Eric Lavigne1, Abdool S Yasseen2, David M Stieb3, Perry Hystad4, Aaron van Donkelaar5, Randall V Martin5, Jeffrey R Brook6, Daniel L Crouse7, Richard T Burnett8, Hong Chen9, Scott Weichenthal10, Markey Johnson11, Paul J Villeneuve12, Mark Walker13. 1. Air Health Science Division, Health Canada, Ottawa, Ontario, Canada; School of Epidemiology, Public Health and Preventive Medicine, University of Ottawa, Ottawa, Ontario, Canada. Electronic address: eric.lavigne@hc-sc.gc.ca. 2. Ottawa Hospital Research Institute, Ottawa, Ontario, Canada; Better Outcomes Registry and Network Ontario, Ottawa, Ontario, Canada; Children's Hospital of Eastern Ontario Research Institute, Ottawa, Ontario, Canada. 3. Population Studies Division, Health Canada, Vancouver, British Columbia, Canada. 4. College of Public Health and Human Sciences, Oregon State University, Corvallis, OR, USA. 5. Department of Physics and Atmospheric Science, Dalhousie University, Halifax, Nova Scotia, Canada. 6. Air Quality Research Division, Environment Canada, Downsview, Ontario, Canada; Dalla Lana School of Public Health, University of Toronto, Toronto, Ontario, Canada. 7. Department of Sociology, University of New Brunswick, Fredericton, New Brunswick, Canada. 8. Population Studies Division, Health Canada, Ottawa, Ontario, Canada. 9. Dalla Lana School of Public Health, University of Toronto, Toronto, Ontario, Canada; Institute for Clinical Evaluative Sciences, Toronto, Ontario, Canada; Department of Epidemiology, Biostatistics and Occupational Health, McGill University, Montreal, Quebec, Canada. 10. Air Health Science Division, Health Canada, Ottawa, Ontario, Canada; Institute of Health: Science, Technology and Policy, Carleton University, Ottawa, Ontario, Canada. 11. Air Health Science Division, Health Canada, Ottawa, Ontario, Canada. 12. Department of Obstetrics and Gynecology, University of Ottawa, Ottawa, ON, Canada. 13. Ottawa Hospital Research Institute, Ottawa, Ontario, Canada; Better Outcomes Registry and Network Ontario, Ottawa, Ontario, Canada; Children's Hospital of Eastern Ontario Research Institute, Ottawa, Ontario, Canada; Public Health Ontario, Toronto, Ontario, Canada.
Abstract
BACKGROUND: Prenatal exposure to ambient air pollution has been associated with adverse birth outcomes, but the potential modifying effect of maternal comorbidities remains understudied. Our objective was to investigate whether associations between prenatal air pollution exposures and birth outcomes differ by maternal comorbidities. METHODS: A total of 818,400 singleton live births were identified in the province of Ontario, Canada from 2005 to 2012. We assigned exposures to fine particulate matter (PM2.5), nitrogen dioxide (NO2) and ozone (O3) to maternal residences during pregnancy. We evaluated potential effect modification by maternal comorbidities (i.e. asthma, hypertension, pre-existing diabetes mellitus, heart disease, gestational diabetes and preeclampsia) on the associations between prenatal air pollution and preterm birth, term low birth weight and small for gestational age. RESULTS: Interquartile range (IQR) increases in PM2.5 (2μg/m(3)), NO2 (9ppb) and O3 (5ppb) over the entire pregnancy were associated with a 4% (95% CI: 2.4-5.6%), 8.4% (95% CI: 5.5-10.3%) and 2% (95% CI: 0.5-4.1%) increase in the odds of preterm birth, respectively. Increases of 10.6% (95% CI: 0.2-2.1%) and 23.8% (95% CI: 5.5-44.8%) in the odds of preterm birth were observed among women with pre-existing diabetes while the increases were of 3.8% (95% CI: 2.2-5.4%) and 6.5% (95% CI: 3.7-8.4%) among women without this condition for pregnancy exposure to PM2.5 and NO2, respectively (Pint<0.01). The increase in the odds of preterm birth for exposure to PM2.5 during pregnancy was higher among women with preeclampsia (8.3%, 95% CI: 0.8-16.4%) than among women without (3.6%, 95% CI: 1.8-5.3%) (Pint=0.04). A stronger increase in the odds of preterm birth was found for exposure to O3 during pregnancy among asthmatic women (12.0%, 95% CI: 3.5-21.1%) compared to non-asthmatic women (2.0%, 95% CI: 0.1-3.5%) (Pint<0.01). We did not find statistically significant effect modification for the other outcomes investigated. CONCLUSIONS: Findings of this study suggest that associations of ambient air pollution with preterm birth are stronger among women with pre-existing diabetes, asthma, and preeclampsia. Crown
BACKGROUND: Prenatal exposure to ambient air pollution has been associated with adverse birth outcomes, but the potential modifying effect of maternal comorbidities remains understudied. Our objective was to investigate whether associations between prenatal air pollution exposures and birth outcomes differ by maternal comorbidities. METHODS: A total of 818,400 singleton live births were identified in the province of Ontario, Canada from 2005 to 2012. We assigned exposures to fine particulate matter (PM2.5), nitrogen dioxide (NO2) and ozone (O3) to maternal residences during pregnancy. We evaluated potential effect modification by maternal comorbidities (i.e. asthma, hypertension, pre-existing diabetes mellitus, heart disease, gestational diabetes and preeclampsia) on the associations between prenatal air pollution and preterm birth, term low birth weight and small for gestational age. RESULTS: Interquartile range (IQR) increases in PM2.5 (2μg/m(3)), NO2 (9ppb) and O3 (5ppb) over the entire pregnancy were associated with a 4% (95% CI: 2.4-5.6%), 8.4% (95% CI: 5.5-10.3%) and 2% (95% CI: 0.5-4.1%) increase in the odds of preterm birth, respectively. Increases of 10.6% (95% CI: 0.2-2.1%) and 23.8% (95% CI: 5.5-44.8%) in the odds of preterm birth were observed among women with pre-existing diabetes while the increases were of 3.8% (95% CI: 2.2-5.4%) and 6.5% (95% CI: 3.7-8.4%) among women without this condition for pregnancy exposure to PM2.5 and NO2, respectively (Pint<0.01). The increase in the odds of preterm birth for exposure to PM2.5 during pregnancy was higher among women with preeclampsia (8.3%, 95% CI: 0.8-16.4%) than among women without (3.6%, 95% CI: 1.8-5.3%) (Pint=0.04). A stronger increase in the odds of preterm birth was found for exposure to O3 during pregnancy among asthmatic women (12.0%, 95% CI: 3.5-21.1%) compared to non-asthmatic women (2.0%, 95% CI: 0.1-3.5%) (Pint<0.01). We did not find statistically significant effect modification for the other outcomes investigated. CONCLUSIONS: Findings of this study suggest that associations of ambient air pollution with preterm birth are stronger among women with pre-existing diabetes, asthma, and preeclampsia. Crown
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