Parental Thyroid Hormone Levels and Brain Development
Adequate levels of in utero thyroid hormones are critical for brain development. Maternal thyroid impairment has been suggested as an underlying mechanism for developmental impairments resulting from exposures to environmental chemicals such as PCBs and polybrominated diphenyl ethers (PBDEs) used as flame retardants (Winneke 2011). Pesticides have been found to interfere with thyroid function by preventing iodine uptake [e.g., mancozeb, thiocyanates, 2,4-D (2,4-dichlorophenoxyacetic acid)] and peroxidation (e.g., aminotriazole, endosulfan, malathion), and by preventing the conversion of thyroxine (T4) to triiodothyronine (T3) (e.g., aminotriazole, dimethoate, fenvalerate) (Colborn 2004). In a review of the effects of mild-to-moderate iodine deficiency in humans, diminished maternal T4 was associated with disorders of mental and/or psychomotor development (Zimmermann 2007).
Roman (2007) hypothesized that even transient intrauterine deficits in thyroid hormones (as little as 3 days) at critical points in gestation could alter the cortical architecture, interfering with neuronal migration and Purkinje cell growth, indications of both of which have been observed in autopsy studies of autism (Fatemi et al. 2002; Wegiel et al. 2010). Because the human fetus does not start producing sufficient thyroid hormones until gestational week 18 (Burrow et al. 1994), adequate maternal thyroid hormones are critical to neurodevelopment in early fetal life, particularly for reelin-regulated neuronal migration (Pathak et al. 2011). Additionally, sex-mediated effects have been observed after exposure to chlorpyrifos on GD17–20, with the induction of increased levels of free T4 in female but not male mice (Haviland et al. 2009).
Environ Health Perspect. 2012;120(7):944-951. © 2012 National Institute of Environmental Health Sciences