|Abstract||Background: Prior animal and human studies of prenatal exposure to solvents including tetrachloroethylene (PCE) have shown increases in the risk of certain congenital anomalies among exposed offspring. Objectives: This retrospective cohort study examined whether PCE contamination of public drinking water supplies in Massachusetts influenced the occurrence of congenital anomalies among children whose mothers were exposed around the time of conception. Methods: The study included 1,658 children whose mothers were exposed to PCE-contaminated drinking water and a comparable group of 2,999 children of unexposed mothers. Mothers completed a self-administered questionnaire to gather information on all of their prior births, including the presence of anomalies, residential histories and confounding variables. PCE exposure was estimated using EPANET water distribution system modeling software that incorporated a fate and transport model. Results: Children whose mothers had high exposure levels around the time of conception had an increased risk of congenital anomalies. The adjusted odds ratio of all anomalies combined among children with prenatal exposure in the uppermost quartile was 1.5 (95% CI: 0.9, 2.5). No meaningful increases in the risk were seen for lower exposure levels. Increases were also observed in the risk of neural tube defects (OR: 3.5, 95% CI: 0.8, 14.0) and oral clefts (OR 3.2, 95% CI: 0.7, 15.0) among offspring with any prenatal exposure. Conclusion: The results of this study suggest that the risk of certain congenital anomalies is increased among the offspring of women who were exposed to PCE-contaminated drinking water around the time of conception. Because these results are limited by the small number of children with congenital anomalies that were based on maternal reports, a follow-up investigation should be conducted with a larger number of affected children who are identified by independent records.|
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|Name||Affiliation||Home page||Total pubs|
|Aschengrau A||Department of Epidemiology, Boston University School of Public Health, 715 Albany Street, Boston, MA 02118, USAfirstname.lastname@example.org||11|
|Gallagher LG||Department of Environmental Health, Boston University School of Public Health, Talbot 4W, 715 Albany Street, Boston, MA 02118, USAemail@example.com||4|
|Janulewicz PA||Department of Epidemiology, Boston University School of Public Health, Talbot 3E, 715 Albany Street, Boston, MA 02118, USAfirstname.lastname@example.org||2|
|Ozonoff DM||Department of Environmental Health, Boston University School of Public Health, Boston, MA, USAemail@example.com||4|
|Vieira VM||Department of Environmental Health, Boston University School of Public Health, Talbot 4W, 715 Albany Street, Boston, MA 02118, USAfirstname.lastname@example.org||4|
|Webster TF||Dept. of Environmental Health, Boston University School of Public Health, 715 Albany Street, Boston, MA 02118, USAemail@example.com||7|
|Weinberg JM||Department of Biostatistics, Boston University School of Public Health, Crosstown, 715 Albany Street, Boston, MA 02118, USAfirstname.lastname@example.org||2|
|Winter MR||Data Coordinating Center, Boston University School of Public Health, Crosstown, 715 Albany Street, Boston MA 02118, USAemail@example.com||2|
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