Endocrine-disrupting chemicals (EDCs) might increase the risk of childhood neurodevelopmental disorders or obesity by disrupting hormone-mediated processes during critical periods of development
The developing fetus, infant and child might have enhanced sensitivity to environmental stressors such as EDCs and increased exposure to some EDCs due to developmentally appropriate behaviour, anatomy and physiology
The available epidemiological evidence suggest that prenatal bisphenol A and phthalate exposure is associated with adverse neurobehavioural outcomes in children, but not excess adiposity or risk of obesity or being overweight
Epidemiological studies show that prenatal PFAS exposure is associated with reduced fetal growth, excess adiposity and risk of being overweight or obese, but not neurobehavioural outcomes
Improving EDC exposure measurement, reducing confounding bias, identifying discrete periods of vulnerability and sexually dimorphic associations, and quantifying the effects of EDC mixtures will enhance inferences made from epidemiological studies
Endocrine-disrupting chemicals (EDCs) might increase the risk of childhood diseases by disrupting hormone-mediated processes that are critical for growth and development during gestation, infancy and childhood. The fetus, infant and child might have enhanced sensitivity to environmental stressors such as EDCs due to their rapid development and increased exposure to some EDCs as a consequence of development-specific behaviour, anatomy and physiology. In this Review, I discuss epidemiological studies examining the relationship between early-life exposure to bisphenol A (BPA), phthalates, triclosan and perfluoroalkyl substances (PFAS) with childhood neurobehavioural disorders and obesity. The available epidemiological evidence suggest that prenatal exposure to several of these ubiquitous EDCs is associated with adverse neurobehaviour (BPA and phthalates) and excess adiposity or increased risk of obesity and/or overweight (PFAS). Quantifying the effects of EDC mixtures, improving EDC exposure assessment, reducing bias from confounding, identifying periods of heightened vulnerability and elucidating the presence and nature of sexually dimorphic EDC effects would enable stronger inferences to be made from epidemiological studies than currently possible. Ultimately, improved estimates of the causal effects of EDC exposures on child health could help identify susceptible subpopulations and lead to public health interventions to reduce these exposures.
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The author would like to thank K. L. Hanson and R. Hauser for their helpful comments and edits on an earlier version of this manuscript. The author acknowledges support from the NIH (grants R00 ES020346, R01 ES025214, R01 ES024381 and R01 ES021357).
The author declares no competing financial interests.
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