Will Simmons1, Shao Lin2, Thomas J Luben3, Scott C Sheridan4, Peter H Langlois5, Gary M Shaw6, Jennita Reefhuis7, Paul A Romitti8, Marcia L Feldkamp9, Wendy N Nembhard10, Tania A Desrosiers11, Marilyn L Browne12, Jeanette A Stingone13. 1. Department of Epidemiology, Columbia University, 722 West 168(th) Street, NY, New York 10032, USA. 2. Department of Epidemiology and Biostatistics, University at Albany, 1 University Place, Rensselaer, NY 12144, USA; Department of Environmental Health Sciences, University at Albany, 1 University Place, Rensselaer, NY, 12144, USA. 3. Office of Research and Development, U.S. Environmental Protection Agency, 109 T.W. Alexander Drive, RTP, NC 27711, USA. 4. Department of Geography, Kent State University, 325 S. Lincoln Street, Kent, OH 44242, USA. 5. Department of Epidemiology, Human Genetics, and Environmental Science, University of Texas School of Public Health, 1616 Guadalupe Street, Austin, TX 78701, USA. 6. Stanford School of Medicine, 453 Quarry Road, Stanford, CA 94305, USA. 7. National Center on Birth Defects and Developmental Disabilities, Centers for Disease Control and Prevention, 1600 Clifton Road, Atlanta, GA 30333, USA. 8. Department of Epidemiology, The University of Iowa, 145 N. Riverside Drive, Iowa City, IA 52242, USA. 9. Department of Pediatrics, University of Utah School of Medicine, 295 Chipeta Way, Salt Lake City, UT 84108, USA. 10. Departments of Pediatrics and Epidemiology, University of Arkansas for Medical Sciences, 4301 W Markham Street, Little Rock, AR 72205, USA. 11. Department of Epidemiology, University of North Carolina, 135 Dauer Drive, Chapel Hill, NC 27599, USA. 12. Department of Epidemiology and Biostatistics, University at Albany, 1 University Place, Rensselaer, NY 12144, USA; Birth Defects Registry, New York State Department of Health, Corning Tower, Empire State Plaza, Albany, NY 12237, USA. 13. Department of Epidemiology, Columbia University, 722 West 168(th) Street, NY, New York 10032, USA. Electronic address: j.stingone@columbia.edu.
Abstract
BACKGROUND/ OBJECTIVE: Research suggests gestational exposure to particulate matter ≤2.5 μm (PM2.5) and extreme heat may independently increase risk of birth defects. We investigated whether duration of gestational extreme heat exposure modifies associations between PM2.5 exposure and specific congenital heart defects (CHDs). We also explored nonlinear exposure-outcome relationships. METHODS: We identified CHD case children (n = 2824) and non-malformed live-birth control children (n = 4033) from pregnancies ending between 1999 and 2007 in the National Birth Defects Prevention Study, a U.S. population-based multicenter case-control study. We assigned mothers 6-week averages of PM2.5 exposure during the cardiac critical period (postconceptional weeks 3-8) using the closest monitor within 50 km of maternal residence. We assigned a count of extreme heat days (EHDs, days above the 90th percentile of daily maximum temperature for year, season, and weather station) during this period using the closest weather station. Using generalized additive models, we explored logit-nonlinear exposure-outcome relationships, concluding logistic models were reasonable. We estimated joint effects of PM2.5 and EHDs on six CHDs using logistic regression models adjusted for mean dewpoint and maternal age, education, and race/ethnicity. We assessed multiplicative and additive effect modification. RESULTS: Conditional on the highest observed EHD count (15) and at least one critical period day during spring/summer, each 5 μg/m3 increase in average PM2.5 exposure was significantly associated with perimembranous ventricular septal defects (VSDpm; OR: 1.54 [95% CI: 1.01, 2.41]). High EHD counts (8+) in the same population were positively, but non-significantly, associated with both overall septal defects and VSDpm. Null or inverse associations were observed for lower EHD counts. Multiplicative and additive effect modification estimates were consistently positive in all septal models. CONCLUSIONS: Results provide limited evidence that duration of extreme heat exposure modifies the PM2.5-septal defects relationship. Future research with enhanced exposure assessment and modeling techniques could clarify these relationships.
BACKGROUND/ OBJECTIVE: Research suggests gestational exposure to particulate matter ≤2.5 μm (PM2.5) and extreme heat may independently increase risk of birth defects. We investigated whether duration of gestational extreme heat exposure modifies associations between PM2.5 exposure and specific congenital heart defects (CHDs). We also explored nonlinear exposure-outcome relationships. METHODS: We identified CHD case children (n = 2824) and non-malformed live-birth control children (n = 4033) from pregnancies ending between 1999 and 2007 in the National Birth Defects Prevention Study, a U.S. population-based multicenter case-control study. We assigned mothers 6-week averages of PM2.5 exposure during the cardiac critical period (postconceptional weeks 3-8) using the closest monitor within 50 km of maternal residence. We assigned a count of extreme heat days (EHDs, days above the 90th percentile of daily maximum temperature for year, season, and weather station) during this period using the closest weather station. Using generalized additive models, we explored logit-nonlinear exposure-outcome relationships, concluding logistic models were reasonable. We estimated joint effects of PM2.5 and EHDs on six CHDs using logistic regression models adjusted for mean dewpoint and maternal age, education, and race/ethnicity. We assessed multiplicative and additive effect modification. RESULTS: Conditional on the highest observed EHD count (15) and at least one critical period day during spring/summer, each 5 μg/m3 increase in average PM2.5 exposure was significantly associated with perimembranous ventricular septal defects (VSDpm; OR: 1.54 [95% CI: 1.01, 2.41]). High EHD counts (8+) in the same population were positively, but non-significantly, associated with both overall septal defects and VSDpm. Null or inverse associations were observed for lower EHD counts. Multiplicative and additive effect modification estimates were consistently positive in all septal models. CONCLUSIONS: Results provide limited evidence that duration of extreme heat exposure modifies the PM2.5-septal defects relationship. Future research with enhanced exposure assessment and modeling techniques could clarify these relationships.
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