MedWire News: Results from a novel Environment-Wide Association Study (EWAS) suggest that exposure to high levels of the pesticide-derivative heptachlor epoxide, polychlorinated biphenyls (PCBs), and the vitamin E compound γ-tocopherol significantly increase the risk for developing Type 2 diabetes.
The effect sizes seen were similar to the best results obtained from Genome-Wide Association Studies (GWAS), note the researchers, who also found that increased exposure to the vitamin A compound β-carotene appeared to reduce the risk for Type 2 diabetes.
Atul Butte (Stanford University School of Medicine, California, USA) and colleagues carried out a pilot EWAS, based on the same principle as a Genome-Wide Association Study (GWAS), which analyzed 266 unique environmental factors potentially linked to Type 2 diabetes.
The team used data from the Centers for Disease Control (CDC) National Health and Nutrition Examination Survey (NHANES) cohorts from years 1999 to 2006 inclusive, with sample numbers ranging from 503 to 3318 per survey (four in total). Degree of exposure to the 266 environmental factors was recorded in the surveys. Type 2 diabetes was defined as a fasting blood sugar concentration of 126 mg/dl or above.
Following adjustment for factors such as age, gender, body mass index, ethnicity, and socioeconomic status, the authors found that a one standard deviation (SD) increase in degree of exposure to heptachlor epoxide, PCBs, or γ-tocopherol increased the relative risk for Type 2 diabetes 1.7, 2.2, and 1.5 fold, respectively, across three of the four cohorts.
Conversely, a one SD increase in exposure to β-carotenes decreased the relative risk for developing Type 2 diabetes in all four cohorts by 40%.
“These results demand a rethinking and restructuring of studies that study disease in the genomics context,” write Butte et al in the journal PLoS ONE.
“The time is ripe to usher in ‘enviromics,’ the study of a wide array of environmental factors in relation to health and biology,” they add.
“Even in this study based on prior collected epidemiological measures, environmental factors can be found with effect sizes comparable to the best loci yet found by GWAS.”
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