Abstract

Background and objectiveManganese, lead, arsenic and mercury are common neurotoxic metals in the environment. Nonetheless, the relationship between prenatal exposure to low doses of neurotoxic metals and neurodevelopment in children is not clear. The objective of this study was to explore the relationship between in utero exposure to environmental neurotoxic metals and neurodevelopment at 2 years of age. MethodsThe population of this study came from the Taiwan Birth Panel Study. We included 230 pairs of non-smoking mothers without any occupational exposure and their singleton full-term children. The information about exposure during pregnancy was obtained using a structured questionnaire, and the manganese, lead, arsenic and mercury levels in umbilical cord blood samples were analyzed using inductively coupled plasma mass spectrometry. We used the Comprehensive Developmental Inventory for Infants and Toddlers (CDIIT) to evaluate the developmental status of each child at 2 years of age, and we examined the association of in utero exposure to environmental metals and neurodevelopment using linear regression models. ResultsThe median concentrations of manganese, lead, arsenic and mercury in the cord blood samples in this study were 47.90µg/L (range, 17.88–106.85µg/L), 11.41µg/L (range 0.16–43.22µg/L), 4.05µg/L (range, 1.50–12.88µg/L) and 12.17µg/L (range, 1.53–64.87µg/L), respectively. After adjusting for maternal age, infant gender, environmental tobacco smoke during pregnancy and after delivery, Home Observation for Measurement of the Environment Inventory results, and arsenic and mercury levels in cord blood, we found that manganese and lead levels above the 75th percentile had a significant adverse association with the overall (β=−7.03, SE=2.65, P=0.0085), cognitive (β=−8.19, SE=3.17, P=0.0105), and language quotients (β=−6.81, SE=2.73, P=0.0133) of the CDIIT. ConclusionsIn utero exposure to environmental manganese and lead may have an adverse association with neurodevelopment at 2 years of age, and there is an interaction effect between the manganese and lead levels in the cord blood that could aggravate the effect.

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