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.

Early-life exposure to EDCs: role in childhood obesity and neurodevelopment.

A global assessment of phthalates burden and related links to health effects.

Abstract In 2015, EFSA established a temporary tolerable daily intake (t‐TDI) for BPA of 4 μg/kg body weight (bw) per day. In 2016, the European Commission mandated EFSA to re‐evaluate the risks to public health from the presence of BPA in foodstuffs and to establish a tolerable daily intake (TDI). For this re‐evaluation, a pre‐established protocol was used that had undergone public consultation. The CEP Panel concluded that it is Unlikely to Very Unlikely that BPA presents a genotoxic hazard through a direct mechanism. Taking into consideration the evidence from animal data and support from human observational studies, the immune system was identified as most sensitive to BPA exposure. An effect on Th17 cells in mice was identified as the critical effect; these cells are pivotal in cellular immune mechanisms and involved in the development of inflammatory conditions, including autoimmunity and lung inflammation. A reference point (RP) of 8.2 ng/kg bw per day, expressed as human equivalent dose, was identified for the critical effect. Uncertainty analysis assessed a probability of 57–73% that the lowest estimated Benchmark Dose (BMD) for other health effects was below the RP based on Th17 cells. In view of this, the CEP Panel judged that an additional uncertainty factor (UF) of 2 was needed for establishing the TDI. Applying an overall UF of 50 to the RP, a TDI of 0.2 ng BPA/kg bw per day was established. Comparison of this TDI with the dietary exposure estimates from the 2015 EFSA opinion showed that both the mean and the 95th percentile dietary exposures in all age groups exceeded the TDI by two to three orders of magnitude. Even considering the uncertainty in the exposure assessment, the exceedance being so large, the CEP Panel concluded that there is a health concern from dietary BPA exposure.

Re‐evaluation of the risks to public health related to the presence of bisphenol A (BPA) in foodstuffs

Phthalate exposure and neurodevelopment: A systematic review and meta-analysis of human epidemiological evidence.

Environmental exposure to low-level lead (Pb) co-occurring with other neurotoxicants in early life and neurodevelopment of children.

Childhood developmental disorders and related problems such as learning disabilities and attention deficit hyperactivity disorder (ADHD) account for a growing burden on the family, education and health care systems. Exposure to environmental chemicals such as bisphenol A (BPA) and phthalates may play a role in the development of child behavioral problems. Using cross-sectional data from Cycle 1 of the Canadian Health Measures Survey (CHMS), we examined the potential association between urinary concentrations of BPA and various phthalate metabolites and child learning and behavioral problems, considering important covariates such as gender, blood lead and environmental tobacco smoke (ETS). The Strengths and Difficulties Questionnaire (SDQ) outcomes of interest were emotional symptoms, hyperactivity/inattention, and a total difficulties score with borderline and abnormal scores grouped together and compared with children with normal scores. Other outcomes studied included any reported learning disability, a subset of learning disabilities reported as ADD/ADHD (attention deficit disorder) and use of psychotropic medications in the past month. Among children ages 6-11 years, the prevalences of any learning disability, ADD, and ADHD were 8.7%, 1.5% and 2.8%, respectively. Estimated prevalences for SDQ hyperactivity/inattention, emotional symptoms and total difficulties scores were 16.9%, 15.0%, and 13.0%, respectively. Child's urinary BPA was associated with taking psychotropic medications (OR 1.59; 95% CI 1.05-2.40). Urinary MBzP concentration was significantly associated with emotional symptoms in girls (OR 1.38 95% CI 1.09-1.75) but not in boys (OR 1.05 95% CI 0.82-1.36).) Blood lead was significantly associated with several of the outcomes examined, with a significant interaction observed between prenatal smoking and blood lead for the total difficulties score (OR=10.57; 95% CI 2.81-39.69 vs. OR=1.98; 95% CI 1.41-2.79 if mother did not smoke during pregnancy). Although limited by the cross-sectional nature of the study which precludes examining causation, the results suggest that although some indicators of child behavior were significantly associated with their urinary BPA and phthalate concentrations, the major chemical associated with adverse behavioral indicators was lead.

Bisphenol A, phthalates and lead and learning and behavioral problems in Canadian children 6-11 years of age: CHMS 2007-2009.

Processed data for CHMS 2007-2009: Bisphenol A, phthalates and lead and learning and behavioral problems in Canadian children 6-19 years of age.

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Bisphenol A, phthalates and lead and learning and behavioral problems in Canadian children 6-11 years of age: CHMS 2007-2009.

Processed data for CHMS 2007-2009: Bisphenol A, phthalates and lead and learning and behavioral problems in Canadian children 6-19 years of age.