Environmental causes may be contributing to the increasing prevalence of type 2 diabetes (T2D).1 Growing evidence suggests that endocrine-disrupting chemicals (EDCs) such as phthalates, dichlorodiphenyldichloroethylene (DDE), and perfluoroalkyl substances (PFAS) are causing people to develop T2D.1 Diabetes is the primary cause of blindness, kidney failure, and nontraumatic amputations in adult Americans.2 The disease is also implicated in the pathogenesis of cardiovascular disease, which is the leading cause of death in the United States.2
In the United States, the diabetes burden is far greater in the African American, Latino, and lower socioeconomic populations.3 While 9.1% of non-Hispanic whites have diabetes, 17.9% of African Americans and 20.5% of Mexican Americans have the disease.3
As the number of diabetes cases in the United States continues to exceed 30.3 million people, with another 84.1 million people with prediabetes, clinicians and researchers are searching for ways to slow this disease, which has an economic burden >$245 billion annually.2 It is a challenge to avoid contact with EDCs because they are found in personal care products, pesticides, food containers, plastic toys, flooring, carpeting, and food products such as meat, dairy, and fish.2 EDCs also indirectly affect people through exposure to contaminated air, soil, and water.2
In water, the chemicals implicated in T2D incidence include arsenic,4 triclosan, perchlorate, alkylphenols, phthalates, cadmium, lead, and mercury.2 “My advice to clinicians who live in areas where arsenic is known to be a problem in drinking water, such as northern New England and the American Southwest, is that they become knowledgeable about the health hazards of arsenic and advise their patients to minimize or eliminate their consumption of arsenic-contaminated water,” suggested
Philip J. Landrigan, MD, MSc, dean for global health and professor of environmental medicine, public health, and pediatrics at the Icahn School of Medicine at Mount Sinai in New York City.
Foodborne and agricultural sources of contaminants include the pesticides dichlordiphenyltrichloroethane (DDT), DDE, trans-nonachlor, oxychlordane, mirex, and dieldrin.2 An extreme example of contamination via air pollution occurred in Italy in 1976 when a chemical plant explosion released 2,3,7,8-tetrachlorodibenzo-p-dioxin into the atmosphere, resulting in an increase in T2D-related mortality over the subsequent 10 years.2
Effect of Environmental Contaminants on T2D
A recent study by Trasande and colleagues found that reducing exposure of Swedish men and women aged 70 years (N=1016) to EDCs led to a 13% decrease in the number of T2D cases in the population (95% CI, 2%-22%).5 When the researchers extrapolated the data to determine real-world cost savings in Europe, they estimated that 152,481 T2D cases could be prevented, saving €4.51 billion (approximately $5.2 billion) per year in related costs.5
As part of the Nurses’ Health Study II, Sun and colleagues discovered 793 incident cases of women (mean age, 45.3 years) with T2D in a nested case-control study.6 The mean 6.7-year follow-up measured levels of 5 major PFASs, including perfluorooctanesulfonic acid (PFOS), perfluorooctanoic acid (PFOA), perfluorohexanesulfonate, perfluorononanoic acid, and perfluorodecanoic acid.6
After adjusting for common T2D risk factors such as body mass index, family history, and physical activity, the investigators found that higher plasma concentrations of PFOS and PFOA led to a high risk of T2D (odds ratio [OR], 1.62; 95% CI, 1.09-2.41; Ptrend =.02 and OR 1.54; 95% CI, 1.04-2.28; Ptrend =.03), respectively.6 The researchers also reported that individuals who consumed certain foods, such as seafood and popcorn, had greater exposure to PFAS compared with participants in the control group. While the chemicals PFOS and PFOA are no longer produced in the United States, they remain in most Americans.6
“According to our study, people with high circulating levels of PFAS are at higher risk of T2D, therefore they may benefit from glucose monitoring for early diagnosis and prevention,” advised study coauthor and research fellow Geng Zong, PhD, in the department of nutrition at Harvard’s T.H. Chan School of Public Health, in Boston, Massachusetts.
Persistence of Effects of EDCs
Indeed, the challenging aspect of EDCs is their persistence and omnipresence in our bodies and in the environment.7 Song and colleagues found in a 49-study meta-analysis of multinational trials that persistent and nonpersistent EDCs contributed to T2D risk. Persistent EDCs including dioxin, polychlorinated biphenyl (PCB), and chlorinated pesticides significantly affected T2D risk: serum concentration pooled relative risks (RRs) were 1.91 (95% CI, 1.44-2.54), 2.39 (95% CI, 1.86-3.08), and 2.30 (95% CI, 1.81-2.93), respectively.7 Urinary concentrations of bisphenol A (BPA) and phthalates also contributed to T2D risk: pooled RRs were 1.45 (95% CI, 1.13-1.87) and 1.48 (95% CI, 0.98-2.25), respectively.7
“I would advise clinicians to review some of the extreme cases of hormonal disorders such as PCOS [polycystic ovary syndrome] in women and Klinefelter syndrome in men for the potential dangers of EDCs, because available data suggest that much of the EDCs exert their biological effects through either the estrogenic or androgenic signaling pathways,” said study coauthor Simin Liu, MD, MS, ScD, MPH, professor of epidemiology, surgery, and medicine at Brown University in Providence, Rhode Island.
Greenery May Be the Pollution Solution
A Canadian study may offer a small antidote to chemical exposure.8 Crouse and colleagues discovered that when urban adults (N=1.3 million) surrounded themselves within greener environments, they reduced their risk of mortality for 6 major causes of death, including nonaccidental causes (HR, 0.915; 95% CI, 0.905-0.924), including cardiovascular disease plus T2D (HR, 0.911; 95% CI, 0.895-0.928).8 The decade-long study measured the amount of green space within 250 m and 500 m of the participants’ residences as recorded by satellite images. The greatest protective effect of living among urban greenness was seen in participants aged 35 to 74 years.8
“The next steps for this field of research are to understand how different kinds of green areas, and the qualities of these green areas, may benefit health differently,” explained sociologist Dan L. Crouse, PhD, from the University of New Brunswick, in
Fredericton, Canada. “For an older person, perhaps having a garden is something that will bring them pleasure and get them out of their house, but for a child, having a place to run and play outside is more important than any flowers or plants in a garden.”
- Lind PM, Lind L. Endocrine-disrupting chemicals and risk of diabetes: an evidence-based review [published online May 9, 2018]. Diabetologia. doi: 10.1007/s00125-018-4621-3
- Shaikh S, Jagai JS, Ashley C, Zhou S, Sargis RM. Underutilized and under threat: environmental policy as a tool to address diabetes risk. Curr Diab Rep. 2018;18(5):25.
- Ruiz D, Becerra M, Jagai JS, Ard K, Sargis RM. Disparities in environmental exposures to endocrine-disrupting chemicals and diabetes risk in vulnerable populations. Diabetes Care. 2018;41(1):193-205.
- Landrigan PJ. The power of environmental protection: arsenic in drinking water. Lancet Public Health. 2017;2(11):e488-e489.
- Trasande L, Lampa E, Lind L, Lind PM. Population attributable risks and costs of diabetogenic chemical exposures in the elderly. J Epidemiol Community Health. 2017;71(2):111-114.
- Sun Q, Zong G, Valvi D, Nielsen F, Coull B, Grandjean P. Plasma concentrations of perfluoroalkyl substances and risk of type 2 diabetes: a prospective investigation among U.S. women. Environ Health Perspect. 2018;126(3):037001.
- Song Y, Chou EL, Baecker A, et al. Endocrine-disrupting chemicals, risk of type 2 diabetes, and diabetes-related metabolic traits: a systematic review and meta-analysis. J Diabetes. 2016;8(4):516-532.
- Crouse DL, Pinault L, Balram A, et al. Urban greenness and mortality in Canada’s largest cities: a national cohort study. Lancet Planet Health. 2017;1(7):e289-e297.