The risk that a 50-year-old white woman will develop breast cancer has soared to 12 percent today from one percent in 1975. Likewise, asthma rates have tripled over the last 25 years and childhood leukemia is increasing by one percent per year.
Such statistics map the alarming rise in incidences of chronic diseases in U.S. populations over the past few decades and are increasingly thought to be linked to the ballooning number of chemicals, including pesticides, that people in the U.S. have been exposed to since the Second World War, reports The New York Times. (HERE)
In a symposium held in November this year, Dr. Philip Landrigan, chair of the Department of Preventive Medicine at New York’s Mount Sinai Hospital, noted that over 80,000 new chemicals have been developed since WWII, of which less than 20 percent have been tested for toxicity to children. One class of chemicals that creates concern — although the evidence is not definitive — is endocrine disruptors, which may fool the body into setting off hormonal changes and can increase incidences of breast cancer.
Endocrine disruptors are found in everyday things like plastic containers, cosmetics and household cleaning products.
Many pesticides — such as atrazine and endosulfan — are potent endocrine disruptors demonstrating health impacts including increased incidences of certain cancers and reproductive harm. The disease incidence numbers and the suffering of countless people speak for themselves:
Pesticide Action Network and other environmental health groups have been calling for adoption of a precautionary approach by regulatory agencies and industry to protect everyone from unnecessary exposures to chemicals that appear likely to cause a wide range of health harms.
Among those who attended Dr. Landrigan’s talk was New York City chef Rob Endelman. He was moved to write about endocrine disruptors in his popular cooking and healthy eating blog, The Delicious Truth, pointing out that until precaution becomes the regulatory standard, consumers must claim their right to a healthy environment by choosing safer products and buying food that is free of pesticides and other harmful additives. “Don’t we owe it to our kids,” chef Rob concluded, “to become more familiar with these issues?”
The world is in the midst of a Type II Diabetes epidemic.
In 2008 and 2009, many new studies have been published concerning links between pollutants and the onset of Type II Diabetes. The key study which got world scientists looking into these links in the last several years was the one conducted by Dr. Duk-Hee Lee (full text of that study is below). She has also published subsequent studies on this topic. Here is a quote from Dr. Miquel Porta from the prestigious journal ‘The Lancet’ regarding Dr. Lee’s findings:
“Another striking finding in Lee and co-workers’ study is that there was no association between obesity and diabetes in individuals with non-detectable levels of persistent organic pollutants. Obesity was a risk factor for diabetes only if people had blood concentrations of these pollutants above a certain level. This finding might imply that virtually all the risk of diabetes conferred by obesity is attributable to persistent organic pollutants, and that obesity is only a vehicle for such chemicals. This possibility is shocking.”
Here also, is the full text of Dr. Porta’s letter to The Lancet regarding that important Lee study. I hope you will share this email with anyone who has not seen it and might find it of interest for their research. All the best to you.
For Land and Life,
John H.W. Hummel,
611 Eighth Street,
Nelson, British Columbia,
Canada V1L 3A6
August 12, 2006
Persistent organic pollutants and the burden of diabetes
Miquel Porta a, b, email@example.com
Studies from the USA1,2 have drawn attention to the possibility that persistent organic pollutants might contribute to cause diabetes.3-6 Dioxins, polychlorinated biphenyls, dichlorodiphenyldichloroethylene (DDE, the main degradation product of the pesticide dichlorodiphenyltrichloroethane [DDT]), trans-nonachlor, hexachlorobenzene, and the hexachlorociclohexanes (including lindane) are some of the persistent organic pollutants most commonly found in human beings.7,8 Lipophilic and highly resistant to degradation, these pollutants are present in many fatty foods, usually at low concentrations.9 Because they contaminate virtually all people, even if they confer only a low individual risk of diabetes, these pollutants might have a substantial overall population effect.10
Dae-Hee Lee and colleagues’ recent study1 is the first to analyse serum concentrations of persistent organic pollutants and fasting plasma-glucose concentrations in a random sample of a general population. Previous studies have focused on selected populations, often occupationally or accidentally exposed to high levels of such pollutants. Not studying a less-exposed group might have led to a blurring of risks. Widely prevalent exposures are particularly difficult to isolate as causal agents.3 Concentrations of persistent organic pollutants in the study are typical of levels in many societies globally, and the risk of diabetes seems higher than ever. After adjustment for age, sex, race, income, lipids, body-mass index, and waist circumference, Lee and colleagues showed that the prevalence of diabetes was more than five times higher in groups with higher concentrations of polychlorinated biphenyl 153, oxychlordane, or trans-nonachlor than in those with lower concentrations. The prevalence of diabetes doubled and tripled in those in the upper quintiles of DDE and other compounds.1
Lee and co-workers adjusted their results by multiple factors.1 Such adjustment is fine if we wish to isolate the “pure” effect of persistent organic pollutants on diabetes separately from that of obesity, age, or income. However, adjustment by body-mass index and waist circumference might be an overadjustment, because dietary fats are the main source of persistent organic pollutants for human beings, and the body burden of these lipophilic chemicals often increases with increasing body-mass index. Crude or less adjusted prevalence odds ratios would provide information about the actual prevalence of diabetes in people with specific concentrations of these pollutants. Indeed, a priority should be to assess the validity of the study’s1 main finding: diabetes might be several times more prevalent in people with higher concentrations of these pollutants than in those with lower or no detectable levels. Causal inferences need to be extremely cautious. The cross-sectional nature of Lee’s study, in particular, prompts assessment of the direction of the association: might diabetes cause a higher accumulation of persistent organic pollutants? Unfortunately, data for the toxicokinetics of these pollutants in patients with diabetes are scarce, while many studies indicate that most persistent organic pollutants are resistant to active metabolism.1,7,8 Even if diabetes is some day shown to be the first major disease favouring accumulation of persistent organic pollutants, patients and clinicians would need to cope with the consequences: individuals with diabetes would be more likely to experience the adverse effects of these pollutants.6
Another striking finding in Lee and co-workers’ study is that there was no association between obesity and diabetes in individuals with non-detectable levels of persistent organic pollutants. Obesity was a risk factor for diabetes only if people had blood concentrations of these pollutants above a certain level. This finding might imply that virtually all the risk of diabetes conferred by obesity is attributable to persistent organic pollutants, and that obesity is only a vehicle for such chemicals. This possibility is shocking. Standard measures were used for body-mass index, but weight changes were not considered. Weight gains and weight losses in individuals with and without diabetes will be difficult to measure in large studies. But cohort studies with repeated measurements of individual weight and blood could help solve the puzzle.
An association between diabetes and blood concentrations of polychlorinated biphenyls has also been reported in a study from Michigan.2 Although the study was prospective, diabetes was self-assessed and participants had had accidental food contamination 30 years previously. Women in groups with higher serum concentrations of polychlorinated biphenyls had a twofold increased incidence of diabetes (again adjusted by several factors, including age and body-mass index). The crude incidence also doubled in men with the highest levels of polychlorinated biphenyls, but adjusted results were non-significant.
Exposure to many persistent organic pollutants has fluctuated in the past 60 years: birth cohort and period effects are plausible. But time-series and age-period cohort analyses of the potential link between persistent organic pollutants and diabetes are not available. Ecological and individual-based studies would allow estimations to be made of the fraction of diabetes that is influenced by persistent organic pollutants, other environmental agents, genetic factors such as susceptibility haplotypes, and by their interactions.3-6
The causal role of persistent organic pollutants in diabetes is more likely to be contributory and indirect-eg, through immunosuppressant, non-genotoxic, perhaps epigenetic mechanisms.3-7,11,12 A proper understanding of how genes and persistent organic pollutants interact to cause diabetes is important both for primary prevention and to advance basic knowledge on diabetogenic mechanisms. When assessing the mechanisms linking diet, fat intake, obesity, and diabetes, persistent organic pollutants should also be considered. We need a better understanding of the burden of diabetes that these pollutants might contribute to cause.
I declare that I have no conflict of interest.
a Institut Municipal d’Investigació Mèdica, Universitat Autònoma de Barcelona, E-08003 Barcelona, Spain;
b University of North Carolina, Chapel Hill, North Carolina, USA
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2 O Vasiliu, L Cameron, J Gardiner, P DeGuire, W Karmaus, Polybrominated biphenyls, polychlorinated biphenyls, body weight, and incidence of adult-onset diabetes mellitus, Epidemiology, Vol. 17, 2006, p. 352-359, .
3 M Rewers, P Zimmet, The rising tide of childhood type 1 diabetes: what is the elusive environmental trigger?, Lancet, Vol. 364, 2004, p. 1645-1647, .
4 D Daneman, Type 1 diabetes, Lancet, Vol. 367, 2006, p. 847-858, .
5 RB Remillard, NJ Bunce, Linking dioxins to diabetes: epidemiology and biologic plausibility, Environ Health Perspect, Vol. 110, 2002, p. 853-858, .
6 MP Longnecker, JL Daniels, Environmental contaminants as etiologic factors for diabetes, Environ Health Perspect, Vol. 109, Iss. suppl 6, 2001, p. 871-876, .
7 LG Hansen, Stepping backward to improve assessment of PCB congener toxicities, Environ Health Perspect, Vol. 106, Iss. suppl 1, 1998, p. 171-189, .
8 Department of Health and Human Services, Centers for Disease Control and Prevention, National Center for Environmental Health, Third National Report on Human Exposure to Environmental Chemicals, http://www.cdc.gov/exposurereport/3rd/, 2005, (accessed July 13, 2006), .
9 KS Schafer, SE Kegley, Persistent toxic chemicals in the food supply, J Epidemiol Community Health, Vol. 56, 2002, p. 813-817, .
10 M Porta, E Zumeta, Implementing the Stockholm treaty on POPs, Occupat Environ Med, Vol. 59, 2002, p. 651-652, .
11 A Luch, Nature and nurture-lessons from chemical carcinogenesis, Nat Rev Cancer, Vol. 5, 2005, p. 113-125, .
12 P Alonso-Magdalena, S Morimoto, C Ripoll, The estrogenic effect of bisphenol A disrupts pancreatic ?-cell function in vivo and induces insulin resistance, Environ Health Perspect, Vol. 114, 2006, p. 106-112,