caring for our world

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Welcome

 

 

 

For additional information email
Dr. Brian Moench, President, at shaunamoench@yahoo.com,
or call
Kira Kilmer at 801.359-8929

 

 

 

 

Scenic photos by Howie Garber
Visit his Web Site at www.wanderlustimages.com

Our Professional Library



Technical references to specific articles and books:

• This linked PDF summarizes peer-reviewed published studies that concluded a link between traffic-related air pollution and health risks.  Information is organized with particular focus on the bulleted points on the cards we will be passing out at the walk on Saturday.  Be very careful not to use language that suggests “cause” as most of these studies only demonstrate “associations” or “increased likelihood.”  Thanks goes to Mark Heileson for the references.

• Air Pollution and Health — Good News and Bad
C. Arden Pope, III, Ph.D. from NEJM, Volume 351:1132-1134 September 9, 2004 Number 11

• Pope CA 3rd, Muhlestein JB, May HT, Renlund DG, Anderson JL, Horne BD.
Related Articles, Links

Ischemic heart disease events triggered by short-term exposure to fine particulate air pollution. Circulation. 2006 Dec 5;114(23):2443-8. Epub 2006 Nov 13.

• Brigham Young University, Provo, UT 84602-2363, USA. cap3@byu.edu
BACKGROUND: Recent evidence suggests that long-term exposure to particulate air pollution contributes to pulmonary and systemic oxidative stress, inflammation, progression of atherosclerosis, and risk of ischemic heart disease and death. Short-term exposure may contribute to complications of atherosclerosis, such as plaque vulnerability, thrombosis, and acute ischemic events. These findings are inconclusive and controversial and require further study. This study evaluates the role of short-term particulate exposure in triggering acute ischemic heart disease events. METHODS AND RESULTS: A case-crossover study design was used to analyze ischemic events in 12,865 patients who lived on the Wasatch Front in Utah. Patients were drawn from the cardiac catheterization registry of the Intermountain Heart Collaborative Study, a large, ongoing registry of patients who underwent coronary arteriography and were followed up longitudinally. Ambient fine particulate pollution (particles with an aerodynamic diameter < or = 2.5 microm; PM2.5) elevated by 10 microg/m3 was associated with increased risk of acute ischemic coronary events (unstable angina and myocardial infarction) equal to 4.5% (95% confidence interval, 1.1 to 8.0). Effects were larger for those with angiographically demonstrated coronary artery disease. CONCLUSIONS: Short-term particulate exposures contributed to acute coronary events, especially among patients with underlying coronary artery disease. Individuals with stable presentation and those with angiographically demonstrated clean coronaries are not as susceptible to short-term particulate exposure.

Dockery DW, Pope CA 3rd, Xu X, Spengler JD, Ware JH, Fay ME, Ferris BG Jr, Speizer FE. Related Articles, Links

• An association between air pollution and mortality in six U.S. cities.
N Engl J Med. 1993 Dec 9;329(24):1753-9.

Am J Public Health. 1989 May;79(5):623-8. Links

• Pope CA 3rd.
Respiratory disease associated with community air pollution and a steel mill, Utah Valley Am J Public Health. 1989 , Vol. 79, Issue 5 623-628 May;79(5):623-8.
Brigham Young University, Provo, UT 84602.
This study assessed the association between hospital admissions and fine particulate pollution (PM10) in Utah Valley during the period April 1985-February 1988. This time period included the closure and reopening of the local steel mill, the primary source of PM10. An association between elevated PM10 levels and hospital admissions for pneumonia, pleurisy, bronchitis, and asthma was observed. During months when 24-hour PM10 levels exceeded 150 micrograms/m3, average admissions for children nearly tripled; in adults, the increase in admissions was 44 per cent. During months with mean PM10 levels greater than or equal to 50 micrograms/m3 average admissions for children and adults increased by 89 and 47 per cent, respectively. During the winter months when the steel mill was open, PM10 levels were nearly double the levels experienced during the winter months when the mill was closed. This occurred even though relatively stagnant air was experienced during the winter the mill was closed. Children's admissions were two to three times higher during the winters when the mill was open compared to when it was closed. Regression analysis also revealed that PM10 levels were strongly correlated with hospital admissions. They were more strongly correlated with children's admissions than with adult admissions and were more strongly correlated with admissions for bronchitis and asthma than with admissions for pneumonia and pleurisy.

* NOTE RATE OF ADMISSION OF CHILDREN TO HOSPITAL WITH RESP DIS WENT UP 300%.

• Related Links
• Respiratory hospital admissions associated with PM10 pollution in Utah, Salt Lake, and Cache Valleys. [Arch Environ
• Health. 1991]

Association between PM2.5 and all-cause and specific-cause mortality in 27 US communities

- Meredith Franklin, Ariana Zeka & Joel Schwartz J Expo Sci Environ Epidemiol 2007 17: 279-287; advance online publication, September 27, 2006; 10.1038/sj.jes.7500530
Abstract | Full Text

When Smoke Ran Like Water, Tales of Environmental Deception by Devra Davis, 2002

Superb book on politics and the history of environmental policy making

Pdf files of Salt Lake Tribune, Catalyst, and Deseret News articles:

http://www.sltrib.com/ci_5800917?source=rss
http://www.sltrib.com/news/ci_5908570?source=email

Tribune article 5/17/07
http://www.catalystmagazine.net/shorts-

 

Common chemicals pose danger for fetuses, scientists warn  LA Times  May 2007 

Exposure to toxic materials in the womb can cause health problems later in life, an international panel declares. From the Los Angeles Times By Marla Cone Times Staff Writer May 25, 2007

In a strongly worded declaration, many of the world's leading environmental scientists warned Thursday that exposure to common chemicals makes babies more likely to develop an array of health problems later in life, including diabetes, attention deficit disorders, prostate cancer, fertility problems, thyroid disorders and even obesity. The declaration by about 200 scientists from five continents amounts to a vote of confidence in a growing body of evidence that humans are vulnerable to long-term harm from toxic exposures in the womb and during their first years.

Convening in the Faroe Islands in the North Atlantic, toxicologists, pediatricians, epidemiologists and other experts warned that when fetuses and newborns encounter various toxic substances, growth of critical organs and functions can be skewed. In a process called "fetal programming," the children then are susceptible to diseases later in life — and perhaps could even pass on those altered traits to their children and grandchildren. The scientists' statement also contained a rare international call to action. The effort was led by Dr. Philippe Grandjean of Harvard University and the University of Southern Denmark, and Dr. Pal Weihe of the Faroese Hospital System, who have spent more than 20 years studying children exposed to mercury.

Many governmental agencies and industry groups, particularly in the United States, have said there is no or little human evidence to support concerns about most toxic residue in air, water, food and consumer products. About 80,000 chemicals are registered in the United States. Yet the scientists urged leaders not to wait for more scientific certainty and recommended that governments revise regulations and procedures to take into account subtle effects on fetal and infant development. Chemicals with evidence of developmental effects include compounds in plastics, cosmetics and pesticides. "Given the ubiquitous exposure to many environmental toxicants, there needs to be renewed efforts to prevent harm. Such prevention should not await detailed evidence on individual hazards," the scientists wrote in the four-page statement.

Genetic concerns The scientists are particularly concerned that the newest animal research suggests that chemicals can alter gene expression — turning on or off genes that predispose people to disease. Although the DNA itself would not be altered, such genetic misfires in the womb may be permanent, and all subsequent generations could be at greater risk of diseases too. "Toxic exposures to chemical pollutants during these windows of increased susceptibility can cause disease and disability in childhood and across the entire span of human life," the scientists concluded.

The "Barker hypothesis," conceived by a British scientist in 1992, says human fetuses are "programmed" for diseases by their early environment. The scientists concluded that this is now well-documented for toxic exposures by a large collection of animal experiments and some human data. "A sad aspect with many of these prenatal exposures is that they leave the mother unscathed while causing injury to her fetus," said Dr. Philip Landrigan, a pediatrician who chairs the Mount Sinai School of Medicine's Department of Community and Preventive Medicine. He was one of the statement's authors.

In a more optimistic vein, the researchers said that if contaminants do play a big role in human health problems, some diseases could be prevented. "Reducing exposure would lead to tremendous benefits," said Dr. Bruce Lanphear, director of the Environmental Health Center at Cincinnati Children's Hospital Medical Center. "We shouldn't wait for an epidemic to fully mature before we develop policies to protect children." For centuries, the basic rule of toxicology has been "the dose makes the poison." Now, the scientists say "the timing makes the poison" — in other words, when a toxic exposure occurs is as important as the amount people are exposed to.
The fetus "is extraordinarily susceptible to perturbation of the intrauterine environment," they wrote. The growing brain is the most sensitive. Mothers' exposure to mercury and polychlorinated biphenyls (PCBs) in fish and other seafood can cause slight declines in a child's IQ and motor skills. In addition, early exposure to pesticides might trigger Parkinson's and Alzheimer's diseases.

Also, children exposed to lead, organophosphate pesticides or cigarette smoke have greater risk of attention deficit hyperactivity disorder. One of every three cases — or an estimated 560,000 children in the United States — can be attributed to lead exposure or prenatal tobacco smoke exposure, Lanphear reported in a study published in December. The immune, reproductive and cardiovascular systems also are vulnerable to early damage. Children exposed prenatally to PCBs have a high rate of infections and weak response to vaccinations. Many chemicals also can mimic hormones, and in animal tests, they feminize newborns, lowering sperm counts and promoting prostate, testicular, uterine and breast cancers. In the newest area of research, metabolic systems, which control how nutrients are converted into energy, have been altered by chemicals administered in animal experiments — changes that may contribute to obesity and diabetes.

Chemical danger -

"These adverse effects have been linked to chemical pollutants at realistic human exposure levels similar to those occurring from environmental sources," the scientists wrote. Among the risky chemicals they named are bisphenol A, found in polycarbonate plastic food and water containers; the pesticides atrazine, vinclozolin and DDT; lead; mercury; phthalates used in some cosmetics and soft plastics; brominated flame retardants; arsenic, which contaminates some water supplies; and PCBs, banned but ubiquitous, particularly in fish.

Some of the chemicals have been regulated in the United States, but many have not. Moreover, the scientists said, tests for developmental effects are not routinely required, so "the potential for such effects is therefore not necessarily considered in decisions on safety levels of environmental exposures." There is "an incredible gap," Landrigan said, because 80% of major chemicals in commerce have never been tested to see if they damage early development.

The conference was funded by the World Health Organization, National Institutes of Health, European Environment Agency and the Centers for Disease Control and Prevention.

Denmark's Faroe Islands, just south of the Arctic Circle, were the venue because the region is home to the longest-running human experiment analyzing prenatal toxic exposure. Since 1986, Grandjean and Weihe have tracked Faroese children from the womb to adolescence to monitor neurological effects of mercury in seafood. Their findings prompted U.S. advisories that children and women of childbearing age avoid swordfish and other highly contaminated fish.

In addition to Landrigan, three Californians and six other U.S. scientists served on the 28-member committee that wrote the consensus: Brenda Eskenazi of UC Berkeley, Irva Hertz-Picciotto of UC Davis, Beate Ritz of UCLA, Jerry Heindel and Kimberly Gray of the National Institute of Environmental Health Sciences, Larry Needham of the CDC, Terry Huang of the National Institute of Child Health and Human Development, David Bellinger of Harvard University and Howard Hu of the University of Michigan.

LA Times Article

marla.cone@latimes.com

 

 

 

 

 

 


Resources

 

A Link to excellent educational resources

• The Physicians for Social Responsibility
The PSR has accumulated excellent articles, training, and information about our environment. Please take a moment and visit their site.

A substantial body of scientific evidence published in the peer-reviewed literature challenges the central tenet of regulatory toxicology, which assumes 'the dose makes the poison.' Experimental data now conclusively show that some endocrine-disrupting contaminants can cause adverse effects at low levels that are qualitatively different from those caused by high level exposures. Regulatory toxicology has assumed that high dose experiments can be used to predict low-dose results. These findings invalidate that assumption. As a result, it is highly likely that health standards established using standard toxicological procedures are too weak.

Experiments with mice show that exposure during pregnancy to very low doses of bisphenol A scrambles the chromosomes of their daughters' fertilized embryos, ie., the pregnant female's grandchildren. This third-generation effect is possible because the eggs of a female mammal, including human, are formed while the female is still in the womb. Exposure to BPA at comparable levels appears widespread among people in the United States, because of its use in common consumer products, including polycarbonate plastic and food cans.