Research on Multiple Chemical Sensitivity (MCS)

Compiled by

Professor Anne C. Steinemann and Amy L. Davis

University of Washington

This document lists scientific citations for peer-reviewed journal articles that support a physiological basis for MCS:

1. Abdel-Rahman A., Shetty A.K., Abou-Donia M.B. 2002. Disruption of the blood-brain barrier and neuronal cell death in cingulate cortex, dentate gyrus, thalamus, and hypothalamus in a rat model of Gulf-War syndrome. Neurobiology of Disease 10(3): 306-26.
2. Abel-Rahman A., Abou-Donia S., El-Masry E., Shetty A., Abou-Donia M. 2004. Stress and combined exposure to low doses of pyridostigmine bromide, DEET, and permethrin produce neurochemical and neuropathological alteration in cerebral cortex, hippocampus, and cerebellum. Journal of Toxicology and Environmental Health Part A 67(2): 163-92.
3. Abdel-Rahman A., Dechkovskaia A.M., Goldstein L.B., Bullman S.H., Khan W., El-Masry E.M., Abou-Donia M.B. 2004. Neurological deficits induced by malathion, DEET, and permethrin, alone or in combination in adult rats. Journal of Toxicology and Environmental Health Part A 67(4): 331-56.
4. Abou-Donia M.B 2003. Organophosphorus ester-induced chronic neurotoxicity. Archives of Environmental Health 58(8): 484-97.
5. Abou-Donia M.B., Wilmarth K.R., Abdel-Rahman A.A., Jenseen K.F., Oehme F.W., Kurt T.L. 1996. Increased neurotoxicity following concurrent exposure to pyridostigmine bromide, DEET, and chlorpyrifos. Fundamentals of Applied Toxicology 34(2): 201-22.
6. Abou-Donia M.B., Dechkovskaia A.M., Goldstein L.B., Shah D.U., Bullman S.L., Khan W.A. July 2002. Uranyl acetate-induced sensorimotor deficit and increased nitric oxide generation in the central nervous system in rats. Pharmacology, Biochemistry, and Behavior 72(4): 881-90.
7. Abou-Donia M.B., Dechkovskaia A.M., Goldstein B., Abdel-Rahman A., Bullman S.L., Khan W.A. 2004. Co-exposure to pyridostigmine bromide, DEET, and/or permethrin causes sensorimotor deficit and alterations in brain acetylcholinesterase activity. Pharmacology, Biochemistry, and Behavior 77(2): 253-62.
8. Abu-Qare A.W., Abou-Donia M.B. 2001. Combined exposure to sarin pyridostigmine bromide increased levels of rat urinary 3-nitrotyrosine and 8-hydroxy-2’deoxyguanosine, biomarkers of oxidative stress. Toxicology Letters 123(1): 51-58.
9. Abu-Qare A.W., Abou-Donia M.B. 2001. Biomarkers of apoptosis: release of cytochrome c, activation of caspase-3, induction of 8-hydroxy-2′-deoxyguanosine, increased 3-nitrotyrosine, and alteration of p53 gene. Journal of Toxicology and Environmental Health Part B, Critical Reviews 4(3): 313-32.
10. Abu-Qare A.W., Abou-Donia M.B. 2008. In vitro metabolism and interactions of pyridostigmine bromide, N,N-diethyl-m-toluamide, and permethrin in human plasma and liver microsomal enzymes. Xenobiotica 38(3): 294-313.
11. Anderson R.C., Anderson J.H. 1999. Sensory irritation and multiple chemical sensitivity. Toxicology and Industrial Health 15(3-4): 339-45.
12. Ashford N.A. 1999. Low-level chemical sensitivity: implications for research and social policy. Toxicology and Industrial Health 15(3-4): 421-47.
13. Baldwin C.M. and Bell I.R. 1998. Increased cardiopulmonary disease risk in a community-based sample with chemical odor intolerance: implications for women’s health and health-care utilization. Archives of Environmental Health 1998 53(5): 347-53.
14. Baldwin C.M., Bell I.R., O’Rourke M.K. 1999. Odor sensitivity and respiratory complaint profiles in a community-based sample with asthma, hay fever, and chemical odor intolerance. Toxicology and Industrial Health 15(3-4): 403-9.
15. Bascom R., Meggs W.J., Framptom M., Hudnell K., Kilburn K., Kobal G., Medinsky M., Rea W. 1997. Neurogenic inflammation: with additional discussion of central and perceptual integration of nonneurogenic inflammation. Environmental Health Perspective 105 (Suppl. 2): 531-37.
16. Bell I.R., Miller C.S., and Schwartz G.E. 1992. An olfactory-limbic model of multiple chemical sensitivity syndrome: possible relationships to kindling and affective spectrum disorders. Biological Psychiatry 32(3): 218-42.
17. Bell I.R., Warg-Damiani L., Baldwin C.M., Walsh M.E., Schwartz G.E. 1998. Self-reported chemical sensitivity and wartime chemical exposures in Gulf War veterans with and without decreased global health ratings. Military Medicine 163(11): 725-32.
18. Bell I.R., Schwartz G.E., Peterson J.M. and Amend D. 1993. Self-reported illness from chemical odors in young adults without clinical syndromes or occupational exposures. Archives of Environmental Health. 48(1): 6-13.
19. Bell I.R., Schwartz G.E., Baldwin C.M., Hardin E.E. 1996. Neural sensitization and physiological markers in multiple chemical sensitivity. Regulatory Toxicology and Pharmacology 24(1), pt. 2: S39-S47.
20. Bell I.R., Baldwin C.M., Schwartz G.E.R. 2001. Sensitization studies in chemically intolerant individuals: implications for individual difference research. Annals of the New York Academy of Sciences 933:38-47.
21. Brandt-Rauf P.W., Andrews L.R., Schwarz-Miller J. 1991. Sick-hospital syndrome. Journal of Occupational Medicine 33(6): 737-39.
22. Bronstein A.C. 1995. Multiple chemical sensitivities—new paradigm needed. Journal of Toxicology: Clinical Toxicology 33(2): 93-94.
23. Brooks S.M., Weiss M.A., Bernstein I.L. 1985. Reactive airways dysfunction syndrome. Case reports of persistent airways hyperreactivity following high-level irritant exposures. Journal of Occupational Medicine 27(7): 473-76.
24. Brown-DeGagne A.M., McGlone J. 1999. Multiple chemical sensitivity: a test of the olfactory-limbic model. Journal of Occupational and Environmental Medicine 41(5): 366-77.
25. Buchwald D., Garrity D. 1994. Comparison of patients with chronic fatigue syndrome, fibromyalgia, and multiple chemical sensitivities. Archives of Internal Medicine 154(18): 2049-53.
26. Caress S.M., Steinemann A.C. 2003. A review of a two-phase population study of multiple chemical sensitivities. Environmental Health Perspectives 111(12): 1490-97.
27. Caress S.M., Steinemann A.C. 2004. Prevalence of multiple chemical sensitivities: A population-based study in the southeastern United States. American Journal of Public Health 94(5): 746-47.
28. Caress S.M., Steinemann A.C. 2009. Prevalence of fragrance sensitivity in the American population. Journal of Environmental Health 71(7): 46-50.
29. Caress S.M., Steinemann A.C. 2009. Asthma and chemical hypersensitivity: prevalence, etiology, and age of onset. Toxicology and Industrial Health 25(1): 71-78.
30. Caress S.M., Steinemann A.C. 2004. A national population study of the prevalence of multiple chemical sensitivity. Archives of Environmental Health 59(6): 300-305.
31. Caress S.M., Steinemann A.C. 2005. National prevalence of asthma and chemical hypersensitivity: an examination of potential overlap. Journal of Occupational and Environmental Medicine 47(5): 518-22.
32. Caress S.M., Steinemann A.C., Waddick C. 2002. Symptomatology and etiology of multiple chemical sensitivities in the southeastern United States. Archives of Environmental Health 57(5): 429-36.
33. Davidoff A.L., Keyl P.M., Meggs W.J. 1998. Development of multiple chemical sensitivities in laborers after acute gasoline fume exposure in an underground tunneling operation. Archives of Environmental Health 53(3):183-89.
34. DeRosa C.T., Hicks H.E., Ashizawa A.E., Pohl H.R., Mumtaz M.M. 2006. A regional approach to assess the impact of living in a chemical world. Annals of the New York Academy of Sciences 1076:829-38. Den ganzen Beitrag lesen…

Ontario, Ministry of the Environment, Press Release:

The ban protects Ontario families and children from the unnecessary risks of cosmetic pesticides by only allowing the use of certain lower-risk pesticides for controlling weeds and pests in lawns and gardens.

The ban prohibits the sale and use of pesticides for cosmetic purposes on lawns, gardens, parks and school yards, and includes many herbicides, fungicides and insecticides. Over 250 products will be banned for sale and more than 80 pesticide ingredients will be banned for cosmetic uses.

There are exceptions for public health or safety reasons such as fighting West Nile Virus, killing stinging insects like wasps, or controlling poison ivy and other plants poisonous to the touch. Other exceptions include agriculture and forestry.

The ban takes the place of existing municipal pesticide bylaws, establishing one clear set of easy-to-understand rules, and providing certainty for businesses operating in different areas of the province.

John Gerretsen, Minister of the Environment:
“We have fulfilled our commitment to ban the sale and use of cosmetic pesticides in Ontario. I’m proud to say that, when the ban takes effect on Earth Day, we will have eliminated this unnecessary risk to our environment, our families, and especially our children.”

QUICK FACTS
Ontario’s pesticide rules are outlined in the Pesticides Act and Ontario Regulation 63/09.
According to the Organic Landscape Alliance, chemical-dependent lawns are highly susceptible to pests and diseases, whereas a healthy lawn can survive several weeks in a dormant state, is less likely to be damaged by pests and is less affected by drought, temperature extremes and general wear and tear.

LEARN MORE
What are the regulatory requirements for retailers, the landscape industry and others?  What are the rules for public health or safety, agriculture, forestry and golf courses?
Get some tips on caring for lawns and gardens without the use of harsh chemicals at the Ministry of the Environment’s web site above.

Reference:
Ontario, Ministry of the Environment, Press Release, 250+ PESTICIDES BANNED FOR COSMETIC USES, March 4, 2009

Pesticide exposure found to increase risk of Parkinson’s disease

Study finds exposure may have occurred years before symptoms appear. The fertile soil of California’s Central Valley has long made it famous as one of the nation’s prime crop-growing regions. But it’s not just the soil that allows for such productivity. Crops like potatoes, dry beans and tomatoes have long been protected from bugs and weeds by the fungicide maneb and the herbicide paraquat.

Scientists know that in animal models and cell cultures, such pesticides trigger a neurodegenerative process that leads to Parkinson’s disease. Now, researchers at UCLA provide the first evidence for a similar process in humans.

In a new epidemiological study of Central Valley residents who have been diagnosed with Parkinson’s disease, researchers found that years of exposure to the combination of these two pesticides increased the risk of Parkinson’s by 75 percent. Further, for people 60 years old or younger diagnosed with Parkinson’s, earlier exposure had increased their risk for the disease by as much as four- to six-fold.

Reporting in the April 15 issue of the American Journal of Epidemiology, Beate Ritz, professor of epidemiology at the UCLA School of Public Health, and Sadie Costello, a former doctoral student at UCLA who is now at the University of California, Berkeley, found that Central Valley residents who lived within 500 meters of fields sprayed between 1974 and 1999 had a 75-percent increased risk for Parkinson’s.

In addition, people who were diagnosed with Parkinson’s at age 60 or younger were found to have been at much higher risk because they had been exposed to maneb, paraquat or both in combination between 1974 and 1989, years when they would have been children, teens or young adults.

The researchers enrolled 368 longtime residents diagnosed with Parkinson’s and 341 others as a control group.

Parkinson’s disease is a degenerative disorder of the central nervous system that often impairs motor skills, speech and other functions. It has been reported to occur at high rates among farmers and in rural populations, contributing to the hypothesis that agricultural pesticides may be partially responsible.

Until now, however, data on human exposure has been unavailable, largely because it has been too hard to measure an individual’s environmental exposure to any specific pesticide.

“Because pesticides applied from the air or ground may drift from their intended treatment sites – with measurable concentrations subsequently detected in the air, in plants and in animals up to several hundred meters from application sites -  accurate methods of estimating environmental exposures in rural communities have long been sorely needed,” said Ritz, the study’s senior author and vice chair of the School of Public Health’s epidemiology department.

So Ritz, Costello and colleague Myles Cockburn from the University of Southern California, developed a geographic information system–based tool that estimated human exposure to pesticides applied to agricultural crops. This GIS tool combined land-use maps and pesticide-use reporting data from the state of California. Each pesticide-use record includes the name of the pesticide’s active ingredient, the amount applied, the crop, the acreage of the field, the application method and the date of application.

Research subjects were recruited between 1998 to 2007; telephone interviews were conducted to obtain their demographic and exposure information. Detailed residential history forms were mailed to subjects in advance of their interviews and were reviewed in person or over the phone. The researchers recorded and added lifetime residential histories and estimated ambient exposures into the system for all historical addresses at which participants had resided between 1974 and 1999, the period covered by the pesticide-use data.

“The results confirmed two previous observations from animal studies,” Ritz said. “One, that exposure to multiple chemicals may increase the effect of each chemical. That’s important, since humans are often exposed to more than one pesticide in the environment. And second, that the timing of exposure is also important.”

Ritz noted that this is the first epidemiological study to provide strong evidence that maneb and paraquat act synergistically to become neurotoxic and strongly increase the risk of Parkinson’s disease in humans.

Of particular concern, Ritz said, and consistent with other theories regarding the progression of Parkinson’s pathology, is that the data “suggests that the critical window of exposure to toxicants may have occurred years before the onset of motor symptoms when a diagnosis of Parkinson’s is made.”

In addition to Ritz and first author Costello, study authors included Jeff Bronstein, UCLA professor of neurology, and Xinbo Zhang of USC. The authors declare no conflicts of interest.

The research was supported by the National Institute of Environmental Health Science, the National Institute of Neurological Disorders and Stroke, and the Department of Defense Prostate Cancer Research Program. In addition, initial pilot funding was provided by the American Parkinson Disease Association.

The UCLA School of Public Health is dedicated to enhancing the public’s health by conducting innovative research, training future leaders and health professionals, translating research into policy and practice, and serving local, national and international communities.

–

UCLA, Press Release, Mark Wheeler, Pesticide exposure found to increase risk of Parkinson’s disease, 4/20/2009

Nanoparticles in cosmetics/personal care products may have adverse environmental effects

SALT LAKE CITY, March 26, 2009 – Using aquatic microbes as their “canary-in-a-cage,” scientists from Ohio today reported that nanoparticles now being added to cosmetics, sunscreens, and hundreds of other personal care products may be harmful to the environment.

Their report was part of symposia that included almost two dozen papers at the 237th National Meeting of the American Chemical Society where scientists grappled to understand the environmental and human health effects of nanotechnology. Hundreds of products utilizing these microscopic particles ”1/5,000th the diameter of a human hair” already are on the market. With many more poised for debut, scientists are seeking to avoid unwanted health and environmental effects in advance.

The study by Cyndee Gruden, Ph.D. and Olga Mileyeva-Biebesheimer focused on nano-titanium dioxide (nano-TiO2) particles found in cosmetics, sunscreens, and other personal care products. The particles are added to those products for their highly beneficial effects in blocking ultraviolet light in sunlight. Excess exposure can cause premature aging of the skin and skin cancer.

Gruden, who is with the University of Toledo, explained that the particles are washed down the drain in homes as people bathe and end up in municipal sewage treatment plants. From there, they can enter lakes, rivers, and other water sources where microorganisms serve essential roles in maintaining a healthy environment.

“When they enter a lake, what happens?” Gruden asked. “Would they enter an organism or bind to it? Maybe they kill it” or have nothing to do with it at all. These are important questions for determining the effects that nanoparticles may have on the environment. Right now, we’re not really sure of the answers.”

Gruden studied survival of Escherichia coli (E. coli) bacteria when exposed in laboratory cultures to various amounts of nano-TiO2. She found surprisingly large reductions in survival in samples exposed to small concentrations of the nanoparticles for less than an hour. “How fast the impact was surprised me,” she said. The findings open the door to future research, including studies to determine whether the same effects occur in the natural environment.

Gruden’s method for pinpointing damage from nanoparticles uses fluorescence to identify when the cell membrane in microbes undergo damage. When membranes – a crucial part of the microbe – are damaged, the cells emit a faint red glow. “Methods based upon fluorescence allow us to obtain results faster, maybe with greater sensitivity,” she said, adding that this approach could speed scientific efforts to understand the threshold at which nanoparticles become toxic to microbes.

In a second study on nanotoxicity at the ACS National Meeting, scientists from Utah described development of a new biosensor that flashes like a beacon upon detecting nanoparticles in the environment.

Anne Anderson and colleagues at Utah State University and the University of Utah have inserted genes into a strain of Pseudomonas putida (P. putida) ”a beneficial soil microbe” so that it emits light upon contact with nanoparticles of heavy metals. They are with Utah State University. The bacteria glow brightly when it is in its normal healthy state. The glow dims upon exposure to toxic substances.

“The novelty of the biosensor is we’re able to get responses very, very quickly,” she said, “and we can get those answers in the absence of other factors that could bind the challenging compounds.” Anderson noted that traditional approaches in measuring bacterial cell growth may take two days. “At the snap of your finger you can see some of these things take place.”

Anderson’s group discovered that P. putida cannot tolerate silver, copper oxide and zinc oxide nanoparticles. Toxicity occurred at levels as low as micrograms per liter. That’s equivalent to two or three drops of water in an Olympic-sized swimming pool. Anderson warns it could spell danger for aquatic life. “If you look up the Environmental Protection Agency’s risk level of Copper to fish and other aquatic organisms, you are at that point of toxicity.”

There’s much debate in the science community about nanoparticle toxicity, Anderson said. Some scientists believe that nanoparticles in nature will aggregate together or bind onto silt and/or other organic matter, greatly reducing their toxicity. “We don’t know if that’s true or not,” she said. So other members of this Utah research group currently are investigating that aspect of the issue.

Although the public is ultimately responsible for understanding the risks of consumer products, Gruden said, science plays a large role in highlighting possible hazards. “It is the scientist’s job to perform good research and let the findings speak for themselves,” she said. And so far the promises of nanotechnology need more evaluation. “To date, it’s unclear whether the benefits of nanotech outweigh the risks associated with environmental release and exposure to nanoparticles.”

Literature:
American Chemical Society, Nanoparticles in cosmetics/personal care products may have adverse environmental effects, Public release date: 26-Mar-2009

FDA Fails to Protect: Remains Silent about Lead in Lipstick

CAMPAIN FOR SAFE COSMETICS – For Immediate Release: February 9th, 2009

Washington – More than a year after the Campaign for Safe Cosmetics reported that popular brands of lipstick contain lead, the U.S. Food and Drug Administration has still not released the results of its own testing of lead in lipstick, despite pressure from senators and repeated calls from health groups.

New reports indicate that the beauty industry’s lead problems go further than lipstick. The Canadian government announced last week it found lead in children’s face paint. The results were publicly announced immediately as the government evaluates next steps. Health Canada also announced last week that it has designated two silicon-based chemicals widely used in personal care products - D4 and D5 – as toxic, an important step toward regulating dangerous substances out of consumer products.

Unlike Health Canada, the U.S. FDA has no such toxic designation, does not conduct routine safety testing of personal care products, and does not publicly report information in a timely manner – as evidenced by the lead-in-lipstick situation.In Oct. 2007, the Campaign for Safe Cosmetics reported that 61% of lipsticks it tested contained lead. In Nov. 2007, Sens. John Kerry, Barbara Boxer and Dianne Feinstein urged FDA to test a range of lipsticks for lead, publicly report the results, and take immediate action to reduce consumers’ exposure to lead from cosmetic products.

Fourteen months later, FDA has made no public statements, issued no reports, and taken no action to reduce consumers’ exposure.

“The typical turnaround time in a laboratory for lead tests is 10 days. There’s no reason for FDA to sit on its lead-in-lipstick research for over a year,” said Stacy Malkan of the Campaign for Safe Cosmetics, a coalition of health and environmental groups.

“FDA appears to still be operating under Bush-era tactics of secrecy and delay. It’s time for new leadership and new direction at FDA, so the agency can do what Americans expect it do to: ensure the safety of cosmetic products.”

“The scientific data is conclusive: Lead in any amount is a health concern. Lead is a proven neurotoxin that can cause learning and behavioral problems, and pregnant women and children are particularly vulnerable.”

The NO/ONOO-cycle has been recognized in many extraordinary ways over the past several months, such that it should be viewed as THE predominant model of this previously unexplained disease.

I was invited to give the initial address at the European Environmental Medicine meeting in Wurzburg, a two day meeting that was largely dominated by the NO/ONOO- cycle mechanism. This was part of a “grand European tour,” giving seven talks in five countries. These included being the only non-European invited to address the European Union Parliament (The Council of Nations) at a special meeting on Environmental Medicine.

There were also two special mini-symposia organized to correspond to my visit in Europe, another great honor. I gave talks in Italy, Germany, Austria, Switzerland and France, including talks at three medical schools. So there has been extraordinary recognition of the NO/ONOO- cycle mechanism, a mechanism that is helping people in many countries around the world to actually lessen their chemical sensitivity responses.

I might add that there was a book written in German on multiple chemical sensitivity, with Hans-Ulrich Hill as first author, that is largely focussed on the NO/ONOO- cycle mechanism of  MCS.

While these are all extraordinary recognition for this science, the most important recognition is elsewhere. I have been asked to write a review on MCS, to be a chapter in a very prestigious multivolume set on toxicology, and that review has been accepted and will be coming out this coming autumn. This is extraordinarily important for at least four distinct reasons.

The first, of course is that MCS has been largely ignored by the toxicologists, despite its high prevalence in the U.S. and in other populations because they have felt that there was no reasonable explanation for it. Now, clearly, they find that we now do have a compelling and well-supported explanation for MCS and therefore it should be integrated into the larger framework of toxicology.

Secondly, the fact that they asked me to write this review is obviously extraordinary recognition for my own work in developing, for the first time, this detailed and well-supported mechanism, as we! ll as for the mechanism itself.

Thirdly, this review is the longest such review on MCS ever written, as well as the most extensively documented, having well over 400 citations in it.

Fourthly, there are several very important types of evidence that were new to me, supporting the NO/ONOO- cycle mechanism that are reviewed in this chapter, including important studies of the mechanism of toxic action of the seven groups of chemicals implicated in MCS, including important animal model studies of MCS implicating almost all of the NO/ONOO- cycle elements and including a series of published studies of various objectively measurable responses to low level chemical exposure, responses that are consistent with the NO/ONOO- cycle and that should be developed as specific biomarker tests for MCS.

When this paper comes out, we as a community concerned about the suffering of the millions of people who are chemically sensitive, will have a unique opportunity to dramatically change the views of the general public, the news media and even the court system of this horrible world-wide epidemic. That opportunity will come because of the essential juxtaposition of rigorous science and extraordinary recognition.

Martin L. Pall

Government bans all use of mercury in Sweden

Press release, 15 January 2009
Ministry of the Environment Sweden

The Government today decided to introduce a blanket ban on mercury.
The ban means that the use of dental amalgam in fillings will cease and that it will no longer be permitted to place products containing mercury on the Swedish market.

“Sweden is now leading the way in removing and protecting the environment from mercury, which is non-degradable. The ban is a strong signal to other countries and a Swedish contribution to EU and UN aims to reduce mercury use and emissions,” says Minister for the Environment Andreas Carlgren.

The Government’s decision means that products containing mercury may not be placed on the Swedish market. In practice this means that alternative techniques will have to be used in dental care, chemical analysis and the chloralkali industry. The Swedish Chemicals Agency will be authorised to issue regulations on exceptions or grant exemptions in individual cases.

In connection with the Government’s decision, waste containing mercury will be disposed of in deep geological repositories in other EU countries. The Swedish market for hazardous waste is small. Last spring, a government inquiry established that there are existing repositories for waste containing mercury in, for example, Germany that more than adequately meet the safety requirements on which Swedish legislation is based. Creating a new Swedish repository would be around 15 times more expensive than depositing waste in existing facilities in the EU. The bodies consulted on this matter shared the inquiry s conclusions.

“By using common solutions and almost forty years of experience of storing mercury in the EU, we are not lowering safety standards. The waste will be transported to a deep geological repository with high safety standards. In accordance with the polluter pays principle, the owners of the waste will be responsible for ensuring that disposal in a repository is arranged and paying for it,” says Mr Carlgren.

The disposal possibilities in other EU countries provide better incentives for the desired development of safe, large-scale technologies to stabilise waste containing mercury.

Since the beginning of the 1990s there has been a ban in Sweden on the manufacture and sale of certain products containing mercury, including thermometers and other measuring devices and electronic components.

The new regulations enter into force on 1 June 2009.

PAN Europe, HEAL and EEB PRESS RELEASE

Brussels, 18 December 2008 – Health and environment non-governmental organisations (NGOs) have cautiously welcomed the proposed EU package on pesticides reached yesterday as a step towards better health through environmental protection.

Following years of political negotiations, the debate on the pesticide package entered yesterday a new stage, with a proposed deal between the Commission, French Presidency and a European Parliament delegation reaching agreement on a Regulation and a Framework Directive on the use and authorisation of pesticides.

Overall, PAN (Pesticides Action Network) Europe, the Health and Environment Alliance (HEAL) and the European Environment Bureau (EEB) consider that the proposed compromise agreement offers positive aspects, first of all because it means the creation of an EU-wide pesticides blacklist, which removes some of Europe’s most hazardous pesticides from the market – and therefore from food products grown in the EU (1).

We are happy to see that the proposed agreement includes criteria for banning pesticides that can cause cancer, DNA-mutation, reproductive problems and hormonal disruption’, says Monica Guarinoni, Deputy Director at HEAL. ‘Only 22 substances will be withdrawn from the market, resulting in a much higher level of health protection, especially for children and vulnerable groups, although we would have liked the list to be larger and include developmental neurotoxic and immunotoxic pesticides’ (2).

The major downside of the deal is that it did not include the Environment committee’s demand to eliminate the division of the EU into three authorisation zones. This omission reduces the control of member states over whether or not to reject a hazardous pesticide within their territory (3).

Regarding the framework directive on sustainable use of pesticides, Member States have to develop National Action Plans with clear targets on how and when to achieve quantitative use reductions.

“Although, we regret the absence of ambitious EU quantified reduction targets and incentives, we welcome the fact that member states will have to prepare national action plans with quantitative use reductions and the idea of applying integrated pest management from 2014″, Hans Muilerman, board member of PAN. “Making Integrated Pest Management (IPM) mandatory for every farmer in Europe presents a unique opportunity to achieve more sustainable agricultural practices,” he continues.

On the Directive, Monica Guarinoni added “Banning the use of pesticides in public areas, such as parks and school grounds, is another measure that would help protect health. Although the current compromise does not include a total ban on pesticide use in public places, we hope member states and local authorities will pick up these measures in their local and national action plans. Some municipalities in Europe are already banning the use of pesticides for cosmetic purposes and our new campaign will encourage others to do so” (4).

Although far from perfect, with a number of loopholes and derogations and based too much on risk rather than hazard and quantitative reductions, the proposed deal will allow the EU to move on to a better system without further delays. Health and environment groups therefore reluctantly advise the EU institutions to officially confirm the deal in January.

Notes to editors:

1 Other positive measures in the regulation are the introduction of mandatory record-keeping throughout the production chain; an obligation on industry to release all scientific articles showing the negative side-effects of pesticide application; consideration of the cumulative effects on health (though not on environment) within the testing and authorisation process; and better protection of bees.
2 The deal does not include developmental neuro- and immunotoxicity in the cut-off criteria, instead these are only taken into account in the setting of health standards.
3 Other negative aspects are that the assessment of endocrine disrupting is also delayed and the Commission has to come up with scientific criteria for their determination in 5 years, after which testing will take even more time to identify this dangerous group of pesticides; some specific categories though are included already in the cut-off.  Nor does the deal get rid of the so-called non-relevant metabolites, which gives the Member States the possibility to ignore toxic effects of metabolites.
4 The “Sick of Pesticides” campaign on pesticides and cancer was launched in November 2008. The campaign website is available in French and English at www.pesticidescancer.eu

Contact:
Henriette Christensen, Pesticide Action Network Europe, Boulevard de Waterloo 34, B – 1000 Brussels, Tel:+32 2 289 13 09, email henriette@pan-europe.info; website: www.pan-europe.info

Monica Guarinoni, Deputy Director, Health and Environment Alliance (HEAL), 28 Boulevard Charlemagne, B-1000 Brussels. Tel: +32 2 234 3643 (direct). E-mail: monica@env-health.org Website: www.env-health.org

Christian Schaible, EU Policy Officer for Industrial Policies and Chemicals,  European Environmental Bureau, Boulevard de Waterloo 34 1000 Brussels ,  Tel. +32 (0)2 289 10 90, website : www.eeb.org

NTEF – National Toxic Encephalopathy Foundation, October 6. 2008

PRESS RELEASE

FDA Agrees Clarins Expertise 3P is a Drug

Las Vegas, NV-AZ (1888PressRelease) October 06, 2008

The National Toxic Encephalopathy Foundation (NTEF) is pleased to announce that the Food and Drug Administration (FDA) has concurred that Clarins Expertise 3P (EP3) is a drug, not a cosmetic as advertised.

In February, the NTEF notified the FDA that Clarins EP3 was making drug versus cosmetics claims and requested an investigation into these allegations. As previously stated: “We are now requesting that the FDA verify the claims made by Clarins, in vitro testing versus in vivo testing, along with compliance, since this product is a new drug under section 201(p) of the FDCA, 21 U.S.C. subsection 321 (p), because it is not generally recognized by qualified scientific experts as “effective” for its intended use.”

On October 1, 2008, the NTEF received the following notification from Patricia A. Hansen, Ph.D. Sr. Advisor for Science and Policy at the FDA:

“The Office of Cosmetics and Colors has reviewed the information at the U.S. website, where products may also be purchased, and consulted with others in the Agency. We are of the opinion that the claims made are drug claims. We have referred the matter to the office that handles these issues, FDA’s Office of Non-Prescription Drug Products in the Center for Drug Evaluation and Research (CDER)”.

“We couldn’t be happier with the FDA’s determination regarding EP3″, said Angel De Fazio, President of the NTEF. “Cosmetic companies have been skirting the drug versus cosmetics claims for too long. It is hoped that as a result of this action, cosmetic companies, such as Clarins, will stop their deceptive advertising. It is expected that in the future they will be forced to submit new drug applications for their products when making medical claims”.

“I extol the opinion of the FDA”s findings regarding EP3 and am confident that they will be of the same mind regarding the two dozen plus other drug versus cosmetic claims that we have submitted. As we will be just as aggressive in having those also being re-classified”, said Dr. Jack D. Thrasher, Ph.D., Toxicologist, Immuno-toxicologist, Fetal-toxicologist and technical director for the NTEF. “Clarins has pushed both the limit of believability and cosmetic references regarding this product. This is not the first time that the FDA has taken Clarins to task for drug versus cosmetic claims and we are highly confident that this will not be the last.”