Rachel's Precaution Reporter #64
Wednesday, November 15, 2006

From: American Journal Of Industrial Medicine ............[This story printer-friendly]
November 14, 2006


[Rachel's introduction: A group of eminent scientists has called for worldwide reductions in exposure to toxic lead, mercury and manganese. They recommend that the U.S. cut its lead standard for children by half.]

By Philip Landrigan and others**

On 17-18 June, 2006, the Scientific Committee on Neurotoxicology and Psychophysiology and the Scientific Committee on the Toxicology of Metals of the International Commission on Occupational Health (ICOH) convened an International Workshop on "Neurotoxic Metals: Lead, Mercury, and Manganese -- From Research to Prevention (NTOXMET)" at the University of Brescia [Brescia, Italy]. Scientists and physicians from 27 nations participated.

Data were presented for each of the three metals on environmental sources, fate and distribution; human exposure; clinical, subclinical, and developmental neurotoxicity; epidemiology; risk assessment; and prospects for prevention. Ongoing and future studies were described and discussed.

For each of the metals, initial recognition of neurotoxicity occurred in the context of high-dose exposure. For example, lead poisoning was first recognized in miners, smelters, and type setters, methylmercury poisoning in inhabitants of the fishing community of Minamata, and manganese poisoning in miners and ferroalloy workers. Subsequent development of more sensitive and sophisticated analytical instruments led to the recognition of subclinical toxicity [toxicity without overt symptoms] and developmental neurotoxicity at progressively lower levels of exposure. In each case, the extent of toxicity was much greater than initially appreciated and the size of the affected population much larger. Many decades typically elapsed between the initial recognition of neurotoxicity and the initiation of programs for prevention. Early warnings were frequently ignored and even actively resisted.

The historical observation that long delays had typically elapsed before the initiation of prevention prompted extensive discussion at the Workshop about the need to develop more effective strategies. From this discussion, a series of recommendations emerged on future directions for research and prevention of the neurotoxicity of metals.

At the closing session of the International Workshop at Brescia, the following recommendations on the prevention of the Neurotoxicity of Metals were adopted by consensus:

Intensified attention must be paid to early warnings of neurotoxicity. Clinical observations or toxicological data suggesting the existence of neurotoxicity including subclinical and developmental toxicity must be taken very seriously. Such observations should prompt consideration of prudent preventive action.

All uses of lead including recycling should be reviewed in all nations and uses contributing to environmental and human exposures, such as uses in toys, paint, water pipes, building materials, solder, electronics, medications, and cosmetics ended. The transfer of these products from one country to another should also be avoided. This approach has been adopted successfully in the EU and needs to be extended worldwide.

In particular, tetraalkyllead must be eliminated without delay from the gasoline supplies of all nations. The removal of organic lead from gasoline has produced declines of greater than 90% in population mean [average] blood lead levels in industrially developed nations, and this success is now being repeated in some of the developing nations. This action represents one of the great public health triumphs of the late 20th century and needs urgently to be extended to all nations.

Current exposure standards for lead need urgently to be reduced. Current standards were established many years ago and do not reflect recent advances in scientific knowledge about toxic effects at levels of exposure below these standards. The Brescia Workshop recommends that:

* For children, the action level, which triggers community prevention efforts to reduce exposure sources, should be immediately reduced to a blood lead concentration of 50 ug/L [50 micrograms/Liter = 5 micrograms per deciLiter] in nations worldwide. This level is proposed as a temporary level that may need to be revised further downward in future years as new evidence accumulates on toxicity at still lower blood lead levels. This reduction of the blood lead action level will reduce the incidence of subclinical neurotoxicity in children as well as the delayed consequences of developmental toxicity.

* For industrial workers, the standard for lead in blood should be reduced immediately to 300 micrograms/Liter in nations worldwide. Additional consideration should be given to further reducing this standard to 200 micrograms/Liter and below in the years ahead. This reduction in exposure standard will reduce the incidence of subclinical neurotoxicity and other toxic effects during the working life and responds to new documentation presented at the Workshop that long-term lead exposure increases the risk of dementia in later life.

* For female industrial workers of reproductive age, the standard for lead in blood should be reduced immediately in nations worldwide to the lowest obtainable, preferably to 50 micrograms/Liter [= 5 micrograms/deciLiter], a level consistent with the recommended blood lead standard for children. Lead passes freely across the placenta from the maternal to the fetal circulation to enter the developing brain where it causes prenatal brain injury. This recommended reduction in maternal lead exposure will reduce the incidence of fetal neurotoxicity in the offspring of women workers.

Exposures of pregnant women and women of reproductive age to methylmercury need to be reduced to prevent subclinical fetal neurotoxicity. Evidence is strong that prenatal exposure to methylmercury causes fetal neurotoxicity. Consumption of fish with high mercury concentration by pregnant women is the primary route of exposure. More than 50% of the mercury in fish may be of industrial origin.

Strategies for reducing mercury exposure recommended by the Brescia Workshop are the following:

* All industrial uses, recycling processes, and other industrial input of mercury into the environment should be reviewed in all nations, and non-essential uses should be eliminated and releases controlled. This approach has been successfully introduced in the EU and is actively promoted by the United Nations Environmental Programme.

* Mercury emissions from coal-fired power plants need to be curtailed.

* All chloralkali plants worldwide should be urgently converted to alternative technologies that are not based on mercury, and mercury stores and wastes must be safely deposited.

* Gold mining with mercury must be controlled and enforced with safety guidelines, and alternative technology should be promoted.

* Dietary advisories should be developed as effective, culturally appropriate means to limit childbearing women's consumption of fish contaminated with methylmercury. Taking into account nutrient contents and availability, healthy diets should be recommended with fish and seafood containing minimal levels of contamination.

Exposures of pregnant women and young children to manganese need to be reduced to prevent subclinical neurotoxicity. Important new data on the neurotoxicity of manganese were presented at Brescia. In adult workers, these data suggest that manganese produces subclinical neurotoxicity at levels of exposure below those that produce parkinsonism. In children, evidence from two recent epidemiological studies suggests that exposure to manganese in early life causes subclinical developmental neurotoxicity.

The addition of organic manganese compounds to gasoline should be halted immediately in all nations. The data presented at the Brescia Workshop raise grave concerns about the likelihood that addition of manganese to gasoline could cause widespread developmental toxicity similar to that caused by the worldwide addition of tetraalkyllead to gasoline. In light of this information, it would be extremely unwise to add manganese to gasoline.

Exposure standards for manganese need to be reconsidered. The drinking water standards for manganese in many countries are not based on health concerns, and those that are, do not protect against developmental neurotoxicity resulting from exposures in utero and in early postnatal life. The current occupational exposure standard may not protect workers against subclinical neurotoxicity. The value for air manganese concentration in inhalable/total dust of 100 mg/m3 should be adopted to protect the workers from prolonged exposure and consequent long-term effects.

Economic impacts of the neurotoxicity caused by metals must be considered. The costs of toxicity may be far greater than the costs of pollution control. The major contributor to these costs is damage to the developing central nervous system. Such injury can result in lifelong loss of intelligence and motor capacities, permanent psychological disturbances, and disruption of behavior. These effects can produce reduction of economic productivity, and when this reduction occurs widely across a society, the resulting economic impacts are great. The costs of pollution recur annually in each exposed birth cohort, adults, and elderly while the costs of control are one-time costs. Need is great for continuing research into the neurotoxicity of metals. Recent studies of neurotoxicology of each of the metals discussed at the Brescia Workshop inform us that we can anticipate harmful effects of increasingly lower levels of exposure to metals, previously f. considered safe as larger studies using sensitive measures of exposure and outcome, and better statistical techniques are conducted.

a. For lead, mercury, and manganese, much remains to be learned about the delayed consequences of developmental toxicity and the prolonged exposure to low levels in the adults, as possible causes of neurodegeneration. This research is critical to guide both future research in metals as paradigms of neurotoxic pollutants and targeted programs of prevention.

b. Prospective cohort studies from birth are needed, parallel to study on adults and elderly with a retrospective assessment of exposure.

c. Neurotoxicological research, including research on developmental neurotoxicology, is needed on metals not considered at the Brescia Workshop -- arsenic and aluminum, in particular, and on interactions with essential elements, pesticides, and persistent organic pollutants.

d. Research is needed into genetic and other factors that contribute to susceptibility to metal toxicity.

e. Research is needed into various determinants of the rearing environment, including the social setting, that can modify the exposure indicators to neurotoxic metals


Philip Landrigan is a member of the ICOH Scientific Committees on Toxicology of Metals and Neurotoxicology and Psychophysiology.

Monica Nordberg is the Chair of the ICOH Scientific Committee on Toxicology of Metals.

Roberto Lucchini is the Chair of the ICOH Scientific Committee on Neurotoxicology and Psychophysiology and member of the Scientific Committee on Toxicology of Metals.

Gunnar Nordberg was the past Chair of the ICOH Scientific Committee on Toxicology of Metals.

Philippe Grandjean is a member of the ICOH Scientific Committees on Toxicology of Metals and Neurotoxicology and Psychophysiology.

Anders Iregren was the past Chair of the ICOH Scientific Committee on Neurotoxicology and Psychophysiology.

Lorenzo Alessio is a member of the ICOH Scientific Committee on Toxicology of Metals.


** Statement authored by Philip Landrigam,[1] Monica Nordberg,[2] Roberto Lucchini,[3] Gunnar Nordberg,[4] Philippe Grandjean,[5] Anders Iregren,[6] and Lorenzo Alessio[1]

[1] Department of Community and Preventive Medicine, Mount Sinai School of Medicine, One Gustave L. Levy Place, New York

[2] Institute of Environmental Medicine, Karolinska Institutet, Stockholm, Sweden

[3] University of Brescia, Institute of Occupational Health, Ple Spedali Civili, Brescia BS, Italy

[4] Department of Public Health and Clinical Medicine, Umea University,Environmental Med- icine, Umea, Sweden

[5] Institute of Public Health, University of Southern Denmark, Winslowparken, Odense, Denmark

[6] National Institute for Working Life, Chemical Risk Assessment, Stockholm, Sweden

* Correspondence to: Philip Landrigan, Department of Community and Preventive Medicine, Mount Sinai School of Medicine, One Gustave L. Levy Place, Box 1057, NewYork 10029-6574. E-mail: phil.landrigan@mssm.edu

The views presented in the Declaration are the consensus reached by the participants in the workshop and do not necessarily reflect the decisions or stated policies of the affiliation organizations.


From: Daily Telegraph (UK) ...............................[This story printer-friendly]
November 9, 2006


[Rachel's introduction: Scientists from Holland and the U.S. have identified 202 industrial chemicals with the potential to damage the human brain and these are likely to be the "tip of a very large iceberg," they say]

By John von Radowitz

Millions of children worldwide may have suffered brain damage as a direct result of industrial pollution, scientists say.

An explosive report talks of a "silent pandemic" of neurodevelopmental disorders caused by toxic chemicals spilling into the environment.

They include conditions such as autism, attention deficit disorder, mental retardation and cerebral palsy. All are common and can result in lifelong disability, but their causes are largely unknown.

The scientists, from Holland and the US, identified 202 industrial chemicals with the potential to damage the human brain, and said they were likely to be the "tip of a very large iceberg". More than 1,000 chemicals are known to be neurotoxic in animals, and are also likely to be harmful to humans.

The researchers made an urgent call for much tighter worldwide controls on chemicals, and a "precautionary approach" to testing. Dr Philippe Grandjean, from the Department of Environmental Medicine at the University of Southern Denmark in Winslowparken, one of the study's two authors, said: "The human brain is a precious and vulnerable organ.

"And because optimal brain function depends on the integrity of the organ, even limited damage may have serious consequences. Even if substantial documentation on their toxicity is available, most chemicals are not regulated to protect the developing brain. Only a few substances, such as lead and mercury, are controlled with the purpose of protecting children.

"The 200 other chemicals that are known to be toxic to the human brain are not regulated to prevent adverse effects on the foetus or a small child." Grandjean and co-author Professor Philip Landrigan, from the Mount Sinai School of Medicine in New York, trawled a range of scientific data sources to compile their evidence.

Five substances for which sufficient toxicity evidence exist were examined in detail -- lead, methylmercury, arsenic, polychlorinated biphenyls (PCBs) and toluene. In each case, the dangers came to light the same way.

First, there was a recognition of high dosage toxicity in adults, and records of isolated episodes of poisoning among children. This was followed by a growing body of epidemiological evidence that lower levels of exposure in children led to neurobehavioral defects.

Pinning down the effects of industrial chemical pollution is extremely difficult because they may not produce symptoms for several years or even decades, said the scientists. This was why the pandemic is "silent". The damage caused by individual toxic chemicals is not obviously apparent in available health statistics.

But the extent of the sub-clinical risk to large populations is illustrated by the legacy of lead. Virtually all children born in industrialised countries between 1960 and 1980 must have been exposed to lead from petrol, said the researchers. Based on what is known about the toxic effects of lead, this may have reduced exceptional IQ scores of above 130 by more than half, and increased the number of scores less than 70.

Other results of lead exposure included shortened attention span, slowed motor coordination and heightened aggressiveness. In later life, early damage from lead can increase the risk of Parkinson's and other neurodegenerative diseases.

Today, it is estimated that lead poisoning in children costs the US economy $A55 billion each year. One in six children is thought to have some kind of developmental disability, usually involving the nervous system.

Developing brains are much more susceptible to toxic chemicals than those of adults, pointed out the scientists. Interference with complex changes taking place in the developing brain can have permanent consequences. And research had shown that this vulnerable period lasts from the foetal stage of life through infancy and childhood to adolescence.

Writing in the online version of The Lancet medical journal, the scientists conclude: "The combined evidence suggests that neurodevelopmental disorders caused by industrial chemicals has created a silent pandemic in modern society.

"Although these chemicals might have caused impaired brain development to millions of children worldwide, the profound effects of such a pandemic are not apparent from available health statistics. Additionally... only a few chemical causes have been recognised, so the full effects of our industrial activities could be substantially greater than recognised at present."

In the EU, 100,000 chemicals were registered for commercial use in 1981, and in the US, 80,000 are registered. Yet fewer than half had been subjected to even token laboratory testing, said the report, and in 80 per cent of cases there was no information about potential danger to children.

Although new chemicals went through more rigorous testing, access to the data could be restricted for commercial reasons. In the EU, a new testing program called Reach is planned under proposed legislation that will enforce tighter controls.

But the scientists said that even this does not go far enough, since it fails to emphasise the importance of testing chemicals for developmental neurotoxicity. "Toxicity testing protocols for chemicals need to be expanded to include examination of neurobehavioral functions," they said.

There was a mixed reaction to the research from other experts.

Professor Mark Hanson, director of developmental origins of health and disease at Southampton University, said: "The authors have put their finger on something which is important and which will not go away. The review, in a way, is timely because it will stir up debate and hopefully generate more research in this area. There is no need to panic, but we can't ignore this possible problem."

Professor Alan Boobis, from the section of experimental medicine and toxicology at Imperial College London, said: "The authors of this review have raised an issue of significant concern, but some of the evidence in support of the conclusions lacks rigour. This is a risk management issue. In implementing the precautionary principle, it is important to take into account all relevant information and not just the potential harm that might result from inaction."

Professor Nigel Brown, head of the faculty of medicine and biomedical sciences at the University of London, criticised the report, saying the authors "verge on scaremongering". He said: "From their assertions, the authors conclude that the combined evidence suggests that neurodevelopmental disorders caused by industrial chemicals has created a silent pandemic in modern society. This is a gross overstatement.

"It is possible that there is a problem. We should be aware of this and we should study the problem, but there is currently not a shred of evidence of a pandemic."

Copyright 2006 News Limited


From: American Legislative Exchange Council ..............[This story printer-friendly]
October 12, 2006


[Rachel's introduction: The chemical industry is conducting a worldwide campaign opposing the precautionary principle. Here is one of the industry's most recent strategy papers.]


The "precautionary principle" is a term invented by environmental alarmists to justify their opposition to technological progress. It essentially states that one must conclusively "prove" that a proposed action or advancement poses no risk of human or environmental harm before being deemed lawful. This asserted burden of proof is deliberately worded to be a very difficult standard to attain. It is impossible to "prove" that a hypothetical result, no matter how far- fetched, absolutely cannot occur (i.e., one cannot prove a negative).

The practical effect of the precautionary principle is to ban almost anything that is not "natural." It prays on irrational fears regarding technology rather than relying on empirical scientific research. An example of the stifling effect of the precautionary principle can be found regarding genetically improved crops. For three decades biotechnology, operating under stringent government regulatory scrutiny, has produced greater yields, higher nutrition, and crops requiring ever-decreasing amounts of pesticides, with not a single person ever experiencing any adverse health effects. Nevertheless, environmental activists operating under the precautionary principle continue to assert that genetically enhanced crops should be banned because such an extensive record of human and environmental success does not constitute "proof" that genetically enhanced crops pose no human health risks. All we have seen, precautionary principle advocates argue, is anecdotal evidence that perhaps no harm has yet occurred.

One need not have an overactive imagination to see the stifling, if not destructive, effect the precautionary principle can have on scientific progress and our standard of living. There is little good that can be accomplished, and much evil that can result, from abandoning our current EPA and FDA regulatory procedures in favor of a "precautionary principle" that, if adopted 10,000 years ago, would have us still living in the Stone Age.

Talking Points:

* Current EPA and FDA rules, regulations and procedures already rigorously ensure environmental health and consumer safety. There is no need to abandon a system that encourages advances in human welfare for an overly alarmist agenda that will stifle scientific and societal progress.

* The precautionary principle itself forbids implementation of the precautionary principle: proponents have failed to conclusively "prove" that the adoption of the precautionary principle will not cause more societal harm that good.

* Application of the precautionary principle 10,000 years ago would have kept us in the Stone Age, as there was no "proof" that mining, using, and disposing of bronze, iron, etc., would not cause environmental or human health harm. Application of the precautionary principle 100 years ago would have banned automobiles, air travel, electricity, and other modern essentials as well. Application of the precautionary principle today will seem just as ridiculous and progress-stifling to our children's children 100 years from now.

* Application of the precautionary principle to biotechnology -- as activists frequently seek -- would have negated tremendous recent gains in global crop yields and nutrition, and would have negated dramatic recent reductions in the need for pesticides.

* Application of the precautionary principle to biotechnology -- as activists frequently seek -- would have negated numerous life- saving medical advances.

* The precautionary principle will outlaw many of the scientific advancements that have come to define modern society.

* From an economic standpoint, studies show that application of the precautionary principle in Europe has the effect of a 15 percent tax on new capital investment.

Additional Sources:

Guldberg, H., "Challenging the Precautionary Principle," Spiked Online, July 1, 2003.

Milloy, S., "U.S. Should Not Import European Laws," November 17, 2005.

"Precautionary Principle," Competitive Enterprise Institute.


From: American Legislative Exchange Council ..............[This story printer-friendly]
October 28, 2006


[Rachel's introduction: The chemical industry wants to halt a trend sweeping the nation that is reducing children's exposure to chemical pesticides in schools. Here is some of the industry's reasoning.]


Anti-chemical activists are pushing for bills to eliminate or drastically reduce the use of pesticides in schools. Some measures attempt to completely ban pesticides in schools, others attempt to greatly reduce pesticides in schools, while others mandate onerous paperwork requirements that discourage pesticide use.

The bills are unnecessary because the U.S. Environmental Protection Agency already requires extensive pesticide testing and conducts risk assessments on various subpopulations, including children, to insure that no sensitive individuals are at risk.

Additionally, the Food Quality Protection Act now requires that manufacturers of pesticides specifically consider the possibility of sensitivity to infants and children from exposure, which often requires an extra 'safety protection factor' for use.

Exposure levels to humans from pesticide use are required to be at least 100 times (required by law and sometimes this increases to 300 or even a 1000 times) below the no-observed adverse effect level in the most sensitive species, using the most sensitive toxicological endpoint. Thus, there is inherent conservatism in the permissible exposure levels established for safe use by humans.

Pesticide restrictions in schools do more harm than good by failing to balance the virtually nonexistent pesticide risks against the very real harm done to children by allowing insects and rodents to thrive, resulting in increased allergy and disease problems.

Talking Points:

* The Environmental Protection Agency rigorously tests all commercial pesticides to ensure that children will not be harmed by pesticide exposure.

* EPA errs on the side of extreme caution in its exposure assumptions, resulting in maximum exposure levels that are typically tens, hundreds, of even thousands of times less than what would be necessary for any plausible health risk to exist.

* Pesticides play a vital role in protecting our children in school. This is especially true considering that most schools provide on-site lunch services that are a magnet for ants, roaches, rats and other disease-spreading pests.

* So-called biological controls -- such as introducing spiders to pray on cockroaches -- are far less effective than safe pesticide treatments and introduce their own set of potential health problems.

* Cockroaches are among the most prevalent child allergens and sources of asthma attacks, with 20 percent of all children being allergic to cockroaches. Without proper pest control, cockroach feces and decomposing cockroach bodies trigger severe allergy and asthma episodes in homes and schools.

Additional Sources:

Assessing Health Risks from Pesticides, U.S. Environmental Protection Agency.

Logomasini, A., "State Legislatures Face Anti-Pesticide Bills," Environment & Climate News, August 1, 2004

Milloy, S., "Pesticides Not a Threat to Students," August 9, 2005

Milloy, S., "Unwarranted Warning," April 21, 2000

Taylor, J., "Pesticide bans put children at risk from roaches, rodents," Environment & Climate News, July 1, 2002


Rachel's Precaution Reporter offers news, views and practical examples of the Precautionary Principle, or Foresight Principle, in action. The Precautionary Principle is a modern way of making decisions, to minimize harm. Rachel's Precaution Reporter tries to answer such questions as, Why do we need the precautionary principle? Who is using precaution? Who is opposing precaution?

We often include attacks on the precautionary principle because we believe it is essential for advocates of precaution to know what their adversaries are saying, just as abolitionists in 1830 needed to know the arguments used by slaveholders.

Rachel's Precaution Reporter is published as often as necessary to provide readers with up-to-date coverage of the subject.

As you come across stories that illustrate the precautionary principle -- or the need for the precautionary principle -- please Email them to us at rpr@rachel.org.

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