Hypospadias and maternal exposure to atrazine via drinking water in the National Birth Defects Prevention study Public Deposited

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  • Meyer, Robert
    • Affiliation: Gillings School of Global Public Health, Department of Maternal and Child Health
    • Other Affiliation: North Carolina Birth Defects Monitoring Program, State Center for Health Statistics, Raleigh, USA
  • Luben, Thomas J
    • Other Affiliation: National Center for Environmental Assessment, United States Environmental Protection Agency, Research Triangle Park, USA
  • Langlois, Peter
    • Other Affiliation: Texas Department of State Health Services, Birth Defects Epidemiology and Surveillance Branch, Austin, USA
  • Mosley, Bridget
    • Other Affiliation: Department of Pediatrics, Arkansas Children’s Hospital, Little Rock, USA
  • Weyer, Peter
    • Other Affiliation: Center for Health Effects of Environmental Contamination, University of Iowa, Iowa City, USA
  • Emch, Michael
    • Affiliation: College of Arts and Sciences, Department of Geography, Carolina Population Center
  • Olshan, Andrew
    • Affiliation: Gillings School of Global Public Health, Department of Epidemiology
  • Winston, Jennifer
    • Affiliation: Carolina Population Center
  • Band, Lawrence
    • Affiliation: College of Arts and Sciences, Department of Geography, UNC Institute for the Environment
  • Abstract Background Hypospadias is a relatively common birth defect affecting the male urinary tract. It has been suggested that exposure to endocrine disrupting chemicals might increase the risk of hypospadias by interrupting normal urethral development. Methods Using data from the National Birth Defects Prevention Study, a population-based case-control study, we considered the role of maternal exposure to atrazine, a widely used herbicide and potential endocrine disruptor, via drinking water in the etiology of 2nd and 3rd degree hypospadias. We used data on 343 hypospadias cases and 1,422 male controls in North Carolina, Arkansas, Iowa, and Texas from 1998–2005. Using catchment level stream and groundwater contaminant models from the US Geological Survey, we estimated atrazine concentrations in public water supplies and in private wells. We assigned case and control mothers to public water supplies based on geocoded maternal address during the critical window of exposure for hypospadias (i.e., gestational weeks 6–16). Using maternal questionnaire data about water consumption and drinking water, we estimated a surrogate for total maternal consumption of atrazine via drinking water. We then included additional maternal covariates, including age, race/ethnicity, parity, and plurality, in logistic regression analyses to consider an association between atrazine and hypospadias. Results When controlling for maternal characteristics, any association between hypospadias and daily maternal atrazine exposure during the critical window of genitourinary development was found to be weak or null (odds ratio for atrazine in drinking water = 1. 00, 95 % CI = 0.97 to 1.03 per 0.04 μg/day increase; odds ratio for maternal consumption = 1.02, 95 % CI = 0.99 to 1.05; per 0.05 μg/day increase). Conclusions While the association that we observed was weak, our results suggest that additional research into a possible association between atrazine and hypospadias occurrence, using a more sensitive exposure metric, would be useful.
Date of publication
  • doi:10.1186/s12940-016-0161-9
Resource type
  • Article
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  • In Copyright
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  • The Author(s).
  • English
Bibliographic citation
  • Environmental Health. 2016 Jul 15;15(1):76
  • BioMed Central

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