Environmental Pollutants: A Risk Factor for Obesity and Diabetes

Pollution has been associated with health complications that can have lingering effects. Air pollution, for example, not only affects the respiratory system, but is also associated with heart disease and stroke. According to a report by the American Heart Association, pollution, from traffic, factory exhausts, power generation, wildfires, smoking, and cooking on wood stoves, can lead to cardiac issues. Elderly heart patients experience the most impact, including the possibility of myocardial infarction. Additionally, pollution-mediated inflammation in the heart can also lead to cardiovascular (CV) complications.¹

Surprisingly, environmental air pollutants also belong on the list of risk factors for obesity, along with the more familiar high-fat diet, lack of exercise, and agricultural policies. Prenatal exposure to polycyclic aromatic hydrocarbons (PAHs; carcinogens and endocrine disruptors produced as a result of incomplete combustion) was found to be associated with childhood obesity in a study that monitored children born to African American and Hispanic mothers living in the Bronx or Northern Manhattan.² By age 5 years, 21% of the children were considered obese, and by age 7 years, 25%, with the children’s obesity found to be associated with the mother’s exposure to airborne PAHs during pregnancy.²

An evaluation of PAHs in the urine of 3189 children and adolescents, aged 6 to 19 years, who participated in the 2001 to 2006 National Health and Nutrition Examination Survey, found total urinary PAH metabolites in those aged 6 to 11 years to be associated with higher body mass index, greater waist circumference, and greater prevalence of obesity. In adolescents (aged 12 to 19 years), a positive but less consistent association was observed for all 3 indices.³ In vitro and in vivo studies have identified the lipogenesis-promoting endocrine effects of PAHs, such as the regulation of PPAR in adipocytes and inhibition of the thyroid hormone receptor.⁴

Scientists at the Institut de Recherches Cliniques de Montréal (IRCM), Canada, found that persistent organic pollutants (POPs) can cause endocrine effects in metabolically abnormal obese (MAO) patients, but not in metabolically healthy but obese (MHO) patients. Serum analysis of these 2 types of patients revealed distinct POP profiles.⁵ The study demonstrated that MHO patients are protected from the effects of POPs, and IRCM is directing ongoing efforts toward identifying the protective factors at work.

POPs—including polychlorinated biphenyls (PCBs), dichlorodiphenyl trichloroethane (DDT), and dioxins—are chemicals produced for use in agriculture, disease control, manufacturing, and industry, among them are. POPs are hard to contain—being easily transported by water and wind–and due to their lipid solubility can accumulate in the body fat of both people and wildlife. Their potential negative effects are multiplied via a process called biomagnification, whereby contaminants present in small amounts at the bottom of the food chain grow increasingly concentrated as they move from one creature to another, ultimately becoming a significant hazard to predators at the top of the chain.⁶

Researchers in Belgium have identified a correlation between POPs, obesity, and diabetes. Following evaluation of 28 different POPs among 151 obese and 44 normal-weight individuals, the authors concluded that exposure to environmentally relevant levels of POPs can be both diabetogenic and obesogenic.⁷

Efforts to Control Pollution-Related Diabetes

A workshop conducted by the National Institute of Environmental Health Sciences (NIEHS), a division of the National Toxicology Program, evaluated the available data on the association between environmental pollution and public health. The participating scientists concluded that several environmental exposures were associated with type 2 diabetes mellitus. Additionally, analysis of the existing literature supported the existence of the “developmental obesogen” hypothesis. According to this hypothesis, chemical exposures can alter adipocyte differentiation, or the development of neural circuits that regulate feeding behavior, and in turn increase the risk of obesity. When combined later in life with a diet that is high in sugar, fat, and carbohydrates, the effect of the chemical exposure may become more obvious.⁸

The workshop identified a critical knowledge gap in the understanding of the effects of pollution on type 1 diabetes mellitus. It also provided suggestions for appropriate end points or biomarkers and clinically accepted measures for diabetes and obesity.

With a mission to further the dialogue on environmental factors influencing human health, the Collaborative on Health and the Environment (CHE) facilitates collaborations that can prevent environmental atrocities and improve health.⁹ The aim of CHE’s Diabetes-Obesity Spectrum Working Group is to stimulate scientific efforts that demonstrate how environmental chemicals and other environmental or societal factors may contribute to the development and management of obesity, metabolic syndrome, and all types of diabetes.¹⁰

Despite the scientific community’s extensive knowledge about the influence of environmental pollution on numerous disease states, there seems to be a lack of public awareness. When contacted by e-mail, representatives at both the NIEHS and the American Diabetes Association informed Evidence-Based Diabetes Management that there were no specific programs at either organization to draw attention to this growing risk in diabetes. Kristina Thayer, PhD, director, Office of Health Assessment and Translation, NIEHS, said in her e-mail that although federal agencies such as the FDA and the environmental health agency regulate environmental pollution measures, none have been regulated based on diabetes or obesity so far.

With obesity and associated metabolic disorders, diet and exercise are emphasized as risk factors, generally to the exclusion of all others. There is a need to adjust this perception to include the daily exposure to pollutants to our list of preventable causes of diabetes, among a host of other diseases.References

1. Air Pollution and Heart Disease, Stroke. American Heart Association. http://www.heart .org/HEARTORG/Conditions/More/MyHeartandStrokeNews/Air-Pollution-and-Heart-Disease-Stroke_UCM_442923_Article.jsp. Accessed June 16, 2014.

2. Rundle A, Hoepner L, Hassoun A, et al. Association of childhood obesity with maternal exposure to ambient air polycyclic aromatic hydrocarbons during pregnancy. Am. J Epidemiol. 2012;175(11):1163-1172.

3. Scinicariello F, Buser MC. Urinary polycyclic aromatic hydrocarbons and childhood obesity: NHANES (2001-2006). Environ Health Perspect. 2014;122(3):299-303.

4. Sun H, Shen OX, Xu XL, Song L, Wang XR. Carbaryl, 1-naphthol and 2-naphthol inhibit the beta-1 thyroid hormone receptor-mediated transcription in vitro. Toxicology. 2008;249(203):238-242.

5. Gauthier MS, Rabasa-Lhoret R, Prud’homme D, et al. The metabolically healthy but obese phenotype is associated with lower plasma levels of persistent organic pollutants as compared to the metabolically abnormal obese phenotype. J Clin Endocrinol Metab. 2014;99(6):E1061-E1066.

6. Persistent organic pollutants: a global issue, a global response. United States Environmental Protection Agency. http://www.epa.gov/oia/toxics/pop.html#pops. Accessed June 16, 2014.

7. Dirinck EL, Dirtu AC, Govindan M, Covaci A, Van Gaal LF, Jorens PG. Exposure to persistent organic pollutants: relationship with abnormal glucose metabolism and visceral adiposity. Diabetes Care. 2014;37(7):1951-1958.

8. Thayer KA, Heindel JJ, Bucher JR, Gallo MA. Role of environmental chemicals in diabetes and obesity: a national toxicology program workshop review. Environ Health Perspect. 2012;120:779-789.

9. Mission. The Collaborative on Health and the Environment website. http://www.healthandenvironment.org/about/mission. Accessed June 26, 2014.

10. Diabetes-Obesity Spectrum. The Collaborative on Health and the Environment website. http://www.healthandenvironment.org/initiatives/diabetes. Accessed June 26, 2014.

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