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UPDATE no. 29 September 2002 INCHES

2002-The International Network on Children's Health, Environment and Safety

Dear member of INCHES,

In this update :
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Article abstracts
Conferences
INCHES funding

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INCHES website
Any items related to children’s are welcome. Someone who wants to do something or knows someone who can do some voluntary work for the website can reply to the secretariat.

News items

INCHES has new member - Center for Infancy and Family Research, Universidad Metropolitana, Venezuela. You can find more information: www.unimet.edu.ve/investigacion/cendif.

UNEP NEWS RELEASE
The Meeting of the Global Mercury Assessment Working Group - Geneva, Switzerland from 9 to 13 September 2002.

A group of some 150 experts meeting in Geneva from 9 to 13 September under the auspices of the United Nations Environment Programme (UNEP) concluded that there is sufficient evidence of significant global adverse impacts to warrant international action to reduce the risks to human health and the environment arising from the release of mercury into the environment.
The risks of mercury poisoning and of chemicals pollution in general gained worldwide attention in the 1960s and 70s when several thousand people living on the shores of Minamata Bay in Japan sickened or died after eating seafood contaminated with mercury from a nearby factory.

"We live now in the 21st century and there can no longer be any excuse for exposing people and the natural environment to dangerous levels of toxic chemicals", said UNEP Executive Director Klaus Toepfer. "In the case of mercury - which has destroyed the lives of thousands of people - we need to make mercury poisoning a thing of the past."

Mercury is a heavy metal that comes from both natural and human sources. Once it has been released into the environment, it cycles between soils, water systems and the atmosphere. It can travel thousands of kilometres from its point of origin, contaminating remote regions such as the Arctic. Mercury also persists in the environment for long periods of time.

Mercury transforms naturally through biological activity in aquatic environments into methyl mercury, a highly toxic organic compound that is absorbed by humans and animals. Because it bio-accumulates up the food chain, the higher carnivores -- especially predatory fish such as tuna and swordfish, freshwater fish such as pike and bass, and mammals such as otters, seals and whales -- can accumulate large quantities in their tissue.

Most people are exposed to mercury primarily through eating fish, as well as some other foods. Responding to findings that freshwater fish as well as marine fish and seafood often contain elevated levels of mercury, a number of Governments have issued health advisories to their citizens recommending limits on how many fish people should eat over certain periods of time. Workers in industries that use mercury face additional exposure risks. Also, in recent years the use of mercury in artisanal gold mining has been polluting the local environment and affecting the health of both the gold miners and their families in an increasing number of developing countries. Chronic, low-level exposures to mercury are known to cause permanent damage to the brain, nervous system and kidneys. Effects on brain functioning may lead to irritability, shyness, tremors, and changes in vision or hearing and memory loss. Pregnant mothers and their foetuses are particularly sensitive to the effects of mercury.

Many Governments have national regulations to control mercury emissions, reduce or eliminate the use of mercury in certain products, and protect workers. Fortunately, effective substitutes for most uses of mercury are now available. Several Governments have succeeded in reducing emissions and uses of mercury by as much as 75% over the past 10 or 20 years.

While mercury is released naturally from rocks, soil and volcanoes, human activities have boosted atmospheric levels to some three times above pre-industrial levels. Estimates vary widely, but some 5,000 to 10,000 tonnes of mercury are thought to enter the atmosphere every year, 50 to 75% of it from human activities. When placed in landfills mercury can slowly seep into groundwater or evaporate into the air. The main human-made source of mercury emissions is coal combustion from electrical power plants and industrial, commercial and residential burners. Other sources include municipal solid waste incineration, mining of non-ferrous metals, and artisanal gold mining.

The UNEP Global Mercury Assessment Working Group is also recommending to Governments a list of options for addressing the dangers of mercury. These include reducing risks by reducing or eliminating the production and
consumption of mercury, substituting other products and processes, launching talks for a legally-binding treaty, establishing a non-binding global programme of action, and strengthening cooperation amongst Governments on information-sharing, risk communication, assessment and related activities.
The Working Group has also recommended a number of immediate actions to enhance outreach to highly vulnerable groups (such as pregnant women), provide technical and financial support to developing countries and to countries with economies in transition, and support increased research, monitoring and data-collection on the health and environmental aspects of mercury and on environmentally friendly alternatives to mercury.
These recommendations, together with a detailed mercury assessment report, are being forwarded to UNEP's Governing Council, which meets 3-7 February 2003 at UNEP headquarters in Nairobi. Based on the Working Group's scientific and technical advice, the Governing Council will adopt political decisions that will set the course for global action on mercury for years to come.
"These recommendations from the scientists and experts are the first essential step on the road to reducing and one day eliminating the environmental and health risks of mercury", said UNEP Executive Director Klaus Toepfer. "Now it is up to the politicians and policy-makers to decide just where we go from here."
For more information, please contact Michael Williams, UNEP Information Officer, at +41-22-917-8242, +41-79-409-1528 (cellular) or Michael.Williams@unep.ch. Official documents and other information are
posted at www.chem.unep.ch/mercury/.

Air Pollutants Tied to Death Risk in Severe Asthma

Exposure to two common air pollutants may increase the risk of death among people with severe asthma, researchers in Spain report. Although air pollution has been linked to asthma exacerbation, the evidence of this effect has not been consistent across studies. One possible reason, according to the authors of the new study, is that much research has focused on people with moderate asthma, while severe asthmatics may be more susceptible to the effects of air pollution. In their study, the Barcelona researchers focused on severe asthmatics and their exposure to two major air pollutants: nitrogen dioxide, a chemical spewed from both automobiles and power plants; and ozone, a chemical formed when sunlight reacts with other air pollutants. Ozone occurs in two layers in the atmosphere--at ground level, where it is an air pollutant that can damage human health, and far up in the stratosphere, where it helps shield the Earth from harmful ultraviolet radiation. The investigators found that deaths among their study patients were correlated with atmosphere concentrations of the two air pollutants. No such link was identified for pollen or spores, Dr. J. Sunyer and colleagues at the Institut Municipal d' Investigacion Medica report in the August issue of the journal Thorax. Asthma is the most common chronic disease in children, and for reasons that are unknown, the number of asthma cases has been on the rise in the US and other developed countries. Sunyer's team evaluated the deaths of 467 men and 611 women who had been diagnosed with severe asthma and died between 1985 and 1995. After looking at levels of common air pollutants on the days of the deaths, the investigators found that patients had a greater risk of dying on days with higher levels of nitrogen dioxide. High-ozone days in the spring and summer were also tied to an increased death risk, according to the report. "The results suggest that severe asthmatics are susceptible to the adverse effects of urban air pollutants, particularly oxidants," the study authors write. Because their research included only patients seen at a single Barcelona hospital, they call for a larger study to look more closely at the connection between the air pollutants and asthmatics' death risk.
SOURCE: Thorax 2002;57:687-693.

Poor air in California leaves children at higher cancer risk, study finds
By Gary Polakovic, Los Angeles Times, 9/16/2002

LOS ANGELES - A report being released today by a Washington, D.C., environmental group says that children in California are at greater risk of contracting cancer from inhaling toxic air pollutants than adults.

The study, which focused on five areas of the state, maintains that a 2-week-old baby in the Los Angeles region has already been exposed to more pollution than the federal government deems acceptable over a lifetime.

By age 18, the same child will have inhaled enough contaminants to exceed the acceptable exposure level hundreds of times over, according to the study.

''The concentration of cancer-causing air pollution in California is so great that, just by breathing this air, children will accumulate cancer risks that are pretty astounding,'' said Andy Igrejas, environmental health program director for the National Environmental Trust, the advocacy group that produced the report.

''This underscores the urgency of efforts to reduce the cancer risks. We have such a long way to go for the air to be healthy,'' he said.

The study examined pollution concentrations in the Los Angeles region, the San Francisco Bay Area, the San Joaquin Valley, the Sacramento Valley, and San Diego. The findings echo those of other studies, including a report prepared three years ago by Representative Henry A. Waxman, Democrat of California.

California is the nation's smoggiest state and researchers have long known that air pollution contains a mix of industrial and automotive chemicals. Solvents, metals, and unburned fuel not only contribute to smog and haze, but can cause cancer, reproductive harm, and neurological damage.

Yet there is disagreement over how harmful toxic emissions are and what should be done to reduce risks.

''If you live in an urbanized, industrialized society with a growing economy you're going to be exposed to some level of toxic air pollution,'' said Jerry Martin, spokesman for the California Air Resources Board.

Each year, 102,000 tons of the most common toxic emissions are released in California. Traces of benzene from gasoline fumes, hexavalent chromium from metal-plating shops, and diesel exhaust from trucks and buses are widespread.

In the four-county Los Angeles region, the state air board estimates toxic air contaminants cause 720 cancer cases per million people annually - a risk almost 1,000 times greater than the federal government's acceptable limit.

That federal benchmark, however, is extraordinarily conservative. It seeks to limit the odds of a person's contracting cancer from contaminants to one chance in 1 million.

Melanie Marty, chief of the air toxicology unit at the California Office of Environmental Health Hazard Assessment, said children are more vulnerable to pollutants. They are more active and inhale relatively more air than adults, have less well-developed immune systems, and undergo rapid growth, during which cells are more vulnerable to attack by carcinogens. Further, she said, some animal studies show that exposure to toxic chemicals early in life increases the
risk of cancer in adult years.

''They are making some leaps in the way they estimate risk'' in the new report, Marty said, ''but their major point, that children have higher exposures than adults, that's not disputed.''

But do children get more cancer as a result? That is unclear, specialists say. Theoretical risks do not always translate into actual cancer cases. In a study published earlier this year, researchers from the California Department of Health Services and the Public Health Institute in Berkeley, Calif., failed to detect any significant increase in childhood cancer among 7,000 children living near freeways, where toxic air pollution is substantial. Similarly, smoggy California communities do not appear to have more deaths caused by lung cancer than other places.
(This story ran on page A2 of the Boston Globe on 9/16/2002. )

Articles
Critical Windows of Exposure to Household Pesticides and Risk of Childhood Leukemia

Xiaomei Ma,1 Patricia A. Buffler,1 Robert B. Gunier,2 Gary Dahl,3 Martyn T. Smith,1 Kyndaron Reinier,1 and Peggy Reynolds2

1School of Public Health, University of California, Berkeley, California, USA; 2Environmental Health Investigations Branch, California Department of Health Services, Oakland, California, USA; 3Stanford University School of Medicine, Stanford, California, USA

Abstract
The potential etiologic role of household pesticide exposures was examined in the Northern California Childhood Leukemia Study. A total of 162 patients (0-14 years old) with newly diagnosed leukemia were rapidly ascertained during 1995-1999, and 162 matched control subjects were randomly selected from the birth registry. The use of professional pest control services at any time from 1 year before birth to 3 years after was associated with a significantly increased risk of childhood leukemia [odds ratio (OR) = 2.8; 95% confidence interval (CI), 1.4-5.7], and the exposure during year 2 was associated with the highest risk (OR = 3.6; 95% CI, 1.6-8.3). The ORs for exposure to insecticides during the 3 months before pregnancy, pregnancy, and years 1, 2, and 3 were 1.8 (95% CI, 1.1-3.1), 2.1 (95% CI, 1.3-3.5), 1.7 (95% CI, 1.0-2.9), 1.6 (95% CI, 1.0-2.7), and 1.2 (95% CI, 0.7-2.1), respectively. Insecticide exposures early in life appear to be more significant than later exposures, and the highest risk was observed for exposure during pregnancy. Additionally, more frequent exposure to insecticides was associated with a higher risk. In contrast to insecticides, the association between herbicides and leukemia was weak and nonsignificant. Pesticides were also grouped based on where they were applied. Exposure to indoor pesticides was associated with an increased risk, whereas no significant association was observed for exposure to outdoor pesticides. The findings suggest that exposure to household pesticides is associated with an elevated risk of childhood leukemia and further indicate the importance of the timing and location of exposure. Key words: case-control studies, child, herbicides, insecticides, leukemia, pesticides. Environ Health Perspect 110:955-960 (2002). [Online 14 August 2002]
ehpnet1.niehs.nih.gov/docs/2002/110p955-960ma/abstract.html

QUESTION to INCHES members: Who of you is working with a environmental history taking tool?

Is this tool available for other members? Where can it be found if it is in electronic format? Can your list be distributed as an example to the other members of INCHES? Can you send us more information?

Conferences

Charting the Course: Birth Defects, Developmental Disabilities, Disability and Health; September 17-19, 2002 ; Atlanta, GA, USA

Hosted by the Center for Disease Control and the National Center on Birth Defects and Developmental Disabilities. The conference will provide the opportunity to reflect on the accomplishments that have been made in the field of birth defects, developmental disabilities, and disability and health, as well as enable attendees to participate in charting the course for future directions. For more information contact Cara Mai (770)-488-3550
Internet: www.cdc.gov/ncbddd/conference.htm

The First Mid-Atlantic Conference on Children's Health and the Environment: Clinically Important Issues in Children's Health and the Environment; September 21, 2002; Washington, DC, USA

Hosted by the Mid-Atlantic Center for Children's Health and the Environment at George Washington University. This conference will discuss topics such as: environmental issues in the school setting, asthma, environmental issues in rural areas, mold, pesticides, and water pollution. The conference program will emphasize small group interactions and opportunities to ask questions directly to the panelists and faculty members.
For more information, contact the Mid-Atlantic Center for Children's Health & the Environment at (202)-994-1166.

Children's Environmental Health Network, 110 Maryland Avenue, NE #511, Washington, DC 20002, USA, 202-543-4033, fax: 202-543-8797, e-mail: cehn@cehn.org, Internet: www.cehn.org or www.health-e-kids.org.

In Harm's Way: Toxic Threats to Child Development; October 12, 2002; Minneapolis, Minnesota,

Hosted by the University of Minnesota School of Public Health. The training focuses on the intersection between common environmental chemicals and child development, clinical interventions to prevent or reduce neurodevelopmental toxic threats throughout the life cycle, and the issue of health practitioners as public health advocates.
For more information contact Kathleen Schuler at the Institute for Agriculture and Trade Policy by e-mail: kschuler@iatp.org or phone: (612)-870-3468.
Children's Environmental Health Network, 110 Maryland Avenue NE #511, Washington, DC 20002 USA, 202-543-4033, fax: 202--543-8797, e-mail: cehn@cehn.org, Internet: www.cehn.org

International Symposium on Children's Health and the Environment; October 18-20, 2002; Istanbul, Turkey

Hosted by the Association of Physicians for the Environment of Turkey. Call for abstracts until September 2, 2002.
Information: SETAC North America Office, 1010 North 12th Avenue, Pensacola,FL 32501-3367, ++90-212-586-1549, fax: 850-469-9778, e-mail: alpincan@yahoo.fr, Internet: www.setac.org/site.html

3rd European Conference on Pediatric Asthma ; October 28-29, 2002; London, United Kingdom.
The Conference will present the latest research findings and discuss their impact on the current understanding of asthma and its treatment. The meeting will consist of interactive teaching sessions with direct audience participation and plenary sessions.
Information: Castle House Medical Conferences, Quint House, Nevill Ridge, Nevill Park, Tunbridge Wells, Kent TN4 8NN, UK, +44-0-1892-539606, fax: +44-0-1892-517773, e-mail: enquiries@castlehouse.co.uk, asthma@castlehouse.co.uk, Internet: www.castlehouse.co.uk

Scientific Symposium on Children's Health as Impacted by Environmental Contaminants; November 1-2, 2002; San Antonio, Texas, USA

The symposium will provide physicians the latest information needed to understand, recognize, and prevent children’s exposure to environmental toxicants. The symposium will address trends, exemplary projects and current research in developmental effects, asthma and respiratory diseases, endocrine disrupters, childhood cancer, biological and chemical terrorism, and ethics in environmental health issues. Participants will be provided with an overview of a Nationwide Environmental Public Health Tracking Network that will document links between environmental toxins and chronic diseases.

Information: The Childrens Environmental Health Institute, PO Box 50342, Austin TX, 78763-0342, 512-657-7405, fax: 512-341-3925, email: Sarah.Jones@CEHI.org, Internet: www.cehi.org/symposium.htm

The Eighth Annual Maternal and Child Health Epidemiology Conference; December 11-13, 2002; Clearwater Beach, Florida, USA

Jointly sponsored by the University of South Florida Colleges of Medicine and Public Health, Center for Disease Control, and the Lawton and Rhea Chiles Center for Healthy Mothers and Babies. Abstracts deadline: May 3, 2002.
For more information contact Erica Thomas by phone at (813)-974-6695, or by e-mail at contend@hsc.usf.edu.

INCHES funding

Did you locate a possible sponsor? Do you a private sponsor? Can we mail some information on INCHES to one of your friends? Any donations (or suggestions of possible donors) are welcome at bank account nr.: 526292490 ABN AMRO (swiftcode ABNANL 2A), Dieren, Netherlands.

Last updated 24 September 2002

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