Maria José Rosa1, Allan C Just1, Itai Kloog2, Ivan Pantic3, Lourdes Schnaas4, Alison Lee5, Sonali Bose5, Yueh-Hsiu Mathilda Chiu1, Hsiao-Hsien Leon Hsu1, Brent Coull6, Joel Schwartz7, Sheldon Cohen8, Martha María Téllez Rojo9, Robert O Wright10, Rosalind J Wright11. 1. Department of Environmental Medicine and Public Health, Icahn School of Medicine at Mount Sinai, New York, New York. 2. Department of Geography and Environmental Development, Ben-Gurion University of the Negev, Beer Sheva, Israel. 3. Department of Developmental Neurobiology, National Institute of Perinatology, Mexico City, Mexico. 4. Division of Research in Community Interventions, National Institute of Perinatology, Mexico City, Mexico. 5. Department of Medicine, Division of Pulmonary, Critical Care and Sleep Medicine, Icahn School of Medicine at Mount Sinai, New York, New York. 6. Department of Biostatistics, Harvard T.H. Chan School of Public Health, Boston, Massachusetts. 7. Department of Epidemiology, Harvard T.H. Chan School of Public Health, Boston, Massachusetts. 8. Department of Psychology, Carnegie Mellon University, Pittsburgh, Pennsylvania. 9. Center for Nutrition and Health Research, National Institute of Public Health, Ministry of Health, Cuernavaca, Morelos, Mexico. 10. Department of Environmental Medicine and Public Health, Icahn School of Medicine at Mount Sinai, New York, New York; Institute for Exposomic Research, Icahn School of Medicine at Mount Sinai, New York, New York. 11. Department of Environmental Medicine and Public Health, Icahn School of Medicine at Mount Sinai, New York, New York; Institute for Exposomic Research, Icahn School of Medicine at Mount Sinai, New York, New York. Electronic address: rosalind.wright@mssm.edu.
Abstract
BACKGROUND: Air pollution exposure in childhood is associated with greater incidence and exacerbation of asthma, particularly in children whose parents report high levels of psychological stress. However, this interaction has not been completely elucidated in pregnancy. OBJECTIVE: To examine whether the association between prenatal exposure to particulate matter no larger than 2.5 μm in diameter (PM2.5) and wheeze in children is modified by prenatal stress. METHODS: Mexican women were recruited during pregnancy (N = 552). Residential prenatal daily exposure to PM2.5 was estimated using a satellite-based spatiotemporally resolved prediction model and averaged over trimesters. Maternal stress was indexed by maternal negative life events (NLE) score (range 0-11) ascertained during mid to late pregnancy. NLE scores were dichotomized at the median as low (NLE score ≤ 3) and high (NLE score > 3) stress. Reports of ever wheeze and wheeze in the past 12 months (current wheeze) for children were obtained using the International Study of Asthma and Allergies in Childhood survey at 48 months. The association between prenatal PM2.5 and wheeze was analyzed using a modified Poisson regression and stratified by low vs high stress. RESULTS: Greater PM2.5 exposure during the first trimester was associated with increased risk of current wheeze among children with mothers reporting high prenatal stress (relative risk 1.35, 95% confidence interval 1.00-1.83, per interquartile range increase 3.8 μg/m3) but not among those reporting low stress (relative risk 0.84, 95% confidence interval 0.61-1.16, per interquartile range increase 3.8 μg/m3; P for interaction = .04). CONCLUSION: Increased prenatal stress enhanced the association between PM2.5 exposure in early pregnancy, and child wheeze at 48 months of age. It is important to consider chemical and nonchemical stressors together to more comprehensively characterize children's environmental risk.
BACKGROUND: Air pollution exposure in childhood is associated with greater incidence and exacerbation of asthma, particularly in children whose parents report high levels of psychological stress. However, this interaction has not been completely elucidated in pregnancy. OBJECTIVE: To examine whether the association between prenatal exposure to particulate matter no larger than 2.5 μm in diameter (PM2.5) and wheeze in children is modified by prenatal stress. METHODS: Mexican women were recruited during pregnancy (N = 552). Residential prenatal daily exposure to PM2.5 was estimated using a satellite-based spatiotemporally resolved prediction model and averaged over trimesters. Maternal stress was indexed by maternal negative life events (NLE) score (range 0-11) ascertained during mid to late pregnancy. NLE scores were dichotomized at the median as low (NLE score ≤ 3) and high (NLE score > 3) stress. Reports of ever wheeze and wheeze in the past 12 months (current wheeze) for children were obtained using the International Study of Asthma and Allergies in Childhood survey at 48 months. The association between prenatal PM2.5 and wheeze was analyzed using a modified Poisson regression and stratified by low vs high stress. RESULTS: Greater PM2.5 exposure during the first trimester was associated with increased risk of current wheeze among children with mothers reporting high prenatal stress (relative risk 1.35, 95% confidence interval 1.00-1.83, per interquartile range increase 3.8 μg/m3) but not among those reporting low stress (relative risk 0.84, 95% confidence interval 0.61-1.16, per interquartile range increase 3.8 μg/m3; P for interaction = .04). CONCLUSION: Increased prenatal stress enhanced the association between PM2.5 exposure in early pregnancy, and child wheeze at 48 months of age. It is important to consider chemical and nonchemical stressors together to more comprehensively characterize children's environmental risk.
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