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A chemical industry consultant with a competing interest (Bond) and his collaborator (Dietrich) dismiss over 20 cross-sectional studies and at least 7 prospective studies that have found links between persistent organic pollutants and diabetes. In this comment, they also ask for experimental studies supporting the view that environmental contaminants could affect glucose tolerance, neglecting more than a dozen of experimental in vivo and in vitro studies (see Ngwa et al 1 for references).
These authors also fail to acknowledge the carefully described reports from the Prospective Investigation of the Vasculature in Uppsala Seniors (PIVUS) study. Our brief report2 recently published in this journal advances knowledge regarding mixtures of chemicals and their collective role in diabetogenesis. Limitations of the PIVUS study which underlie our estimates of disease burden and costs have been carefully described previously,3–6 following scientific reporting criteria which Bond and Dietrich falsely accuse us of violating.
The authors of this letter fail to note that we acknowledged our ‘extrapolation on limited data’. We agree that further longitudinal studies are needed, ideally with: thousands of cases from several countries across the globe; higher participation rates; several 100 contaminants measured at repeated time points; and measurement of all potential confounders. These will serve to improve precision of the disease burden and cost estimates we have described,2 not to zero out the costs of chemically induced diabetes. Other studies have suggested that these costs are in the billions of dollars annually,7 and used the same economic methods we did.
Bond and Dietrich also fail to recognise the broader array of known health effects of the diabetogens we examined. Endocrine disrupting chemicals (EDCs) are likely to cost $340 billion in the USA8 and $163 billion in Europe.9 The main drivers of these costs are effects on the developing brain, but effects on male and female reproduction also contribute substantially. Phthalates were also identified to contribute to early cardiovascular mortality, independent of increases in diabetes and obesity, through reductions in serum testosterone.
Much of the doubt surrounding the effects of endocrine disruptors raised by the industry consultant and his colleague has been documented in this journal and others to be ‘manufactured’.10 ,11 In contrast, independent scientific entities, including the International Programme on Chemical Safety,12 Endocrine Society,13 ,14 the WHO and United Nations Environment Program15 and the International Federation of Gynecologists and Obstetricians,16 have reviewed studies demonstrating the relationship between EDC exposures and endocrine diseases in controlled animal studies and human populations, and called for the reduction in prenatal EDC exposures to prevent a broad array of problems across the life course. Consistent exposure–response data cohere with existing knowledge and document substantial effect sizes, after consideration of alternate explanations. Bond and Dietrich fail to present any data that contradict our findings, advance scientific knowledge or to reduce the urgency for prevention of chemical exposures that contribute to diabetes or any other metabolic, reproductive and neurodevelopmental disease and disability.
Twitter Follow Leonardo Trasande @leotrasande
Contributors LL wrote the first draft with PML. LT substantially revised and amplified the response, in consultation with EL.
Competing interests None declared.
Provenance and peer review Commissioned; internally peer reviewed.
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