic and Fluoride Exposure in Driniking Water: Children's IQ and Growth in Shanyin County. Shanxi Province Ghina San-X13119 111121119,f Zheng- Xiao- Tian Cheng.,J11n Li,? Zhi-Ping Sang.? Xiang? Dong Zheng, Ling? Ling Xiao- Yan 121117510,1r Zhao-Ming Wu.? and Zhi-Ouan Wang? 1Sha nxi Institute for Prevention and Treatment of Endemic Disease, Linfen. Shanxi Province. People? 3 Republic of China: 2Shanyin Center for Disease Control and Preventio n. Shanyin Shanxi Province. People' 5 Republic of China BACKGROUND: Recently. in a cross-sectional study of 201 children in Araihazar, Bangladesh, exposure to arsenic (As) in drinking water has been shown to lower the scores on tests that measure children?s intellectual function before and after adjustment for sociodemographic features. We imcstigatcd the ellircts ofAs and ?uoride exposure on childrenl's intelligence and growth. We report the results ofa srudy of 720 children between 8 and 12 years of age in rural villages In Shanyin county. Shanxi province, China. The children were exposed to A5 at concentra- tions of 142 106 pg?. (medium-As group) and 190 1 13.5 (high- -As. Mgroup) drinking water compared with the control group that was exposed to low concentrations ofAs (Z a 3 pgiL) and low concentrations of ?uoride 1 0.2 mglL). A study group oi'childrenI exposed to high concen- trations of ?uoride (8. 3 a 1. 9 mglL) but low concentrations ofAs (5- was also included because of the common occurrence of elevated concentrations of fluoride to groundwater to our study area.1\ standardized lQ(iutelligence quotient) test was modi?ed folr children In rural China and was based on the classic Raven' 5 test used to determine the effects 0- these exposures on chil- dren's intelligence. A Standardized measurement procedure for weight. height. chest circumference. and lung capacity was used to determine the effects of these exposures on children?s growth. RESUITS: The mean 1Q scores decreased From 105 1 15 for the control group. to 101 16 for the medium-As group (p 0. 05). and to 95 17 for the high- -As group (p I: [ll 01). The mean 1Q score For the ltigh- -iiuoride group was 101 16 and significantly dili'erent From that of the control group (p 0. 051. Children In the control group were taller than those In the high- -iluoride group (p 0. 05): weighed more than the those In the high-As group (p 0. 05); and had higher lung capacity than those In the medium-As group (p 0. 03). CONCLUSIONS: Children 5 intelligence and growth can he allected by higlt cancentrations oFAs or ?uoride. lite 1Q scores of the children In the high As group were the lowest among the four groups we investigated. It 15 more signi?cant that high coucentrations ofAs achct children' 5 intelligence. It indicates that arsenic exposure can affect children intelligence and growth' KEYWORDS: arsenic. children. fluoride. growth. 1Q. water. 51111111111 ?with Perspecr 115:643?647 (2006). available via blip. Weir. dot. org/ [Online 9 Jairtuaty 2007] Exposure to arsenic (As) in drinking water has been associated with a decline in intellectual ?tncrion in children. This association has been csrablishcd recently on the basis of a cross- scctional Study of 201 tcn-ycar?old children in Bangladesh (Wasserman et al. 2004). The authors point out the absence of research on the effects ofAs on children's intellectual Func? tion. They attribute the lack of data to poorly described in reported studies on the neurologic consequences of acute and chronic exposures in adults. Only two other srudics, one in Mexico (Calderon et al. the other in "l'aiwan (Tsai et al. 2003). have estab- lish ed tentative adverse associations between A5 exposure and children's intellectual Function although both studies evaluated only a small number oi' subiccrs (11 100). Signi?cant impairments ofhcigbt. body weight. brain, anti intelligence were reported in children poi- soned by mill-I powder containing As in Japan when compared with that of the control group of tilt; same age 16 years after the poisoning event (Wang 199?). in the 19805 in China. it became known that arsenicosis was occurring in individuals I drinking groundwatc'r containing As (\X?ang and Huang 1994). Sitanxi province, where our study was 'conducied. has been .recognircd as an area with signi?cant exposure in terms of both As concentration (lup to 4, 4-10 ng?L) and population (Sun 2004). individuals with arsenicosis were ?rsr correctly diagnosed bya team of Chinese endemic disease experts dur- ing a survey in 199-1 in Shanxi. Groundwater 1515 data that accumulated over the years point to two sedimentary basins. Darong (1,350 km") and Jinzhong (800 km2 where tube well water drawn from. depths beIWeen 20 and 50 to often contaitis As concentrations 50 which is the Chinese drinking water standard (GB 5749-85: Ministry of Health 2007). Groundwater from these basins also contains elevated of ?uo- ride up to 10 nIgfL) but not always together with elevated concentrinions 0M5. The popu- lation residing In Dato:ng and )inzhong basins is 932. 086, although l'only II or rhe total population (569, 685) was exposed to high-As concentrations in groundwater because of the heterogeneity of groundwater As distriburion. To date. 3.998 indiViduals with arsenicosis, Environmental Health Perspectives - including children. have been identified, with mosr living in rural areas. Here, we report the results of an ccologic study on the intelligence and growth in 720 children between 8 and 12 years oFagc from Shanxi province, China. Subjects Were drawn from control (11 high-?uoride (II 253). medium-As (11 911. and high-As (11 180) groups. Our study expands the exist- ing but very limited literature base on the cliect oi'As on the intellecrual function of children. and reports a measurable reduction of IQ, (intelligence quotient) scores due to As expo- sure. We initially included fluoride in our investigation because of the high tions of ?uoride contained in some of the groundwater wells in our study area. To the best of our knowledge. there is no literature published in English that shows liu'oride expo- surc'has an cilia-ct on the function of children. although literature published in Chinese points to significant impairment of children?s intellectual function (Li et a1. 2004; Liu er al. 2000; Yu et al. 1998). and growth (Qian et al. 1989: Xu and him 2000). based on studies with Huorosis. Methods Overview. Our current projecr is part larger ongoing evaluation of the health ciiccts ofan As study supported by the Shanxi Natural Science Foundation. The. srudy was approved by our institute-'5 Institutional Review Committee. As in most rural areas in Shanxi in central northern China. people in villages live in brick?concrete houses with ?oors made of brick and roofs made of tiles. Members of extended families live in clusters of individual houses surrounded'by family Farmland. liaclt cxrendcd household has one or more tube wells. This region is very poor even by Chinese standards. with an annual This .Irricle is pan of the mini-monograph "Occurrence and Health Effects oI?ArseniI: in China.? Address correspondence to S-X. Wang. institute for Prevention and of Endemic Disease. lini'cn. Shanxi {11111110,C111rtt. Telephone [86 55F-23151131. Fax (86 357-23131 18). ii -mail: 51(de public lilsx .cn - We thank Y. XJIeng. the guest editor oi this mini~ monograph. Forltercrirical comments and wooden- tions regarding this manuscript. This work was supported by SlIanxi Natural Science Foundation grant 20051093. llII: authors dIclarc have no competing financial interests. Reec-ivcd 1? April 2006; accepted 3 Ocrohcr 2006. 643 ?agg er al. income of approximately per Family. Before conducting this study, we obtained informed written consent From parents and children by arranging meetings through local health clinics, village leaders, and teachers - from children's school. Subjects. ln 2003. 524 children between 8 and 12 years of age were recruited From Gucheng township in Shanyin county to Form the srudy groups comprising individuals who had been exposed to either As or ?uoride. There are 23 villages in Gucheng, with a pop? ulation of 17.321 and a land area 01:2203 Previous survey tiara on water-containing As and ?uoride were used to identify 9 villages as target-areas for recruitment. The average content oFAs and fluoride in drinking water in the village was used as the basis to form the three study groups: high As group from Dongxingahuan (DXZ) Nanwanzhuang (NWZ) and Siliahuang (SI. Z) villages: medium-As group from Yangjuantou (YJT), Yangjuanpu (UP). and l'longqitun villages: and high??uoride group l?rom I-lousheduo (HSD), Nanjufang (NJF), and Yuanying (YY) villages (Table 1). Approxi- mately 80% of children in the 8- to 12?year- old age group in the 9 Villages agreed to participate in this study( (Table 1). \Vith this large number of recruited individuals we hope to avoid sampling bias. (I From the control group (n r: 196) Were enrolled From 3 villages in nearby Heshengbao town- ship (-- 13.8 km From Gucheng] with a popu- lation 0F 1 1,601 and a land area If 1 (59.3 km?i. 3130 in Shanyin county. Approximately 75% of the children between 8 and 12 years of age From these villages in Heshengbao were recruited. We chose Heshengbao as the con- trol group because the data on ?rs-and ?uoride in water showed uniformly low and l'luo- ride concentrations (Table 1; \?(iang er al. 2003). In addition, all groups lived in rural areas with similar geographic and cultural Con- ditions and :1 comparable level of socioeco- nomic development (Table ll. All children were currently attending school. Procedure. Children participated in the assessments described below and I'eCeivcd medical examinations by a team of trained personnel with medical backgrounds. Each team member was assigned to a single task that included administering the .IQtest, mea- suring height, weight. chest circumference. and lung capacity. In addition, all Children agreed to provide Spot urine samples For the measurement of urinary As and urinary ?uo? ride. Urine samples were stored and trans- ported on ice to the laboratory. Information on family demographics parental age, education, occupation, housing type) was obtained from interviews of parents during enrollment of their children in the study (Table 1). Informatiou on income was based on 2000 census data (Table 1; Statistical litforrtiation ol' Shanxi 2007). Unfortunately, we did not- include questions on other sources of drinking water For each child other than on the household well. Measures. Water analyses. We collected water samples from 10?30% ofWells ran- domly selected From our study area during a groundwater sampling study that was shown to provide a statistically representative mean for each village (Sun et shortcom- ing oi? this srudy design was that we could not evaluate and individual child 5 level of expo- sure. This prevented us from establishing a dose?response relationship. Briefly. samples were collecred in 50?1111. plastic bottles and l-mi. of 7 high-purity HCI was added for preservation. Water containing As was ana- lyzed by hydride generation atomic Fluores- cence spectrometry (HG-AFS) on an 820 Uitian Instrument Company, Beijing, China) with a limit of detection (LOD) 06 Water containing fluoride. was ana- lyzed by a ?uoride ion selective electrode with an L013 0130 Urinary measurements. we determined As content in urine using HG-AFS, actor-ding to a standard protocol {Cheng et al. 2004), with an 1.01) ofU.06 The fluo- ride content in urine was also determined usinga ?uoride ion selective electrode with an 1.013 050 pg/I. a 2% Children 1Q scores. The scores From chil- dren 5 intelligence tests were measured by the Combined Ravenfs Test The Rural in China (CRT-RC2) method. This method is based on the Ravens Standard Progressive Matrices (5PM) and Color Progressive Matrices (CPM) (Raven etrai. 1983) For fluid intelligence and was widely adopted in China a?er modifica? tions were made For cultural, ethnic. anti lan? guage differences (Chen 2002). Briefly, 72 questions' in sixgroups of the CRT-RC2 corte- sponded to the CPM groups A, :13. and B, and the 5PM groups C. D, and in the original Raven matrices. A rural vetsitIn oi the test was used For this Study because it was the Standard test for children between 4 and 15 years oi" age who lived in rural settings in China. This ver- sion has also been widely used For 1Q tesrs For children in China with heating and speech dis- abilities and mental retardation. Children?s 1Q scores Were calculated from the raw scores .oF the CRT-RCltests by applying the 1997 ver-- sion (IF :1 common model established For Chinese children. The common model is essen? tially :1 Standardized scale For Chinese children established luring the same methodology as the Wechsler Intelligence Scale Weehsler 19911. The children's ltheores were divided accord- ing to the scale into the following categories: low intelligence, 5 (I9: marginal intelligence. ?0?79; below medium, 80~89; medium, 90?109; above medium, 110?119; good, 120-129; excellent, 2 130. Werecogniae that this scale is' For nonverbal reasoning and is only measures certain aspects of intelligence. However, no other Standardized IQ tesrs or common models have been developed For rural Chinese children. Children?s growth. Children?s growth ?mcrion was grouped according to ?ve levels (He 1994) by applying a Z-score method (2. 11. 12) using a standardized proce- dure for Chinese children (Ye 2.000). Brie?y, dimensionless Z?scores were calculated on the basis ofmeasurement values using the follow ing equation: I where is the individual child's growth meas? ure height, weight), Mdis the medium. Table 1. Study parameters for villages in Gueheng township? .. .. 4'5 919191. . 11.191.199.168 group? -. Central VIIlage 0X2 $12 r1111? ill-130 NJF YY group nValue No. of males 'females 'Sum" 46158] 24 21 1261 681111} 1271156} 681651 3? {4161 831112}- 55169} 196125?) Average age {years} 10.0 1.3 10.0:12 9,811.2 113.0112 10.1 1.3 10.01- 1.6 10.1 11.51 9.91 1.6 10.1 1.5 9.9-1: 1.5 0.65? Average income 1,129: 223 1,240: 13? 1.1941235 1,150i205 1.2331241 1.1641216 12391252 1.166121? 1.2091122 1.2401216 11.06? Parents' education {years2.6 9.15? Water 1181ng 1661.160 2502.230 171M101 1512120 141211] 1291-103 311 3:2 51.4 213 Water fluoride {8111le 1.6 a. 0.6 0.9-: 0.5 0.9 0.3 1.5 1.I12 Exposurellmelyearsl 10.0112 9.81112 111W 101:13 10.l+.15 Abhrevi'ations: DXZ. .Housheduo; NW2, Silizhuang; YJT. Yangjuantou; .YJP Yangjuanpu; HOT. Hengqituri; NJF Nanjulang; Yuanyr'ng, ?Values are reported as mean 2 SD for all parameters unless otherwise noted. bMean water manganese concentration across all viliages was 43.- 36. 5 ngL?SIudy groups vs. control groups, 0.115; lhereis no statistical difference for age, income, or parents'- education I?l'he total number of children between 3 and 12. years of age 111. each village Is listed In parentheses. 644 - Environmental Health Perspectives and 5 the standard deviation. Therefore. posi- tive Z-scores represent above-median values and negative Z-scores represent below- median values. The Z-score transformation above allowed us to Convert the measurement data into rank data. We ranked the children?s growrh firnctions according to the Following ?ve categories: lower growdt. 2; lower- medial growth. ?2 to medial growth, -1 to l; upper-medial growth, 1 to 2; and upper growth, a 1. Sratisrical analysis was then performed on the rank data. Statistical anabrses. Data were analyzed by SPSS For Windows 10.0 (SPSS, Chicago, IL. USA) and CS2000 [Department of Public Health, Shandong University, Shandong, China) by the Statistics Teaching and Research Section of Public Health College of Shandong Unis?ersity. One-way analysis of variance (ANOVA) was performed en the log-transformed data; the Krusl-tal-Wallis test was also used. Regression ANOVA was per? Formed on the log-transformed data. Paired q-tCSt, chi?square tesr, and t?test were used to compare differences between any of the two study groups. Coefficients were calculated using the Spearman rank-order correlation test. All values were transformed hack to the arithmetic scale for reporting purposes. \We ditl notper?irm a analysis. Results Sample characteristics. In Table 1 we present descriptive information on demographics, income, parents? education, and the variables for As. fluoride. and manganese in water. The average age of children was 10 Years, and approximately hall" the samples were male. Children on average have been exposed since birth to the well being used by the household. On average, patents reported having 6 years of" primary school education, with an average income from farming of- approximately per year (1,200 Yuan RMB per year). The average household consisted of 3.6 persons residing in a brick?concrete dwelling. Evposurc characteristics The mean water ?ts concentrations were 2, 3. 142. and 190 pg?. in the control. high-fluoride. medium-As, and high-As groups, respectively (Table 2). The mean urinary As concentra? tions were 10, 6. 46. and 73 in the con- trol, high?fluoride, medium-As, and high-As groups, tespecrively. The mean water fluoride concentrations were 0.5, 1.7, and 0.9 rug/1.. in the control, medium-As. and high-As groups, respectively, but was 8.3 for the high? fluoride group (Table 2). The mean urinary fluoride concentrations were 1.5, 2.8. and 1.0 mgll. in the control, medium-As. and high-As groups, respeCtively. but was 5.1 mgf'L in the high??uoride group. Thus, chil- dren in the medium-A5 group were exposed to some amount of ?uoride and showed elevated Low IQ urinary ?uoride concentrations. Fewer water samples than urine samples were analyred For As and ?uoride. Bo:h water and urine were randomly selecred For sampling in order to determine the meat values of the exposure group. An unfortunate shortcoming is that the nature of this study design prevented us from establishing a dose?r?sponse relationship. The distribution I scores. in each smdy group, the number of children who were administered 1Q teats was greater than the number of analyses performed on water and urinary As and fluoride that represented the and growth in children exposed to high-As or high-fluoride water mean values of exposure lTablesZ The dis? triburion of children' 1Q scores is skewed in the control group: 15% (n 30} with IQ score 5111:4406 (u 37") with 1Q score .90 and 109; and 41?? with 1Q score [09 (Table Figure 1). The percent- age of children with IQ score 109 decreased to 30. 30. and 1996111 the high-?uoride group. the medium-As group. and the high-As group, respecdvely. A chi-square test (signi?cance level, at 0.01185) shows that this dismrhingly low percentage of children with IQ score 109 in the high-As group is signi?cantly lower than Table 2. Arsenic fluoride (mgle concentrations in drinking water and urine from subjects in Shanxi province, China, Water As Water ?uoride Urinary As Urinary ?uoride Group In {mean a [11 [mean 301] [11 9.- 801] [anM High-As 50 [1 30 1 1331" 5010.9 1: 0.51 80113 i 31? '13 11.0 21.11 [14, 502] 1.8] [11595] 3.5] Medium?As 301142 1051' 30 11.11' 50140 .t 31' 511 [2.3 1E1]il 303] 3.0] 315] 5.6] Higl?e?uoride 21 13 31 21 [3.3 $1.91" 101 a 21 10515.1 a 2.01' - i 11]] 11.5] 20] 11.0] Control - 11125-31 1111155112] 1211110121 11011511131 . [1 .10] 1.11 GM geometric mean Numbers 111 brockels are lowest and highest observed values. Significant difference from control group: ?p 0.115. 'p 0. 01. Table 3. Distribution of children 0 ?12 years of age based on intellectual function. 5913 In rears ?0 We. Group or [rrioan i so} {mean 5.551 59 15-35 55:99 90?159 115?119 125?129 2 135 High-As 155 9.9 11.5 95.1 5 15.5 4 5.3 9.4 13.3 49.4 15.5 2.5 1.1 Medium-As 91 9.5 a 1.4 155.5 15.5 4' 9.3 5.5 11.11 49.5 17.5 9.9 2.2 High-?uoride 253 9.9 5.1.4 155.5 15.5 .. 4 5.9 12.3 45.2 22.9 4 7 2.5 Control 195 9,9: 1.5 154.5 5141.? 44.4 24.5 12.5 3.1 Shamti 1,2?4 9.5 2 5.52 105.5 114.11" 1.3 2.5 5.7 44.5 25.4 15.5 China 35255 9.5+o.94 1035mm 3.5 54 15.5 431 195 12.5 50 ?Number of children tested "The average 10 of children' In Shanxi was determined to be 100.+0 14.0111 2005 which 15 sta- tisticaIly different from that of the control group lo: 3. 2, 11.011.th average ll] of Chinese children was determined to be 103. 5 in 2005 which Is not statistically different from Signi?cant difference from control groupPercentage distribution 8 1 11.111? 1?11 that of the control group {um 0. 995, p) D. 051. - High-Asfrt=100] Medium-As [11:91] High-fluorideln_= 2531 C3 Control group 1114:1901 r" 111:1 Shanaipmvinceln?l?] 1 I {1511' l? Il i 5 EB 1043 911-109 110-119 120-129! 2130 Children's 11] scores Figure 1. Frequency distribution of 111 in 10-vear-old children from Shanvi county, Shanxi, China, who were exposed to high-As water, medium-As water, and hig fluoride compared with control group with low-As and low-fluoride, as well as children residing in Shanxi province, China. Environmental Health Perspectives - votunit1151Nuraara4 Apr112007 645 Wang et al. that in the high?fluoride group (:42 53?. 0.05) and that in the control group 19.33, 0.01) but not different from that of the medium?As group. The per- centage oi'children with IQScore 70, or chil- dren with intellectual disabilities, increased signi?cantly from 0% in the control group to 4, 5.5, and 8.3% in the high?uoride, lTICdiillTerS, and high-As groups, respecrively. Based on a sampling of1,274 children in Shanxi, the percentage of children with 1Q score .70 is 1.3% (Chinese Center for lilisease Control and Prevention 2006). in the four groups. the change in the dis- triburion oiiehildren's IQ scores is also reflected in the mean values of 1Q scores in decreasing order From 105 a 15 (n 196) in the control group to 101 16 (a 253) in the high-fluoride group and 101 s: 16 (n 91) in the medium-As group, and finally to 9.5 1 17 (n r. 180) in the high-As group. The lD-point reduction in IQ scores in the high- As group with a I90-pg/L mean exposure to water As (Table 1) compared with the control group is signi?cant (if 8.42. 0.01). The 4?point reduction in scores in both the high-fluoride group (4 4.99, 0.01) and the medium?As group :2 2.94. 0.05) ceinpared with the control group is also sig- nificant. The difference in IQ scores between any of the two groups except that-betWeeu the high-fluoride group and the medium?As group is significant by the q?test 0.05 or 0.01). The distribution afcbr'la'ren ?5 growth. The disrtibution of the four parameters that indi- Cate children's growth and development. gen- erally showed that exposure to As and ?uoride in water had a negative impact, although the efTeCt is neither as striking as the impairment of IQ nor always-statistically significant (Table 4). Chest measurements showed the least difierence or no statistically signi?cant difiiererlces in average rank values among the four groups (Table 5). Average weight, height and lung capacities in children exposed-to either As or fluoride, or both. however. are always than the average rank values For children in the control group (Table 5). The statistically signi?cant diliizrenccs were found in the Following comparisons: Children?s height in the. control group was signi?cantly higher than that in high?fluoride group (p 0.05); children?s weight in the control group was signi?cantly higher than that in the high? As group (p 0.05); children?s lung capacity in the control group was signi?cantly higher than that in the medium-As group (p 0.05). Reirrtionsbip between As and?rroride capesme and Urinary As concentrations correlated positively with water As concentrations in children in all study groups. Similarly, urinary fluoride con- centrations also correlated positively with Table 4. Rank distribution of children 8?12 years of age based on growth and development factors. Distribution 1%1" Indicator, group Lower Lower medial Medial Upper medial Upper Height Medium-As 111? 2.5 18.? 211.1 1} High~f1uoride' 228 2.2 28.4 611.1 2.9 1.4 l-Iiph-As 1911 2.9 21.6 6?.4 3.2 11 Control? 2115 5.4 211.1] 135.9 5.9 2.9 Weight Medium-As 111?. 11.9 15.9 High-fluoride 278 11.4 14.1] 210 5.8 2.9 l-ligh~As' 1911 11 18.4 28.9 2.6 11 Control? 205 1 l] 5.4 81.5 6.3 5.9 Chest circumference Medium-As 1116 1] 1114 82.1 2.8 High-?uoride 228 11.? 13.3 29.1 5.4 1.4 High-r15 191] 8 11.6 82.} 5.8 0.5 Control 2115 1.0 16.1 25.1 4.9 2.9 lung capacity MediumsAs' 89 11 19 88.8 2.2 1.1 High-?uoride 0 5.1 13.1] 3.2 High-As 1118 11 3.7 813.1 8.3 1.9 Control? 205 1.5 2.8 64.9 18.11 13.8 a: number of children tested. ?Values are based onpercent of median value for each indicator. 'Signi?eant difference. 4: 0.115. Table 5. Average rank of growth and development indicators. Height Weight Chest measurement Lung capacrty Groups Average rank :1 Average rank it Average rank it Average rank Medium-As 111? 399 11131 1116 ?114 89 294' High-?uoride 279 369 2?8 389 228 38? 343 High-As 1911 388 1911 355' 191] 395 1118 32? Control 205' 418* 2115 3130' 2115 3811 205 382? number of children tested. difference, 11.05. 646 water fluoride concentrations in children in all study groups. ?Zl-?heSpearman correlation coef? ?cient thatwas calculated hethen urinary As ennCenrrations and children?s in the con- trol and high-As'groups was -?0.201 (p 0.01) and was unadjusted for other factors that may contribute to IQ. This negative correlation suggests that As exposure via water lowers 1Q score. Similarly, a Spearman correlation coeffi- cient 0130.10? (p 0.05) was found between urinary Fluoride and 1Q scores in children in the control and the high-fluoride groups. This negative correlation suggests that fluoride exposure also lowers IQ. These negative corre- lations betxveen IQ and urinary As and between and urinary ?uoride indicate that exposure to high levels ofAs or fluoride. or both. could affecr children's intelligence. No Statistically significant negative correlations were found between and urinary As .or betWeen 1Q and urinary fluoride in children in the control and medium-As groups. This, in part, is because of the small sample size of the medium?As group comprising only 91 children (?liable 5). Discussion This study indicates that exposure to ?uoride in drinking water is associated with neuroroxic efi?iacrs in children. A iireratute search on fluo- ride and intelligence in the l?ubMed database returned srudics conducted only in China and none From w'esrern literatures. Animal experi- ments showed that fluoride is neurotoxic .to rats and damagesbrain functions (Cheng et a1. 2002). A survey of newborn infants from Zhao county in Heilongjiang province in northeast- ern China, an areawith a high rate offiuoroco? sis, found that earn'isurc of mothers to high concentrations offluoride-afiitcred neurobehav? ioral development'and agonistic muscle tension development in infants. Agonisdc muscle ten- sion is often affected when brain damage occurs, which is consistent with the finding that. in China, exposure to ?uoride afiects chil? dren?s intelligente (Liu et 211.3000: 1?u er al. 1998). in our Follow?up study of this populad tion, we are working toward establishing a dose?responserelationship between exposure to fluoride in water and children's'IQ. It is less surprising that exposure to fluoride affected children?s growrh Funcrion, especially height. l?rcviousstudies have demonstrated multiple effects of exposure to high concen? trations of fluoride on children?s morphology. growth and development, and on bones and teeth (Qian er al. 1939: Xu and Huo 2000). This is because fluoride accumulates in bone and reduces calcium uptake. thereby influenc? in growrh. When Ma etal. (1994) exposed adult rats to As, the authors found- thar baby rats devel- oped abnormal nerve consrruction in the - Environmental Health Perspectives brain cortex and were slower to gain weight compared with normal rats. Although the results of thii animal study of Ma et :11. suggest the possibility that brain damage in children could be caused by maternal exposure to As, there. is-no evidence to date to support this hypothesis. Li and An (2005) found that His can pass through the blood-brain barrier and the placenta barrier, thereby, porentially affecting fetus brain development. Because of the decline we found in the intellectual function of children from expo- sure to As, it appears that this exposure is more signi?cant than fluoride exposure. W'e note that urinary flouridc in the medium-As group displayed a geometric mean of 2.8 mgi'L and is approximately twice that of the control group. with a geometric mean of 1.5 mg! (Table 2). This somewhat elevated level of fluoride exposure did nor appear to greatly alien the IQ of children in this group. because the decline in IQ scores from 105 to 101 to 95 was observed in the control group. The mean values for water As in the three groups are as follows: control group, 2. medium-As group, 142 ngL; and high-As group, 190 (Table 2). In other words, the medium-As group would have even lower IQ scores if exposure to higher concentrations led to severe impairment ofintelligence. but it did not. Taken together, our results highlight the signi?cant impact of As exposure on chil- dren's intelligence. Even in water that may contain other agents such as fluoride that also impair intelligence, As remains the primary lite-tor in ailccting children's intelligence. Limitations. Children's intelligence, growd1, and development can be influenced by many factors such as inheritance, nutrition. geography, education, and society. Our current study sampled a homogcnous rural population in Shanxi, and therefore, the influence of socioeconomic and genetic factors was expecred to be minimal, but we cannot completely Low [0 and growth in children exposed to high-As or high-fluoride water exclude the in?uence of such facrors. After adjustment for these Factors, et al. (2004) found that exposure ofa Bangladeshi 10?year?old child to of drinking- water As led to a reduction in intellectual Func- tion. A report from pointed out that the intellectual function of children correlated with As exposure, with about 14% of variance resulting from As exposure after removing con- founding factors (Siripitayakunkit 19.99). Additionally, we recognize that children in our study groups attend :school and therefore are exposed to different levels ol?As while not at home. All the complications and limitations of our srudy design. however, would not lead to systematic errors that would challenge the main ?ndings: that 10-year-old Chinese chil~ dren IQ scores were lowered by 5?10 points when they were exposed to drinking water containing As. However, we emphasize the need fir more careful evaluation of the effects of fluoride on intelligence. Even though urinary As 10w (Table 2) In 101 of 233 children In the high- fluoride group, we cannot exclude the possibility that the urinary As could be higher 111 the 142 children who were not evaluated. REFERENCES Calderon J, Navarro ME Jimenez- ME Santos Diat MA. Goldan. Rodrigueo? Leyva at al. 2001. Exposure to arsenic and load and development in Mexican children. Environ Res 85121335415. Chen Z-P. 2002. Mitigation Approach to Address Iodine De?ciency Disorders in China. '?aann. China:1'lanjin Science and Technology Press. Chang X-T. Wang S-X. Bao JG. 2002. Analysis oi M8P.NSE.F- content and CHE activity in brain tissue of rats with chronic ?ucrosis [in Chinese}. ChinJ Endomiol 211512350. Chang X-T. Zhang J, Li J. 200-1.chteImination of total arsenic in urine by HE-AFS [in Chinulsu]. Chin Chinese Center lor Disease Control and Prevention. 2006. Surveillance oi Health Eliuct of iodine Dc?cicncy' In China: Summary Flopori. Boiling: Center for Disease Control and Prevention. He D-F. 19941113 Z-score analytical method ol child's physique dovelopmontIin Chinescl.'J Prev Med lniorrn Environmental Health Perspectives - Li 0-8. An D. 2005. Progress in mechanisms leading to Monica- sis. Chin Curt Clin Med Li J. You Shao 11-L2004. Eilecls of high ?uoride on neonatal neurohchavioural development [in Chinese].l Chin Endemic! 23464?455. Liu S- 5. Lu Sun ER. 2000. The investigation oil children's intel- lective level in high lluoridc area. Chin .1 Coca Endem Dis 15231?232. Ma Zhang C. Liu W?d.1994. The in?uence of arsenic on growth oi the mice subgeneratlcn. Chin Prev Med 28:20-21 Ministry at Health. 2007. Drinking Water Standards. Beijing. ChinatMlnistryol Health of the People?s Republic 111 China. Dian C. Li J. Doi (H. 1989. Ellect of high ?uoride in drinking water on sexual and physique development ol children and adolescent. Chin Contr Endern Dis 4:36-37. Haven JC, Court JH. Haven .1. 1903. Manual for Raven's- Ptogrossive Matrices and Vocabulary Scales. London. UK: Lewis Siripitayaltunkit U. 1999. The relationship between chronic expo- sure on arsenic and children's intelligence in Thailand. in: Fluorine and Arsenic of the Pon~Asia Paci?c 1993. Shenyang. China:Ptoiessional Committee o1 Fluorincand Arsenic of Endemiological Society at Chinese Medical Association. 22. Statistical information of Shonxl. 2000. Available: stais-sxgovcry' [accessed 10 March 2002!. Sun 6.2004. Arsenic contamination and arsenicosis in China. Toxicol Appl Pharmacol Sun G-F, 11x. Zhou J-Y. 2003. Study of using-101E sampling method to identify the high arsenic exposure area. Chin Dis Contr Prev 73180?433. Tsai S-Y, Chou H-Y, The H-W. Chen C-M, Chen C-J. 2003. The Effects of chronic arsenic exposure from drinking water on the neurobohavioral development in adolescence. NeuroToxicolugy 24l4?5l:74??753. Wang Huang J. 1994. Chronic arsenic from drinking water in some areas of Xiniiang, China. In: Arsenic in the Environment Pan ll: Human Health and Ecosystems Effects [Nriagu JD. ed}. New Wiley 8. Sons. 159-112. Wang L-F. 1097. Endemic Arsonism and Blackfoot Disease, Xinjiong, Chinadlinjiang Science and Technological Medical Publishing House. Wang Z-H. Li J. Cheng X-T. 2003. A survey of water arsenic and arsenicosis in Shanyi county. Shanxi. China. Chin Court Endem Dis 18151233495. Wasserrnan GA. Liu X. Parvor F, Alison H, Factor-Limk P. van Been A, or 31. 2004. Water arsenic exposure and children's intellectual iunclion in Araihatar. Bangladesh. Environ Health Perspac11121329?1333. Wechslor D. 1991. Manual [or the Antonio. Corp. Xu N-Y. l-luo J-X. 2000. Eliect of high ?uoride on growth 01 chil- dron and adolescentJ Baotou Med Coll 1532-95. Ye G-J. 2000. Child and Adolescent Health. BeijingMidi'slry of Health. People's Republic of China. Yu Y-N. [long 2, Liu J-L. 1998. Measurement 11! embryo thyroid stereopsis parameters in fluorosis area. Gulzhou Province. ChinJ Cont: Endem Dis 13:148-149. 64? epartment of the Planet Earth 701 Street, SE - Suite 200, Washington, DC 20003 (301) 475-8366 - planetbartl1?erols.com; December 16, 2006 Dear Board, . Best of the Holidays and the New And it?s going to be a ?girmuch better year. Senator Tim Johnson, Democrat of South Dakota, had a stroke and is recovering in the hospital. If he stays alive for the next two years, the Democrats will hold all the committee chairs in the US Senate. I am sure that the religious right Republicans will be asking for withdrawal of life support. At the very minimum, we will have the opportunity to persuade the chairs to investigate the White House. I plan to ask for an inquiry into the FDA. Joe writes that Elizabeth ran for the greens in the London by-election and nearly won, taking many votes from a Conservative. That produced a win for a Liberal. Congratulations for putting the crunch on. 1. GM Wine: It has been proposed to use genetically modified yeast to make wine, with the claim that it might prevent headaches among some consumers. Joe points out that yeast is genetically unstable and can produce toxicity. Also, yeast is what makes wine taste good, and wineries are particular about their yeast types. Contamination with genetically modified strains would cause serious problem. Also, the market for wine depends upon consumer belief in the product, and markets could be severely affected. This is an issue that we could take to the Committees for investigation, since many Congressmen drink wine, and wine drinkers tend to be richer. As Joe points out, most wine producers in California, South Africa, Australia- New Zealand and EU have rejected GM wine. 2. Governors and Kyoto Protocol: Dave Shiah and myself are getting prepared to call all the new Governors and provide them educational material, with the request that they sign Kyoto Protocol executive orders for their states. As you may have noticed, the amount of bad news about global warming has sharply increased. Likewise, news about peak oil is also intensifying. A just published article in Science finds that we are now risking climate change of a magnitude last seen 50 million years ago. Another predicts the end of the barrier islands along the US coast by 2100: i.e. just another generation. Another shows carbon dioxide emisisons up by 25 percent globally since 1990. Wow. Acidification of the oceans is being measured. And a lot of fraud. The hydrogen economy may actually generate more carbon dioxide than if the fossil fuel was burned by itself. Planting trees in the temperate zone may increase temperatures, since they are dark colored. I am putting together a short paper of recent findings in capsule form for distribution. 3. Aluminum and Alzheimer?s: I will soon get started preparing another scientific article on the subject. At the conference in Merida, Mexico February 24?27, Dr. Chris Exley has put me into the second to last slot as cleanup speaker, to propose to the scientific community that they now need to take action to regulate aluminum. We are past the study stage - time for action. This should be fun. 4. Patuxent River as National Demonstration River: Here is an issue that has come up that would be a good project. The Chesapeake Bay and tributaries require a 50 percent reduction in nitrogen loading to restore aquatic life. Stormwater and non-point sources are the largest sources: i.e. 78 percent in the Patuxent River watershed. The river lies totally within the State of Maryland. An in?uential retired politician, Senator Bernie ?Fowler, proposes to make the Patuxent a national demonstration river for control of nitrogen. I have drafted raingarden legislation that would replace the usual stormwater pits with rain gardens, and there seems to be interest. We?ll see. 5. Board Meeting: Let?s aim for a board meeting rather soon. Will get back to you with some suggestions. May Santa Claus bring good things to environmentalists in the New Year. Have fun. Best, (2,5 Erik urea-n; . . P. Main Identity 3 From: "jcurnmins" To: "Erik Jansson" Sent: Tuesday. December 12. 2006 2:35 PM Subject: gm wine . The dangers of genetically modi?ed wine yeast By Erica Martenson Tuesday, December 12, 2006 6:39 AM PST Despite the Wine Institute?s recent statement that no genetically modi?ed organisms (GMOs) should be used in winemaking, the Sacramento Bee recently reported that, according to American Tartaric Products, the ?rst wines made with a genetically modi?ed wine yeast, will be released this year. This yeast is available only in North America where GMOs are unregulated. It was modi?ed by inserting two foreig'n genes, one from the pombe yeast, a yeast found in Africa and used to make beer, and one ?om the bacteria 0. oeni, so that the alcoholic and rinalolactic fermentations, normally a two-step process, occur at the same time. While this may be a convenience towinemakers, especially those producing large quantities of wine, I am concerned for both consumers and our local economy. - The designation of this yeast as GRAS (Generally Recognized as Safe) is questionable for a few reasons. First of all, the FDA approved the yeast based on data supplied by the developer, based on its own study or an independent study. A developer has an ihterest in getting its product to market as soon as possible, whether it has been proven safe or not. Secondly, according to Professor Joseph Cummins, emeritus genetics professor at the University of Western Ontario, wine yeasts are unstable, and genetically altering them can lead to unexpected toxicity in the ?nal product. He states that there is no evidenize that the - developer did any animal feeding studies to test for such toxicity and that there is no proof that the yeast and yeast DNA will not be present in the wine. I I A few wineries? decision to use this yeast could affect the entire North American market. Since these wines are unlabeled, the only way people can avoid them is to avoid all wines ?om North America, except those labeled organic, and few wines are labeled organic, due to the addition ,of sul?tes during the winemaking process. Consumei?s in Europe and Asia' are very informed regarding GMOs and have resoundingly rejected them. American consumers are becoming more aware, and polls show that a majority of Americans would prefer to avoid them. I A few wineries? choice to use MLOI could also be a nuisance to other wineries, because this GM wine yeast could contaminate native and traditional wine yeasts through the air, surface waste ?and water runoff. Page 1 of2 Page 2 of 2 Many wineries here in the Napa Valley are very particular about their choice of wine yeast, and contamination of these various yeast strains would truly be a shame. I contacted many of the large producers of Napa Valley wine asking whether or not they have used this GM yeast or plan to in the future. All that responded stated emphatically that they have not used it and do not plan to. To help-consumers who'would prefer to avoid consuming genetically modi?ed products make an informed wine choice and to provide an avenue for our local wineries to distinguish their wines from wines that may be using GM yeast, those that responded were listed, with their permission, on a ?Shopper?s Guide to Buying at on the FAQs page. In our society, we often talk about our rights and discuss very little our responsibilities to 'our neighbors, to the enVirornnent and to the community as a whole. In considering the issue of GMOs and their use, all of these factors should be taken into account. (Martenson lives in Napa.) 16.20 Discussion 16.30 COFFEE 17.00 JD Birchall Memorial Lecture Professor Tom Kinraide Personal experiences analyzing the interactive toxic and ameliorative effects of aluminum species and other ions. 18.00 Discussion 18.30 General Discussion and Closing Remarks 20.00 Conference Dinner SESSION EIGHT Aluminium and Alzheimer ?s Disease 14.00 Platform 21 Walter Lukiw Alterations in micro RNA complexity in Alzheimer?s disease (AD) and in metal-ion stressed human brain cells. 14.20 Discussion 14.30 Platform 22 Paula Goncalves Neurotransmission impairment: an accomplice .to aluminium neurotoxicity. 14.50 Discussion 15.00 Poster 20 Carmelo Abbate Neurocognitive effects in workers exposed to aluminium. 15.05 Discussion 15.10 Poster 21 Salvatore Polizzi Dust exposure to iron and aluminium and impairment of lung function in apprentices living near a foundry. 15.15 Discussion 15.20 Platform 23 Paolo Prolo Aluminium vs. Alzheimer?s disease: The evidence- based approach. 15.40 Discussion 15.50 Poster 22 Erik Jansen A review: Aluminium A causative co-factor of ?dementia? of Alzheimer?s disease. 15 .55 Discussion 16.00 Platform 24 Arthur Dalton Aluminium chelation therapy: Past, present and future. 10.25 10.30 11.00 11.20 11.30 11.35 11.40 11.45 11.50 12.10 . 12.20 12.40 13.00 Lunch Effect of aluminium on intestinal calcium absorption in pregnant and actating rats. Discussion COFFEE SESSION SEVEN Human Exposure to Aluminium Platform 18 Christopher Exley The body burden of aluminiumzwhat is it? i Discussion Poster _1 8 Usman Ahmed Elevated urinaryi aluminium in past and current users of heroin. i Discussion Poster 19 Lisa Charles Aluminium in breast cancer tissue. Discussion Platform 19 Elisabet Berfors . What happens when children sensitised to aluminium receive aluminium adsorbed vaccines. Discussion 5 Platform 20 Judie Walton . Aluminium in osteoporotic vertebroplasty specimens. Discussion 20.00 09.00 09.05 09.10 09.20 09.40 09.50 10.10 10.20 FREE AFTERNOON Dinner Light and Sound Experience of Uxmal!? Tuesday 27th February 2007 SESSION SIX Animal Models of Aluminium Toxicity Poster 15 Goran Kova?evi? The effect of aluminium on green and brown hydra?s: preliminary observations. Poster 16 Goran Kova?evi? The effect of aluminium on the planarian Polycelis felina. Joint Discussion Platform 16 Judie Walton? An aluminium-based rat model for Alzheimer-type dementia exhibits oxidative stress, inhibition of PP2A activity and hyperphosphorylated tau. Discussion Platform 17 Jose-Luis Esparza Effects on locomotor, spatial learning and proliferation 'in a transgenic mouse model of Alzheimer?s disease after exposure to low dose of oral aluminium. Discussion Poster 17 Daniel Orihuel'a 11.00 11.20 11.30 11.35 11.40 12.00 12.10 12.15 12.20 12.40 12.50 14.00 SESSION FIVE Aluminium Biochemistry Platform 13 Kelly Elkins Designing and testing peptides with aluminium speci?city. Discussion i Poster 13 Rachel Bongini Analysis of computational site-directed mutagenesis of ligands in the metal-ion binding site in an isolated EF-hand from trpponin C. Discussion I Platform 14 Vasu Appanna Aluminium-induced metabolic in hepatocytes mimics obesity-like conditions. Discusswn I Poster 14 Ziqiang Meng Effects of aluminium chloride on Na+ current and transient outward current and delayed recti?er current in acutely isolated rat hippocampal CA1 neurons. 1 Discussion 1, Platform 15 Walter Lukiw Mechanism of in?ammatory gene expression in aluminium- or iron-stressed aging human brain cells; rescue with desferrioxamine and Feralex-G. 1 Discusswn . Lunch 09.00 09.20 09.30 09.50 10.00 10.05 10.10 10.15 10.20 10.25 10.30 Monday 26?1 ebruarv 2007 SESSION FOUR Plants Platform 11 Thomas Kinraide Metal ion binding to some organic and inorganic ligands and to plant cell walls and membranes. A scale for binding strength closely related to charge and Pauling electronegativity. Discussion Platform 12 Jimmy Ramirez-Benitez The role of organic acids in aluminium tolerance in cell suspensions of Co?ea aribz'ca L. Discussion Poster 10 Radhouane Chaffai Alteration of the pro?le of organic acid content and exudation in maize, Zea Mays under aluminium stress. Discussion Poster 11 Faezeh Ghanati Aluminiumeinduced changes in the polysaccharide components of cell walls of suspension-cultured tobacco cells. Discussion Poster 12 Leticia Chee Physiological response in suspensions of Co?ea arabica L. cells exposed to different chemical forms of aluminium. Discussion COFFEE 17.05 17.10 17.15 17.20 17.25 17.30 17.50 18.00 18.05 18.30 20.00 1 Discussion Poster 7 Antonin Nikodem Aluminium speeiation in forest soils of a mountainous . region with relatively low effects of acid deposition. Discussion Poster 8 Lubos Boruvka Grass cover on forest clear-cut areas ameliorates soil chemical properties. Discussion Platform 10 Hails-Christian Teien Mobilisation of river transported colloidal aluminium in estuaries and subsequent deposition on ?sh gills sodium silicate as a countermeasure. Discussion Poster 9 Patricia Quiroz-Vazquez Temporal ?uctuations of Al and Si in the epilimnion of a freshwater lake: uptake and accumulation by plankton. Discussion . 1 End of First Day I Dinner 1 Poster Session and Tequila! 14.50 15.00 15.20 15.30 15.35 15.40 15.45 15.50 15.55 16.00 16.30 16.50 17.00 Discussion Platform 8 Jiri Kopa?ek Photochemical source of aluminium for lakes and its impact upon phosphorus cycling. Discussion Poster 3 Arja Sarpola Identi?cation of hydrolysis products of aluminium and iron in. water. Discussion Poster 4 Peter Mat?? Analytical chemistry of aluminium its total determination, ?'actionation and speciation analysis as different approaches for Al routine environmental pollution monitoring. Discussion Poster '5 Changqing Ye A113 and the speciation of other polymeric forms using the ferron reaction. Discussion COFFEE Platform 9 David Sigee Energy and wavelength-dispersive X?ray microanalysis of Al and associated elements in freshwater phytOplankton. Discussion Poster 6 Jaroslav Vrba A key role for aluminium in phosphorus availability, food web structure, and plankton dynamics in strongly acidi?ed lakes. 11.00 COFFEE SESSION TWO Aluminium Chemistry 11.30 Platform 5 Oleg Antzutkin An 27Al and MAS NMR surface study of adsorbed? aluminium species at ?uor? and hydroxy -apatite. . 1 1.50 Discussion 12.00 Poster 1 Kirill Shafran and characterisation of pure monodisperse aluminium polyoxocation and aluminium hydroxide solutions using anovel technique based on static anion exchange. - 12.05 Discussion 1 12.10 Poster 2 Xiao-Di Yang Aspects of the structural speciation of complexes with bi-ligands in aqueous solutions. 12.15 Discussion - 12.20 Platform 6 Kirill Shafran Interactions of pure Al hydrolytic species Keggin polyoxocations and hydroxide with biomolecules. 12.40 Discussion 13 .00 Lunch SESSION 3 Environmental Bioinorganic Chemistry 14.30 Platform 7 Michael Anderson Alum treatment oilf lakes to control phosphorus recycling:Forms and'transformations of Al. cw 351'. PRELIMINARY TIMETABLE Saturday 24?? Februarv 2007 17.00 Registration and Poster Assembly 20.00 Welcome to Meeting Welcome Buffet Sunday 25?? February 2007 09.00 Conference SESSION ONE In Silico Approaches to Understanding Aluminium 09.00 Platform 1 Christopher Exley A systems biology approach to the biological availability of aluminium. 09.20 Discussion 09.30 . Platform 2_ James Beardmore Solving the blood-aluminium problem. 09.50 Discussion 10.00 Platform 3 Elixabete Rezabal Protein side chains that facilitate metal exchange in model protein binding sites. 10.20 Discussion 10.30 'Platfonn 4 Jerry Winter Towards improved understanding of the molecular genesis and acid-base properties of aluminium polyoxocations using various computational approaches. 1 10.50 Discussion _Page 1 of 1 Main ldenti? From: ?David Shiah" To: "Erik Jansson" Sent: Monday, February 05, 2007 4:36 PM Subject: SC follow-up .Hi Erik. Just wanted to forward the below message from oun South Carolina contact. I responded to him that the next packet would be the same as the original one. Thanks again for putting together such an informative packet Erik! I Best, Dave S. David 1 Will this package be similar to the one I received? Your package to me was very informative. Thanks again for all your help, I Justin jaw/A Chm/?an ofIZic?t? 2/3/2007 . \r ?Ta .11? [1:31 3: '1 ?1384.313? 1 Limos: [?ll I ain Faujas Must Business Be Ecological? Page 1 of? truthoul?cditorial El Print {Story [23 Go to Original Must Business Be Ecological? By Alain Faujas Le Monde Monday 05 February 2007 In his "ecological will." published February ?lst by Le Nouvel Observateur, Jacques Chirac repeats an idea expressed by his prime minister in November 2006. "We could tax imports from countries that do not conform to Kyoto (an international protocol that provides for greenhouse gas reduction) with speci?c additional duties." That's the planned "Kyoto" or "carbon tax." On their side, American Democrats want to match any liberalization of their trade with the demand that their partners respect the environment. just to counter China, which manufactures products at low lcost because it exempts itself from expenses that the United States compels for protecting the air and water. If these trade protections with environmental goals were to be adopted. they would inevitably be attacked before the World Trade Organization (WTO) as contrary to free-trade rules. That tax "would be very problematic and almost impossible to implement," warned European Trade Commissioner Peter Mandelson. Not for certain. retorts Daniel Esty, Yale University Professor of Environmental Law, who bases his view on the General Agreement on Tariffs and Trade (GATT). GATT. the keystone of the WTO, authorizes countries to take measures ?necessary to the protection of life and health of people and animals and the preservation of vegetation." I Thus, in 1998, the WTO acknowledged the United States's right to prohibit shrimp imports from four Asian countries. including Thailand, since those countries ?shed for the crustaceans with nets dangerous to turtles. American Joseph E. Stiglitz, Nobel {Economics 2001 Prizewinner, has turned this argument against his own country, which obstinately rejects the Kyoto Protocol. "By getting off from paying for the damage they in?ict on the environment, American companies in fact receive a subsidy." he writes in his book, Another World (2006. Fayard). "Now. one of the WTO's main objectives is to equalize business conditions: subsidies introduce distortions; that's why countries are allowed to respond to them with countervailing duties." Imagine the following equation: exempted from reducing their carbon emissions the way businesses from countries adhering to the Kyoto Protocol must. American steel manufacturers enjoy an advantage of sixty dollars per ton of steel over their European competitors. Europe would have a basis for raising a tax of 60 dollars a ton on transatlantic steel - 10 percent of its cost. This would be a commercial 2/6/2007 Alain Faujas Must Business Be Ecological? weapon to incite polluters to respect the planet's equilibriums. Translation: 1? tFrench language correspondent Leslie Thatcher. about it's. Jump to today's Truthout Features: Today's Truthout Features (In accordance with Title 17 U. S. (3. Section 107, this material is distributed without pro?t to those who have expressed a prior interest in receiving the included information for research and educational purposes. tr at th 0 thas no af?liation whatsoever with the originator of this article nor is tr th 0 endorsed or sponsored by the originator.) "Go to Original" links are provided as a convenience to our readers and allow for veri?cation of authenticity. However; as originating pages are often updated by their originating host sites, the versions posted on T0 may not match the versions our readers view when clicking the "Go to Original" links. Print This Story r: . I 1 1' issues environment labor] women health voter rights] donate cmnact subscribe about us 2/6/2007 . . . . Viv-M I Fan-?Lam a? - - .. - ?Quasi-bunny ?Wilt-id? The Iranian petroleum criSils and United States national security Eng em/Lew WM, iron Roger Stem" 5?7 210/443 Department of Geography and Environmental Engineering, The Johns Hopkins University, 3400 North Charles Street, Baltimore, MD 21218 Edited by Ronald W. Jones. University of Rochester. Rochester, NY, and approved October 31, 2006 (received for review May 16, 2006) The U.S. case against Iran is based on Iran's deceptions regarding nuclear weapons development. This case is buttressed by asser- tions that a state so petroleum-rich cannot need nuclear power to preserve experts. as lran claims. The U.S. infers, therefore. that - Iran's entire nuclear technology program must pertain to weapons development. However. some industry project an Irani oil export decline ie.g.. Clark .IR (2005) Oil If such a decline is occurring. lran's claim to need nuclear power could be genuine. Because Iran's government relies on monopoly proceeds from oil exports for most revenue. it could become politically vulnerable if exports decline. Here, we survey the political econ- omy of irani petroleum for evidence of this decline. We define lran's export decline rate (edr) as its summed rates of depletion and domestic demand growth, which we find equals 10-12%. We estimate marginal cost per barrel for additions to lrani production capacity, from which we derive the "standstill" investment re- qulred to offset edr. We then compare the standstill investment to actual investment. which has been inadequate to offset edr. Even if a relatively optimistic schedule of future capacity addition ls met. the ratio of 2011 to 2006 exports will be only 0.40?0.52. A more probable scenario is that, absent some change in Irani policy. this ratio will be 0.33-0.46 with exports declining to zero by 2014- 2015. Energy subsidies. hostility to foreign investment, and inef- ficiencies of its state-planned economy underlie lran's problem, which has no relation to "peak oil." market power I Middle East oil 1 sanctions The U.S. has projected military force in the Persian Gulf for two decades. The policy aims to preempt emergence of a regional superpower (1). However, preemption of Iraq has been accom- plished only after two wars and an occupation. These costly exercises have not slowed Iran's procession toward regional super- power status but rather may have accelerated it (2). Iran?s rise illuminates a flaw in preemption policy. The flaw is that force projection is not a remedy for the underlying economic problem, market power. Oil cartel states exert market power to collect monopoly rents. In a lawless region such as the Gulf, each states? rents are a potential war prize to another. If rents could be aggregated by wars of seizure, a Gulf superpower would emerge, as was iraq?s aim in invading Iran and Kuwait. Yet, although U.S. force projection prevents wars of seizure, rents still flow. Force projection thus keeps a peace in which cartel states can collect monopoly rents sufficient to attain near-superpower status, even without wars of seizure. Market power thereby perpetuates the need for force projection, whereas force projection protects the cartel states that exert market power. This paradox guarantees that the U.S. militarywill remain in the Gulf until some policy is adopted to reduce market power. U.S. failure to confront market power is not an oversight. however. It is a policy whose premise is that cartel states must be appeased to secure their oil exports (3). This conception is based in turn on the perceived threat of an ?oil weapon? (4), a fiction U.S. of?cials have believed for ?ve decades. Whatever the shortcomings of past policy, the present concern is how to prevent a terror sponsor from attaining nuclear weapons or contain it if it does. 1 04 The U.S. case for action against Iran is based on its deceptions with respect to the Treaty on the Nonproliferation of Nuclear Weapons (NPT). HOWever, this case is buttressed with assertions about Irani petroleum: Finally, there is Iran's claim that it is building massive and expensive nuclear fuel cycle facilities to meet future electricity needs, while preserving oil and gas for export. All of this strains credulity. Iran?s gas reserves are the second largest in the world. [Yet] Iran flares enough gas annually to generate electricity equivalent to the output of four Bushehr reactors.?r Given historic dif?culties that U.S. policymakers have had with petrole economics, it seems possible that these assertions are wrong. Iran is guilty of NPT deceptions, but it cannot be inferred from this that all Irani claims must be false. The regime?s depen- i dence on export revenue suggests that it could need nuclear power as badly as it claims. Recent analyses by former National Iranian Oil Company (NIOC) of?cials project that oil exports could go to zero within 12?19 years (5, 6). It therefore seems possible that Iran's claim to need nuclear power might be genuine, an indicator of distress from anticipated export revenue shortfalls. If so, the Irani regime may be more vulnerable than is presently understood. Here we survey Iran?s petroleum economy for evidence of oil export decline that might suggest such vulnerability.t . Petroleum Sector Overview IMost Irani oil export revenues are monopoly rents, which com- ;prised 63% of Irani state revenues in 2004 (4). Rents derive from lthe difference between market price and competitive price, which Iis the sum of marginal production cost plus return to capital. For states like Iran that subsidize domestic petroleum demand, such dependence can be problematic. If subsidies call forth demand growth in excess of production growth, the exportable fraction of production will decline. This is what happened to Iran. Since 1980, energy demand ?growth has exceeded supply growth (5, 7, 8), with :exports stagnant since a 1996 peak (Fig. 1). A component of this imbalance is Iran?s recent oil production decline and consequent failure to meet Organization of the Petroleum Exporting Countries Author contributions: 0.5. designed research, performed research. and wrote the paper. The author declares no conflict of interest. This article is a PNAS direct submission. Freely available online through the PNAS open access option. Abbreviations: bid. barrels per day; fie, fuel efficiency; LDV. light-duty vehicle; LNG. liquefied natural gas; NIOC. National Iranian Oil Company; NPT, Treaty on the Nonprolif- eration of Nuclear Weapons; OPEC, Organization of Petroleum Exporting Countries. I ?E-mail: rstern?jhuedu. ?from a U.S. State Department transcript of remarks by Ambassador John Holton to the Hudson Institute, August 17, 2004 (available at 35281.htmii. 'Our survey uses some data from the Irani press. Although this press is largely statHontrolied. its energy reportage offers insights unavailable elsewhere. Quantitative data in Irani reportage usually correspond with trade press or agency reports when comparable 2006 by The National Academy of Sciences of the USA PNAS I January 2, 2007 vol. 104 no.1 377?382 Em ES c?2 gm Meter Reader Page I .4 ?itinerary Slut/(x i sing the lie/k7) Rulm January RU. 2007 Cantarell over the Cliff Summary and Recommendation Accelerating decline in Mexican oil production reminds us of hidden value in proven oil and natural gas reserves in buy-recommended producers including mega cap Total S.A. (TOT). large cap Anadarko Petroleum (APC), and small caps Berry Petroleum (BRY) and Cimarex (XEC). The Wall Street Journal calls attention to the "Plunge in Production "(see graphic) after highlighting potential acceleration of decline a year ago (see Meter Reader, February 15, 2006). For the four stocks, McDep Ratios at 0.85. 0.74. 0.74 and 0.58, respectively. point to increasing undervaluation (see table Rank bv McDep Ratio). We suggest full unlevered weightings in the illustrative McDep Energy Portfolio for TOT. APC. XEC and a half weighting for BRY (see table Portfolio Composite). Below the 200 day average. stock price below trend indicates the stocks are out of favor and investors may need more patience. Kurt H. Wulff. CFA Six-Year and One-Year Natural Gas and Oil Futures Plunge in Production . 'l,l .- I, '3 fl. ll'Loy-T (1 - lh (xi ?1 Latest Data Points and Trend 1300 Dollars Per Million BTUs 7?12 Mo Natural Gas 722? 7.23 72 M0 Natural Gas 7.34 7.41 12 Month Oil 64.85 60.48 ?3-372 Month_0_il_?t_np _6618_ 62.85_ 1100' tx 900 i 12/29306 118/07 ?12/07 1/22/07 . 11'29/Dollars Per Barrel A 7.32 782 7.54 7.53 I 7.50 743 5614 55.48 5711' 5962 50.98 59.41 Historical independent energy investment analysis by Kurt Wulffdoing business as McDep Associates is posted at 0 ms .mcdepcom. Analyses are prepared from sources and data believed to be reliable, but no representation is made as to their accuracy or completeness. Mr. Wulfi? is not paid by covered companies. Neither he nor his spouse trade a subject stock within a week before or after a change in rating. Page 1 of3 Main Identity From: "jcummins" To: "Erik Jansson" Sent: Friday. January 12. 2007 11:24 PM Subject: yeast for high ethanol production ISIS Press Release 12/01/07 Yeasts Targeted for High Ethanol Production Metabolic engineering of yeasts for high ethanol biofuel production may generate toxic metabolites and pose unique threats to agriculture Prof. Joe Cummins A fully referenced version of this article is posted on ISIS members? website. Yeast genetic manipulation more precise than crop plants. but.. Fermentation of plant materials to make ethanol has been greatly promoted as a means of producing sustainable biofuel Biofuels for Oil Addicts . 30) Production of ethanol during fermentation has been limited by the inability of yeast to grow at high ethanol levels, and a great deal of effort is being devoted to creating yeast strains that tolerate high ethanol levels, so they can continue fermentation to produce higher concentrations of alcohol. This has the major advantage of saving on energy involved in distilling and re?ning the ethanol. Yeast genetic manipulation is far more precise than can be achieved in crop plants, and the genes in yeast have been precisely altered by mutations. One method developed for making high ethanol yeast, for example, involves site-speci?c mutagenesis (see below) of regulatory proteins controlling a metabolic network for ethanol production, to make the yeast tolerate high levels of ethanol and glucose Although genes can be altered precisely to avoid collateral genetic damage, changing a metabolic network will still result in unexpected metabolic effects. The reason is that because genes are connected in a complex functional network, one gene cannot be altered without affecting many others Living with the Fluid Genome . 1818 Publications). Twelve years ago, Japanese scientists reported that a transgenic yeast engineered for increased rate of fermentation with multiple copies of one of its own genes ended up accumulating the metabolite at toxic, mutagenic levels As the yeast is not intended for making very strong beer for consumption but ethanol biofuel. toxin production may seem less of a problem, provided the yeast strain can be completely contained, which is well nigh impossible. GM yeast is likely to contaminate or cross with native yeasts. If unexpected toxins are produced because of metabolic network alterations. then we are in real trouble. Bakers yeast is not a pathogen, but may become one as the result ofcontamination. And toxic ethanol yeast in 1/13/2007 the human gut would be hardly desirable. What if this yeast escapes into the general environment and contaminate the soil as it might well do? Some years ago, a GM bacterium, Klebsialla planticola engineered to produce ethanol from wood wastes was found to inhibit the growth of wheat plants in every microcosm tested 6] Ethanol from Cellulose Biomass Not Sustainable nor Environmentally Benign, 30). A GM yeast engineered to produce high concentrations of ethanol released into the soil may spell catastrophe for agriculture and food production. Manipulating metabolic networks is a brand new ?eld and clearly here to stay. Organic farmers and the organic industry will soon be faced with dif?cult decisions about organic foods. Can genes and networks manipulated by precisely engineered DNA changes be considered organic? We will have to decide soon, before the bureaucrats decide for us. Legitimate Recombination and Site Speci?c Mutagenesis Site-speci?c mutagenesis has been used to make yeast produce and tolerant high levels of ethanol The process involves changing speci?c DNA code words in a particular gene. In the case of the high ethanol yeast, a commercial kit called the quick change site-speci?c mutagenesis kit was used. Short DNA chains (oligonucleotides) with desired mutations were ?rst prepared by the experimenters or purchased at the oligonucleotide store. The quick change kit provides the tools for changing the wild type gene carried on a bacterial plasmid. The mutant oligonucleotide is annealed to the wild type gene in the plasmid, which is ampli?ed to produce plasmids carrying the gene with the speci?c mutations. Next, the mutant gene is inserted into the yeast at a speci?c locus, a step that involves legitimate recombination. Genes to be inserted by legitimate recombination need to be ?anked by short sequences of the gene at the insertion site. Homologous recombination inserts the DNA and disrupts the target gene, allowing rapid selection of cells with the inserted gene. In the case of the regulatory protein gene targeted to the uracil locus, the transformed yeast colonies would be identi?ed using replica plating on growth medium lacking uracil. The colonies with the disrupted gene do not grow on the medium lacking uracil but leave a ghost like pattern on the agar. These colonies are picked off the uracil?containing master plates, and grown up for fuller testing. The main concern about the manipulation of metabolic network regulators is that the genes have multiple effects and changing the activity of one gene inevitably alters that of many others. Consequently, it may lead to production of unpredicted toxins (see above). Conventional mutagenesis still effective Ultraviolet light has been used for many years to generate mutant strains for laboratory and commercial applications. This technique has created strains of brewer's yeast that produce high levels of ethanol 1/13/2007 Page 3 of 3 for brewing and bioethanol production ?Petite yeasts are mitochondria-de?cient strains that can be produced by either nuclear or mitochondrial mutations. One nuclear petite increased ethanol production when it was cultivated on starch GM yeasts to ferment cellulose for bioethanol Amorphous cellulose was digested to produce ethanol by Saccharomyces cervisiae modi?ed with endogluconase genes from the fungus Trichoderma and a wild yeast Saccharomycopsis . The two genes were inserted in the uraFURl gene A number of genetic . modi?cations are designed to make Saccharomyce's cervisiae metabolize the sugar xylose found in lignocellulose in agricultural and forest wastes. Xylitol dehydrogenase and xylitol reductase genes from the yeast Pichia stipilis were integrated into the chromosomes of S. cervisiae . Xylose was converted to ethanol in the modi?ed strain [1 1-13]. Not much thought seems to have been given to the consequences of releasing such modi?ed yeast to the environment. S. cervisiae hasinot been pathogenic in plants or animals but modi?ed yeast may create novel pathogens, or simply prevent crop plants from growing (see above). Mutations and genetic modi?cations of Saccharomces cervisiae are being promoted to boost ethanol production from fermenthtion of crop and forest waste products. However, critical evaluation bf the human and environmental consequences of releasing the novel organisms has not been forthcoming. Furthermore, it has been shown recently that ethanol from cellulose biomass is neither sustainable nor environmentally benign 1fl3/2007 Main Identity From: "jcummins" To: "Erik Jansson" Sent: Wednesday. January 10. 2007 12:03 PM Subject: gm grapes and toxici wine ISIS Press Release 10/01/07 GM Grapevines Toxic Wines genes, toxins and cyanide gas are some of what to expect from wines on your dinner table Prof. Joe Cummins and Dr. Mae-Wan Ho A fully referenced version of this article is posted on ISIS members? website. Many ?eld trials commercial approval imminent A number of genetically modi?ed (GM) grapes have been created, though none is yet commercialised. There were 25 ?eld test releases in USA between 1999 and 2005, and a small deluge of commercial releases is expected any time now. The bulk of the test releases were of GM grapes resistant to diseases including powdery mildew, Botrytis Agrobacterium Clostridium Xylella nepovirus and closterovirus. There was one application for improved fruit quality, but the transgene was designated con?dential business information. The disease resistance genes antimicrobial peptides encoded by genes. The majority of the applications for release permits were from Cornell, California and New York State Universities, the rest were from Vintners or wine research companies In Europe, Italy conducted trials of grape modi?ed with a gene regulating the plant hormone auxin. Germany tested grapes resisting fungal diseases and France tested grapes resisting nepovirus Australia has ?eld-tested grapes modi?ed for fruit colour or quality most of them carrying antibiotic resistance genes as selectable markers, which would very likely spread to other organisms during wine making. There has been a hiatus in the commercial approval of GM cr0ps recently despite a very large number of ?eld trials. Bureaucrats may regard the low frequency of commercial approvals to be a ?log jam? and facilitate a ?ood of new approvals without warning. It is something that the concerned public should be prepared for. GM grapes potential hazards not addressed GM grapes carry all the potential hazards of other GMOs Horizontal Gene Transfer - The Hidden Hazards of Genetic Engineering ISIS Report; GM Food Animals Coming 32), but because GM grape juice and GM wine come as a clear liquids, many people may assume it is safe to drink; not so. 1/10/2007 Page 2 of 4 DNA from a GM grape persisted for over a year after wine fermentation, contradicting claims that wine fermentation elimin'ates DNA GM DNA in wine carries all the risks of horizontal gene transfer and recombination: creating new viruses and bacteria that cause diseases, triggering cancer in the case of GM DNA with promoters jumping into the genome of human cells Other potential hazards from GM grapes are toxins and allergens from the transgene products, or from unexpected metabolic disturbances to the host plant. Toxic antimicrobial peptides Chardonnay grapes have been modi?ed with genes for magainin and peptidyl-glycine-Ieucine carboxyamide, both antibiotic peptides originally ?om frog skin, and neomycin resistance and GUS were included as selectable markers. The GM grape was found to be more resistant to bacteria than to ?Jngi The toxicity of the GM grape to mammals has not yet been investigated. 1 Patent applications have been made for producing transgenic grapes with a version of a cecr0pin-1ike toxin, shiva The transgenic grapes resisted bunch rot, powdery mildew and downy mildew 10]. Shiva 1 is an experimental antibiotic peptide for treating mammals, and treatment of rabbits revealed a narrow range between effective and toxic doses [1 Great caution is needed in evaluating GM grape with genes for toxins that could endanger domestic and wildlife, as well as human beings. Grapevine fan leaf virus resistance was achieved by transforming grape with a coat protein gene from the fan leaf nepovirus 112,13]. The coat protein gene conferred resistance most likely through an suppression of virus replication [14] Subverting the Genetic Text 24). Disease resistance with bacteria and viral genes Grapevines are susceptible to infections with Agrobacterium causing - . . . crown gall (tumour) disease (the same Agrobacterium 1n a dlsarmed form that's commonly used in genetic modi?cation of plants). The plant tumours are initiated when the bacterium injects plant cells with a DNA Ti (tumour?inducing) plasmid carrying genes for plant cell proliferation. A portion of the Ti plasmid is transferred into the plant cell genome, and depends on the forming a DNA single strand intermediate that is protected from degradation in the plant cell by'a coating of vir gene protein produced by the bacterium. The protected single strand of DNA integrates into the plant chromosome and begins activating genes that initiate tumour formation. Agrobacterium -resistant grape vine was made by inserting a gene for a mutant form of the virigene into the plant genome. The transgenic grape produces the mutant vir protein continuously, which attaches to the infecting part of the Ti plasmid, causing it to be inactivated and destroyed rather than being integrating into the chromosome 1/ 10/2007 Grape bunch rot Botrytis is caused by the fungus Botrytis cinerea while the fatal Pierce's disease is caused by the bacterium Xylella . Both pathogens use enzymes that degrade the plant cell wall to invade the grape tissue. A gene for an inhibitor of the pathogen wall-digesting enzyme (polygalacturonase inhibiting protein) from pear fruit was used to transform grape vines. The transgenic DNA included the promoter, a TMV enhancer, the pear gene, and octopine terminator, accompanied by the GUS gene and a neomycin resistance gene as selectable markers. The transgenic grape was reported to resist both the bacterial gene and the fungal gene Cyanide-producing grape Grape has also been genetically modi?ed to resist insects by making them produce hydrogen cyanide when attacked by insects. Cyanogenic plants are characterized by the liberation of HCN in the course of tissue injury, due to the hydrolysis of cyanogenic glucosides. Most of our knowledge of cyanogenicity comes from Sorghum bicolor which contains large quantities of the cyanogenic glucoside, dhurrin. Prussic acid, a derivative of cyanide, is also a serious potential problem. Crop species most commonly associated with prussic acid poisoning are sorghum, Johnsongrass, and Sudangrass. Grain sorghum typically has more potential for toxic levels of prussic acid than forage sorghum or Sudangrass. Young, rapidly growing plants are the most likely to contain high levels of prussic acid. Cyanide is more concentrated in young leaves than in older leaves or stems. New sorghum growth following drought or frost is dangerously high in cyanide. Generally, any stress condition that retards normal plant growth may increase prussic acid content. Hydrogen cyanide is released when plant leaves are damaged by trampling, cutting, crushing, chewing, or wilting. Drought-stunted plants accumulate cyanide and can possess toxic levels at maturity. Prussic acid poisoning is most commonly associated with regrowth following a drought-ending rain, or the ?rst fall frost. New growth from frosted or drought-stressed plants is palatable, but dangerously high in cyanide. After a killing frost, at least four days should pass before grazing to allow released hydrogen cyanide to dissipate. A multigenic trait responsible for of the secondary metabolite, dhurrin cyanogenic glucoside was engineered in grapevine with three genes sequences from sorghum Sorghum bicolor two cytochrome P4505 (CYP79A1 and CYP71E1) and a The grapevine was modi?ed using a two-step process involving whole plant transformation followed by hairy root transformation. The two step process make sure that the whole plant could be transformed with the dhurrin pathway, while the secondary transformation of the hairy root culture allowed fuller study of the dhurrin produced in roots which had been challenged with the root pathogenic insect Phyloxera . One dhurrin-positive line was tested and found to release cyanide upon maceration. Co-culture of a cyanogenic hairy root line or a non-cyanogenic line with the specialist rootsucking, gall-forming, aphid-like insect, grapevine Daktulosphaira vitifoliae) 1/10/2007 gave no evidence that the cyanogenic plant-tissue was protected from insect infestation. Consistently high levels of dhurrin accumulation may be required for that to occur We are not sure at all about the ultimate purpose of the modi?ed grape but will cei'tainly avoid drinking juice and wine made from it, provided that it is labeled as such. If it is not labeled, we may all have no choice over cyanide poisoning. For crying out loud The modi?cation of grapevines has gone beyond the humdrum of Bt and herbicide tolerance of most GM food crops. The new emphasis is on genes and proteins, and virus resistance using coat protein gene modi?cations. The introduction of a cyanogenic toxin into grapevine may be a sign that genetic engineers are growing ever more daring in the recognition that regulators are standing with them against the public. Clearly these new developments are crying out for GM labelling at the very least, and a clean sweep of the regulatory regimes would not come amiss. Page 4 of 4 1/ I 0/2007 Main Identity From: "jcummins" To: "Erik Jansson" Sent: Monday, January 08, 2007 2:56 PM Subject: self cloned wine yeast ISIS Press Release 08/01/07 'Self?Cloned? Wine Yeasts Not Necessarily Safe Yeast genetics is more precise, but altering the expression of a single native yeast gene can change the entire metabolic network in an unexpected way. Prof. Joe Cummins A ?rlly referenced version of this report is posted on ISIS members? website. Self cloned versus genetically modi?ed yeast The ?rst genetically modi?ed (GM) wine yeast, and the only one commercially released so far has been described earlier (GM Wine Sold Unlabelled in the United States, this series). In 2006, FDA designated another wine yeast generally recognized as safe (GRAS), and this is the second to be released for commercial use. Saccharomyces cerevisiae was derived from Davis 522, a strain commonly used in the wine industry, and carries a recombinant genetic insert composed of three elements, the gene, a promoter, and a terminator, each of the three parts derived from a different strain of S. cerevisiae. Davis 522 actually has its own gene, which is not normally active during alcoholic fermentation. The purpose of creating is to increase the expression of urea amidolyase, which catalyzes the hydrolysis of urea produced by the wine yeast during alcoholic fermentation. Urea is a precursor of ethyl carbamate (urethane), a suspected human carcinogen formed in the wine from the reaction of urea and ethanol; so hydrolyzing urea should signi?cantly reduce the potential for the formation and accumulation of ethyl carbamate in the wine The gene under control of the S. cerevisiae promoter and terminator signals was integrated into the URAS-locus of Davis 522. In vivo assays showed that the GM strain reduced ethyl carbamate in Chardonnay wine by 89.1 percent. Analyses of the genotype, phenotype, and transcriptome revealed that the GM yeast is substantially equivalent to the parental strain Publications were cited to indicate that is a powerful carcinogen in animal and humans, and there is general agreement about those ?ndings. Interestingly, mice given ethyl carbamate and wine had signi?cantly reduced incidence of cancer compared with mice given ethyl carbamate alone. Wine components other than ethanol seem to play a role in suppression tumours 1/8/2007 ?Self?cloning? yeasts The term self-cloning has been coined to describe genetic modi?cation by gene transfer within the same species, as in the 'case of Saccharomyces cerevisae genes from different strains being incorporated into the GM strain l. The issue of self-cloning arose recently in Japan, where a sake (rice wine) yeast was modi?ed to enhance ?avour by incorporating a mutant fatty acid gene along with an antibiotic resistance gene. A counter selection procedure was then used to remove the antibiotic resistance gene but preserves the fatty acid mutant in the chromosome. The Japanese government has decided that the sake yeast is a ?self-cloning organism? not covered by regulations Eover GM organisms Self-cloning covers a growing class of GM wine yeasts that are under development to enhance or improve the ?avour of wines and distillates. Yeast genes encoding enzymes or degiading esters are targets of manipulation. The genes made to over-express include alcohol acetyl-transferase and ethanol hexanoyl- transferase. Additional copies of the genes introduced into GM strains were driven by the yeast PGKI promoter and PGK terminator. A dominant selectab'Ie marker was a mutant of the yeast acetolactate gene (ilv2) that pr'ovides resistance to the herbicide sulphmeturon. A cassette containing all of the yeast genes to be integrated was inserted at the ilv2 locusl[6]. Even though bacteria had been used in preliminary cloning, the modi?ed yeast contained only yeast genes and in that sense it may be comparable to the sake yeast. i Transgenic yeasts 1 Grapes with high sugar content may produce wines ivith excessive ethanol leading to public health problems and in impaired ?avour. A champagne strain of wine yeast was modi?ed using the NADH oxidase gene from Lactococcus lactis under the control of a yeast glyce'raldehyde 3 phosphate dehydrogenase promoter integrated into the yeast URA3 locus. The transgenic wine yeast consumed the high sugar of the must without producing excessive ethanol The anti-oxidant resveratrol is a wine component of proven health bene?t. In a novel apprdach, a coenzyme-A ligase gene from hybrid poplar and resveratrol gene from grapevine were both added to the yeast chromosomes. The coenzyme?A ligase gene with a yeast alcohol dehydrogenase promoter and transcription terminator was inserted at the URA3 locus of the wine yeast. The resveratrol gene under the control of the yeast enolase promoter and terminator was inserted into the LEU2 locus of the wine yeast. In that way the yeast biochemical pathway was restructured for enhanced resveratrol presumably to; produce a double whammy anti-oxidant. But is it safe? Transgenic vs self-cloned yeasts A recent review listed recombinant wine yeasts produced since 1993 to ?improve? wine quality or technology. 0f the 14 recombinant wine yeasts, Page 2 of 4 1/8/2007 seven were transgenic and seven were modi?cations of the genome using the genes of wine yeasts It seems sensible for the wine industry to present the ?self cloned? strains as distinct from the transgenic ones. Both transgenic and self-cloned require careful safety evaluations, though of the two transgenic wine is probably the greater concern. Direct comparisons of self-cloned and transgenic wine strains regarding their commercial and environmental characteristics have not been reported so far. However, there is a comparative study of the commercial Baker?s yeast with a transgenic strain and a self-cloned strain altered for improved frozen bread dough. The yeasts are made resistant to freezing by disrupting the acid trehalose gene through transformation with either a yeast uracil 3 gene or a bacterial gene consisting of a fragment of a gene specifying antibiotic resistance which were directed to the yeast trehalose gene by short fragments of the trehalose gene at each end of the disrupting gene sequence . The freeze-resistant strains were compared in a contained soil environment to determine if the self-cloned or transgenic strains survived better in the natural environment than did the wild type yeast. Both the cells and the DNA of the self cloned and transgenic strains behaved similarly to the wild type yeast in the simulated natural environment This type of experiment might prove informative in wine yeasts. ?Cisgenic? cr0ps In a related development, the developers of GM crop plants have used the term ?cisgenic? to describe genetically modi?ed crops derived from sexually compatible lines. The developers argued that there was no need for regulatory approval of cisgenic crops provided they are shown to be free of foreign DNA There was strong support for the proposal to deregulation cisgenic crops from industry representatives Molecular geneticists David Schubert and David Williams made cogent arguments against the unregulated release of cisgenic Cisgenic plants suffer from practically all the major shortcomings of GM organisms. Cisgenic plants still require the transformation of cells with DNA, a process widely documented to result in large-scale translocations of the plant DNA, and scrambling and fragmentation of the transgene, with frequent random insertions of the plasmid DNA. In addition, a cisgenic plant would likely lack rigorous, tissue-speci?c expression of the introduced gene, thereby allowing aberrantsecondary modi?cations of proteins, such as glysosylation, that can cause serious immunogenic responses in animals. Furthermore, regardless of the presence of regulatory elements, the pattern and level of gene expression can vary greatly depending upon its insertion site Cisgenic crops should not be confused with self-cloned yeasts. Crop genetic engineering differs ?rndamentally from yeast genetic engineering. Crop genetic engineering is based on illegitimate recombination while yeast genetic engineering employs legitimate homologous recombination allowing gene insertions at speci?c sites in contrast to the unpredictable, uncontrollable insertions in crop genetic 1/8/2007 Page 4 of 4 Nevertheless, even self-cloned yeasts must be subject to rigorous and comprehensive safety tests, as it has already been demonstrated that changing the expression of a single gene in yeast clan have unexpected effects. In 1995, Japanese researchers reported that a transgenic yeast engineered for increased rate of fermentation with multiple copies of I one of its own genes ended up accumulating the metabolite at toxic, mutagenic levels modi?cation. 1 I 1/8/2007 December 16, 2006 Prof. Joe Curnmins Genetically Modified Yeast and Grapes for Drink and Fuel Genetically Modi?ed Grapes A number of genetically modi?ed (GM) grapes have been created and tested but these varieties have not been approved for commercial release. There have not yet been commercial releases of GM grapes but there have been numerous ?eld test releases of GM grapes in USA which may signal a deluge of commercial releases. There were 25 ?eld test releases of GM yeast in USA between 1999 and 2005. The bulk of these releases were to test grapes resistant to diseases including powdery mildew, Botytis, Agrobacterium, Clostridium, Xylella, nepovirus and and closterovirus. There was one application for improved fruit quality whose donor gene was designated con?dential business information (CBI). The disease resistance genes included antimicrobial peptides determined by genes, specifying peptides. The institutions applying for release permits included Cornell, Califomia and New York State Universities and theirs were the majority of applications, others applying were vinters or wine research companies (1).In Europe, Italy conducted trials of grape modi?ed with a gene regulating the plant hormone auxin, Germany tested grapes resisting fungal diseases and France tested grapes resisting nepovirus (2).Australia has done a number of ?eld tests of grapes modi?ed for grape fruit color or quality (3). Most of the tests included antibiotic resistance genes as selectable markers which would very likely be spread among other organisms during wine making. Recently, there has been a hiatus in approvals of GM crops for commercial release, that relatively tiny approval frequency in the face of a very large number of ?eld trials suggests that bureaucrats may regard the low frequency of approvals to be a ?log jamb? and for that reason facilitate a ?ood of new approvals that will be dif?cult to evaluate because there has been no warning and relatively few have the time and ability to carefully evaluate the numerous releases. It is something that the concerned public should be prepared for. A number of transgenic grapes have been created and some current examples of these will be described below. Before describing those GM grapes it is worth keeping in mind that the DNA from a GM grape persisted for over a year a?er wine fermentation (4) rendering claims that wine fermentation eliminates DNA to be invalid .Chardonnay grapes have been modi?ed with a magainin and Peptidyl-glycine-leucine carboxyamide (antibiotic peptides isolated from frog skin) the genes also integrated include neomycin selectable marker and a GUS marker gene The grape was found to be more resistant to bacteria than to ?rngi The toxicity of the GM grape to mammals has not yet been reported. Patent applications has been made for producing transgenic grapes bearing a version of a ceeropin like toxin shiva The transgenic grapes resisted bunch rot, powdery mildew and downy Shiva is an experimental drug for treating mammals, treatment of rabbits showed a narrow range between effective and toxic doses (9). Caution is needed in evaluating GM grapes bearing genes for toxins. Grapevine fanleaf virus resistance was achieved by transforming grape with a. coat protein gene from the fan leaf nepovlirus The coat protein gene conferred resistance to the virus (10,11), The coat protein gene conferred resistance most likely, - through an RNA I suppression of virus replication. Grape vines are infected with Agrobacterium causing crown gall (tumor)l formation on the vines. The plant tumors are initiated when the bacterium injects plant cells with a DNA plasmid bearing genes for plant cell proliferation. The plasmid transfer a portion of the plasmid from bacterium to plant cell, this transfer depends on the part of the plasmid transferred forming a DNA single strand intermediate that is protected from degradation in the plant cell by a coat of vir gene protein produced by the bacterium. The protected single strand of DNA integrates into the plant chromosome and begins activating genes that initiate tumor formation The resistant grape vine is made by inserting a gene for a mutant form of the vir gene into the plant genome which continuously produces the mutant vir protein which is able to attach to the infecting part of the} plasmid causing the infecting part of the plasmid to be inactivated and destroyed in the plant cell rather than being integrating into the chromosome and causing plant cell to proliferate as a tumor (12). The crown gall disease caused by the plant tumors is signi?cant in vineyards. Grape bunch rot (Botrytis) is caused by the fungus Botrytis cinerea while Pierce?s disease is a fatal bacterial (Xylellal) disease of grape vines. The pathbgens employ plant cell wall degrading enzymes Iare used by the pathogens to invade the grape tissue, a gene for the enzyme inhibitor of the pathogen wall digesting enzyme. (polygalacturonase inhibiting protein) from bear fruit was used to transform grape vines. The grape transformation included the promoter, a TMV enhancer ,the pear gene, and octopine terminator, the transformations also contained the GUS .gene and a neomycin resistance gene. The transgenic Igrape line resisted both the bacterial gene and the fungal gene(13). Cyanogenic plants are characterized by the liberation of HCN in the cou'rse of tissue injury. This cyanogenesis is caused by the hydrolysis of cyanogenic glucojsides. Most of our knowledge of cyanogenicity is based on investigations of Sorghum bicolor, which contains large quantities of the cyanogenic glucoside, dhurrin. Prussic acid, a derivative of cyanide, is a serious potential p'roblem. Crop species most commonly associated with prussic acid poisoning are sorghum, Johnsongrass, and sudangrass. Grain sorghum typically has more potential for toxic levels of prussic acid than forage 'sorghum or sudangrass. New regrowth from Johnsongl'ass and shattercane can also pose problems for grazing animals because of toxic levels ofprussic acid.Young, rapidly growing plants are the most likely to contain high levels of p'russic acid. Cyanide is more concentrated in young leaves than in older leaves or stems. New sorghum growth following drou'ght or frost is dangerously high in cyanide. Generally, any stress condition that retards normal plant growth may increase prussic acid content. Hydrogen cyanide is released when plant} leaves are physically damaged by trampling, cutting, crushing, chewing, or wiltirig. Drought-stunted plants accumulate cyanide and can possess toxic levels at maturity. Prussic acid poisoning is most commonly associated with regrowth following a drought? ending rain or the ?rst fall ?'ost. New growth from frosted or drought-stressed plants is palatable, but dangerously high in cyanide. After a killing frost, wait at least four {days before grazing to allow the released hydrogen cyanide to dissipate. A multigenic trait of the secondary metabolite, dhurrin cyanogenic glucoside) was engineered 2 in grapevine (Vitis vinifera L.).Using three genetic sequences from sorghum (Sorghum bicolor): two cytochrome P450-encoding (CYP79A1 and CYP71E1) and a UDPG- grape was modi?ed using a two-step process involving whole plant transformation followed by hairy root transformation, which was used to transfer the three sorghum sequences to grapevine. One dhun'in- positive line was tested and found to release cyanide upon maceration .Co-culture of a cyanogenic hairy root line or an a cyanogenic line with the specialist rootsucking, gall- forming, aphid-like insect, grapevine (Daktulosphaira vitifoliae,), there was no evidence for protection of the cyanogenic plant tissue from infestation by the insect. Consistently high levels of dhurrin accumulation may be required for this to I am very uncertain about the ultimate purpose of the modi?ed grape and the juice or wine made from the GM grape. One fervrently hOpes that the wine will be labeled in the market As Rev. Jim Jones used to say ?try a little grape Kool-Aid?. but' in spite of what Rev Jim Jones believed we should be warned before we drink such a drink. The modi?cation of grape vines has gone beyond the hum drum modi?cations for Bt and herbicide tolerance of most GM food crops. There has been a new emphasis on genes and proteins along with virus resistance using coat protein gene modi?cations. The introduction of a cyanogenic toxin into wine yeast may be a signal that genetic engineers are growing ever more daring and they recognize that regulators stand with them against the public. Clearly these new developments cry out for labeling of the foodstuffs at the very least, but a clean sweep of the regulatory regimes followed by a replacement with competent regulators would be a real salvation. References 1. Grape Field Test Release Permits Database for the US. 2005 2. Grape International Field Test Sources Last checked September 20, 2005 3. Australia Evaluation of transgenes in grapevine No. 3 CSIRO Plant Industry Horticulture Unit 2001and 2002 4. Savazzini,F and Martinelli, L. DNA analysis in wine: Development of methods for enhanced extraction and real-time polymerase chain reaction quanti?cation Analytica Chimica Acta 2006,563,274-82 5. Vidal JR, Kikkert JR, Wallace PG and Reisch BI High-ef?ciency biolistic co- transformation and regeneration of 'Chardonnay' (Vitis vinifera L.) containing npt-II and antimicrobial peptide genes. Plant Cell Rep. 2003 6. Vidal,J,Kikkert,J,Malnoy,M Barnard,J and Reisch,B. Evaluation of Transgenic ?Chardonnay? (Vitis vinifera) Containing Magainin Genes for Resistance to Crown Gall and Powdery Mildew Transgenic Research 2006,15,69-82 7. Scorza,D and Gray,D. Disease resistance in vitis United States Patent Application- 20010047522 8. Scorza,D and Gray,D. Disease resistance in vitis United States Patent Application 20030182686 9. Shahsavari M, Peyman GA, Niesman MR, Miceli MV and Jaynes J. Shiva-l: in vitro and in vivo tests of the effects of a novel, lytic peptide on ocular cells. Int Ophthalmol. 1995 and Fuch,M. Grapevine fanlcaf virus resistance in grapevine United States Patent Application 20030226172 11. and Fuch,M Grapevine fanleaf virus resistance in grapevine expressing grapevine fanleaf virus coat protein US Patent 6,667,426 2003 . 12. Burr,T,Gonsalves,D and Pang,S. Bacterial resistance in grapevine United States Patent United States Patnet 6,172,280 2001 . 13. and Dandel To: "Erik Jansson" Sent: Tuesday, December 12, 2006 2:35 PM Subject: gm wine The dangers of genetically modi?ed wine yeast By Erica Martenson Tuesday, December 12, 2006 6:39 AM PST DeSpite the Wine Institute?s recent statement that no genetically modi?ed organisms (GMOs) should be used in winemaking, the Sacramento Bee recently reported that, according to American Tartaric Products, the ?rst wines made with a genetically modi?ed wine yeast, MLOI, will be released this year. This yeast is available only in North America where GMOs are unregulated. It was modi?ed by inserting two foreign genes, one from the pombe yeast, a yeast found in Africa and used to make beer, and one from the bacteria 0. oeni, so that the alcoholic and malolactic fermentations, normally a two-step process, occur at the same time. While this may be a convenience to winemakers, especially those producing large quantities of wine, I am concerned for both consumers and our local economy. The designation of this yeast as GRAS (Generally Recognized as Safe) is questionable for a few reasons. First of all, the FDA approved the yeast based on data supplied by the developer, not based on its own study or an independent study. A developer has an interest in getting its product to market as soon as possible, whether it has been proven safe or not. Secondly, according to Professor Joseph Cummins, emeritus genetics professor at the University of Western Ontario, wine yeasts are unstable, and genetically altering them can lead to unexpected toxicity in the ?nal product. He states that there is no evidence that the developer did any animal feeding studies to test for such toxicity and that there is no proof that the yeast and yeast DNA will not be present in the wine. A few wineries? decision to use this yeast could affect the entire North American market. Since these wines are unlabeled, the only way people can avoid them is to avoid all wines from North America, except those labeled organic, and few wines are labeled organic, due to the addition of sul?tes during the winemaking process. Consumers in Europe and Asia' are very informed regarding GMOs and have resoundingly rejected them. American consumers are becoming more aware, and polls show that a majority of Americans would prefer to avoid them. A few wineries? choice to use could also be a nuisance to other wineries, because this GM wine yeast could contaminate native and traditional wine yeasts through the air, surface waste and water runoff. 12f 13/2006 Many wineries here in the Napa Valley are very particular about their choice of wine yeast, and contamination of these various yeast strains would truly be a shame. I contacted many of the large producers of Napa Valley wine asking whether or not they have used this GM yeast or plan to in the future. All that responded stated emphatically that they have not used it and do not plan to. To help consumers who would prefer to avoid consuming genetically modi?ed products make an informed wine choice and to provide an avenue for our local wineries to distinguish their wines from wines that may be using GM. yeast, those that responded were listed, with their permission, on a ?Shopper?s Guide to Buying at on the FAQs page. I In our society, we often talk about our rights and discuss very little our responsibilities to our neighbors, to the environment and to the community as a whole. In considering the issue of QMOS and their use, all of these factors should be taken into account. (Martenson lives in Napa.) 1 Page 2 of 2 12/13/2006 5 u. -c U-?ulo amwmaeauq-?u-q magnum-?- .awmtw?hu Vlh?-vahy -w-ug-r. ABGUT i ARCHIVE i CONTACT US BONEFE i WELCOME (3M grapes earn wrath of growers {2351052006} 5) ?ll-t INTRODUCTEON FROFELES FOCUS on AFRICA SAY NO TO GM Wnes of South Africa'. the body for exporters of South African wines. inexplicably seems to be backing GM trials -just click the link below to automatically send them an email. It only takes a minute: (please paste this link into your browser, if necessary) FOCUS ON ASIA GM grapes earn wrath of growers BOBBY JORDAN The Sunday Times. 22 October 2006 The University of Stellenbosch's planned planting of 'super-grapes' has top wine exporters seeing red AN EFFORT to produce South Africa's ?rst genetically modi?ed . Chardonnay wine has sparked ferment among top winemakers, who want the country's wines to remain 'pure'. The 'super?grapes' already in incubation inside a greenhouse at the University of Stellenbosch. are due to be grown at the university's experimental farm. But the trial ?rst needs the go-ahead from the government's Executive Council on Genetically Modi?ed Organisms. which will debate the matter next month amid a chorus of opposition from wine authorities, including premier estates such as Spier. Lanzerac and Distell. This week the national Wrne Council, chaired by former Cabinet minister Kader Asmal, opposed another application from the university - to use genetically enhanced yeast in wine production. The row over super-grapes highlights a broader spat over GM foods such as maize, soya and cotton, which are already widely cultivated in South Africa despite concerns about possible health risks and environmental contamination. A Free State University study has found traces of GM ingredients in 90% of soya products and 61% of maize products tested from the local market. Maize meal is one well-known GM product. 1 8 1 1 2/1 3/2006 1v; vv albll.U1 Page 2 of 3 South African companies at present do not have to label?food products containing GM mate'rial unless they show 'signi?cant difference' from other products - a term ye"t to be clearly de?ned. Vl?ne farmers opposed to GM foods fear their non-GM grapes might become contaminated by GM seed, which in the case of wine would be a disaster for the country's eco?friendly reputation. Anti-GM lobby groups such as Biowatch South Africa also warn of intellectual property issues - the patents on GM organisms are retained by the companies that produce them. i However. pro-GM scientists and companies believe GM drops offer signi?cant bene?ts such as resistance to disease and higher nutrient content. They argue that GM products are already widely lavailable throughout much of the developed world as well as in South Africa. About 30% cf yellow maize and 10% of white maize is already derived from GM crops. . I Among other things, GM grapes could lower alcohol content in wines and reduce headaches resulting from particular grape sugarsl GM maize is resistant to some harmful weeds and bugs, thereby reducing the need for pesticides. Some GM herbicides contain insect genes that make crop sprays more effective. Dr Sarita GroenewalJ. GM ?eld trial manager at Stellenbolsch University Institute for Vl?ne Biotechnology, said the whole point of the GM trials was to produce more environmentally friendly grapevines. Groenewald said: 'It is really vital that we do these trials. The actual aim is to produce a grapevin:e that can be used in more environmentally friendly production on wine farms. These trials are for research purposes only.? Groenewald said the trial site would be completely sealed off to minimise the risk of contamination. All ?owers would be bagged andugrapevines covered with nets to prevent seed dispersal by birds or other animals during fruiting stages. 'The genes that have been inserted into these plants [come from] from E. coli. which is generallyI present in nature anyway,? Groenewald said. But Leslie Liddell, director of Biowatch South Africa. said: 'The nets and bagging of ?owers will 'Inot ensure that small insects and micro-organisms don't get to the GM plants.? GM vineyard trials are a thorny issue in several other wine-producing countries. including the US and France, where science is making inrOads in the ?ght againSt harmful crop viruses. - i . A GM vineyard under lock and .key in Colmar, the heart of France's famous Alsace wine region, has angered ?ercely traditional French farmers. some of whom say they'd rather live with viruses. South African winemakers this week expressed concern about the university's ability to completely isolate its vineyard trial. The head red 8 1 12/13/2006 GMWatchorg Page 3 winemaker at Spier Estate, Kobie Viljoen, said even the slightest exposure to genetically modi?ed organisms (GMOs), such as a GM yeast, could contaminate a wine cellar and have serious repercussions for wine exports. 'For us on the production side, GMOs are a no-go.? he said. The head of grape and wine buying at Distell. Ernst le Roux. said consumer doubts about GM products outweighed the need for innovation in agriculture. 'From a commercial point of view we can't afford to even say we are thinking of using this material,? Le Roux said. adding that Distell had no plans to buy GM grapes. 'We won't be pressing to make it legal either.? Consumer doubts are well founded. according to Chris Viljoen, head of the University of the Free State GMO testing facility in the faculty of Plant Sciences. 'Most scientists who are pro-GM have no problems with GM plants. But when you talk about producing GM babies then suddenly vieWpoints become quite varied. One wonders if people would want labels on GM human beings.? he said. 'This debate is not about accepting or rejecting technology. It's about making sure that technology is relevant. One can't just say because we used technology to produce something then we have to use it because it's be?en' Back to the Archive Go to a Print frlendly Page Email this Article to a Friend GM Watch Nit-$11 13 December 2006 8 1 . 12/ 3/2006 rDepartment of the Planet Earth 701 Street, SE- Suite 200, Washington, DC 20003 (301) 475-8366 - - Aluminum: A Causative Co-Factor for ?Dementia? of Alzheimer?s Disease Presentation at the ?7th Keele Meeting on Aluminum, Uxmal, Mexico. 2/27/07 Erik Jansson, Pres. Department of the Planet Earth, Washington; DC Brie?ng Paper General Findings: 1. Alzheimer?s disease and Alzheimer" 3 disease ?with dementia? are different medical conditions. The later condition sends people to the nursing home. 1 2. The ?dementia? of Alzhelmer is produced by gross brain atrophy and loss of brain connectivity rather than by senile plaques. Neurofibrillary tangles participate in both brain atr0phy and loss of connectivity. (Walton, 2006) The ?dementia? of Alzheimer? is substantially preventable. Epidemiology indicates that restriction of aluminum intake and absorption from food and drinking water additives can reduce Alzheimer?s ?dementia? risk by as much as 50 to 80 percent, at least 1n the United States and Canada. 5. Abundant evidence supports a primary role of aluminum 1n co-productio?n of the ?dementia? of Alzhe1mer 5: 1e it? no longer controversial. There 13 suf?cient evidence to initiate govermnental actions to protect the public health. Observations on Aluminum?s Role in 0' DRC McLachlan, Canadian pioneer (1993): Aluminum is a ?necessary but not suf?cient risk factor for Alzheimer?s?. ?Because aluminum has co-exlisted with life for so long, it must have some role in biology. Perhaps its purpose is to kill cells.? 0 R. Deloncle et al (2001): After chronic exposure of rats to aluminum L-glutamate and examination' I of the hippocampus it is concluded: ..These results are consistent with' aluminum-induced acceleration of the aging process.? I I Lukiw et al (2005): After exposure of human neural cells to 100 nano- molar aluminum sulfate to an array of human genes: Of the most altered genes expression. levels, 71 percent of aluminum- affected genes and 87 percent of aluminum induced genes exhibit expression patterns similar to those observed 1n AD. A Review: Aluminum - A Causative Co-Factor 0f ?Dementia? of Alzheimer?s Disease. Erik Jansson, Department of the Planet Earth, 701 Street, SE, Ste. 200, Washington, DC 20003, Alzheimer?s Disease (AD) and the ?dementia? of AD have been confused as having identical causation. Disagreement between the clinical identi?cation of persons with dementia using cognitive testing, and brain autopsy ?ndings based on plaque and tangle deposits reveals that AD, as presently de?ned, and its dementia lack identical causation. Study of 56 religious sisters (age of death 88 to 93) from the Nun Study found that fourteen died with AD measured by brain deposits, but with normal cognition. Another nineteen sisters had AD with dementia. The difference between the two AD groups was hippocampal volume, i.e. brain atrophy. Aluminum is an effective killer of brain cells in laboratory animals and humans. Dementia of AD is prevented by restriction of aluminum exposure. Brain atrophy is prevented by folic acid, also an aluminum chelator. Aluminum should be viewed as a causative co-factor in generation of brain atrophy and dementia. . Alzheimer?s Disease is Substantially Preventable As Indicated By Many Epidemiology Studies. 0 Prevention of 50 to 80 percent of AD incidence appears to be feasible. The more than twenty different prevention approaches listed below suggests a linear disease process. 0 There are four basic categories of opportunity for prevention identi?ed by epidemiology. 1. Aluminum Avoidance: Avoidance of intake of aluminum from food and drinking water prevents AD. There are 22 published drinking water epidemiology studies and one food study linking aluminum: intake to either elderly cognitive impairment or to AD. Fifty to 80 percent prevention appears possible. Suf?cient epidemiology studieis exist to justify governmental regulatdry actions. . 2. Antioxidants. Anti-in?ammatories and Aluminum Chelatorsd A wide range of food products and supplements have the capacity to chelate aluminum or abate the oxidation and in?ammation produced by the metal. 3. Fat and Calories: of ?sh, DHA, and avoidance bf obesity and the metabolic can prevent AD. 4. Exercise of the mind: Intellectual and social activity and physical exercise can postpone the onset of by creating a cognitive reserve. Further detail is provided below - based upon published studies. For one example, the Framingham study ?nds that the daily consumption of one ?sh pill can reduce AD risk by 50 percent. A study ?'om a Syracuse,.New York geriatric center founthhat food prepared with aluminum additives such asl aluminum constituted baking powder can increase the risk of AD by as much as one hundred percent: i.e. all participants consuming this food developed AD and none of the controls. See chart. Epidemiology Studies Identify theE Following Preventative Programs That Can Reduce the Risk of Devel0ping AD by 50 Percent or More, After Control for Other Factors. I i Category 1: Aluminum Avoidance: i . 0 Reduction of aluminum intake from food ._and drinking water. I 1. Maintenance of the pH of the municipal water supply in a band close to 7.9 to reduce aluminum absorption (likelyfvia skin, lung and nose). 2. Elimination of food containing aluminum additives from the diet, and regulatory action to phase out such additives such as aluminum based baking powder. Consumption of silicic acid containing mineral waters to chelate aluminum, prevent absorption and increase excretion. (Can reduce risk by 50 percent.) Category 2. Use of These Dietany Items With Biological Importance But Which Also Cltelate Aluminum or Compete in Biology. Normal or high intake versus low intake of folic acid, with combined folic acid supplements and additional quantity from food shown effective in one study. (Folic acid is also a brain chelator for aluminum and associated with reduced brain atrophy.) In contrast, mixed results are shown for vitamin and niacin. Consumption of vitamin or vitamin and supplements together or from foods enriched in the vitamins, with indication that allele carriers may be poor responders to vitamin E. Alpha lipoic acid supplements: ALA is a likely preventative supplement with a published successful clinical trial- for AD therapy completely halting progression. Animal studies are available but human epidemiology is lacking. ALA capably chelates brain iron and likely also aluminum, and it rescues the mitochondria.) The Indian diet containing curry, and water supply with too high ?uoride. (Curcumin bonds to aluminum, and curry contains high levels of silicon.) See next chart. Mediterranean diet which includes more vegetables and wine. Consumption of food in highest two thirds of ?avonoid content, including light to moderate amounts of wine, but no effect shown by wine for APOE84 allele carriers. (Alcohol consumption in general may reduce atrophy of the hippocampus and amygdalar in APOE84 allele carriers, but epidemiology is mixed on the relation of alcohol to AD as compared to drinks containing ?avonoids such as wine.) High consumption of polyphenols as in wine or fruit and vegetable drinks. Maintenance of normal zinc serum levels in older persons showing zinc malnutrition, through modest (close to the RDA level) supplementation. Normal zinc levels may also reduce age based copper overload. Zinc competes with aluminum for enzymes and is part of the CulZn SOD. (RDA zinc ingestion reduces senile plaque deposits.) Category 3. Alternative Fat, Especially is}: Oil, and Caloric Intakes. Consumption of ?sh, fish oil or DHA supplements, or potentially ?ax seed oil, walnuts, and vegetable sources of n?3 PUFA such as DHA produced by algae. (One ?sh pill per day reduce AD risk by 50 percent in Framingham study.) Reduction of fat and caloric intake for persons carrying the allele. Reduction of obesity in older populations. Reduction of metabolic incidence. Reduction of intake of saturated or trans-unsaturated (hydrogenated) fats. Category 4.. Other Options. . Cognitive, social and physical activity throughout life including education: :i.e one example a large preventative effect shov'm in one study by frequent dancing which combines social, physical and cognitive and reduced risk by 76 percent. Bilingualism can postpone AD onset byv4 years. Prevention of elderly loneliness which can double risk of late-life ?dementia?. Past vaccinations for in?uenza and other diseases. Control of high blood pressure or extremely low pressure or sharply falling blood pressure in mid-life. Antihypertensive medication use especially potassium sparing diuretics. NSAIDs use well before age of dementia onset of two or more year duration. Early estrogen replacement well before age of dementia onset in Cache County Study. But there are inconsistent reportsI and other adverse health effects of estrogen. 1 Category 5. Detrimental Iterlns hat Can Increase Incidence of AD or Reduce Brain Size. Mid-life high consumption of tofu or soybeans compared to low. Late estrogen replacement with progestin for 5.6 years, initiated after the age of 65. The use of progestin and the late use timing distinguishes this study. Possible Options But With Little Human Epidemiology: Alpha-lipoic acid and L-camitine supplements; Magnesium, selenium and other aluminum competing metal supplementation; Curcumin, constituent of tunneric a spice used in Indian cooking; Blueberries, strawberries, and spinach; Melatonin intake or reduced night light. Best Low Cost Therapy Alternatives 1. new Alpha-lipoic acid supplementation. This is the only program shown to completely halt disease progression in a clinical trial in Germany. An ALA ?sh oil clinical trial is in progress at Oregon Health and Science University. Both can be purchased over the counter and are not pat'entable. Fish consumption and avoidance of beans 1 . I Zinc supplementation at 2 times RDA. i . Quite Likely Best Therapv: Peptide YY nose spray (soon available commercially for I obesity control). . Mineral water rich in soluble silicon in combination with vitamin or similar product that can reach the nuclear matrix? Why Are Age Adjusted AD Rates in North India 73 Percent Less Than One of the lowest age adjusted AD rates in the world was recorded in a rural community of northern India by Chandra. Incidence was 4.7 per 1000 person-years for persons aged 65 and over, as compared to an incidence rate of 17.5 per 1000 percent years in the Monogahela Valley of It is a 73 percent reduced rate, which is remarkable since 71 percent of the Indian study population was illiterate, and education is partially preventative of AD. (Likely elderly family life in India is more social and less isolating which could compensate for a lack of education.) AD cases determined by clinical evaluation were con?rmed by MRI, to reduce misdiagnosis which could be a problem in cross cultural studies. This study, as do others, standardizes for age, since people live longer in the United States than India on average. Age is the largest risk factor for AD. Comparison of lifestyles of the two locations gives us some insight into prevention opportunities. 1. ?is_h; The Indian diet carries a higher ?sh to animal fat ratio. Fish is partially preventative of AD. But, the American consumes vastly larger quantities of both meat and ?sh annually, 268 pounds of meat per capita compared to 9 pounds in India, and 46 pounds of ?sh per capita compared to 11 pounds in India. So, it is dif?cult to assess this risk factor in comparing the Indian experience. 2. Aluminum: Aluminum content of the diet, another risk factor, is much reduced. Daily dietary and air pollution intake of aluminum in Mumbai, India was calculated at 6.4 mg/day, compared to dietary intakes of 9 mg/day for adult American females and 12-14 mg/day for adult males. 3. Curcumin: It is a major constituent of the spice turmeric used in the yellow curry that is a staple of the Indian diet, and may reduce AD rates as it reduces soluble and insoluble amyloid (AB) levels and plaques in laboratory mice genetically altered to produce brain plaques. It has anti-in?ammatory and anti-oxidant properties. Curcumin bonds to aluminum attached to chromatin DNA. Curry contains some of the highest levels of silicon of any food product, which can both reduce aluminum absorption from the diet and enhance excretion. 4. Fluoride: North India lies on the ?uoride belt that stretches from north and east Africa through India and Pakistan to Southeast Asia and south China, and ?uorosis is common. High ?uoride facilitates excretion of aluminum, and has been correlated with reduced AD risk in Canadian drinking water studies. An American study found an 80 percent reduction in AD risk in a South Carolina county with high drinking water ?uoride (4.3 ppm). But, ?uoride is linked to adverse health effects and is best avoided as a prevention method. 5. Melatonin: Rural India has reduced indoor electric lighting, increasing melatonin exposure which may reduce AD risk. It is also an aluminum brain chelator. Part 1. 0 Brain Atrophy and Loss of Connectivity Are the Key Issues In the ?Dementia? of Alzheimer?s Disease. 0 Aluminum Is A Major Causative Player of These Conditions. . ApOptosis Some Mechanisms By Which Aluminum Exposure Kills Brain Cells In Vivo Caspase induction, release of cytochrome c, and suppression of feedback mechanisms preventing programmed cell death such as Bel-2. Induction and suppression of genes involved in AD. Adverse effect on ?mction of mitochondria and endoplasmic reticulum. Decrease of glutathion regeneration in mitochondria. Peri-nuclear clustering of mitochondria. Impairment of the ion pumps. Calcium homeostasis disruption. Oxidation of membranes and generation of soluble AB. . Necrosis. In?ammation and oxidation. Induction of in?ammatory genes. Impairment of the ion pumps. . Combination of apoptosis and necrosis. . Glial cell death or impairment leading indirectly to neuron death. . Hypoxia: heme, blood ?ow, genes. Nuclear translocation of HIF -1 alpha and promotion of anaerobiosis. Heem and red blood cell depletion. Interference with Slowing of cerebral blood ?ow due to damage to cerebral microvessels v'ia in?ammation, occlusions and amyloid angiopathy. Induction and suppression of genes irivolved in AD. . Enucleation by mechanical action of neuro?brillary tangle excessive accumulation. . Death by loss of connectivity and lack of stimulation. Clogging of axons with neuro?brillary tangles to impede chemical communication and ?ow of building material to the synapses. Glial cell death or impairment reducin'g brain communication. . Damage to synapses directly or via reduction of axon ?ow. Dendritic pathology and reduction of dendritic connectivity. Effect on mossy ?bers. Interference with neurotransmitters. Oxidation and depletion of myelin and fatty acids. Disruption of the perforant path. Death of connective layers of brain. Isolation of hypocampus from the remainder of the brain. . Abstract?Hippocampal is a marker of Alzheimer disease (AD). Ital-?- Hlppocampal atrophy remains unclear whether this holds true for younger patients as well. Hip. 111 AIZh-elmer dlsease: pocampal volume was measured on MRI scans of 103 clinically diagnosed AD Age matters patients and 73 controls (aged 51 to 85 years). Aging and AD were indepen. dently associated with smaller hippocampal volume. Both young and old AD patients have hippocampal atrophy abnormal for age. Age-dependent criteria for hippocampal atrophy, suggestive of AD, are needed. NEUROLOGY L.A. van de Pol, A. Hensel, F. Barkhof, MD, H.J. Gertz, MD, P. Scheltens, MD, and van der Flier, Pathologically, the ?rst degenerative changes in Alz? heimer disease (AD) occur in the medial temporal lobe structures, including the hippocampus.1.. Hip- pocampal volumes, measured on MRI, correlate with 5000? neuropathologic changes in AD2 and can be used as a diagnostic marker to differentiate AD patients. from controls.3 However, hippocampal atrophy also occurs in normal aging, and it has been speculated that 3-4000- hippocampal atrophy loses its sensitivity at an older age.? E, Most studies investigating hippocampal atrophy 2 have focused on elderly AD patients. However, AD 2 may also develop at an earlier age, and medial tem- 2 3000 poral lobe structures may be less involved in younger 3 AD patients.6 For diagnostic purposes, it is impor? g' tant to distinguish the effects of age and AD on hip- 8 pocampal volumes. We therefore measured a 3100- hippocampal volumes in AD patients and controls, .9- including a large cohort of relatively young subjects. a: 1000- .L - I AD 5am?- EI Controls 0 I I I I I 5.40mAge (yrs) Figure I. Scatter plot of hippocampal volume by 3m_ age. The parallel regression lines of Alzheimer disease pa- tients (bottom line) and controls (top line) indicate that 3- hippocampal volume is similarly affected by age in both 5 groups. Raw data are presented, whereas in the multivari- a?m ate statistical analysis, intracranial area, sex, Mini- Mental State Examination score, and type of scanner were corrected for. I I I I Controls young AD wrung old an old Figure 2. Box ptots of total hippocampal volumes (mms) by group. Old subjects show more hippocampal atrophy than younger subjects. Alzheimer disease (AD) patients show more hippocampal atrophy than.- controls. Raw data are presented, whereas in the multivariate statistical anal- ysis, intracranial area, sex, Mini-Mental State Examina- tion score, and type of scanner were corrected for. The Importance of Brain Cell Death (Brain Atrophy) in Alzheimer?s and Dementia: The Two Tracks of Dementia. I Gosche obtained postmortem MRI scans of the head of the ?rst 56 participants from the Nun?s Study before autopsy The question was whether volumetric measure of the hippocampus provided a sensitive and speci?c indicator of AD neurbpathology. Matching the MRI with autopsy results} the proposition was con?rmed. I The MRI predicted the AD neuropathological criteria for all 56 participants i.e. the 24 'sisters who were demented and the 32 sisters who remained nondemented. 1. Of the nondemented group, 44 percent met the AD neuropathological criteria upon autopsy, which is not unusual since the average age of death ranged from 88 years to 93. . I 2. It was found that a reduced hippocainpal volume has a substantially adverse effect on MMSE cognition scores a year before death in persons with AD i.e. with high deposits of plaques and tangles. Brain volume was more important than Braak stage in explaining low cognition scores in both AD and in dementia without AD. 1 Age of Braak Hippocampal Death Stage Volume, Left MMSE . Non-Demented With AD (14 sisters)! 88 4.07 2,206 mm3 . 23.93 0 Demented with AD: (19 sisters) 1 91 5.00 1,778 8.95 I Non-Demented Without AD: (18 sisters) 88 1.78 2,557 I 25.3 - Demented Without AD: (5 sisters) 93 1.00 2,234 . 14.0 K.M. Grosche et al, Hippocampal volume as an index of Alzheimer neuropatholbgy, Findings from the Nun Study, Neurology 58 (2002) 1476-82 Brief Communications Brain volume 105 Abstrac't?Rates of temporal horn volume change were signi?cantly greater in . the subjects with mild cognitive impairment who were developing dementia vs 1n MCI those who remained stable. dementia NEUROLOGY D. Erten-Lyons, D. Howieson, M. Milar Moore, J. Quinn, G. Sexton, L. Silbert, and J. Kaye, MD Patients with mild cognitive impairment (MCI) have impairment in memory or other cognitive domains but otherwise function well.1 The clinical outcome of MCI is variable, and not all patients develop demen- tia.2 Patients with MCI may present with regional brain atrophy on MRI that differs from age-matched healthy individuals.3 In this study, we examined whether rates of regional and total brain volume loss distinguish MCI subjects that sub- sequently decline to dementia. In this study, of persons with average ages of 83-88 years, persons with mild cognitive impairment with declining hippocampus and total brain volume and increasing ventricular and temporal lobe volumes were most likely to progress to ?dementia?. A .. 0.00- .. a- g-ozs? g: 5-0.50- 5- .E-OJS- 4' I E-mo- .151 3' 3.3- 2-1.25- - at as. -1.50MCI-S MCI-D NC MCI-S ?can Figure. Annualized percentage change in brain volumes by group: (A) total brain volume change, (3) ventricular vol- ume change, (C) hippocampal volume change, (D) tempo- ral horn volume change. *Accounting for age, sex, and interval between scans di?iars from the NC and MCI-S groups. NC normal cognition; CI-S mild cognitive impairment?stable; MCI-D mild cognitive impairment?declining. Table 2Baseline volumes for hippocampi and for all other regions of interest (emf?) Volume NC MCI stable MCI decliner Total brain 921.4 (93.4} 905.1 (96.1] 825.2 (103-4) Ventricular 39.2 117.3) 37.2 14) 41.6 (16.7) Hippocampal 1.34 (0.18) 1.34 {0.13) 1.16 (0.13? Temporal horn 1,511.1) 1.7 1.9 (1.1) White matter high signal 514.5) 12.8 12.??r 110.9) Total intracranial 1,193.4 (128.1) Values are mean SD). 1,094.9 (136.2} Accounting for sex and age differs from NC and stable MCI groups 1,0 0.007). MCI mild cognitive impairment; NC normal cognition. Hippocampal disconnection contributes to memory dysfunction in individuals at risk for Alzheimer's disease Travis R. Stoub'. Leyla deToledo-Morrell?, Glenn T. Stebbins*. Sue Leurgans?. David A. Bennett**.' and Raj C. Shah?? Departments of *Neurological Sciences and ?Family Medicine. and ?Rush Alzheimer's Disease Center, Rush University Medical Center, Chicago. IL 60612 Communicated by Richard F. Thompson, University of Southern California. Los Angeles, CA. April 26. 2005 (received for review October 2005) This is a study comparing white and gray matter brain volumes of two regions pf 50 healthy controls against 40 individuals with: MCI, both of approximately 78 years of age with similar education and sex. i l. The Authors Find That Both White Matter Connectivity of the Hippocampu's to the Rest of the Brain and Gray Matter Volumes- Makes a Difference in Memory Even for Persons With Mild Cognitive Impairment. i The concept of amnestic mild cognitive implairment (MCI) describes older people who show a decline predominantly in memory function, but who do not meet criteria for dementia. Because such individuals are at high risk for developing Alzheimer?s disease, they are of great interest in for understanding the prodromal stages of the disease process. in brain structures were assessed with two imaging techniques: whole- brain, voxel-based morphometry to determine regions of reduced white matter volume and (ii) sensitive volumetric segmentation of the entorhinal cortex and hippocampus, gray matter regions that are critically important for memory function. 2. Atrophy of Both White and Gray Matter Adversely Affected Memory: Impcirtance of Perforant Path in Linking Hippocampus to Rest of Brain. In participants with amnestic MCI, compared with age-matched controls, results showed a signi?cant decrease in white matter volume in the region of the parahyocampal gyrus that includes the perforant path. There was; also signi?cant atrophy in both the entorhinal cortex and hippocampus. Regression models demonstrated that both hippocampal volume and parahippocampal white matter volume were signi?cant predictors of declarative memory performance. These results suggest that, in: addition to hippocampal atrophy, disruption of the of parahippocampal white matter ?bers contributes to memory decline in elderly individuals with MCI by partially disconnecting the hippocampus from incoming sensory information. 3. Loss of Layer II Cells in Entorhinal Cortex and Implications . investigation by Hyman et al, carried out on postmortem tissue, showed that in patients with very mild AD there is disconnection of the hippocampus from cortical inputs as a result of loss of layer 11 cells in the entorhinal cortex. exact underlying mechanism of the volume loss in parahippocampal white matter cannot be determined in vivo with the tools currently available to us. One can speculate that a decrease in white matter ?bers. . .may cause a disruption of input to the hippocampus from the entorhinal cortex. Because these incoming white matter ?bers arise from cells in the entorhinal cortex, entorhinal atrophy may, in part, re?ect changes in afferent connections. . .Furtherrnore, the white matter volume change may re?ect. . .also partial demyelination in the remaining ?bers. 4. Importance of Both White and Gray Matter in Distinguishing Controls From MCI Table 2. Location and size of signi?cantly reduced white matter voxels in patients with amnestic MCI, relative to controls Stereotactic white coordinates, mm matter 10* Region 2 2 score 159 Rightparahippocampalgyrus ?24 ~23 ?19 5.37 Leftparahippocampalgyrus 24 ?17 -24 4.48 Stereotactic coordinates and scores are for voxels of maximal statistical significance for each region. Each region is defined in accordance with the Talairach Daemon (38) by using the corresponding stereotactic coordinates. *No. of voxeis per cluster1.5 gray '2 04 a- matter .. Aged Controls MCI Aged Controls MCI Left Hemisphere Right Hemisphere Fig. 3. Mean normalized entorhinal (A) and hippocampal (3) volumes in participants with amnestic MCI and healthy age-matched controls. Volumes are st for each hemisphere separately. Vertical bars represent the standard error of the mean. significantly different from controls (P a: 0.001). Proceedings National Academy Science, USA 103/26 (June 27, 2006) 10041?5 Qualitative Estimates ofl edial Temporal Atrophy as a Predictor of Progression From Mild Cognitive Impairment to Dementia Charles DeCarli, Giovanni B. Frisoni, Christopher M. Clark, Danielle Harvey, I Michael Grundman, MD, Ronald C. Petersen, MD, Leon J. Thal, Sheliajin, MD, Clifford R. Jack, jr, Philip Scheltens, MD, for the Alzheimer's Disease Cooperative Study Group Background: Individuals diagnosed as having mild cog-I nitive impairment (MCI) have a high likelihood of pro-' gressing to dementia within 3 to 5 years, but not all in- dividuals with MCI progress to dementia PrognosticI uncertainty suggests the need for additional measures to' assist the clinician. Oiledlvo: To assess the added value of qualitative mea-: sures of medial temporal atrophy (MTA) to estimate the, relative risk of progressing from MCI to dementia. I Design: A 3-year, double-blind, placebo-controlledi Alzheimer?s Disease Cooperative Study initially designed to evaluate the efficacy of donepezil hydro-l chloride or vitamin vs placebo to delay progression o? MCI to dementia. So?lng: Memory assessment centers. Fallon?: A total of 190 individuals with MCI. Mall: Oukomo Measures: Ratings of MTA per- formed using magnetic resonance images obtained at base- line. Log-rank tests and Cox proportional hazards ra- tios examining the significance of MTA estimates in predicting progression of MCI to dementia. Results: A mean MTA score greater than 2.0 was asso- ciated with a greater than 2- fold increased likelihood of progression to dementia during the observation period (hazards ratio, 2. 30: 95% confidence interval, 1. 09- 4. 92; P: .03) after controlling for age, education, sex, and baseline Mini-Mental State Examingation score. Canola-Ions: Adjusted estimates were associated with signi?cantly increased risk ofdevelhping dementiawithin 3 years, suggesting that obtaining a1 magnetic resonance image during the evaluation of MCI may offer additional independent information about the risk of progression to dementia. Given the relatively high prevalence 1n the genetalp0pulation, useoithis methodaspartofroutine clini- cal evaluation may help identify individuals who might bene?t from increased surveillance and future treatment 'I'rlcl clinicaltrials.gov Identifier: NCT00100022. Arch Neurol. Table 1. Medial Temporal Atrophy Hating Algorithm I 1 width ol 1Width at Height ol . Score Choroidal Fissure Temporal Hum Hippocaml?ls 1] Normal Normal Normal 1 Mildly widened Normal Normal 2 Moderately widened Mildly widened Mildly reduced 3 Markedly widened Moderately widened Moderately reduced 4 Markedly widened Markedly widened Markedly reduned The amount of brain atrophy at the commencement of the study determined what percent of the patients progressed to dementia within 3 years. For individuals with a mean rating of 1.0 or less, only 29.1 progressed, compared to 75 percent for those with a rating greater than 2.0. Vitamin and donepezil had no effect on progression. Mean Rating $2.0 Mean Rating >21! Proportion oi Nondemented Patients no 1125 1:0 1. 5 are is 3.0 Years Figure 4. Kaplan- -Meler curves for particlliants with medial temporal atronlly ratings of 2.0 or less compared with those with ratings greater than 2. n. Part 2. 0 Alzheimer?s Disease Can Be Partially Diagnosed By Measuring Blood or Urine Aluminum Levels, or Absorption From an Aluminum Spiked Citrate Drink. 0 Brain Aluminum Increases 19 to 28 Fold in Normal Persons From Middle Age Adults to Elderly. The Initiation of Alzheimer?s May Involve Only Another Doubling of Brain Aluminum. Arch. Gerontol. Geriatr. Suppl. a moon 393-402 0167-49435 sea front matter 2004 Elsevier Ireland Ltd. All rights reserved TRACE ELEMENTS AND COGNITIVE IMPAIRMENT: AN ELDERLY COHORT STUDY Chart 1 c. SMORGON. E. MARI. AR. ATTI, E. DALLA NORA, P.F. ZAMBONI, F. CALZONI. A. abd R. FELLIN Second Department of Internal Medicine, University of Ferrara. We Savonarola. 9 - 44100 Ferrara. ltaly author Phone: +(30-05321-236-291 Fax: E-mall psn@unife.it SUMMARY . .Thirty-?ve patients were enrolled-in this study. . . .Patients were then divided into 4 groups according to the obtained diagnosis (Controls, CIND, AD, blood sample was In our cohort we found a positive correlation between cognitive ?mction; expressed as the MODA scoreserum levels, while a negative correlation was observed between MODA score, Cu and Al serum levels. Moreover, some statistically signi?cant differences concentration were found among the groups. According to these results, we may suppose that Se, Cr and Co protect cognitive function, Cu influences the evolution of cognitive impairment, while Al contributes to the pathogenesis of AD. 1.0- 0.9- I . I 0.0- 0.7? 0.6' 0.54 0.4- 0.3? 0.2? 0.1~ Alumlnlum on. Controls 0an 3 AD Figure 5. Aluminium serum levels. Statistical comparisons: ?p 0.001 . Table THE RESULTS OF THE TRACE ELEMENT ANALYSES IN THE FOUR GROUPS. mgl'ml. mean SD. Controls CIND AD Se 0.303 0.044 0.240 a: 0.039 0.157 1: 0.048 0.122 1 0.022 Co 0.030 0.014 0.0133 1: 0.004 0.0010 0.001 0.0022 0.002 Cr 0.017 1: 0.003 0.013 0.001 0.005 0003 0.007 .t 0.004 Cu 1.059 0.081 1.170 0.118 1.457 1 0.250 1.400 0.210 Al 0.215 0.106 0.352 0.145 0.735 0.158 0.303 i 0.103 Increased absorption of aluminium from a normal dietary intake in dementia N.B. Roberts A. Clough J.P. Bellia 3, J.Y. Kim '3 Department of Ciinicui Chemistry. Royai Lit'erpooi University Hospitai. Liaerpooi. UK Preventiw Medicine. Dong-A. University Scitooi of Medicine. Pusan. South Korea Source: Journal of Inorganic Biochemistry, 69 (1998) 171-176 Chart 2 Abstract Serum aluminium was signi?cantly raised (p 0.0 l) up to 2?3-fold. in patients with dementia including Alzheimers Disease (AD) 0.66 .4: 0.2 mean i 1 and patients on regular aluminium hydroxide therapy 0.54 i 0.17. compared with healthy vol- unteers 0.21 i 0.13. although not as high as in patients with end stage renal failure on regular dialysis 0.88 i 0.42. The urine outputs mean i of aluminium and silicon. respectively. were also signi?cantly increased up to 5-fold in dementia 3.89 1.78 (a 23) and 1587 i 645 (a 22) and patients on regular aluminium hydroxide therapy 5.03 i 2.08 (n 8) and 998 i 364 (it 21) compared with healthy volunteers 0.95 i 0.1-14). The increase in urine aluminium was thus associ- ated with a similarly marked increase in the output of silicon. The increased absorption of aluminium in dementia patients is equiv- alent to the intestinal loading in Aludrox therapy. Also silicon appears to be important in the renal excretion of the absorbed aluminium. Whether this is a phenomenon related to the elderly or the process of dementia warrants further study. 1998 Elsevier Science Inc. All rights reserved. Serum and Urine Aluminum in Dementia About 3 Times Higher Than Controls and Similar to Ulcer and Renal Failure Patients Table 1 Summary of analytical data for serum and urine aluminium and silicon Serum aluminium Urine amminium Urine Urine silicon L'rine SiiC Control 0.21 i 0.13 114) 0.95 i 0.82 tn=$4) 0.13 i: 0.16 tn=84) i 322tn=1151 411 i 30 lu= 31) Dementia ,2 0.66 i 0.2 (-7 2.84 i 1.68 tit-=23) 0.6? i 0.52 18) 1.158? 645 3611 158 In: 18] Aludrox treated 0.54 i 0.17 5.03 i 2.68 (11:3) 0.66 i 0.35 998 i 440 (it: 11] [-12 5? in 8) Renal failure 0.88 i 0.42 20) Vaiue as mean :1 email] and umolimmol creatininc Tlte dill?erenees for each analyte were highly signi?cant at 0.05 between control and the patient groups. N.B. Renal failure patients studied were in end stage renal failure on regular dialysis and do not produce urine. ?585 0 3" 0301' Serum aluminium tun-told) 0.40 0.10 1N Fig. 3. The relationship between serum alttminium and age in years: healthy controls and patient groups (n 130) correlation ,0 0.01. the regression analysis gave 0.008. 0.003. Gastrointestinal Absorption oil? Aluminum in Alzheimer?s Disease: Response to Aluminum Citrate Geoffrey A. Taylor, I. Nicol Ferrier, Ian J. McLoughlin, Andrew F. Fairbaim, lan G. McKeith, Debra Lett, James A. Edwardson. Age Ageing 21/2 (1992) ?81-90 MRC Neurochemical Pathology Unit, Newcastle General Hospital, Newcastle upon Tyne. Alzheimer's disease (AD) has been linked to genetic defects on chromosome 21 in some families. but most elderly cases appear to be sporadic and may, at least in part, involve environmental risk factors. Several lines of evidence suggest that aluminium may be involved in the aetiology of AD. However, despite universal exposure to aluminium in the diet, only some people develop the disease. We have developed a test of aluminium absorption using an aluminium citrate I drink, to examine the hypothesis that sufferers from AD show increased aluminium absorption. In a younger group of AD patients aluminium absorption was signi?cantly raised compared with age-matched controls. Aluminium absorption increased with age in the control group but was not significantly raised in older AD patients when compared with age-matched controls. Blood aluminum levels 60 minutes after drinking an aluminum citrate drinking (290 mg 4.8 citrate) increases in normal people over the age of 70 in an exponential fashion similar to increased rates of Alzheimer?s in the same age group. EL sour AGE :yurl Figure 2. Increase in blood aluminium 60 min after an aluminium citrate-containing drink (290 mg A1, 4.8 citrate) in normal subjects, plotted against age. Increases in aluminum blood level in AD patients and in the older controls 60 minutes after consumption of a citrate drink spiked with 290 mg Al were much larger than in the younger controls (less than 77 years of age). Ferritin levels were also higher in the younger controls. Table Mean data of SDAT patients aged 76 and under and 77 and over compared with data from age-matched control subjects Younger group Old'?r group Mean' (range) (a Patients Controls Patients Controls (SD) (n=10) (n=10) (n-10) (nu-I10) Age 71.4 . 72.0 83 .3 82.3 (years) (65?76) (69-76) (79?89) (77-88) (3.9) (2.4) (3.8) (3.8) Weight 61 .5 72.8 51.3 57.6 (kg) (47?81) (51-90) (40-62) (52-68) (10.5) (13 .7) (8.2) (6.4) MTS 13 .6 36.3 18.0 - 34.6 (n137) (7-22) (33-37) .- (10-24) (31-37) (5.5) (1.3) (4.5) (2.2) Creatinine 91.3 92.3 95.5 101.0 (mom) (71 -l 14) (81 ?1 06) (75-109) (75-127) (13.2) (12.8) (11.6) (15.9) Albumin 40.3 42.8 39.8 40.9 (gll) (3 6?43) (40?46) (37-42) (36-46) (2.5) (2.9) (2.0) (2.9) Ferritin 101.7 167.5 64.4 57.9 (20-205) (57?760) (12-210) (15-185) (67.8) (21 1.9) (67.7) (48.7) Al (pg/l) 8.6 7.7 5.8 6.8 Baseline (5.6?13.9) (5.2?10.8) (3.8-12.8) (2.8) (1.8) (1.1) (2.8) 60 min 104.5 37.9 79.8 101.3 (30.5?332.4) (20.8-60.9) (18.8-373.2) (l9.4?232.0) (100.1) (14.2) (107.0) (63.6) Increase 95.9 30.3 74.1 94.5 (16.6-321 .0) (15.6-54.0) (14.8?336.0) (15.5-228.2) (99.3) (14.0) (106.3) (63.0) People Over the Age of 60 l_ose Their Capacity to Exclude Aluminum - Comparison With Dementia Rates 1) Increase in blood aluminum levels 60 minutes after drinking an aluminum citrate containing drink (290 mg Al. on the chart). over the age of 60. (1 0 2) Estimated increase in "dementia? rates chart shows an uncanny parallel. (Dementia 4.8 citrate) in normal people AGAINST): European cities.(2) The double every 5 years.) leven rates 70 l' Charm 300 200 citiesaluminum blood 0 levels YEARS (1) Taylor. Geoffrey et al. "Gastrointestinal absorpton of alumin (1992) 81-90. (2) Hoffman. A. et al. ?The prevalence of deme (1991) 736-748 um in Age and Aging. 21. nlial in lnt. J. of Epidemiol. 20/3. INCREASE IN BLOOD ALUMINUM .- ug/I EW STUDY Absorption of Aluminium-26 in Alzheimer's Disease, Measured Using Accelerator Mass Spectrometry P. Brian Moorea J. Philip Dayb Geoffrey A. Taylora I. Nicol Ferriera L. Keith Fifieldc James A. Edwardsona Neurochemical Pathology Unit. Newcastle General Hospital. Newcastle upon Tyne, I?Department of Chemistry, University of Manchester. UK: ?-?Department of Nuclear Physics, Australian National University, Canberra. Australia Key Words - AMS is capable of determining <10"ag of with Alzheimer's disease - Aluminium, isotopic - Accelerator many orders of magnitude more sensitivity than other mass spectrometry - Gastrointestinal absorption techniques. Using this sensitivity, we have shown. under normal physiological conditions, that the ability of the GI tract to exclude Al is reduced in AD. possibly leading to Abstract greater systemic exposure to Al. Public health measures Although chromosomal abnormalities underpin some to limit Al dietary uptake or bioavailability may decrease early onset cases of familial Alzheimer's disease (AD). the prevalence of. AD in the community and should be most cases are sporadic and not associated with such considered. abnormalities. Aluminium (Al) is a signi?cant but contro- versial risk factor for sporadic AD. and studies have 5 reported associations between AI and the principal pathological features of AD, senile plaques and neurofi- brillary tangles. The present study measured gastroin- testinal (GI) absorption ofAl under normal dietary condi- tions using tracer and accelerator mass spectrome- try (AMS). Following overnight fast, 13 AD patients (aged 63-76 years) and 13 age-matched controls (aged 62- 76 years) ingested a fruit drink containing 27 ng 26AI. Plasma samples were obtained before and 1 after the drink and fromthese the fraction of 28Al absorbed across the GI tract was estimated. The GI tract rigorously excludes AI with only of the ingested Al being absorbed. The mean fraction absorbed by AD subjects exceeded controls by a factor of 1.64 (p 0.05, Anova). 1 - Relative gut uptake factor (F1) - I Is an Original Research Article a 9" Dement Geriatr Cogn Disord 2000;11:5549 Fig. 1. Relative Gl uptake factors in the control and AD patient groups. The samples were analysed in two groups, each consisting of patients and controls. The relative 61 uptake factor was calculated for each subject, by dividing the GI uptake factor, F., by the mean control value of in that group of analyses (see ?Methods'). Mean 1: 1 SD are shown on each data set. the difference between the means is signi?cant. 0.048 (Anova). Chart 12. I Brain Aluminum Levels Sharply Increased' 111 the ?Non-Demented? (Aged 75 to 101) Compared to Younger ?Non-Demented? Adults, (Aged 32 to 1) Hippocampus aluminum content 28 times higher 1n non-demented elderly. I 2) Cortex of frontal lobe aluminum content 19 times higher. 3) Non-demented elderly showed many changes typical rof Alzheimer?s and they were associated with aluminum concentration - including neurofibrillary tangles in some persons: 4) No such aluminum ?uorescence reaction was found for the younger adults. Mppon Ranen Igoldrai Zasshi 1994 1 correlative study of the aluminum contenit and 11 elderly subjects]. .J Hazime Shimizu?, Talrashi Mori Mine Koyama?, Masao Sekiya 1 i Ghe interrelation of the aluminum content and aging change of the nerve cells was studied with special reference to the neurofibrillary tangle (NFT) and occurrence of senile plaque (SP), in 15 autopsied brains (cerebrum) of non- demented elder-l ly subjects varying in age from 75 to 101 years old and 10 cases of non-demented non-elderly adult subjects. 1) In the brain of non-demented non-elderly adult subjects, the aluminum content of the: hippocampus was 14.4 i 1.39 and that of the cortex of the frontal lobe was 20.4 i 2.54 ppb. In the brain of the non?demented elderly subjects, the aluminum content of the hippocampus was 401.7 60.05 and that of the cortex of the frontal lobe was 373.29 72.35 ppb. Comparison of the two groups showed obviously higher levels in the latter; group, being 28 times in the hippocampus and 19' times in the cortex of the frontal lobe. 2) The. histochemical demonstration of the aluminum local- ization by the Morin method disclosed the positive ?uorescence reaction along the part of the disinte-; grating neuro?brillary tangle and amyloid core ini the senile plaques of non- demented elderly subjects. In the normal brain tissue, positive ?uorescence reaction was observed in the wall of the capillary vessels of the blood brain barrier, perivascular glial supporting tissues, the nuclei of the astrocytes and nuclei. nucleoli of the nerve cells partially. No ?uo- . IDivsion of Pathology] Institute of Gerontology, Nippon Medical School Division of clinical Medicine, Institute of Geron- tology, Nippon Medical School and Hi roshi Ooami? rescence reaction was observed in the non-demented adult subjects. 3) Morphologically, the appearence ofwthe neurofibrillary tangle was noted in some cases of non-demented elderly group with higher aluminum levels. Classical and diffuse type senile plaques were dispersed in the let to 4th zone of the cortex of the frontal lobe. However, diffuse type senile plaques 1n the hippocampus appeared to a lesser extent. Neurof? br1llary tangles were noted in the cortex of the frontal :,lobe however marked 1ncrease was confirmed' 1n the CA1 to CA3 zones of the hippocampus. UltraStructurally, paired helical filaments (PHF) were noted' 1n the neurof- brillary tangle constituent and the increase of amyloid fibrils in senile plaques was-confirmed. In this study, high levels of the aluminum content of the brain were confirmed in the non- demented elder- ly subjects. Moreover, the histochemical demonstra- tion of aluminum localization by the lIVlorin method disclosed a positive ?uorescence reaction along' the sites of neurofibrillary tangles and amyloid core in \ythe senile plaques of non- demented elderly subjects. 1 Based on these observations, the accumulation" of aluminum plays a role" 1n the appeare1ice of neurofi- brillary tangles and' 1ncrease of senile plaques sug- i gating the possible mechanism of interaction with the causative factor of senile dementia of the Alz- heimer type (SDAT). Key words: Aluminum, Aging brain, Non- demented elderb, Neuro?br?laty Seniie piaque (Jpn Geriat 1994: 31: 950?960.) I ging changes of the brain in non-demented Chart 12. (continued) Dramatically Higher Aluminum Brain Levels in Non- Demented Elderly Compared to Younger Adults Table 1 Quantity of Aluminum in Non-demented Adult Group Examirled area Cases Age ?Sex Clinical Diagnosis . Brain Weight Hippocampus .. Frontal lobe 1 32 Kidney Cancer 10.8 14.0 1.380 2 33 a CML . 20.0 31.1 1.220 . 3 36 d? CML 7.0 35.6 1.145 4 37 3' CML 15.2 16.0 1.410 5 41 .1- . M. 15.5 22.3 1.400 5 43 . Bact. Endocarditis 12.7 19.2 - 1.580 7 45 8? Pyothorax 20.6 10.0 1.360 8 45 8' AMI - 10.3 20.0 1.450 9 45 6" Lung Cancer - 13.5 12.7 1.210 10 46 6" Lung Cancer 17.6 18.7 . 1.250 MeaniSE 14.4i1.39 20.022.54 l.340:l:41.85 (Wet weight ppb/g) (2) Table 2 Quantity of Aluminunl in Non-demented Elderly 9" Examined area Cases Age Sex Clinical Diagnosis Brain Weight Hippocampus Frontal lobe 75 3. AMI 739.4 439.4 1.260 2 75 Cardiac Failure 199.4 100.8 1.210 3 77 -T- LIME Cancer 160.4 130.3 1.320 4 la 2 Lung calmer 200.9 150.5 1.300 5 so .2 Liver Cirrhosla?nloc 500.0 525.9 ?1.010 5 81 Sup. V. Cava - 169.0 161.3 1.250 7 85 8' 120.5 110.6 1.165 8 86 A-V Block 769.3 618.8 1.210 9 37 a Pnemzioniaa 509.9 473.7 1.350 10 87 Hemtitis 585.9 474.2 1.300 11 90 d" Pneumonia 458. 6 388451.4 335.5 1.140 13 93 3 Acute Renal Failure 182.6 122.3 1.010 14 100 a" Multiple MYeloma. 724.8 1162.3 1.350 15 101 0" DM - 253.4 340.2 1. 285 MmisE 401. 7:150. 05. 323. 29:72. 35:: 232320. 37 .. . . . (We: weight ?rm/3395 . .- ., Elevated Aluminum in ?Non-Demented? Elderly Correlates; With AD Type of Brain Changes in Frontal Lobe and Hi Table 5 Relationships between Aluminum content and mo Chart 12. (continued) rphological ?ndings of Frontal lo?e in Non- lppocampus demented Elderly Aluminum . INFT Case Age Sex Plaque Diffuse Plaque 71 1 75 51- 48931- 160119474388335122.3 i: - 14 100 d" 1162340.2 - - - - MeaniSE 3732917235 (Wet weight ppb/s) Not observed in 10 ?elds (X200). :0-1 in 10 61316131311200). 1~3 in a ?eld (x2011). :4--81n10 ?elds (x200), in 10 ?elds (x2011). Senile Plaque NFT Neuro?brillary tangle I Table 6 Relationships between Aluminum content and morphological ?ndings of Hippocampus in Non- demented Elderly $.17 Aluminum Case Age Sex Classical Diffuse Quantity Morin CA1 CA2 FCAS CA4 CA1 CA2 CA3 CA4 CA1 CA2 CA3 CA4 1 75 2 739199.4 - 3 77 ?7 106.4 - 4 7s 200.509.9 - :t 6 81 .7- 169129.5 d: i 86 i- 769509585458151182.6 .t 196 a 724253.4 - 1- - Mean:SE 191.7 :66. 05 {Wet weight ?31 :Not observed in 10 ?elds (X200). :0~1 in 10 ?elds (X200). ?3 l~3 in a ?eld (x200). :4~3 in 10 ?elds (X200), in 10 ?elds (X200). I Senile Plaque Neuro?brillary tangle Initiation of Alzheimer?s Disease May Involved Only Another Doubling of Brain Aluminum Beyond That Experienced During Normal Aging. agannatha Rao reported that the bulk of metal accumulation in the brain during the development of AD is primarily attributed to two metals, aluminum and iron. There is an exponential acceleration of brain deposition of aluminum between the moderate and the severe AD stage as indicated by Figure 2. The changes in copper and zinc is likely from SOD which initially increases to deal with oxidation generated by aluminum and iron, and as the brain is atrophied falls to near zero. Brain Increases in Aluminum Measured in Mole Percent of Total Metals: To put the brain aluminum buildup into perspective, the team from India presented the issue in mole percent of total brain metals. The mole percent for aluminum in the hippocampus of the normal brain was 1.6 percent, rising to 8.1 percent in moderate AD, and then to 48.4 percent in severe AD. Mole percent for the frontal cortical region increased from 2.8 percent in normal controls, to 4.6 percent in moderate AD, to 65.6 percent for severe AD: i.e. 65.6 percent of all metal content could be attributed to aluminum. In this study of persons from cognitive good health to moderate AD, brain aluminum increases relatively to all metals by 5 fold in the hippocampus and about 64 percent in the frontal cortex. Other studies con?rm the differential accumulation of aluminum in different parts of the brain, and suggest that total brain accumulation of two fold may be suf?cient to initiate Front-loom60- 60- ?35m +Cu+2n .n 50? +Cu+2n .. .0. 3 40 E2304 ?5an- 220Carma rMothrlio?illi ScwroAD Gum 801;!? Figure 2. Levels of Al and Cu Zn drains the progression in AD in frontal cortex and hippocampus. Al start: accumulating in moderate AD along with Cu and Zn, while Al is signi?cantly deposited in severe AD. However, Cu and Zn levels were decreased in both ?ontal cor- tex and hippocmrm Gupta VB, Anitha S, Hegde ML, Zecca L, Garruto RM, Ravid R, Shankar SK, Stein R, Shanmugavelu P, Jagannatha Rao KS, Aluminum in Alzheimer?s disease: are we still at a crossroad? Cell Mol Life Sci 62 (2005) 143-58 2 Additional Studies Supporting a Doubling of Brain Aluminum to Initiate Alzheimer?s Disease. Bouras found an approximate doubling of aluminum in AD and the Delmentia puglistica (DP) along with iron, and concluded that the evidence suggested the possibility of a ?global dysregulation of Al and Fe transport in DP and (See chart.) 0 McLachlan found about a doubled aluminum level in the brain of 80 year old AD patients which could be restored to normal for that age group by chelation with desferrioxamine.(3) Crapper reported grey matter aluminum in AD brains approximately twice that of controls and a variation between brain regions. Chart presented in McLachlan, RDC, Aluminum and the risk for Alzheimer?s Disease, Environmetricsl? 91995) 233-75 1 A similar picture is presented by An'drasi, with a 2 to 7 fold increase in aluminum in AD patients compared to controls' in different parts of the brain.(5) (See chart.) - Srivastava and Jain found a doubling of aluminum in the parietal cortex} in (1) Jagannatha Rao KS, Rao RV, Shanmugavelu P, Menon RB, Trace in Alzheimer?s disease brain: a new hypothesis, Alz Rep 2 (1999) 241-6; (2) Chart reproduced in: VB. Gupta et al, Aluminum in Alzheimer?s disease: are we still at a crossroad? Cell Mol Life Sci 62 (3) C. Bouras et al, A laser microprobe mass analysis of brain aluminum and iron in Dementia puglistica: Comparison with Alzheimer?s disease. Eur Neurol 38 (1997) 53-8; (4) DRC McLachlan et al, Desferrioxamine and Alzheimer?s disease: video home behavior assessment of clinical course and measures of brain aluminum. Ther Drug Monit 15 (1993) 602-7; I . (5) Andrasi E, Naoemi P, Molnar Z, Kosel S, Brain aluminum, magnesium and? phosphorous contents of control and Alzheimer-diseased patients, Alzheimer?s Dis 7 (2005) 273-84 (See next chart.) (6) Srivastava RAK, Jain JC, Scavenger receptor class type I expression and elemental analysis in cerebellum and parietal cortex regions of the Alzheimer?s disease brain, Neurological Sci 196 (2002) 45-52 Joumal ofAllhcirncr's Disease '3 20051 273-284 105 Press Brain aluminum, magnesium and phosphorus contents of control and Alzheimer-diseased patients Erzs?bet Andrasia-? Noemi Par, Zsuzsa Molnarb and Siegfried Kosel? aInstitute of Inorganic and Analytical Chemistry, L. o'tvo's University, Budapest. Hungary l?Institute afNuciear Techniques, University of Technology and Economics, Budapest. Hungary ?Institute of Neuroparhoiogy, University of Munich, Munich. Germany Communicated by by Sharon Moalcm Abstract. A study was undertaken to determine A1. Mg and concentrations in 5 different brain regions of 3 control and 3 Alzheimer-diseased patients. One of the aims of this work was to evaluate the performance of applied analytical techniques. The digested samples were analyzed by inductively coupled plasma atomic emission spectrometry for AI, Mg and P. The dried samples were measured by instrumental neutron activation analysis for Al and Mg. The determination of human brain A1 levels is complicated by the interfering reaction of We have previously worked out an analytical method which can eliminate this interference. The accuracy of the measured data was investigated by the analysis of biological standard reference materials. Our second goal was to study the possible elemental concentration changes in Alzheimer-diseased patients. Signi?cantly higher A1 and lower Mg and values were found in some AD brain regions compared to the controls. Two to Seven Fold Increase in Aluminum Measured in Alzheimer?s Brain Compared to Controls Andrasi?s study is one of the best controlled, as methods were found to adjust for brain weight, magnesium and phosphorous. The controls averaged 61 years of age (55-71)_ compared to average age of the AD patients of 77 years (72-80). Whereas the last two minerals were distributed relatively evenly among brain regions, this was not true of aluminum which selectively accumulated at a higher concentration in different brain regions, especially the entorhinal cortex, a brain region heavily involved in the development of Alzheimer?s since it is linked to the hippocampuss As Table 7 illustrates, aluminum was measured at concentrations 1.910 6.8 times higher in different portions of the brain compared to controls, with the entorhinal cortex at the highest concentration. Table 7 Al. Mg and contents in ?ve control and AD brain parts measured by ICP-AES and INAA methods (mean :t dry weight) Brain part Control value AD value A1 Mg 1? Al Mg Ammon's horn 1.4 :t 0.6 680 100 13190 :11000 480 Cortex cntorhinalis 1.5 0.9 666 106 12560 i 900 ?10.2 9 540 55 10700 500 Cortex frontalis parasagittalis 1.8 2120.6 606 89 12040 10860 :t 550 Cortex frontalis basalis 2.5 :t 0.7 673 :t 48 12500 940 6.4 2.9 623 53 10650 730 Globus pallidus 1.8 0.7 628 80 13000 1000 3.5 0.4 552 48 10850 :t 860 Original Paper Chart: 13 1 i . Eur Neural 19971.3353-58 EIIrOpean Neurology mamas; I 11th *5 193353.513" gamma?; A Laselr Microprobe Mass Analysis mum anode of Brain Aluminum and lr'on' In Amy Hm? mm Home Dementia pugilistica: Comparison Daniel P. PerlbWIth AlzheImer DIsease Department HUG Belle-ld?e. - I University of Geneva School of Medicine. Geneva. Switzerland; 5 Fishberg Research Center for Neurobiology and Neurobiology of Aging Laboratories, and Departments of Pathology (Neuropatholosr). Geriatrics and Adult Development. and Ophthalmology, Mount Sinai School of Abstract I We report a laser microprohe mass analysis ofaluminum and' Iron content in York- USA the hippocampus and' In the inferior temporal cortex: in 2 cases of dementia pugilistica (DP), 4 cases of Alzheimer's disease and 3 controls. There was a predommant accumulation of Al and Fe within neuro?brillary tangles In both DP andAD cases. High levels of Al and Fe werealso detected' the nuclei of NPT- free and NFF-containing neurons, as well as in neuropil Key Words probe sites in these cases. In both regions, NFT contained substantially higher Alzheimer?s disease levels of Al and Fe In DP compared to AD cases. These ?ndings suggest the Dementia pugilistica existence of an association between the deposition of Al and Fe and NET laser microprobe mass analysis formation, and support the possibility of a global dysregulation of Al and Fe Trace elements transport in DP and AD. 1 i Table 1. Content ofAl and and control cases 1 NFT Nuclei Nuclei ofNFf-l'tee Neuropll I containing neurons neunons camera Aluminum DP 45.5 $3.8 23.4:t:2.l 17.1 3:2.7 [5.9 AD 33.5 :25 21.9: 1.9 16.61522 15051.3 Control - 7.5 10.4 4.4 Iron I 114. 72s II .5 25.1 :t2.6 12.0 '103 12.7 :05 AD 2 30.4:15 15.4%13 15.11503 Control - 7.3 6.7 10.8 Area 20 Aluminum I . DP 612:6.8 22.5 :l:2.2 14.8: 1.5 12.2 .4 AD 50.0153 22312.1 19.9 5:2.6 13.4: 1.3 Control - - 9.0 $0.6 5.11:1? Iron I 212.3 19.9 25.1 12.6 12.01103 1 [2.7 $0.5 AD 83.3 5:82 24.1: 1.5 1511'1 3 [5,810.7 Control - - 3.35::1 1 5. 35:0. 3 Results are expressed In volts and represent the mean integrated peak intensity of all laser probe sites directed to each given site In the temporal cortex. Note the high Al and Fe levels In In both DP and AD cases. No NFTwere observed In the temporal cortex In controls. See text for details. Part 3. The United States Has One of the Highest Dietary Aluminum Intakes and High Alzheimer?s Rates As a Result. - Epidemiology Identi?es Aluminum in Food and Drinking Water As a Primary Causative Agent for the Dementia of Alzheimer?s. l. Twenty two drinking water and one food epidemiology studies are available. 2. Drinking water constituents such as pH, silicic acid and ?uoride can markedly affect AD risk. 3. Chartbook available upon request and mailing address to: Mnetearth?krol5.00m A Range of Dietary Factors Chelate Aluminum, Can Reduce Risk, and Offer Partial Therapy. 0 Naturally Present Body and Secreted Brain Chemicals Also Offer Partial Aluminum Chelation and Prevention for Alzheimers. Estimates of Daily Dietary Adult I1 Nations 1. United States: 2. Mumbai, India: 3. Japan: 4. United Kingdom: 5. France: 6. Italy: 7. Romania: Sources: 7.7 mg/ day for teenage and - females aged 25 to 45 11.5 mg/day for teenage and c. 8-9 mgI/day . adult males aged 25 to 45 Ages of Initiation and Progression o?EIderly ntake of Aluminum in Various c. 7 nag/day adult' Cognitive Impairment and Alzheimeri?s Disease 6.9 mg/day for 60-65 year old females! 9.4 mg/day for 60-65 year old males 1 7.2 mg/ day for 70 year and older females 7.8 mg/day for 70 year and older males 6.4 mlg/day: diet and air pollution 3.5 mg/ day (range 1.8 to 8.4) 3.4 Ins/day I 1 4.2 mg/day . 2.3 6,3 mg/day. (Even if all foods prepared a a "and stored 1n aluminum containers: :6.0 mg/ day) 0.8 2.4 mg/day I 1. .A. Pennington and SA. Schoen, Estimates of dietary exposure to aluminum, Food Addit Contam 12 (1995) 119-28': and, J.A.T. Pennington, Food Ad'dit and Contam, 5 (1987) 161-232. Figures 11'} table based on 1991 USDA Total Diet neweww Study and retesting of aluminum content of key food items. (See Folder 55} RM. Tripathi et al, Sci Total Environj299 (2002) 73-7 M.R. Sasaki et a1, Shokuhin Eiseigaku Zasshi, 42 (2001) 18-23 G. Ysart et a1, Food Addit Contam, 17 (2000) 775-86 G.H. Biego et a1, Sci Total Environ, 217 (1998) 27?36 L. Gramiccioni et 31, Food Addit Contam 13 (1996) 767-74 . R. Cuciureanu et a1, Rev Med Chir So:c Med Nat Iasi 104 (2000) 107-12 1 RISK AMONG 73 YEAR OLDS TO CONTROLS WITH REGARD TO ALUNIINUM INTAKE DURING PREVIOUS FIVE YEARS - Syracuse, New York Food Items Consumed - Adjusted Odds Ratio for AD 1. Pancakes, waffles, biscuits, muffins, ?All got Alzheimer? cornbread, corn tortillas. if consumed. 2. Doughnuts, cookies, cake, pastry 34.6 times more likely to have AD. 3. American cheese, mixed dishes 7.9 times more likely with cheese to have AD. 4. Chocolate chocolate 77.7 times more likely milkshake or hot chocolate to have AD. (aluminum based food coloring) 5. Salt 47.5 times more likely (anti-caking aluminum) to have AD. 6. Pepper 1.1 times more likely 7. Tea .(hot or iced) 0.7 times (less likely) (?uoride limits absorption) 8. Chewing gum 3.3 times more likely 9. ALL HIGH-ALUMINUM FOOD 8.6 times more likely (as above combined) to have AD. - 10. FOOD 32.3 times more likely IN ALUMINUM CONTAINERS to have AD. Small sample sizes limits values. However, category #1 was statistically significant at P: 0.025 Age and Ageing I999: 28: 205-209 I999. British Geriatrics Society A preliminary study of dietary aluminium intake and risk of Alzheimer?s disease . Food Aluminum and Alzheimers MARY A. M. ROGERS. DAVID G. SIMON . . Department of Medicine. State University of New York Health Science Center. Syracuse NY. l32l 0. USA Address correspondence to: M. A. M. Rogers. Fax: (H) 31 5 464 8290. Email: i Abstract Background: epidemiological studies of Alzheimer?s disease and aluminium intake have realised on aluminium in drinking water. There have been no studies Investigating the relation between the disease and the consumption of foods containing large amounts of aluminium additives. ll Objectives: to conduct a pilot study to determine whether dietary intake of aluminium additives differs in individuals with and without Alzheimer?s disease. Design: matched case-control study. Controls were matched to cases on centre. Setting: Syracuse. New York. USA. Subjects: 46 participants comprising 23 matched sets.? Methods: residents of the Loretto Geriatric Center with and without newly-diagnosed Alzheimer's disease were selected. Next-of-kin were asked to complete informatldn on the resident's medical history; lifeistyle behaviour and dietary intake before admission to the centre. An. expanded form of the Health Habits and History Questionnaire was used to determine dietary intake. Consumption of foods containing elevated levels of aluminium additives was compared between cases and controls. Results: the crude odds ratio for daily intake of foods- containing high levels of aluminium was 2.0 and. When adjusted for covariates. was 8.6 (P 0.19). Intake of pancakes. waf?es. biscuits. mu??ins. cornbread and/or corn tortillas differed signi?cantly (P 0.025) between cases, and controls. Adjusted odds ratios we're also elevated for grain product desserts. American cheese. chocolate pudding or beverages, salt and chewing 'gum. However. the odds ratio was not elevated for tea consumption. Conclusion: past consumption of foods containing large amounts of aluminium additives differed between people with Alzheimer's disease and controls. suggesting that dietary intake of aluminium may affect the risk of developing this disease. larger studies are warranted to corroborate or refute these preliminary ?ndings. - age. gender and date of adnu?ssionnto the - I Table 2. Odds ratios for aluminium-containing foods and Alzheimer's disease I . No. of ratio Food categoryI discordant pairs Crude Adjusted" ,0 Pancakes. waf?es. biscuits. muf?ns. cornbread. corn tortillas 5/0 .oa - 01,25 Doughnuts. cookies. cake. pastry . 7/4 1.75 54.6 i an American cheese. mixed dishes with cheese 1.5 7.5? 0.41 Chocolate pudding. chocolate milkshake or hot chocolate I 20. 1.0 717' 024 Salt . . 4/2 2.0 47.5 0.26 Pepper Ira/s 1.6 0.36 Tea (hot or iced) .4/7 0.6 0.7- 0.69 Chewing gum 5/3 1.7 5.3 0.51 All high-aluminium food (above) combined 6/3 2.0 8.6 0.19 14/2 - 2.0 azaj 0.22 Foods stored/baked/cooked in aluminium containers 'For all high-aluminium food and for foods in aluminium containers. 1+ servings/day was compared with <1 (reference integer-y). For salt and never'. For chewing gum. once per week or more was compared with less - pepper. ?always. often or sometimes? was compared ?seldom or than once per week. For all other items (grain products. dairy and tea). 22 senrings/week was compared with I?Odds ratios were adjusted for kilocalories. body mass index. education and intake of vitamins A. and E. Further Thoughts On the Aluminum-Alzheimer?s Disease Link W.F. Forbes and D.R.C. McLachlan Epidemiol Commun Health, 50 (1996) 401 -3 Chart 3 SUMMARY This study compares drinking water aluminum exposures in Ontario with cases of Alzheimer?s disease, as ascertained by death certi?cates. (The AD patients had an average age of 85 and over.) Additional modifying drinking water components which affect the absorption and speciation of the aluminum are included in a multi-factor analysis of the relation of drinking water to AD in Ontario. Note that a neutral pH of about 7.9 reduces risk of AD by about 52 percent. Table 1 77:: mm between 3mg mm m; ,?pmhg of Alzheimer?s dame (ICD 0) an dank m?mmfor aged 35 and were mm A1 :3 67 (1.00) (1.00) (1.00) (1.00) (1.00) (1.00) (1.00) 68-250 0351- 0.88 0.9] 0.89 0.91 0.90 0.89 . 250 4.761 4.931' 5.071- 6.271- 7.381' 7.561- 'Source: - Ground (1.00) (1.00) (1.00) (1.00) (1.00) (1.00) Surface 0.91 0.76 0.82 0.77 0.76 0.88 Silicic acid 1.5 . (1.00) (1.00) (1.00) (1.00) (L00) a 1.5 0.811- 1.01 0.96 l.03 1.10_ Iron (alga): 6.2 (1.00) (1.00) (1.00) (1.00) 15.2-18.0 0.721' 0.751' 0.84 0.95 . 18.0 0.711- 0.641- 0.76 0.94 pH: 7.85 - (1.00) (1.00) (1.00) 7.85-7.95 0.531 0.501- o.4s+. 4" 7.95 0.82 0.78 0.521'_ Fluoride 0.5 (1.00) (1.00) 0.5-0.98 0.83 0.711- 0.98 1.231' 1.20 1hrbidity(formazin . units): . 33 (L00) . 33 0.581- n=104l;1' 0.05. Substances in Biology, Food or Drugs That Chelate or Interact With Aluminum Body Chemis?; Transferrin, Citrate APP, A Neuro?brillary (bonding with aluminum) I Phosphates: (Aluminum bonds with phosphates) Peptide YY (Appetite hormone powerfully removes brain aluminum) Praline-rich peptide-l (Powerful brain based aluminum chelator) Alpha-lipoic acid (strong chelator for iron and copper, removes iron from the brain of laboratory animals, moves vitamin into the cell and therefore, is at minimum an indirect chelator of aluminum)I 7. Melatonin, Serotonin, 8. Dopamine, Epinephrine, No'repineprine 9. GDNF I I I 1 Dietary, Drug. or Supplemental Dietary Items: I 10. Curcumin an ingredient of turmeric (chelator of iron and bonds with aluminum). I 1. Magnesium D-aspartate combined with sodium L-glutamate (removes brain aluminum) 12. Polyphenols?'om wine, grape juice, grapes l3. Des?rrioxamine (used successfully in human clinical trail to remove brain aluminum), deferiprone, eralex 14. Vitamin I 15. Vitamin i . 16. Folic Acid (reduces brain aluminum) I 17. Vitamin B-6 (antidote for aluminum generated dendrite toxicity). 18. Fluoride (facilitates excretion) I 19. Soluble Silicon (reduces absorption and facilitates excretion) I 20. Aspirin (inhibits aluminum produced aggregation) I 21. Other candidates?? Blueberiries, other flavonoids, Colostrinin I Metals That Compete or Interact With Aluminum in Biology 22. Iron: Aluminum depletes heme and enhances iron oxidation. I 23. Magnesium, Chromium, Selenium, Cobalt: Dis?placed or depleted by aluminum. I 1 24. Zinc: Displaced by aluminum. I 25. Calcium: Aluminum moves it into the cell to cause apoptosis. 26. Copper: aluminum enhances copper oxidation. In laboratory animals. it has been found that GDNF, cyclosporine A. and lithium (combined with anti-oxidants) can inhibit aluminum induced neuronal cell apoptosis. Osthol improves memory in aluminum trebted mice. as does ginkgo biloba in aluminum treated rats. Mechanism are no:t explored. Chart 14 I High Silicon in Mineral Water Reduces Alzheimer?s Risk at Age 80 Years By About 50 Percent in French Study. 1. Sili Al min In Ab ti Enhance Excr A number of human and laboratory animal trials have discovered that ingestion of soluble silicon will reduce the absorption of aluminum, and also enhance excretion of aluminum through the kidneys, most likely through the bonding of silicon and aluminum (1). (Soluble silicon and aluminumcombine to produce clay.) 2. Mineral Water High in Silicon: Mineral water is very popular in France, with 31 percent of this sample of people drinking only mineral water, and another 20 percent both mineral water. and tap water. Aluminum levels in French mineral water are Very low and silicon-levels are very high. Table 1. 3. Mineral Water Prevents AD: In confirmation of previous studies from France, this human epidemiology study ?nds that the consumption of drinking water high in silicon (primarily mineral water) reduces the risk of Alzheimer?s, almost certainly by reducing aluminum loading. 4. Low Silicon Intake Associated With Doubling of AD Risk: After control for the usual variables such as age and education, silicon intake of less than 12 mg/day was associated with a doubling of Alzheimer?s disease risk, with intake levels of 4 or less mg day statistically significant in .this sample, as well as the trend. See Table 5. - Cognitive impairment and composition of drinking water in women: findings of the EPIDOS Study?3 Am Clin Nutr 81 (2005) 897-902. Sophie Gillette-Gwonnet, Sandrine Andi-fen, Fatemeh Nourhashemi, Viviana de La Gu?ronni?re, H?l?ne Gramb?ean, and Bruno Vellas ABSTRACT Background: The concentration of aluminum or silica in drinking water may be a potential environmental risk factor for Alzheimer disease (AD). Objectives: The objective .was to investigate at baseline the poten- tial association between the composition of drinking water and the level of cognitive function in women taking part in the Epidemiology of Osteoporosis (EPIDOS) Study and to determine during follow-up the effects of the composition of drinking water on the risk of AD. Design: Women aged 2-75 (n 7598) were recruited between 1992 and 1994 in 5 geographic areas of France. The participants from one center (I: 1462) were followed for 57 y: during this time. an active search for incident cases of AD was conducted. The initial questionnaire comprised a food consumption survey with speci?c ques tions about the daily?consurnption of tap and mineral water. The evaluation of cognitive function was based on the Short Portable Mental Status Questionnairelnuring follow-up, the diagnosis of dementia was made by a geriatrician and a neurologist. Results: A low silica concentration was associated with low cog- nitive performance at baseline. Compared with the nondemented subjects. the women with a diagnosis of AD during follow-up were older at inclusion. had a lower ?nancial status and educational level. had a poorer perception of their own health, and had a more dif?cult time performing activities of daily living. A multivariate analysis including potential confounding factors showed that women with AD appeared to have been exposed to lower amounts of silica at baseline. Conclusions: Silica in drinking water may reduce the risk of devel- oping AD in elderly women. The results corroborate those of another epidemiologic study carried out in France. The potential effect of silica needs to be confirmed in additional investigations. Am Clin Nutr (Over) DJ Ch rt 14 (continued) Relation between AD and water composition - - - - The women who developed AD during follow-up were sig- Multlvana'ie analy?fu? uificantly older at inclusion than were those with normal cogni- Consumptlon 0f Slhcon tive function (81.1 4.3 compared with 79.2 $13.3 y;P 0.02). to Si gnificant reduction of They also had a lower income and educational level and Alzheimer?s Disease had greater dif?culty with IADL (Table 4). (See Table 5) TABLE 4 Comparison of characteristics observed on inclusion in the study of TABLE 1 women who developed Alzheimer disease (AD) during follow-up and of Aluminum. silica, and calcium concentrations of mineral waters and city . women who maintained normal cognitive function? water supplies . Women Aluminum Silica Calcium - normal cognitive Women with function Mineral water' nag/L . - .. .L. adoit Undetectable 33.4 187 3 Characteristic on inclusron AD (11 60) (n 323) Contrex <0.003 8.6 480 . Age 81.13: 4.3 79.2 i 3.3 0.002 Evian Undetectable 15.2 82 Education to school-leaving 83.3 91.1 0.068 Perrier 0.013 10 152 1 age (96) Vichy Q?lestin 0.032 36.4 98 income >?9lS 21.7 49.8 0.0008 Ville! Grands Source <0.003 95 204 i Abnormal mm. (as) 13.3 6 0.022 Vittel H?par <0.003 8.8 563 I Volvic 0.005 35.7 11 City water supply. 1992?19942 TABLE 5 Paris (Orly-Venue. Loing) 0.013 5.2 93.6 Factors associated with Alzheimer disease (AD) in 383 women aged ails Boulogne Biliaucourt 0.061 5.1 86 in the Toulouse cohort of the Epidemiology of Osteoporosis (EPIDOS) Toulouse 0.063 4.6 41.? Study? Toulouse. 1999?2000? 0.060 4 39 Moutpellier 0.052 6.4 118.6 I M?d?l 231:? 3:3: 1:2 I (153 Variable to be explained? Odds ratio 95% - See text for manufacturers. ?Giff? ?551 - 0-52 0.35. 0.79 0.0019 3 Time of enrollment in the Epidemiology of Osteoporosis (EPIDOS) . Age (3) . 1'15 1'06- 1-24 (3-0004 Study. -. income (reference: >6915) 0.00365 Time period of the prospective study of Alzheimer disease risk factors I 647-915 3'72 1'73! 8-00 09003 and (1313110518. I (6547 4.46 ?102. 19.52 0.0470 - Unknown 3.19 1.47. 6.95 0.0035 Silica (reference: 12 mg/d) 0.18815 . 9?12 mgId" 2.00 0.56. 7.07 0.2829 TABLE 2 . 5?8 lug/d 1.81 .033. 4.48 0.1986 Daily intakes of aluminum. silica. and calcium supplied by drinking 54 mg/d 234 1.09. 6.86 0.0316 water? . Trend test 1.36 1.02, 1.83 0.0378 Amount supplied by i Women who consumed ?other" mineral waters or Vichy Graude Element Intake mineral water . Source were excluded from the analysis because the composition of these rug/d I waters was unlmown. To study the relation between water composition and Aluminum 0.0231 3: 0.0252 5.6 I d15119111113113":I" 01' AD during follow-up. we excluded those women who ini- . tially had what we considered to be an abnormal Pfei??er score 10.17 10.01 72Calcium 134.8 i 154.1 69.1 Multivariate analysis based on logistic regression. Dementia of AD type 60) was compared with normal cognitive function 323). i 6135. 0.41 (Hosrner and Lemeshow test). 2 i i 5130111 such values). After adjusunent for confounding factors (age. Pfeiffer score. and I income). . i Overall P. - (1) J.P. Bellia et al, Role of silicic acid' in the renal excretion of aluminum, Ann Clin Lab Sci 26/3 (1996) 227?33; M. Belles et a1, Silicon reduces aluminum accumulation in rats; relevfance ot the aluminum hypothesis of Alzheimer?s disease, Alzheimer Dis Assoc Disord 12/2 (1998) 83-7 Source: Am Clin Nutr 81 (2005) 897-902 Nutrition 2: (2005) 405?510 Basic nutritional investigation Effect of folic acid supplementation on aluminum accumulation in rats Terken Baydar, more, Land Nagymajt?nyi, Askin Isimer, Gonul Sabin, Deparnnenr of Toxicology, Faculty of Pharmacy, University of Hacettepe. Ankara, Thrkey Department of Public Health. Faculty of Medicare. University of Szeged. Szeged. Hungary Depamnenr of Toxicology. Guiirane Military Medicine Acadennv. Ankara. Turkey Manuscript received December 30. 2003: accepted July I. 2004. Chart 16 Abstract Objective: Exposure to many xenobiotics may cause depletion of folie acid (folate), which is an essential vitamin for humans. Replacement of folate can be effective in protection against some diseases and in partial or total prevention of adverse effects related to xenobiotics. Aluminum (Al) is the most widely distributed metal in the outer crust of the earth. Its toxicity in humans is well known. However. there is no evidence that folate can decrease accumulation of Al to which humans can be exposed in many ways. The aim of the present study was to quantify organ Al accumulation and to evaluate whether there is any protective (or reductive) effect of folic acid on Al accumulation. Methods: Male Wistar rats were assigned oral Al chloride (200 mg - kg"l 10, group 1) alone or in combination with folic acid (20 mg - kg" - 10, group the period, bone. kidney. brain. and blood samples were collected. and Al concentrations were determined by electrothermal atomic absorption spectrophotometry. Results: Mean values of Al in the tissue samples from group I were higher than those from group 2 (all 0.05). No difference was observed in serum Al levels between groups (P 0.05). Conclusion: These results suggest that folate supplementation might be useful to decrease Al accumulation in its main target organs. hone. kidney. and brain. 0 2005 Elsevier inc. All rights reserved3.2_ 1? 1 - oJ Fig. 2. Comparison of Al concentrations in serum (A). femur (3). brain (C). and kidney (D) in group 1 (black bars) and group 2 (gray bars). Data are presented as mean 1' standard deviation. 0.05. Al. aluminum. Part 4. . The Time for Regulatory Ac?on Seems Overdue. 1 SPECIAL REPORT ON LEAD POISONING IN QHILDREN Standing Up to the Lead Industry: An Interview with Herbert Needleman i Dawn ROSNER. INTRODUCTION Genus) Herbert Needleman. MD. is a pioneer in the history of medicine who has helped transform our understanding of the effect of lead on children's health. In the 19705, he revolutionized the field by documenting the impact of low lead exposure on the intellec? tual development and behavior of children. In 1979. he published a highly influential study in the New ofrlal'cdicim" that transformed the focus of lead research for the next generation'and played a critical role in the elimination of lead in gasoline and the lowering of tlre.CDC's blood lead standard for children. Building on a study by Byers and Lord in 1943 ?and those ofjulian Chisolrn and others in the 1950s and lilli?s. which had documented a variety oi'chrunic damage alfecting children who shpwed acute of lead poisoning, Needleman's innova- tive study analyzed the lead content of the teeth of schoolchildren. correlating it with the children?s behatior, IQ. and school performance. Not surprisingly. Needleman became the focus of the lead indusuy's ire. Beginning in the early 19805. the industry's attacks on his research and use of public relations firms and scienti?c consultants to under- mine his credibility became a classic example of how an industry seeks to shape science and call into question the credibility of those whose research threatens it. Industry consultants demanded that the Environ- men tal Protection Agency and. later, the Of?ce ofScienti?c Integrity at the National Institutes of Health. investigate Neetllernan?s work. And then, inl 199], under pressure from industry consultants. the University of Pittsburgh formed a committee to evaluate the integrity of his lead studies. Ultimately the federal government and the university found no basis for questioning Needleman's integrity or the results of his re- search. But the impact of the industry?s actions affected both Needleman's academic life and the field of lead research. On the one hand. the industry explicitly showed the power it had to disrupt re- searchers' lives if they dared to question the safety of its products. On the other hand. Needle-man?s experience galvanized a generation of researchers who were profoundly influenced by the implications; of his studies. In the quarter century since ?De?cits in and.Class- room Performance of (.Il'rildrerr with Elevated Dentine Lead Lewis"I I ?Certter [or the History and Ethics of Public Health and Department oIIStrcionredical Sciences. Mailman School of Public. Health. Columbia University. New York, NY . Columbia University. New York. NY I ?johnjay College and The Graduate Center. City University of New ?r'ork. New York. NY Address correspondence to: Dar-id Center for the l-listory and Ethics or Public Health. Mailman School ol'l?rrblic Health. . Columbia University. 3'22 W. llililh Rm. 934. New York. NY 10032: tel. lax 212-342-1986: e-mail @2005 of Schools of Public l-leallh 330 Pursue l-Ir-zarmr REPORTS Mar?lunrc 2005 Vt'rursn-t' I20 INTERVIEW WITH HERBERT NEEDLEMAN 331 was published. Philip Laudrigan._lolnt Rosen. Brute Lan- phear. Kim Dietrich. and others have built on Needleman's work. continuing his ?ndings as well as opening new areas of research that have shown that lead, at virtually any level. has negative, life?altering consequences for children. This interview. conducted on the eve of his 733th birthday, re- counts :1 small part of l-lerb Necdlernan?s experiences over the course of the last halt?centuty. Editors' note: Dr. Needletnan was interviewed in his of?ce at the University of Pittsburgh on December 11. 2003, by Drs. Rosner and Markowitrt. PHR: Let's start with a little background about your family and your education. I'm a Philat'lelphian by birth. lwas born in 1927. My-Iatl'ter was in the furniture business. I was the first person in my family to go to college. I went to College in Allentown. and tlten to the University of Pen n- syhania Medical School. I interned at Philadelphia General Hospital. I had initially intended to be an internist, but I discovered lwas having much more fun in pediatrics. [did a fellowship in rheumatic fever research at Children's Hospi- tal in Philadelphia. I then went into the Anny and was an Army pediatrician. I hadn't been trained yet, but I worked under aboard pediatrician. When he was discharged [from the Army], I became the chief of pediatrics. I had 12 in pa- tient beds. and a big, and very busy. outpatient clinic. We had a hundred deliveries a month at Ft. Meade. so that meant we had seven preemies [a month]. I learned about pediatrics in a hurry. I had a consultant from johns Hopkins who came once a week?a very line. distinguished pediatrician. Barton (jltilds, who helped me survive that period. Then I went back and ?nished my training at Children's l-lospital, where I became the Chief Resident. The experience that turned me. toward lead is very clear itr my mind. I was working on the infant ward at the Children's, and a child was bought up from the ER with severe acute lead toxicity. I did what. I'd been trained to do. Igave her [chelation therapy}. She was stuporous and very ill. Slowly she got better. it wasa gratilying experience, and I felt very smug. I told the mother that she had to trtove out of that house: ?You can not go back to that house be- cause if she has a second episode she's going to be re- tarded." This was what I'd been trained to do in medical school. She looked at me and said, ?Where run I going to move to? All the houses I can afford are the saute age.? I suddenly realized that the issue was not just making diag- noses and treating thetn. The issue was in the life story of people. This was a very powerful learning experience. Then I practiced pediatrics in the suburbs of Philadel- phia for a *ar or two. I practiced with Bill Rashkiud. who was a pediatrician and physit'rlogist. Bill developed the Rashkind prettedure. which saved the lives of thousands of babies with congenital heart disease. He became a professor of pediatrics full-time at Children 's Hospital. and suddenly I was left with a practice. I discovered that a lot of the parents who were coming in to See me. mothers. were courting be- cause they were themselves anxious or depressed. These were suburban housewives. and those days they didn?t havejobs. A lot of my discussions were around issues, so I took a residency. In those days, the goverru'nent was subsidizing general practitioners and pe- diatricians to go into because they thought we needed more was going to be a child analyst. I went to St. (Zln'istoplrer's to begin a child try residency anti discovered that because I made house calls I knew more about family structure and dynamics than the I could go into people's ltontes and size up the family. whereas in the clinic the modrcr would bring the child, the child would talk to a the mother would talk to a social worker, and the father would somehow get evaluated. In a half hour in a borne you learn much more than in that whole intake procedure. [was very unhappy with the training, and the theoretical basis of child didn't satisfy me. I kept think- ing. ?How many of these kids who are coming in with learn- ing problems have lead poisoning?? The inner city we sen'tlead. People thought that was a craav idea. In my residency. I turned to the labonuory. I did some still? with invertebrates: Memoir: and morphine addiction. I had another formative experience. I was in the commu- nity program in North Philly. the inner city. I was the Director of Consultation Education, which ?as the out- reach part of the community health center. I gave a talk at a black church one night to a group of adolescents?tnostly boys. At the end of the talk. a kid came up to me and started telling me about his ambitions. He was a very nice kid. but he was obviously brain-damaged. He had trouble with words. with propositions and ideas. I thought. how many of these kids who are coming to the clinic are in [her a missed use of lead poisoning? My ollicc looked on a school ground. I watched the kids every morning line up atrd go to school. I said, ?I'm going to go that school and identify the children who have elevated lead and see what their 1915 are." Then it occurred to me that the blood lead at 6 years of age might be normal if the exposure occurred at less than 2 years of age. So I began to think: ?What can I use to read back in their exposure history?" Iwent up to Boston to see a guy named Louis Kopito about hair lead levels. But hair-lead has serious tnetl'todological issues: you can't tell how much is deposited from the outside and how much reflects what?s in the blood and brain. Finga-nails have the saute problem. Fingemails are keratin. high-protein. They have a lot of lead in them. but they also have a lot 01 external dirt. Lead goes to bone it's treated like calcium. but you can't do a bone biopsy. Then it occurred to me there?s a way to do a sponta- neous bone biopsy. It's universal, spontaneous, and painless. You just have to catch a deciduous tooth. There actually had been one paper in the 19605 on high tooth lead levels in kids who had been poisoned.? collaborated with a dentist in the dental school. [We] collected a lot of teeth from inner-city and suburban kids. The sources were a suburban periodontist and two inner-city dental clinics. The tooth lead levels in the inner city kids were live times what they were. in the suburban kids. ll" got a ntedical student. Bruce Dobkin. who WL?l'll. to St. Christopher's l-Iospital and ob- tained the names of children who had been discharged with lead poisoning. We idenlilied five kids with lead poisoning. and we paid $5 per tooth. The lowest lead concentration in Pursue HEALTH Rtmon'rs Mav?lurst?. 2005 VOLUME 12!] 332 Senor-u. Lean Porsonrxc. IN the poisoned children was (if-.5 parts per million and the l'Iigltest was something like Twenty percent 01? the kids in the whole sample in the inner city had levels higher than 63 ppm. The exposure prevalence was very high. We published a very short paper in Nature.? PHR: It seems like this work originated in large part from your clinical experience of doing home visits. My practice in pediauics was irt Mainline Philadelphia. an uppcr?middle?class are: . i did have experience visiting homes in the inner city. and I did my pediatric residency irt the' middle ol'the black ghetto in South Philadelphia?l 7111 and llainln'idge streets. was single then and would walk hack' through there after a date. i knew that pretty well, and i knew the quality of the homes. I did another study it: Philadelphia. it was witl't [wing Shapiro. a pediatrician whom i knew, and Ed Sewell. who was the head doctor of the school system. Ed collaborated with us because he wanted to use the school system to do health research in children. We colleCLed teeth from six or seven inner-city schools and three or four schools in North- east Philadelphia, which had experienced a population ex- plosion and building boom after World War Because the city had a contract with the Catholic schools. Ed asked me to include some Catholic schools in the project. This was very important. The dill?erences in teeth from the inner city and North- east Philadelphia were so great that I ttsed to play a little garlic. Irving Shapiro would collect teeth. analyze them. attd send me the results. I could gttess the kith' race anti where they lived. if [the lead level] was over fill ppm, it was a black kid from the inner city. If it was under 5, it was a white kid from Northeasr Philadelphia. It was so clear-cut?the separa- tion was extraordinary. Then a bunch of teeth came in that were Very high from kids with ltaliart or irish names who all lived on three streets in East Kerrsingtou. So irving and i went to St. Anne's School. which was right ttext to the Na- tional Lead Company. These kids were living in the. shadow of the NL. stacks. Ni. had a [itctoty that spanned both sides of a huge street. The children ill-St. Anne's were getting as much lead from industrial emissions as the inner?city kids who got lead from paint. Ol?conrse it caused a little loo, the city didn't do a thing about it.l thought this was going to open the doors to lead control. PHR: How did you publicize your ?ndings? We talked to the city. and we published in the Nita: England journal at] rl?lr'dt'cirrc. Years later there was a lawsuit on behalf of the people who lived there. A Washington law ?rm won an award of a million dollars. PHR: Did the community get involved at the time of your study? It turns out that the [community] residents knew that there was a lot ol'lead: they were not surprised by it. I had another experience: i was collecting lead from the gutters in these neighborhoods to see what the levels were. The workmen canre out of the [National Lead] factory. and they were very menacing: ?What are you doing here?" ?l?m from the city." I said. ?just collecting some samples." They told me. ?Get. the hell out of here." CHILDREN This work got me an invitation to Boston (liltiidren's Hospital [and Harvard Medical School] to do this? work. in I finally got a big grant. 1 collected teeth from school systems in Somerville and Chelse' . In those days, those were white, industrial. working-class neighbor- hoods. I collected something like teeth from 2.500 children. The teachers were terri?c. very cooperative, very well motivated. ma.- how did it work? Did the teachers ask the children to bring in their teeth? had posters placed around the city in store windows. My secretary's husband was a commercial artist. He drew us a tooth that looked like Mickey Mouse. It had .1 missing tooth. and it said. "i gave." The communities were aware of the campaign. We gaveas a reward a little kit?toothbrush. tooth? paste?and a badge. in Philadelphia. [we had given out] solid silver Kennedy halfdollars. which were quite rare. Tire kids. after they gave the tooth. were given this half dollar and a certi?cate by the dental clinic. I discovered that some of the dentists were givingr the kids two quarters and keeping the half dollars. 1 Spoke at a meeting anti 1 said. ?How?d you like that Kennedy half dollar?" And [the kids] said. ?What do you mean? i got two quarters." This was my ?rst experience with the corrupting power of cash in science. [it] the Somerville and Chelsea study]. instead ol'cash we gave a toothbrush and a badge. We got some funny things from the kids. We got some dogs? teeth and some adult molars that they'd found lit the house. Even some white stones. The toothpaste and badge were a powerful motiva- tor. The teachers were wonderful. They each had a shoe box ?lled with coded envelopes. On the envelope was a diagram of the human mouth with a big smile. They would look in the kids? mouth. [hid the space. and then mark the space on the envelope. When my chemist would open the envelope. he would look at the type tooth and the space and see if they were consistent. At the peak. we were ahle to do, i think. till teeth per week. We had no idea what a normal tooth lead level was or what the range was. We ltad to develop a rolling standard. As we did teeth. we?d see what the mean was and then establish the upper E-lUth percentile and the lowest 10th percentile. But then we would do another 100. and the mean would move around a little bit. This is important because this is out: of the issues raised during the investiga- tion of scienti?c misconduct. I had to make up the rules myself as to which children were classifiable and who were not. initially i said that if a child gave four samples, then three out of four had to he Consistent. Otherwise we'd say "unclassified? and exclude the child. But that excluded too many children. We made it two out of three. Thatt *as raised lit the investigation. and was a little hazy on it; i couldn?t remember. At any rate, we identified. 1 think. 2'50 kids who were at the highest or lowest end of the distribution and brought them into Boston Children 's Hospital. adult! in? terview the mother. git-e her an IQ test and a medical ques- tionnaire. The kid had a four-hour examination by well trained and then we?d get the data crunched. Wt'd pay to have all of the teachers dismissed for half a day and hire substitute teachers. All they had to do was [ill l?unmc Rat-ours Mar?June. 2005 Vows?; wn'n HERBERT "b 333 out a questionnaire for every child in the class, whether they were in the study or not. The questions were very simple: Is the child distractihle? Y?s or No. Disorganized? Yes or No. Follow simple directions. complex directions. etc. There were 11 questions like that. to. had 2,146 good datasets, that is. a good tooth analysis and a good questionnaire. Then we arrang'd the subiects in six groups oi ~12 ascending tooth levels. Class 1 was the low est. Class 2. up to ti. Wit-just counted the negative reports by teachers for each ol'the six groups. As tooth lead went up. the rate of bad reports went up, too. It was extraordinary. The teachers, who didn't know [the kids'] lead levels. could identify ail these non-adaptive be- haviors [that were] in direct relationship to the level of lead in the teeth. That Convinced me that was right. The evi- dence came of the computer: there it was. So we pub- lished it with the IQ and lat'tguage data in It?t?iti in the. Non I had a very good organic chemist. Neil Maher, who was doing the tooth analysis. in 1976. I got a call from David Schocnhrod, a lawyer at the Natural Resources Defense (loun- cil. He had sued to write an air lead standard. EPA had drafted the ?rst version, and he asked me to take a 10er at it. It was such a bad piece oi'work that it was clear to too that it was an industry pass-through. Probably an industry-scientist had written it and given it to EPA and they had incorporated it. Neil and lwrote a rather strong report, and we both went down to City, Virginia. as part of the Clean Air Sci? ence Advisory Committee's (GASAC's) review of this docu- ment. The chairman of the was Roger McClellan. lie later was the head of the Chemical lnstittlte of Toxicology. A very nice fellow. but very pro-industry. Most of the people on the (IASAC were pro-industry except Sam Epstein from Boston Children's. Ruth Diamond, who was the Dean ol? Boston University School of Public Ilcalth. and Bailns Walker. who is now at i-ioward University College of Medicine. After a very strenuous debate and at the conclu- sion oftwo days. the CASAC totally rejected the document and decided not to revise it?that is they decided to get rid of it, Start again. and get some new people involved. They get a new coordinator for GASAC to produce the EPA criteria document. They wrote a thicker one: it was better. it still wasn't good enough. and again said this needs to be tightened up and we need new consultants. I was appointed. anti then Sergio Piomelli from Columbia, who was a pediatrician. was appointed as w-ll. I't?e went down to North Carolina. It was the year of the big hrownout in New York City. 19?? We went down just alter that. We spent three or four days in North Carolina. and it was terri- bly hot. They had also appointed two pro-industty consult- ants?l?nn'nettJacobs. who was the. vice president for petro- leum all'airs at Dupont. and a young guy named Ed MeCabe. PHR: What did the pro-industry people say? They really weren't on firm ground. They didn't hav . the background. McCabe was appointed because he had partici- pated in one epidemiologic study that bad measured blood leads across the countty." lie was not the senior Ilc didn?t design the study. He hecam - a consultant to the industty?wrote letters to the editor and that kind of stull?. Jacobs was a smart cookie, but he was no pediatrician or biologist. I said to hitn. "You have these l?hDs, these smart chemical engineers. why don?t you develop a better anti- knock agent [one without lead]? And he said. ?Well, Herb. to tell you the truth, our economists are looking at the gasoline market. It's beginning to flatten out. There's not going to be the same kind of detnand. And we?re not going to pot 100 million dollars into Rand This is what he said. This was my post-postgraduate education. That all this s?ittg in the criteria docutuent [about the lack of any danger From lead in gasoline] didn't mean anything. Dupont's sci- enti?c position was determined by the company's economists. I had worked at Dupont when I was in medical school. Between my first and second years as a medical I worked as a laborer at Dupont?s Deepwater plant. where they made tetraethyl lead. I didn?t know anything about it at that time. I shoveled chemicals: backbreaking. awkward. dangerous work. carried cigarettes in a plastic case be- cause if you didn?t you would dissolve the tobacco?you sweatcd so much. It was so hot there. i would walk out into a summer evening and it would feel like I was walking into air-conditioning. We weren't allowed to carry matches. We were allowed to smoke at IO. lunch time, and The smok? ing whistle would blow anti all these guys would pour out of the (lill'crent buildings. They had a wooden shack where they would have two cigar lighters and a Coke machine. Everyone would smoke two cigarettes back-to-back and drink Coke, then go back to work. There was a group of workers who always sat in one place in the corner. They didn 't talk to anyone. They just stared out in to space. They were obvi- ously out of contact. So I said to some of the old guys, ?What's going on?" and one said, ?Oh, they're front the House of Butterflies [where tetraethyl lead was fabricated]? I knew nothing about the House of Butterflies; I just knew these guys were brain-damaged. When I left thatjob (after two months) . the sector head?- he was a PM), I guess a chemical engineer?asked me to come up and talk to ltitn. He asked me. "What do you do think about this job?" said, don't think any human should do this work. I mean it?s hot, dangerous. anti nasty." I said, don?t think any animal should do this work. No- body with a nervous system should be exposed to this kind of work." He was kind of shocked. It wasjust horrible, but it put some money in my pocket for school. I worked in what was called the house. We were always moving. You would have to wear a hat and goggles and gloves all the time. Hard toe shoes. You would go in to work and change your clothes and in about 30 minutes you were soaked. Absolutely drenched with sn'eat. At the end of the day you'd shower and go home. I couldn't eat when I had thatjob. I'd drink a quart of milk at lunch and some crackers. I would go home and think and drink and drink. My tl'tirstt-vould be enortrtous. [would lose like 13 pounds a day and then gain itback. As lsaid, I don't think anything with "a nervous system should be doing that work. PHR: Were there any issues with the industry other than at government meetings? In 1979. when I published that paper [no the Someniile and Chelsea Study] the lead industry was silent. They didn?t say anything for about sis months. I expected that there would he a big response. but there was nothing. Then?lerome Cole of the International Lead Zinc Organization called and Politic: i?ileAIJ?li REPORTS MAY?just: 2005i \"ommv. 1330 33-4 SPECIAL REPORT on Lean PorsoNtN-t?: lr?\ CHILDREN wrote a letter to the editor?tire usual stuil'. Then they started? to call [or my data, my printouts, and I said. ?No. I?ll shartl them with arty legitimate scientist, but I'm not going tol share thetn with the lead industry becatwe they don?t qualify.?r . PHR: How did they request your data? In public. Then in the writing or the ?nal EPA criter'iai document, I testi?ed and was questioned about my work. Claire Ernhart testified. presented-and was questioned about her work. It was a very strange thing. Lester Court had been. at the University of North Carolina. then he went over to: EPA. He asked me to criticize her work and her to criticize my stuff. I thought that was kind of strange to set up thist kind of due]. So I presented my stuff. and l-Zr'nhart raised: questit'n'ts about tutcorrtrolled variates. ett . PHR: Can you explain? Claire Ernhart is a who published in 1974 what was the best paper at that time in the journal of Learning Disabilities." She and joseph Perino examined the IQ scores in children on Long Island whose blood leads were over 40 or under 30. [t was a more sophisticated analysis than any- thing that had been done before because she used multiple . regression analysis and included a number ol'variable:. in- . eluding maternal IQ. There was a significant effect; the high I lead subjects had signi?cantly lower IQ scores than the low - lead subjects. She said that while this may not be visible in the clinic. it has important effects on arid public health authorities should pay attention to it. Then, itr at the American Association for the Advancement of Scient in Toronto, Ellen Silbergeld. Debbie Rice. and I were part. ofa symposium on lead toxicity. Ernhart got up in the audience and said she was publishing a paper [showing] that if there I is any effect it is ?tninintalfjerome Cole was on the panel; he was the head of the International Lead Zinc Research I Organization. Six months later she had a grant from ILZRO and became their principal spokesperson. In her later paper, Ernhart presented her data in an way.7 She did not present rand values. which is the customary any. Site gave some other metric to it that cart be transformed. which I did and there was a signilicant ell'ect. ll'iust was blurred out by her: When Ernhart criticized my work in the. EPA hearings. she said Something about inadequate control of confound- ers. When I criticized her. I said. ?ou didn?t even control for socioeconomic status. which is traditional." She said. ?Well. that?s because all of rny subjects were of the same socio- economic status.? 1 said, ?Well. I've read your paper and apparently i know your paper better than you. I have a Copy of it here. and it says the parents of these subiects Were teachers. postal workers. and welfare mothers." This was kind of dramatic. There was one incident that was most revealing about Ernharl. It involved a lawsuit about a kid lrotn (.Ileveland. was asked by a lawyer for the plairttil'l'ii'l would he an expert witness for the use. I read the case and said absolutely. I thought this was art opetnatrdoshut case. This was a child named Danita R. She was described as singing nursery rhymes, dancing. being a very bright kid. Then site got sick. She was taken to Rainbow Children's Hospital with a fever and sore throat. She was stuporous. A neurosurgeon looked at her and thought she had a brain tumor because site had signs of increased intracnmial pressure. They took her to the (JR as an emergency. 0n the way up, they drew her blood for lcatl. In the 0R. they opened her head, and they saw severe swelling of the brain and some dead cerebellar tissue, which they excised. They closed her up. and she had a very stormy post-op period. Then they inserted a shunt to decrease the. in tracranial pressure. After recovery. she had hyperactivity, attention deficit disorder. and a low IQ. I-ler blood lead [level] returned while she was the OR and ras as high as they cotrld measure. It was over That was the ceiling of their measurement. So here was a case of a kid with an extraordinarily high blood lead and evidence of dead brain tissue. 1 said. ?Sure, I'll testify.? (Ilaire testified for the defense. PHR: When was this trial? Mid-19803. hert in 1991 I was approached by a guy named Benjamin Fisherow, a senior attorney at the Department of justice. He asked ifI would be the principal medical witness in a suit against. the owners of a mill in Midyale, Utah. The owners were Sharon Steel. a local Pittsburgh steel com pany: Gulf Resources: and a third group. The suit was not for damages to people but to get the owners to pay to clean up the place. They had mined and smelled the lead there and left a mountain of tailings. Houses were built on them. ltwas felt to be a hazardous waste dump. Fisherow prepared a very good case. Lots of good witnesses on the environmental side. I was deposed here irt town at_]ones Day. Twenty law- yers in a room where the conference table is like a bowling alley. Claire Ernhart was there for my deposition. PHR: She was in the room? In the room. She was seated and taking notes. A few months later. a lawyer from Philadelphia sends me a copy ofa sub- mission Lo the National Institutes of Health accusing me of scientific misconduct. Sandra Scott. who had worked as a consultant to EPA during the drafting of the [1986] criteria document. had been a member of a special ad hoc committee sent by Lester Grant to interview the and Claire Ernlrart. The committee wrote a report which savs you cart not make any conclusions from the data of Needleman or Ernhart. The report con- tained ll factual errors. The deal was that they could come and I'd give them the data and they could ask any questions they wanted but I would have a chance to see this and comment on it before it was published. It was sent to me the day of publication. I wired Grant that ifhe didn?t correct :tll these errors. Iwould make him send an errata sheet; to the entire distribution. PHR: This was being published where? . Distributed by EPA as art addendum to the ??83 criteria document. So Lesrer corrected all of thos?e things because they were lactnal. but he didn?t change the Conclusion; it tras still left a little vague. I-Iowev then the (IASAC met in North Carolina and I was asked to come down anti corn- rnent. Ernhart and Scarr were there. I got up and said the report was erroneous and here are the facts. In the mean- I??unrar: Rr-zr'ok'rs ,3 Mar?Jenn 2005 I?ll) INTERVIEW WITH HERBERT NEEIJLFMAN time, the EPA had ghen us some money to reexamine the data and-sent two EPA staffers to help with it: Joel Scl'twartz and Hugh Pitcher. They analyzed the data and got the same results. They recorded that the conclusious I drew and pub? lished were accurate. The ?nal version in that 1986 criteria document says this is pioneering work and it does support the conclusion that low levels of lead affect children's IQ. etc. It also said that Ernhart's data support that. too: they looked at it and found the same thing I did. [In 1991]. I got a brief that accused me of scienti?c misconduct. It was submitted by a guy named David Geneson. He is an attorney with l-Ittnton and Vi-?illiams. l-Iunton and Williams is interlocked with Ethyl (.quroration of America through its board of trustees. So he was the. person who sent the charges down to NIH. The next thing I know. I was called by a reporter from Science magazine. Isaid, "Come on, this isjust the industry trying to get me.? I didn't realize how serious it was. The university called me and said. this is nothing to worry about. It will pass. The next thing I know they?re. going to have. an inquiry. The NIH referred the investigation to the university. That's their procedure. My ?les were locked. and I could only look at my data in the presence of a representative of the Oliice of'Scienli?c Integrity of the ttnivetsity. I had to call her up and say I wanted to look at some data: can you come and unlock the ?les? They put bars on my ?le cabinets. The inquiry committee was cmnposed of three people frotn the University of Pittsburgh: two epidemiologists and a statisti- cian. They looked at my data tapes and regressions and got the same results. They reported that they found no evidence of scienti?c misconduct but they could not rule out scien- ti?c misconduct. But the university said there was enough reason to go ahead with an investigation, which is the. sec? ond phase of a scientific misconduct inquiry. It's like the deciding whether there is a reason to go fonvard, and what the university found was that there was no miscon- duct but they should go fonvard anyway. Do you have any sense on who was pressing them on this? Yes. I do. I think it was the guy who recruited tne to the university. I think I displeased him because there was certain research he wanted me to do that I said. ?No, that's not my bag and Iwon?t do it.? A lot of this is surmise, but I told him no and think I made a serious enemy. Also, Sharon Steel is a local firm. and I had cost them $20 million in the environ- mental lead lawsuit that I had testified in. There are local industry connections to the ttniv usity. So I think those two things together are adequate to explain why this thing was pulled off. PHR: What was it like for you during this period? I-lorriblc. It was absolutely horrible. I was so angry, and it's not good to be that angry and worried: it's had for your health. I was mostly fun'ons because I thought, they're not going to find anything because there isn't anything to Iind. What I discovered is that not only did the university not come to defend the but they wouldn?t give me an even playing ?eld. I went to the dean. and I said. I want the intestigation to be public. I want to have scientists. the press. and my colleagues here at the university monitor this. The university guidelines for scienti?c misconduct state that that the university can bring in outside ?experts. I want you to bring the top people in lead toxicology and neurotoxicology and put them on the panel." The dean refused my request to open it up and bring in appropriate experts who knew the ?eld. He said. ?We don't need them. We have our own experts.? This is hard to believe. but one of their experts 'as Robert McCall. a who had worked on American Association panels with Sandra Scarr. I brought this up. I said this guy has a conflict. He knows her and has been working with her. Another was Roseucranz. a toxicologist who had been head of eudrontnental health at Case Western Reserve. where Claire I?lrnhart was. So I said he should not be on this panel either. They responded. ?We know about that?, and there is no conflict of interest.? PHR: Did you have a group who you were supported by? Other professors and medical people? it is a very clarifying moment when this happens. You learn who your friends are. My friends were not people in the medical school. but the faculty in the university at large. in the liberal arts and sciences, etc. They-really stood behind me. The major issue was having an open hearing. I knew that if we went in to executive session. I was through?I meijustjudging by the report that the inquiry committee wrote. I cam pal gned to get it open. and the university faculty senate was behind me 100%. It became a big issue here. The chanCellor was challenger! in public. About 400 scientists from around the country petitioned. The beatings were then declared open. at which point Sandra Scarr and Clair - Ernhart said they would not come. They did not want to be questioned in public. All we kn cw. my lauyer and I. was that there were meet? ings between the investigation committee and the adminis- tration. the science integrity officer. and Scarr and Embart. They were having discussions and they finally persuaded them to come. because if they didn?t they would have had to drop the whole thing. Ifl couldn?t confront my accusers. then there would be no case. The -.al was that they would come but they could refuse to answer any questions that they didn't want to answer. So how do you confront some- body when they can say, I'm not going to answer that? I had a lawyer. a very good lawyer. but he was not allowed to speak. He cottld only sit there and whisper in my ear. PHR: How long was the hearing? A day and half. It should have been longer. Really, we should have just them. We should have said. you have to answer that question. They accused me of not controlling for age in my study. But the le are normed for ago. So I asked, did you control forage in your paper such-and-such? They answered, that's not relevant. So that was the kind of thing that went on. The main issue as that they said I?d chosen my snbjecrs knowing who had high lead and low IQ. So when I got my printouts out and read through them again, I saw on the front page of every data mu a piece of computer Code in SPSS which said, select the subjeCts if the lead is high or low. That was in the computer code. I asked Scan; ?Did you see this code?" She said. don?t know.? I Rspowrs Vow 121) hilt?) x) SPECIAL REPORT on LEAD POISONING tn CHILDREN said, ?Do you know that it?s at the front page of every sub- routirte of the data you examinet She wouldn't answer. It'went on for a day attd a half. The press was very favor- able and kind. It took a longtime for the committee to it around. They said there was no evidence of scienti?c misconduct in terms ofl?alse application or plagiarism; how-l ever. the way I reported my control group was misrepre-, That was important because I had brought tltis up tol them at the beginning. I said tltere is an error in reporting tlte range of tooth lead levels in my control group. There were a couple of things. One was where I changed in the middle from three out of four teeth to two out of three. 'I?ltat was unclear; it was not dishonesr. It had no impact [0n 5 the results]. As I told you. I was doing it in a kind of rolling sequence of admitted subjects. I said, 'ah. I was uncertain about that. It was the ?rst time. that this had ever been done, and we were only doing (it) teeth a week, so the allies changed with titne. But the industry ttutnpeted that ltad deliberately misrepresented the data. PHR: So you are at the university and sonte of your colleagues have abandoned you?what?s happening? At that. point, I spent most of my titne with my staff. They were vety helpful to me. The research coordinator helped me a great at]. Two younger people did a lot of research and brought stuff together: they prepared it for me for my hearing. I had asked for help from the Tenure anti Academic Freedom Committee (TAFC). The chair. Richard Tobias. who was a former president of the faculty senate. a professor of English. was a great support, and the TAPE was supportive of me. The faculty senate tally backed me up completely. I felt I had friends. The Dean of the School of Public Health at that time. Dott Mattison, was a good friend of mine. I ltad knowtt him for a long time. His interests and mine were similar. After this was all over. he called me up because he had a research project he wanted the to partici- pate itt. Months had gone by of absolute silence. and now he took to lunch and we talked. I said, ?Hey. Don. how come you never spoke to me when I was in the middle of all that melodrama?? He said, ?Well, my wife thought I should, but I guess I was afraid.? At least that was honest. PER: 50, in your relationships new with the faculty. have there been lingering issues? No. Because of this experience, because they were so helpful to me, I ran for a position on the TAFC. I served for many yeats. was chairman for four years. I'm going to tell you another stoty. There was a guy named Erdetn Cantekitt who was a whistle-blower?a bio? I medical engineer who was the science director for an ear. nose. and throat research project. A huge Millions of dollars to study th'- antibody of otitis media, a common ittfectious disease in childhood. Halfway through the study, the [researchers] stopped the data collection and did an analysis and found a marginal improvement for their drug over the control group. \r'ety small difference. They wanted to submit it to the Netak'ttgfamf loaned, but Cantckin wouldn't sign offon it. He said. ?First of all, we broke the code. We said we were going to do 1.000 subjects but we did 500." attd a lot of other things. Suddenly Cantekin became I persona non grata. He had tenure; they couldn't ?re him, they-dismissed him from the head ofthis project. By the way. it turned the principal investigator was taking money from Glaxo at the saute time he was accepting federal sup- port and not reporting it. He was found guilty of iscientiI-ic misconduct. he sutvived. Erdetn was sent to ?an otlice over what used to be the Giant Eagle grocery market with a ?ling cabinet and a phone. sued and won a big. bigr settlement. No one would talk to Et?dem. I used to go to lunch with him once a week the cafeteria. I joined the TAFC and I became the chairman. and I've been in those kinds of arbitratiou since. PHR: So what happened in 1991, after the investigation? The investigation committee found no misconduct. They just let [the inquity committee?s ?ndings] stick. I continued to get grants after that. I was allowed to apply for grants because only if you?re found guilty of scientific misconduct do they say you'are barred from research, but that never happened. PHR: You were a hero outside of the university. The reason I told you the Erdent Canti ken story is because it contains a diagnostic episode. When the principal investiga- tor was found guilty of scienti?c misconduct, the medical director of Children's Hospital wrote a public letter to the editor itt his defense. I wrote a letter subsequent to that in which I said that the real hero was Erdem (lantikett. who was punished and should have been applauded for his courage. Also that the university had to be very careful about doing a minuct with the drug companies. [wanted Erdem to know that he wasn?t totally alone. I got an anonymous letter from a faculty member thanking tne for that etlitotial. That tells you what the climate was. He didn't even sign his name. PHR: It raises the question of what effect you think the assault on you had. Was it meant to scare younger scholars away from doing controversial research? I wrote about that in a piece in Pediatrics.? If this is what happens to tne, what is going to happen to somebody who doesn't have tenure? I'm worried that people who are ttyingr to get a niche attd don't have tenure are asked?and I?ve seen it as a member of the. do things that they question the ethics of. They are intimidated. It's a real force. PHR: What were the repercussions after 1991? Were you able to continue your work? I think. all in all, that throwing light on [my expetiett'lt e] was healthy for the medical see the any that certain people operate. So I think that was good. i i PHR: Has there been any effort to apologize to ypu? You know, it says in the faculty handbook that if someone is found not guilty ofscientilic misconduct, the univetsity will make a public statement. But they never did. It got lost in a committee. Subsequent to that. however, I did win the Chancellor?s Award for Community and a handshake. Punctc Rtteott?t's 2005 INTERVIEW WITH Hatteras-r NEEDLEMAX 33.: PHR: Do you think we are ever going to ?nd a threshold below which lead has no effect on children? Most of the damage is dot'te at very low levels, which is what we. showed in our study in 1987." it is Schwartz has shown in his meta-analysis.? It?s a very intriguing physiologi- cal problem. Why is it that the toxic effect of lead is stronger at lower doses? I have a couple of ideas. I think there is an early mechanism that is important and powerful that can be saturated by only a little bit of 1 *ad; yott do that damage and then you need more lead to get the other targets activated. 1 think that?s what some smart molecular biologist will be able to show. As a matter of Schneider has shown that lead at picogtam influences the length of branches oi'nen'es in tissue cultures." I think that at very small doses. these things happen because you don't need much. Then the next damage occurs on a dili?cret'tt mecha- nism at a different level. All altmg there are dill?erent mecha? nisms that come into play tltat end in the neurophysiologic deficit. I don't think there is a threshold. Barry Commoner. who made tne see this, says that we?ve had a billion years to adapt to natural molecules. We?ve had a couple thousand years to adapt to lead. Fifty years to adapt to pesticides. All of these are toxic at some level. W: have developed no adaptive biological mechanism For lead. which has no purpose at all in the body. Nobody has ever been able to discover an enzyme that is activated or influenced by lead. There is no biological function. so any amount is going to be deleterious. We are now able to look at at lower doses For a couple of reasons. One is that we have better statistics. ana- lytic methods. especially since the removal of lead from gasoline has now given us comparison groups with blood leads of or below. W- never had that before. When I did my in the lil?i'fls. my control group had a mean blood lead of 15. Now we have a large number of people walking around with blood leads of or below. PHR: So you?re siill working away. You?re now 75 years old. You certainly started a school. i didn?t Start it. There were maybe six or seven papers before mine. Phil Landrigan had a nice paper in the ?Flls.?2 Claire Ernhart's paper was a nice piece of work for the time." A woman in Virginia, Bridgette de la a pediatrician, looked at some kids with high lead levels."5 But above all. there was Randolph Byers in 1943 and after. who said he wondered how many of the kids walking around with school or behavior problems were lead-poisoned. That was really where it began. What I did was develop a tooth assay, which was very useful. I had a vety good epidemiologist in Boston, Alan Leviton, who helped me develop a rigorous study. It answered the questions that were around at that time. PHR: Does that explain in some sense why you became such a focus for the industry? Yes! Sure. it's very clear to me that in there were now 30 papers ll'uln around the world all sayingr the same thing? except for Claire Ernhart. The [lead industry] couldn't cou- test that. so what were they going to do? If they could dis- credit my work. the whole thing would collapst- or he Funda- mentally revised. I'm sure that was it. That?s why they kept saying they had to have my original data because they had planned to make a concerted attack on [my ?ndings]. Then all the other work that grew out of it would be . . . PHR: Suspect? Discredited. The authors would like to acknowledge the support ol?the Robert \l'oodjohnson Foundation's Investigator Awards Program in Health Policy Research. REFERENCES I. Necdlt?man l-ll.. {ittnnoe (I. Let-hon A. Reed R. ll. Mahnr l. rt :11. De?cits in and classroom pt?t?lht?ntamt? ol t'ltil- (iron with elevated dcntinc lead levels [published erratum a ppcars in Ettgl_] Med New Englj Med 95. 2. Altshuller LF. Halak DB, Landing BH. Kchoc RA. Deciduous teeth as an index of body burden l?cdiatr 3. Necdletnan L. Tuucay OC. Shapiro 1M. Lead levels in deciduous teeth of urban and suburban American children. Nature ltl'Fil: 235:111-2. ll. l-lL. Davidson 1. Sewcll EM, Shapiro l-M. Subclinical lead exposure in Philadelphia Identi?cation by dcntine leatl analysis. New EnglJ Med 5. Clark jL. Challop RS. McCain: EB. Elevated blood lead levels in children?a 274in neighborhood Health Serv Rep ?53:88:419-22. ti. Pcrino j. Ernhart (SB. The relation of subclinical lead level to and scnsorituotor impairment in black presrhoolrrs. 1 Learn Disahil F. Ernltart Lands ll. NB. Subcliult?al levels of lead and developmental deficit: a multivariate follow-up reassessment. Pedi- atrics 8. Necdletnatt Hl-. Salem comes to the National Institutes ot?Hcalth: notes Front inside the crucible of scientific integrity. Pediatrics I 992:901177-8] . 9. Bcllinger D. Leviton A. Watcrnaux t1, Ncedlcman H. Rabinmvita M. Longitudinal analyses ol'prcnatal and postnatal lead exposure and early in?nitive development. Engl] Med 1987:316: ?13143. 10. Schnarts]. Beyond LOEL's. values. and vote counting: methods For looking at the shapes and strengtl'ts of associations. Neurotoxi- colony 1993: ??3346. ll. Huang FN. Vemuri MG Elli-rts oi low-icu?l lt?ud exposure on cell sunital and neurite length in pn?tnaty tnt'sen- cephalic Nt'ttroltmirol 'l?cralol 20033255533. 12. Land?gan Whitworth Rll. Baltfah RW. Staehling NW. Barthel Rosenhhun BF. Neuropsyt?hological dysfunction in children with chronic lowch-?cl lead absotprion. Lancet 12. 13. De la Btn'de l5. Choatc Docs lead exposure in children have latent Petliatr Editor's note: For :tst-Iected bibliography ol? related lite more. see to PUBLIC REPORTS I MAY?just: 2005 VOLUME 120 Partial Bibliography A. Aluminum Induced Brain Cell Death 3May Involve Both Apoptosis and Necrosis 1 Johnson, VJ, Kim S-H and Shanna RP, Aluminum-maltolate induces apoptosis and necrosis in Neuro-2A cells: potential role for p53 signaling. Toxicol Sci 83 (2005) 329- 39 B. Aluminum Induced Brain Cell Death by Either Apoptosis or Necrosis (In?ammation Initiated). 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Alzheimer 5 Dis 8 (2005) 117-27 Becaria A, Lahiri DK, Bondy SC, Chen D, Hamadeh A, Huihui L, Taylor R, Campbell A, Aluminum and copper interact in the promotion of oxidative but not in?ammatory events. implications for Alzheimer? 3 disease, Alzheimers Dis 5 (2003) 31?38 Campbell A, Becaria A, Sharman K,'Bondy SC, Chronic exposure to aluminum in drinking water increases in?ammatory parameters selectively in the brain, Neurosci Res 75 (2004) 565-72 Deloncle R, Huguet F, Fernandez B, .Quellard N, Babin Ph, Guillard O, Ultrastructure study of rat hippocampus after chronic of aluminum L?glutamate: an acceleration of the aging process, Experimental Gerontology 36 (2001) 231-44 Dewitt DA, Hurd JA, Fox N, BE, Grif?oen KJ, Ghiribi O, Savory J, Peri-nuclear clustering of mitochondria 15 triggered during aluminum maltolate induced apoptosis, Alzheimers Dis 9/2 (2006) 195-205 Ghribi O, Herman MM, Savory J, The endoplasmic reticulum 15 the main site for caspase-3 activation following aluminum-induced neurotoxicology 1n rabbit hippocampus, Neurosci Lett 324 (2002) 217-21 Ghribi O, Hermann MM, Forbes MS, DeWitt DA, SavoryJ, GDNF protects against aluminum induced apOptcsis in rabbits by upregulating Bcl- 2 and Bel-X and inhibiting mitochondrial Bax translocation, Neurobiol Dis 8 (2001) 764? 73 Ghribi O, Herman MM, Spaulding NK, Savory J, Lithium inhibits aluminum- induced apoptosis 1n rabbit hippocampus by preventing cytochrome c, Bel-2 decrease, Bax elevation and caspase-2 activation, Neurochem 82 (2002) 137- 45 Ghribi O, DeWitt DA, Forbes MS, Herman MM, Savory J, Co- involvement of mitochondria and end0plasmic reticulum in regulation of ap0ptosis: changes in cytochrome c, Bcl-2 and Bax in the hippocampus of aluminum?treated rabbits, Brain Res 903 (2001) 66-73 Ghribi O, DeWitt DA, Forbes MS, Arad A, Herman MM, Savory J, Cyclosporin A inhibits Al?induced cytochrome release from mitochondria in aged rabbits, J. 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Nehru B, Bhalla P, Reversal of an aluminum induced alteration in redox status in different regions of rat brain by administration of centr0phenoxine, Mol Cell Biochem 290 (2006) 185-91 Nehru B, Bhalla P, Garg A, Evidence for centrophenoxine as a protective drug in aluminum induced behavioral and biochemical alteration in rat brain, Mol Cell Biochem 290 (2006) 33-42 Sarin S, Julka D, Gill KD, Regional alterations in calcium homeostasis in the primate brain following chronic aluminum exposure, Mol Cell Biochem 168 (1997) 95-100 Satoh E, Okada M, Takadera T, Ohyashiki T, Glutathione depletion promotes aluminum-mediated cell death of PC12 cells, Biol Pharm Bull 28/6 (2005) 941? 946 Savory J, Rao JKS, Huang Y, Letada PR, Herman MM, Age-related hippocampal change in Bcl-2/Bax ratio,oxidative stress, redox-active iron and apoptosis associated with aluminum induced neurodegeneration: increased susceptibility with aging, Neurotoxicology 20 (1999) 805-18 Savory J, Herman MM, Ghribi O, Intracellular mechanisms underlying aluminum induced apoptosis in rabbit brain, Inorg Biochem 97 (2003) 151-4 0 Savory, J, Ghribi 0, Forbes MS, Herman MM, Aluminum and neuronal cell injury: inter-relationships between neuro?lamentous arrays and apoptosis, Inorg Biochem 87 (2001) 15-19 0 Silva VS, Goncalves PP, The inhibitory effect of aluminum on the (N ATPase activity of rat brain cortex synaptosomes, Inorg Biochem 97 (2003) 143-150 0 Silva VS, Duarte AI, Rego AC, Oliveira CR, Goncalves PP, Effect of chronic exposure of chronic dietary exposure on isoforrn expression and activity of rat ATPase, Toxicological Sciences 88/2 (2005) 485- 94 - Somova LI, Missankov A, Khan Chronic aluminum intoxication in rats: dose-dependent morphological changes, Methods Find Exp Clin Pharrnacol 19 (1997) 599-604 I C. Glial Cell Death or Impairment by Aluminum (Leading to Neuron Impairment or Death and Axon Damage and Death) 0 Aremu DA, Meshitsuka S, Some aSpects of astroglial functions and aluminum - implications for degeneraton: review, Brain Res Brain Res Rev 51/1 (2006) 193? 200 - Aremu DA, Meshitsuka S, Accumulation of aluminum by primary cultured astrocytes from aluminum amino acid complex and its ap0ptotic effect, Brain Res 1031/2 (2002) 284- 96 Fields DR, The other half of the brain, Scienti?c American (April 2004) 54-61 Guo-Ross SX, Yang EY, Walsh TJ, Bondy SC, Decrease of glial ?brillary acidic protein in rat frontal cortex following aluminum treatment, Neurochem 73 (1999) 1609-14 0 Hoke A, Neuroprotection in the peripheral nervous system, Arch Neurol 63 (2006) 1681 -5 - Nedzvetsky VS, Turzu M, Yasar A, Tikhomirov AA, Baydas G, Effects of vitamin against aluminum neurotoxicology 1n rats, Biochemistry (Moscow) 71/3 (2006) 305-11 - Theiss C, Meller K, Aluminum impairs gap junctional intercellular communication between astroglial cells in vitro, Cell Tissue Res 310 (2002) 143- 154 D. Cell Death Related to Hypoxia (Blood Flow, Heme, Gene Expression) Promoted by Aluminum 0 Atamna H, Killilea DW, Killilea AN, Ames BN, Heme deficiency may be a factor in the mitochondrial and neuronal decay of aging, Proc Nat Acad Sci USA 99/23 i (2002) 14807-12 - Bazan NG, Palacios-Pelaez R, Lukiw WJ, Hypoxia signaling to genes: signi?cance 1n Alzheimer? disease, M01 Neurobiol (2002 283-98 0 Challa VR, Lovell MA, Moody DM, Brown WR, Reboussin DM, Markesbery WR, Laser microprobe mass spectrometric study of aluminum and silicon 1n brain emboli related to cardiac surgery, Neuropathol Exp Neurol, 57/2 (1998) 140- 7 Exley C, Esiri MM, Severe cerebral congophilic angiopathy coincident with increased brain aluminum in a resident of Camelford, Cornall, UK, Neurol Neurosurg 77/7 (2006) 977-9 0 Florence A, Gauthier A, Ponsar C, Van den Bosch de Agilar P, Crichton RR, An experimental animal model of aluminum overload, Neurodegeneration 3 (1994) 315-23. (Note: Authors propose that aluminum depletion of heme may be a mechanism in brain cell death.) 0 Ganchev T, Dyandov E, Zacharieva R, Pachalieva, Velikova M, Kavaldjieva B, In?uence of aluminum on iron metabolism and some functional characteristics of in rats, Acta Physiol Pharmacol Bulg 23/1 1998) 27-31 . Garbossa G, Galvez GT, Castro ME, Nesse A, Oral administraton to rats with normal renal function. 1. Impairment of Hum Exp Toxicol 127/6 (1998) 312-7 0 Grammas P, Samary PG, Thirumangalakudi L, Thrombin and in?ammatory proteins are elevated in Alzheimer?s disease microvessels: implications for disease pathogenesis, Alzheimer?s Dis 9/1 (2006) 51-8 I Granadillo VA, Tahan JE, Salgado O, Elejalde LE, Rodriguez-Iturbe B, Romero GB, Robero RA, The in?uence of the blood levels of lead, aluminum and vanadium upon the arterial hypertension, Clin Chim Acta 233/1 -2 (1995) 47-59 0 Mailloux RJ, Appana VD, Aluminum toxicity triggers the nuclear translocation of HIF-lalpha and promotes anaerobiosis in hepatocytes, Toxicol In Vitro 21/1 (2007) 16-24 0 Mailloux RJ, Hamel R, Appana VD, Aluminum toxicity elicits a dysfunctional TCA cycle and succinate accumulation in hepatocytes, Biochem Mol Toxicol 20/4 (2006) 198-2008 0 Ono T, Goto K, Takagi S, Iwasaki S, Komatsu H, Schlorsing effect of OC-108, a novel agent for hemorrhoids, is associated with gra?nulomatous in?ammation induced by aluminum, Pharmacol Sci 99/4 (2005) 353-63 0 Rapino C, Bianchi G, Di Giulio C, Centurione L, Cacchio M, Antonucci A, Cataldi A, alpha cyctoplasmic accumulation is associated with cell death in old rat cerebral cortex exposed to intermittent hypoxia, Aging Cell 4/4 (2005) 177-85 0 Vittori D, Nesse A, Perez G, Garbossa G, Morphologic and functional alterations of cells induced by long-term ingestion of aluminum, Inorg Biochem 76/2 (1999) 113-20 0 Vittori D, Pregi N, Perez G, Garbossa G, Nesse A, The distinct functions that promote cell survival and proliferation are affected by aluminum exposure through mechanisms involving receptor, Biochim Acta 1743/ 1-2 (2005) 29-36 E. Brain Cell Death Due to Enucleation by Neuro?brillary Tangles Walton R, A longitudinal study of rats chronically exposed to aluminum at human dietary levels, Neurosci Lett 412/1 (2007) 29-33 Walton JR, Aluminum in hippocampal neurons from humans with Alzheimer?s disease, Neurotoxicology 27/3 (ZOC 6) 385-94 F. Adverse Effect of Aluminum on Connectivity, Neurotransmitters, and Eventual Neuron Death for Lack of Stimulation Colomina MT, Roig JL, Sanchez DJ, Domingo JL, In?uence of age on aluminum- induced neurobehavioral effects and morphological changes in rat brain, Neurotoxicology 23 (2002) 775-81 I Cordeiro JM, Silva VS, Oliverira CR, Goncalves PP, Aluminum?induced impairment of Ca2+ modulatory action on GABA transport in brain cortex nerve terminals, Inorg Biochem 97 (2003) 132-42 Fattoretti P, Bertoni-Freddari C, Balietti M, Giorgetti B, Solazzi M, Zatta P, Chronic aluminum administration to old rats results in increased levels of brain metal ions and enlarged hippocampal mossy ?bers, Ann Acad Sci 1019 (2004) 44-7 Forbes MS, Ghribi O, Herman MM, Savory J, Aluminum-induced dendritic pathology revisited: cytochemical and electron micrOSCOpic studies of rabbit cortical pyramidal neurons, Clin Lab Sci 32 (2002) 75-86 Jing Y, Wang Z, Song Y, Quantitative study of aluminum-induced changes in synaptic ultrastructure in rats, Synapjse 52 (2004) 292-8 Kaizer RR, Correa MC, Spanevello RM, Morsch VM, Mazzanti CM, Goncalves JF, Schetinger MR, activation and enhanced lipid peroxidation after long-term exposure to low levels of aluminum on different mouse brain regions, Inorg Biochem 99/9 (2005) 1865-70 Murayama H, Shin R-W, Higuchi J, Shibuya S, Muramoto T, Kitamoto T, Interaction of aluminum with PHF in Alzheimer?s disease neuro?brillary degeneration evidenced by desferrioxamine-assisted autoclave method, Am Pathol 155 (1999) 877-85 Pandya JD, Dave KR, Katyare SS, Effect of long-term almninum feeding on lipid/phospholipids pro?les of rat brain myelin, Lipids in Health and Disease 3/ 13 (2004) Open Access BioMed Central Platt B, Fiddler G, Riedel G, Henderson Z, Aluminum toxicity in the rat brain: histochemical and immonocytochemilcal evidence, Brain Res Bull 55 (2001) 257- 67 Sarin S, Gupta V, Gill KD, Alterations in lipid composition and neuronal injury in primates following chronic aluminum exposure, Biol Trace Elem res 5 9/ 1-2 (1997) 133-43 . Shea TB, Wheeler E, Jung C, Aluminum induces neuro?lament assembly, I cytoskeletal incorporation, and axonal transport, Mol Chem Neuropathol 32 (1997) 17-39 . Sreekumaran E, Ramakrishna T, Madhav TR, Anandh D, Prabhu BM, Sulekha S, Bindu PN, Raju TR, Loss of dendriticiconnectivity in CA1, CA2, and CA3 neurons in hippocampus in rat under aluminum toxicity: antidotal effect of pyridoxine, Brain Res Bull 59 (2003) 421-7 Stokin GB, Lillo C, Falzone TL, Brusch RG, Rockenstein E, Mount SL, Raman R, Davies P, Masliah E, Williams DS, Goldstein LSB, Axonopathy and tranSport defects early in the pathogenesis of Alzheimer?s disease, Science 307 (2005) 1282-8 Verstaeten SW, Golub MS, Keen CL, Oteiza PI, Myelin is a preferential target of aluminum-mediated oxidative damage, Arch Biochem Biophys 344 (1997) 289- 94 Walton JR, Aluminum in hippocampal neurons from humans with Alzheimer?s disease, Neurotoxicology 27/3 (2006) 385-94 Wang M, Chen -T, Ruan D-Y, Xu Y-Z, Vasporessin reverses aluminum-induced impairment of synaptic plasticity in the rat dentate gyrus in vivo, Brain Res 899 (2001) 193-200 Zatta P, Ibn-Lkhayat?Idrissi M, Zambenedetti P, Kilyen M, Kiss T, In vivo and in vitro effects of aluminum on the activity of mouse brain Brain Res Bull 59/1 (2002) 41-5 How long can China pollute for free? - MSN Money Jubak'sJournal 2,?9f200? 12. 00 AM ET How long can China pollute for free? countries is growth that?s virtually unchecked by! ant may be forced to change. One of the nation?s big iI'Idustrial advantages over other environmental laws. Here's how and when the waking BY Jiteiubak These are boom times for Shanxi province in northern country's coal in 2005 at a time when coal prices were 2005, well ahead of even the astonishing 10% growth Or maybe not. The province is home to LII-den, Yangquan and Datong, expectancy in Linfen is 10 years below the Chinese nat province closed 4,800 illegal mines in 2005 -- and the chronic water shortage and a steady loss of farmland drained aquifers. If you subtract the costs of air and water pollution from Deutsche Bank, the province's real economic growth Net growth? Almost nil Understandably, those officials have chosen to remain Page 1 of 4 i i China. The province produced 25% of the soaring. Shanxi's economy grew by 12.5% in for China?s economy as a whole. the three most poliuted cities in China. Life tional average. Unchecked coal mining -- the . drilling of illegal wells for water have createdia as it subsides into underground mine shafts and Shanxi' 5 growth rate, local officials have told is close to zero. anonymous, but of?cial numbers on the national economy confiirn the drift of their figures. The central government's most Iecent report put the cost of pollution at $64 billion in 2004 Subtract that rom the country' 3 gross domestic product and growth in 2004 was closer to That's still a growth rate that most countries in the world would love to have, but it's far short of the 10% annual growth that China reports in its headlines and frighteningly similar to the 7% rate of growth that most economists calculate as the minimum necessary to create enough jobs for the country?s growing population. It's easy to find economists outside China who are even costs of China' poilution at 8% of GDP. Some econom to this accounting, China isn growing at all. Getting it on the books more pessimistic. The World Bank puts the ists peg it as high as 10% of GDP. According On one level of course, this is all academic. No country -- certainly not the United States uses accounting like this to calculate its gross domestic product or the growth rate of its economy, although China' 5 Environmental Protection Administration is trying to implement some kind of green accounting. Polluting the air or water, releasing toxic amounts of mercury, using so much water that a river runs: dry -- these are all what economists call externalities. The costs of these externalities aren 't paid by the producers of the pollution but are passed along to third parties the general public, in most cases .. in the form of increased illness or higher death rates, and they remain external to the country?s GDP accounts. However, today's externality has a way of becoming to morrow's cost. Just ask any U.S., European or Japanese company about what it costs them to clean up their wastewater, scrub 21/9x2007 How long can China pollute for free? - MSN Money Page 2 of 4 their emissions and safely dispose of their toxic waste today. Those were once externalities -- companies used to simply dump their waste into the air, water and ground. Now disposal is part of the cost of doing business. Closing the ?externality gap' That will happen in China, too, someday. Today, however, Chinese companies have a sizable cost advantage over their rivals in the developed world because many of the environmental costs of doing business in the United States, Europe and Japan are still externalities in China. Polluting the air, water and gtbund at no co'st to the company's bottom line makes it easy to undercut the prices charged by companies that don't have a right to pollute for free. Closing the "externality gap" between China and the developed world would eiiminate one source of China's cost advantage and slow the country's economic growth rate. If we want to know how sustainable China's current growth rate of 10% per annum is, we need to look at how quickly current environmental externalities will get on the corporate books. Death by pollution There are two factors that determine the speed of that process. First, how long will it take until China's environment is at a breaking point that will force an end to polluting for free? Second, how quickly will the global economy force the Chinese economy to change its ways? The environmental figures out of China, even the official ones, are appalling. More than 400,000 of China's 1.3 billion people die from air-pollution?related illness each year, according to the Chinese Academy on Environmental Planning. About 300 million Chinese don?t have access to clean drinking water, and 400 of the country's 668 largest cities are short of water. Acid rain falls over 30% of the country. 0f the 20 most polluted cities on earth, according to the World Bank, 16 are in China. Video on MSN Money yer :i Any-- ?mun-- ?we" n-vuw \"Jr; . if?: i . .r?ha Eire. estate baton China To make a smart investment in China's complex and growing economy, you have to understand some of the key trends affecting business there. MSN Money?s Jim Jubak lays out five areas to watch. The situation is getting worse fast. By 2020, 550,000 Chinese a year are likely to die from air? pollution-related illness. Human health costs from air pollution, according to the Chinese Academy for Environmental PlanningChina's GDP, will reach 13% of GDP by 2020, if current trends continue. Power sector runs amok But I'm pretty sure that as bad as things are, they aren't bad enough to force much change yet. Oh, the central government in Beijing is convinced of the need to clean up the country's environmental act, but as always in China, what the center wants isn't necessarily what the center gets. As the saying goes, "The mountains are high, and the emperor is far away." Consider what has happened in the country's power sector. The Beijing government estimates that 20% of China's power plants are illegal and operate in clear violation of China's environmentai regulations. The state Environmental Protection Administration knows where these companies are but has been unable to shut them down. Environmental enforcement is in the hands of local officials who routinely protect big polluters because they produce jobs and taxes for the province and big payoffs for local officials. Finally, in desperation, the Beijing agency said that it wouldn?t approve new projects by four of China's top power producers unless they met environmental rules. 2/9/2007 How long can China pollute for free? - MSN Money Page 3 of 4 Are you surprised that the country didn't meet its goal of a 2% reduction in major pollutants in 2006? Instead, by office! count, pollutants climbed A looming water crisis Unfortunately, the part of the environment nearest til) crisis also presents the toughest nut to crack. China is rapidly running out of water. Industries can?t get enough. City dwellers can't get enough. Farmers can't get enough. Parts of the country look like they're headed into permanent drought as surging demand teams up with falling supply -- fromidesertification and wasteful water-diversion projects to produce scarcity no matter how much Water the clouds bring. For the past 25 years, China has been able to feed itself one of the country's greatest achievements. But the water shortage is bad enough to put this in doubt According to James Kynge in his 2006 book, "China Shakes the World," China uses seven to 20 times more water per unit of I GDP than the developed countries oI the world. All you have to do to fix that is start charging a market price for water that's high enough to produce major gains in the efficiency of water use. Simple, eh? Well, we haven?t managed to do that in the U.S., where water is still priced as if it were in inexhaustible supply. And we don?t have 400 million people on the edge of survival. For China's . rural and urban poor, and especially for its peasant farmers, a market price for water would push them over the edge. Transition takes time I Fortunately for China, the global economy may provide the push when Beijing's officials can't provide the shove. It is undoubtedly unfair that China is being asked to make the transition from externality to environmental- -income statement in just a few decades, when the developed world had centuries to make the transition. The air in London, for example, was a miasma unfit to breathe and its water a stew of deadly microbes for centuries before the government forced 'polluters to spend money to clean up their waste streams. It took a century or more to turn the Cuyahoga River where it flows through Cleveland into such a brew of chemicals that the river. would burn and the cleanup began only a few decades ago. . The world isn 't inclined to give China the luxury of its public air, water and land for centuries. The leaders in Beijing, astute as ever at grabbing the "main chance, see this as an opportunity. If the world wants to slow global warming and reduce the global emission of greenhouse gases, Beijing is happy to comply by improving its environmental practices -- as long as the world is willing to put cash into the deal. Cash incentives Beijing is working with the United Nations to set up the first carbon-trading exchange in a developing country. The exchange would trade the carbon credits;set up under the Kyoto Protocol on climate change. Under the trading system, companies that reduce greenhouse gases generate credits that they can sell to companies that are over their greenho1use-gas quota. China's industries are huge emitters of greenhouse gases, but even small investments in emission controls can yield big improvements. Carbon credits can be quite a tidy profit center. In the first nine months of 2006, developing countries generated $3 billion in carbon credits, and China accounted for about 41% of the total Video on I-ii?i?xi Honey I if; ?r ?Mam _-sa video; .Fi.ye_ways_. to. bet on China To make a smart investment in China's complex and growing 2/9/2007 How long can China pollute for free? - MSN Money Page 4 of 4 economy, you have to understand some of the key, trends affecting business there. MSN Money's Jim Jubak lays out five areas to watch. This will give many of China's companies the cash incentives they need to get started on converting environmental externalities into income statement items. And as more Chinese companies develop global brands, they'll get another push from consumers in the developed world, who increasingly want to feel good about the companies they buy from. Global standards . . . eventually But this will be just a start. And the cash it will provide to China?s companies is just a drop in the bucket. expect that local officials and local company executives will fight tooth and nail for their right to pollute for flee. Eventually, though, Chinese companies will adopt something like the global economy's standards of accounting for pollution. That will help further narrow the cost gap between China and the rest of the world, and slow China's growth rate from the current breakneck pace.The alternative is business as usual in China, with growth at all costs. Go far'enough down that road, and the costs of paying for those environmental externalities gets big enough so that even China's booming economy can't pay it. Coming Feb. 13: China?s financial window: thinking about capital as a limited resource. New developments?on past columns "State of the nation? Broke": President Bush has thrown down the gauntlet. If the Democratic majority in Congress is serious about reducing the long?term deficit created by Medicare, he said with his 2008 budget, it should apply a means test to those programs and Social Security. Under the president's plan, Social Security payouts for higher-income workers would grow more slowly than those for. lower-income workers, and wealthier Medicare recipients would pay higher premiums for their coverage. The percentage of Medicare recipients paying higher premiums would rise over time as inflation pushed more over the "wealthy" threshold. Editor's note: A new Jubakfs Journal is posted every Tuesday and Friday. Please note that lgbak?s Picks recommendations are for a 12- to 18?month time horizon. For suggestions to heip navigate the investors For picks with a truly long-term perspective, see Jubak's 50 best stocks in the world or Futui e. Fa E-mai'l Jubak at 2/9/2007 epartment of the Planet Earth 701 Street, SE - Suite 200, Washington, DC 20003 (301) 475-8366 - planetbarth?crols.com; February 8, 2007 Dear Board Members, Let's aim for March or April for a telephone board meeting. I would suggest that we focus on just three issues in 2007: 1. Global Warming at the State and Federal Level: Dave Shiah and I have mailed new packages of information to all the governors, including the executive orders by the eleven governors Signing a Kyoto Protocol. Also, we are sending information on why action is needed within ten years, using James Hansen?s analysis, and what can be done. Dave will be calling each office in the next few weeks. Here is a note he received back from South Carolina. Governor Stanford is appointing a committee to look at options for his state. I see that Jay is featuring global warming at the next Beyond Pesticides national forum in Chicago. Warming will have an big effect on agriculture and pest management. The issue of the production of ethanol using corn is a matter of concern. Burning the food supply will produce nutrition problems, and there are already riots in Mexico. 2. Genetic Modification of Wine Grapes and Yeast: Enclosed is some information from Joe on various GMO programs for wine grapes and yeast. Because President Bush has adopted several directives to make regulation of any toxin impossible (see enclosed), a petition to FDA or EPA on GMO for grapes would be a waste of time. However, getting an investigation by an Congressional committee of the FDA and EPA programs might be useful. I?ll give it a try. 3. Aluminum in Food and Drinking Water: I'm a platform speaker on February 27th at the annual Keele Conference on aluminum and silicon, this time held at Uxmal, Mexico. It is a meeting of experts from around the world. I will make the pitch that now is the time that they get inspired by the example of Dr. Herbert Needleman who began the regulatory program for lead and childhood learning disabilities. A friend produced a powerpoint for me. Enclosed is a handout. Once again, it is unlikely that our FDA petition will produce results until we have a new president. Will get back to you about possible dates for a telephone board meeting. Best regards, 201/ Erik FHOTODISC CHANGING THE RULES ON REGULATIONS WHITE HOUSE: Bush directive riiakes it harder for agencies to issue rules NEW DIRECTIVE from President George W. Bush to federal agencies adds layers of bureau- cracy to the process of issuing regulations and gives the White House greater control over agencies? own rule making. Critics say the directive, issued Jan. 18, willi slow down regulation. They say it also shifts regulatory priorities, which were set by Congress in fede:ral laws, away from protection of health and environment to economic rationales. Some industry groups praise the directive. ?It?s the ?rst truly signi?cant attempt by an Administration to hold federal bureaucrats to account and insist they act with discretion when imposing new and expensive burdens on businesses and consumers,? says William Kovacs, vice president of environment, energy, and regulatory affairs for the U.S. Chamber of Commerce. Under the new directive, agencies can regulate only when they can demonstrate to the White House Of?ce of Management Budget (OMB) that the free market is not producing the desired results of a proposed rule, such as one on health protection. To show that a new rule is warranted, agencies must identify what econo- mists call ?market failures??such as when an indus- trial sector with unfettered pollution sells its products more cheaply than it would have had it included the cost of pollution control into the price of its goods. Also, the directive requires agencies to calculate the costs and bene?ts of each of the upcoming rules they plan to issue in a calendar year. The Administration will use these numbers to set regulatory priorities. ?These cost-bene?t analyses are notoriously biased against regulation,? says Joan Claybrook, president of the activist group Public Citizen. . In addition, the directive requires each agency have a presidentially appointed ?regulatory policy of- ?eet.? The agency cannot begin work on a new rule? even one required by Congress through a law?until it gets a green light from this policy of?cer or unless the head of the agency gives approval. Under the directive, agency guidance documents must undergo the same rigorous economic cost-bene?t analysis and White House review as regulations now HOGUE 1:0 JANUARY 29. 2007 . .: . - er Rips EPA Chief as Bowing to Industry Page 1 of 3 i: 0 environment trmitour IE1 PrintThis Story E-mail This Stery I . I And to read more articles on the Environment, please visit the envrronment page. Also see below: . Mm Gore Says Bush Administration Paying Scientists to Dispute Global Warming - Go to Original Boxer Rips EPA Chief as Bowing to industry By Zachary Coile The San Francisco Chronicle subscribe Wednesday 07 February 2007 . Official says policies speed up bene?ts to the environment. I 1 Washington - California Democratic Sen'. Barbara Boxer ripped the Environmental Protection Agency's top of?cial Tuesday for rules changes that could limit the input of scienti?c advisers into issues agency decisions and reduce public access to information about toxic substances in communities. Boxer. using her clout at her second hearing as the new chairwoman of the Senate Environment and Public Works Committee, accused EPA Administrator Stephen Johnson of bending to the wishes of industry rather than protecting public health. 6 want to send a clear signal to EPA and to this administration: We are watching." she said. "No longer will EPA rollbacks quietly escape scrutiny." Johnson defended the Bush administraticgin's record on the environment, saying his agency had pursued policies aimed at cutting the costs of regulation and giving companies incentives toreduce their pollution. I I I "These decisions and actions all accelerate the pace of environmental protection," Johnson said. . . "They all deliver environmental results." . Boxer devoted the hearing to shedding light on half a dozen controversial decisions made by the EPA late last year, which she said received little scrutiny from the formerly Republican?led Congress. Among them: I i The decision to shut down or cut access to seven EPA libraries across the country. The libraries are used by scientists, agency employees and citizens looking for information'about mm public health and environmental hazards in their neighborhoods. 0 The agency in December eased the rules on industry for the reporting of their discharge of toxic chemicals. Previously, companies that released 500 pounds of chemicals were required to ?le a detailed report. Under the new rule. ?rms would ?le detailed accounts only afte'r releasing 2,000 pounds of chemicals. 2/11/2007 Boxer Rips EPA Chief as Bowing to Industry 4336th Us? Page 0 The EPA in December proposed changing its decades-old policy that asked scienti?c advisory boards to study and develop new air quality standards before the agency would announce them. The move to lessen the in?uence of the advisory boards would strengthen the hand of the agency's political appointees in setting policy. Democratic senators on the committee complained that the agency's decisions seemed designed to satisfy the requests of key industry groups. The Battery Council International. a trade group of battery manufacturers and lead smelters. sent a letter to the EPA in July urging it to revoke the ambient air quality standard for lead - which the agency said in December it is considering. The trade group also asked the EPA to expedite the decision by changing how the agency and scientists review its proposals. Boxer warned that "if the standard is revoked, there is no assurance that lead will- be monitored in air across the country. Polluters could emit dangerous levels of lead without being detected." Johnson insisted he is committed to reducing emissions of lead, which pose health risks to humans, especially children, even at low levels. In written testimony. he noted that lead concentrations in the air had fallen by 95 percent since leaded gasoline was banned but said it was too early to say whether the lead standard would be revoked. Boxer and Johnson got into a testy exchange over the EPA's closure of its libraries. Johnson called it an effort to modernize the libraries now that many people are accessing agency data and scienti?c reports on the Internet. He said the reports kept in the libraries either would be made available online or would be donated to other libraries. But Boxer read e-mails from EPA librarians that detailed the destruction of agency reports and other documents. "There's something about Americans. they don't like things being destroyed - libraries, books, movies. things like that," Boxer said. "The image of it is discomforting." "We have not been disposing of documents," insisted Johnson, who noted that the agency halted plans to close more libraries because of the outcry. I But Johnson received a little help from Republicans on the committee. Sen. James lnhofe. R- Okla.. the panel's ranking Republican, accused critics of the EPA's library plan of being "hysterical" and motivated by the desire to save a few union jobs. lnhofe asked Johnson if he knew that the EPA's libraries held titles including "Memoirs of a Geisha." "Fat Chicks Rulel: How to Survive in a Thin-Centric World." and the Dr. Seuss book. "The Lorax." Johnson smiled as each title was read, saying he was aware the EPA had those books. Boxer, annoyed by the scripted exchange with lnhofe, commented sarcastically: "I'm amazed that the administrator of the Environmental Protection Agency would know what books are in the You're a multitasker, that's for sure." It's not the first time Boxer and Johnson have clashed. The California Democrat held up Johnson's nomination to head the EPA until the agency dropped a program that paid parents to monitor the health effects of pesticides on their children. Boxer warned Johnson that he should expect to spend more time in her hearing room explaining his agency's decisions. 2/7/2007 Page I of 2 Main Identity From: "cvs" To: "Erik Jansson" Sent: Saturday. February 03. 2007 7:48 PM Subject: Fw: [pestinform] Check out this Conference in Chicago in early June Have you heard about this? i -- Please distribute widely -- Apologies for cross postings -- Changing Course 1n a Changing Climate: Solutions for health and the environment The 25th National Pesticide Forum Loyola University (Water Tower Campus), Chicago, IL June 1 2007 Visit for online registration and more details. Please join us in for Changing Course in a Changing Climate: Solutions for health and the environment, the 25th National Pesticide Forum, at Loyola University (Water Tower Campus)' 1n Chicago's Magni?cent Mile neighborhood, June 1-3, 2007. This exciting event is convened by Beyond Pesticides and co- Sponsored by the Chicago- based Safer Pest Control Project. Coming Clean 5 Pesticide Working Group (PWG) will hold its meeting on June 3rd, immediatelyfollowing the Forum (see below). Forum tochs: Global warming: consequences and the organic connection; Environmental justice; Nanotechnology; Health and environmental effects of common antibacterials; Asthma; Increased risks of pesticide mixtures; New legislative opportunities;: Passing local policies; Great Lakes/water contamination; and more. i Featured Speaker: Samuel S. Epstein, M. D. (2007 Dragon?y Award recipient), author of The Politics of Cancer, professor emeritus at the Universny of Illinois School of Public Health and chairman of the Cancer Prevention Coalition; Rolf Halden, Ph. D. ., professor at Johns Hopkins Bloomberg' School of Public Health; Tyrone Hayes, Ph. D, professor of Integrative Biology at the University of California Berkeley; Paul Hepperly, Ph. D., Rodale Institute' 5 research and training manager, Peter Orris, M. D., associate director of the Great Lakes Center for Occupational and Environmental Safety and Health of the University Of Illinois School Of Public Health and director of HS Occupational Health Service Institute and Global Toxics Policy Program; and, Jennifer Sass, Ph. D., Natural Resource Defense Council (NRDC) senior scientist and director of NRDC's scienti?c integrity project. Updated list at . beyondpesticides. org/forum. Green Rooftop/Garden Tour: The Forum will begin with an afternoon tour of the Chicago City Green Roof http: asla. html) and other community gardens. Contact jkepner@beyondpesticides. org for details. - _R_at_es: Members: $65; Non? members: $75 (includes one-year membership); Business: $175 (includes one-year membership for non-members). Forum registration includes a welcome reception with hors d'oeuvres, beer and wine, breakfast and lunch on Saturday and breakfast on Sunday, plus all panel sessions, keynotes and workshops. All food will be organic. 2/18/2007 Lifegand Living ii En ?he Aluminiu Age Saturday 24'? to Wednesdlay 28"1 February 2007 Hofei Misic?m Uxmal Yuc?tan, M?xico I ~41 ALUN. ii 1 3E Court Halt on GMO Alfalfa Shows USDA Failure Page 1 ON C. truthout?issues Also see belowgil Court Halt on GMO Alfalfa Shows USDA Failure By Carey Gillam Reuters Thursday 15 March 2007 Kansas City, Missouri - A court decision overturning US government approval for a biotech alfalfa underscores complaints made for years that the USDA is failing to adequately oversee genetically altered crops, biotech crop critics said on Tuesday. And the critics believe it sets a precedent that should prompt more stringent oversight of these controversial crops. ?It is a big deal for the court to do that. It is the ?rst time it has happened in the said Margaret Mellon. director of the Union of Concerned Scientists Food and Environment Program, which is not a party to the case. There have been concerns for years about the USDA's lack of proper oversight. lndeed, other recent court rulings have leveled criticism against US government oversight of biotech crops. "There are some serious problems there," said Mellon. "They need to be ?xed." USDA of?cials would not comment Tuesday. a day after US District Court Judge Charles Breyer of the Northern District of California issued an order on Monday that vacated USDA approval of Monsanto Co's "Roundup Ready" alfalfa. The crop. genetically altered to withstand treatments of Monsanto's Roundup herbicide, was approved in 2005. But Judge Breyer immediately halted any more seed sales and ordered that any planting must cease after March 30 after he determined that the USDA violated the law in allowing unrestricted commercial planting of the crop. The judge said the USDA should have prepared an environmental impact statement before deregulating the Roundup Ready alfalfa. Such a statement is designed to explore negative consequences that might result from a release. In the case of biotech alfalfa. a perennial livestock feed crop. several farm. environmental and consumer activists groups said there were many potential problems, including contamination of organic and conventional alfalfa supplies with the biotech version. 5i2007 Court Halt on GMO Alfalfa Shows USDA Failure .ti: *ur in Other crops, including most notably corn and rice, have already been contaminated with biotech varieties, forcing in some situations costly recalls and lost export sales. challenged them over and over to give us any scienti?c evidence that they can control the gene flow from these crops. So far they haven't been able to do that," said Andrew Kimbrell, executive director of The Center for Food Safety, which led the lawsuit against the US Agriculture Department. "This technology was put out into the environment without any idea of how to control it,? he said. "Now the agency for the ?rst time will have to come up with some sort of answers as to how you can control this and be accountable for it." Like USDA, Monsanto of?cials also declined to discuss the potential rami?cations of the ruling Tuesday, but company spokeswoman Lori Fisher said Monsanto was informing Roundup Ready alfalfa seed dealers of the court order and outlining actions they must take. "Basically, this communication informs dealers to stop sales of Roundup Ready alfalfa under court order, to secure Roundup Ready alfalfa seed not sold in inventory and to expect further instructions as the situation develops," Fisher said. Over the last decade, the USDA has approved applications for more than 70 genetically modi?ed organism (GMO) crop lines, many of which have been embraced by farmers because they are easier andlor more pro?table to grow. Sharon Bomer, a vice president at the Biotechnology Industry Organization (BIO), said her group, which represents the interests of biotechcompanies, including Monsanto, said that the safety of alfalfa and other commercialized biotech crops was not an issue. And she said the court ruling on alfalfa appeared limited. "We think this deals with only one situation," she said. Still, the oversight, primarily handled by the USDA's Animal Health and Plant Health Inspection Service, has been repeatedly criticized as lacking. An Of?ce of Inspector General audit of and its biotechnology regulatory services unit found numerous holes in oversight efforts in'a report issued in December 2005. The government is currently reviewing and rewriting the regulations for ?eld testing and for deregulation of- genetically modi?ed crops with a ?nal report on the overhaul due out in the next few months. In the meantime, Kimbrell said he was dismayed that the USDA appears to remain more focused on supporting Monsanto's commercial needs than on protecting the interests of others in agriculture. have never seen a government agency so openly and unashamedly defend the interests of a corporation and not represent the interests of farmers," he said. Go to Original Judge Halts Sale of Biotech Alfalfa Seeds By Marc Lifsher 1 3/ 1 5/2007 . Court Halt on GMO Alfalfa. Shows USDA Failure Page 3 of 4 I The Los Angeles Times . Tuesday ?13 March 2007 Activists applaud the preliminary ruling as first ban 0 genetically manipulated cr ips. A federal judge Monday overturned the Bush administration?s 2005 approval of genetically engineered alfalfa seedsl and stopped their sale for now, in what activists hailed as the ?rst ban on selling such crops. U.S. District Judge Charles R. Breyer in San Francisco found that the US. Department of Agriculture failed to adequately conduct an environmental impact study before approving them for sale. . Monday's ruling grew out of the ju'dge's decision last month that the USDA failed to take seriously concerns that genetically altered seeds could migrate to other alfalfa crops. Nothing in the National Environmental Protection Act, "the relevant regulations, or the case law support such a cavalier response," he said. The seeds, developed by agribusiness giant Monsanto Co., are now in their second season of use. Such genetically engineered seeds are grown in 200,000 of the nation's 23 million acres of alfalfa, widely grown for hay and animal grazing. The seeds were re-engineered so that alfalfa plants can resist the ill effects of another Monsanto product, a widely used herbicide known by the trade name of Roundup. As a result, some farmers say, they can get greater crop yield and better quality alfalfa. ?f . California is the nation's No. ?l alfalfa producer with about 1 million acres under cultivation. The state's 2004 harvest .was worth $853 million. Breyer's preliminary injunction came in a lawsuit brought by the San Francisco? based Center for Food Safety and otlher environmental groups. It is the ?rst ban on the genetic manipulation of traits of basic crops, such as corn. canola, soybeans and cotton, people familiar with the case con?rmed. Boosters of organic foods Called tlje judge's order a landmark in protecting the public interest. A representative of the Agriculture Department in Washington could not be reached. But some farmers, agricultural scientists and of?cials at Monsanto said the ruling, if upheld, would pose a major setback for the burgeoning U.S. biotech industry. "It?s a very signi?cant development, the next step in the pushback by the federal court system for the grossly inadequate environ mental review of genetically engineered crops." said Charles Benbrook, chief scientist of the Organic Center, a nonpro?t Rhode Island-based group that does research into the bene?ts of organic food. I The ban will remain in effect until thejudge considers lifting it or making it permanent. Monsanto is banking on increasing the acreage by convincing Breyer at an April hearing that farmers can use so-called Roundup Ready alfalfa seeds without contaminating neighboring ?elds. 3/15/2007 Court Halt on GMO Alfalfa Shows USDA Failure Page 4 of Researchers have developed "stewardship" practices that provide "a robust and responsible approach to managing the environmental questions raised by the plaintiffs in this case.? said Jerry Steiner, Monsanto's executive vice president. hope this is just a bump in the road." added Phillip Bowles, who grows Roundup Ready alfalfa on about one-tenth of his 6,000-acre alfalfa farm in Los Banos in Merced County. Without the new seeds, farmers will be forced to use herbicides that are far stronger than Roundup if they want to control weeds, Bowles said. Allen Van Deynze, a biotechnology scientist at UC Davis who's done extensive research on genetically modi?ed alfalfa. said that genetic plants could be managed effectively so that less than 1% of the seeds would contaminate other crops. "We've managed gene flow in the seed industry for 100 years now," he said. Although Van Deynze con?rmed that he received some of the ?nancial support for his research from the seed industry. he stressed that all his papers had been thoroughly reviewed by other scientists in the ?eld. Van Deynze said that he and his colleagues at UC Davis also had developed management plans for using Roundup Ready seeds that have been accepted by alfalfa growers. who use conventional and organic methods. But Jim Rickert. who raises 3,000 acres of organic and conventional alfalfa in Siskiyou and Shasta counties in Northern California, was skeptical. "l've heard this particular statement made before." he said. ?ii. a Jump to today's Truthout Features: Today's Truthout Features (In accordance with Title 17 U. S. C. Section 107, this material is distributed without pro?t to those who have expressed a prior interest in receiving the included information for research and educational purposes. tr th 0 at (has no af?liation whatsoever with the originator of this article nor is tr endorsed or sponsored by the originator.) "Go to Original" links are provided as a convenience to our readers and allow for veri?cation of authenticity. However, as originating pages are often updated by their originating host site'snthe versions posted on T0 may not match the versions our readers view when-clicking the "Go to Original" links. - - - Print This Story El 't 9? . tl' t] issues environment] labor women health voter rights] multimedia donate I contact] subscribe about us 3/ 1 5/2007 nanotechnology policy, oversight and risk analysis. The history of other voluntary regulation proposals is bleak; voluntary regulations have often been used to delay or weaken rigorous regulation and should be seen as a tactic to delay needed regulation and forestall public involvement. Nanotechnology's rapid commercialization requires focused environmental, health and safety research, meaningful and open discussion of broader societal impacts, and urgent oversight action. Unfortunately, the DuPont-ED proposal is, at best, a public relations campaign that detracts from urgent worldwide oversight priorities for nanotechnology; at worst, the initiative could result in highly reckless policy and a precedent of abdicating policy decisions to industry by those entrusted with protecting our people, communities, and land. We strongly urge all who have an interest in nanotechnology's future to reject this proposed framework. Respect for adequate worker safety, people's health, and environmental protection demands nothing less. Respectfully submitted, American Federation of Labor and Congress of Industrial Organizations Beyond Pesticides Brazilian Research Network in Nanotechnology, Society and Environment Center for Environmental Health Center for Food Safety Corporate Watch Edmonds Institute Environmental Research Foundation ETC Group Friends of the Earth Australia Friends of the Earth EurOpe Friends of the Earth United States Greenpeace Institute for Agriculture and Trade Policy International Center for Technology Assessment International Union of Food, Agricultural, Hotel, Restaurant, Catering, Tobacco and Allied Workers? Associations Natural Resources Defense Council Sciencecorps Silicon Valley Toxics Coalition Third World Network United Steelworkers of America Return to Table of Contents Page ii of 15 From: Rachel's Democracy Health News #992, Apr. 12, 2007 [Printer-friendly version] To All Interested Parties: We, the undersigned, submit this open letter to the international nanotechnology community at large. We are a coalition of public interest, non-pro?t and labor organizations that actively work on nanotechnology issues, including workplace safety, consumer health, environmental welfare, and broader societal impacts. DuPont Chemical Company (DuPont) and Environmental Defense (ED) jointly have a voluntary "risk assessment" framework for framework both in the U.S. and abroad for consideration and/or adoption by various relevant oversight organizations, including the U.S. Environmental Protection Agency (EPA). 45132007 Sticker Shock El (tricity including tat-.25, paid ay industry, in dollars Dr-r mP-ia'aett hour" Denmark XVMRETE $148.3 Darn-tn 123019 at curt-C41! ifu?re: "Line: floor space in buildings and homes was built during that period, according to the Danish Energy Authority. Torben Mikkelsen, a veterinary sur- geon and father of two, spent $105,000 last year to insulate his white single- level house and to replace sliding- glass doors and floor-to-ceiling win- dows with airtight models. Mr. Mikkelsen expects to save at least 60% on his heating bill, which last year to- taled $5,400. Mr. Mikkelsen says it doesn't bother him the project will take 30 years to pay for itself. For years, his family couldn?t stay warm enough no matter how high they turned up the heat. ?It's much more comfortable in the house now.? he says. Some local of?cials have taken con- servation even further. In 2001, Willy Eliasen, then mayorofthe townofSten- lose, some 25 miles from Copenhagen, decided to develop a new parcel ot'land. Homes on the land, he decreed, would have to be 50% more energy-ef?cient than what the building codes required. Some construction companies balked, saying the new rules would cost too much. and didn?t bid. But today the parcel has some 250 houses and apart- ments, many made of yellow brick and all with thick insulation panels. All have been sold and construction is under way for another 500 homes. in the mid-19903, the Danish govern- ment turned to energy-guzzling appli- ances, which consumers bought even when more ef?cient models were avail- able. All appliances sold in Denmark hear an efficiency label that. according to EU standards. rates the ippliance :rom for the best to for the worst. In 1995, a government tndy found that only one quarter of the fridges and Freezers sold in Denmark had ratmgs of or B. :ili-d Sayings Fx'nst intro- duced .I .- prnizrmn that ?lm] mimic-s. payable at the Emil?! t) people .vlio hiltlillt ippii- .u1u. "ill A l?l inns. in urn-hange- for [he 'lzo .mrt-spruni'wrl truth-v. ic 'ntl :ni'mrtisirie - in :it ipizliain': - .Imi .al :1 a stock a wider variety of models. ?There are many options to choose from." said Greta Andrcasen as she was shopping for a fridge at an appliance store in Copenhagen last month. Be- fore her were l0 refrigerator models? all with ratings of or better, and half with grades of or The most on? ergy-efficient models cost from $75 to $150 more than the other models. With three national rebate carn- paigns from 1999 to 2005, the Trust passed out some $20 million in subsi- dies to consumers. In 2005, 92% of the freezers and fridges sold in Denmark had A ratings. Denmark?s center-right govern- ment, elected in 2001, has adopted more of a market-oriented approach to conservation. its key target: utilities. which until recently, played mostly an advisory role. They would lend meters to households, for example, so resi- dents conld pinpoint which appliances in their homes were sucking up the most electricity. But the utilities, which distribute oil. electricity and gas, were never held accountable for whether their counseling worked or not. in 2005, the government ruled that utilities would have to meet a certain level of energy savings every year by law. Utilities can meet their targets any way they want. An electricity com- pany, for example, can persuade an in- dustrial client to introduce more eco- friendly machines into its factory. But some are skeptical the conserva- tion goals can be met. "All the easy en- ergy savings have already been imple- mented in many industries," says Ole Sundman, head of energy services at the giant state-owned energy com- pany DONG Energy. "it will be more and more dif?cult to find energy sav- ings, and more expensive.? Utilities aregetting help. Along with the new targets, the government has set up a virtual exchange whereby utili- ties that have trouble saving energy can buy credits from any company that has saved energy. Last year, Dalum Pa- pir was able to recover much of the 31 million it spent to replace electric dry- ers with those that run on natural gas It did this by s: lling energy savings to a natural-gas company that needed to meet its annual energy-savings target. The company paid Dalum $625,000. Mr. Bach. who has been working on Denmark's energy-conservarion drive for a quarter nil; century, scoffs at up;- gestions that all the feasible sauiz. r- have already been made. He neiitves companies more, wipe: iallv on homes and Cars. ?It's like tin-apple trees 111V he says. "'i?heygrow 1: vwirtng- tie avert." 11?. ONL.NE TODAY: 'let?ni .. . titular "ll [hr n: [it 'c i ll?? ., Hay WELL 101.: ilnlioeTJ 1.va Denmark?s Energy Independence Continued from Page One Danish homes and other buildings are warmed by surplus heat from power plants. Government policies have spurred developers to build homes with thick insulation, and consumers to buy energy-ef?cientappliances. Util- ities that can?t meet government en- ergy-savings guidelines can buy cred- its from companies that have invested in ef?ciencies. The result of these and other poli- ciesisthatDerunark?s energyconsump- tion?the amount of fuel it uses to heat its buildings, drive its cars and power its economy?has If . \5 held stable for more 4' -- 3 than 30 years, even 3 as the country's I. 1331"?) gross domestic a? product has. dou- - bled. according to 72/ thelnternationalEn' 1" ergy AgencgaParis .. groupthattracksen- A ergy prices and poli- cies. During the same period, en- ergy consumption in the U.S. has risen 409.3, while its GDP has quadrupled. The coverage Dane uses 6,600 kilowatt hours of electricity 3 year, compared with 13,300 for the average Ameri can. ?You can?tjust sit back and wait for market forces to do this for you,? says Peter Bach, a civil engineer who has worked as a regulator at the Danish En- ergy Authority for 26 years. Some of Denmark's approaches can?t be easily replicated elsewhere. U.S. policy makers and businesses have resisted the type of aggressive inter- vention and regulation behind Den- mark's successes, concerned about higher costs and taxes, reduced com- petitiveness and slower growth. But in Denmark, much of the coun- try?s energy sector is in the hands of nonprofit cooperatives. with residents .is shareholders. which makes it easier tle opposition from business interests. With a population of5.5 million people. Denmark also is a social welfare state that puts a higher priority on things like generous health care. free schools and guaranteed pensions than on prof - its. low taxes and individualism. Danish consumers and businesses clearly pay a price for the energy pro- grams. A Dane buying a new car must pay :1 r: aistration fee ofapproximately 105 .oflhc car?s value. plus additional taxes on tutl. Danish companies pay ltl'u nu Ire 1:01? megawatt hour of elec- tricity companies in the U.S., 24 more than in France and 19? more than .n England, .n-r'Ul'tliltr-t To Dunsk an inrlust: trade association. Den? -r::n'lt's high and its costly uni-1 Welfare sy