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Prenatal fine particulate exposure and early childhood asthma: Effect of maternal stress and fetal sex - 04/05/18

Doi : 10.1016/j.jaci.2017.07.017 
Alison Lee, MD, MS a, Hsiao-Hsien Leon Hsu, ScD b, c, Yueh-Hsiu Mathilda Chiu, ScD b, c, Sonali Bose, MD a, Maria José Rosa, DrPH b, Itai Kloog, PhD d, Ander Wilson, PhD e, Joel Schwartz, PhD f, Sheldon Cohen, PhD g, Brent A. Coull, PhD h, Robert O. Wright, MD, MPH b, c, Rosalind J. Wright, MD, MPH b, c,
a Division of Pulmonary, Critical Care and Sleep Medicine, Icahn School of Medicine at Mount Sinai, New York, NY 
b Department of Environmental Medicine and Public Health, Icahn School of Medicine at Mount Sinai, New York, NY 
c Department of Pediatrics, Kravis Children's Hospital, Icahn School of Medicine at Mount Sinai, New York, NY 
d Faculty of Humanities and Social Sciences, Department of Geography and Environmental Development, Ben-Gurion University of the Negev, Beer Sheva, Israel 
e Department of Statistics, Colorado State University, Fort Collins, Colo 
f Department of Environmental Health, Harvard T.H. Chan School of Public Health, Boston, Mass 
g Department of Psychology, Carnegie Mellon University, Pittsburgh, Pa 
h Department of Biostatistics, Harvard T.H. Chan School of Public Health, Boston, Mass 

Corresponding author: Rosalind J. Wright, MD, MPH, 1236 Park Ave, First Fl, New York, NY 10029.1236 Park Ave, First FlNew YorkNY10029

Abstract

Background

The impact of prenatal ambient air pollution on child asthma may be modified by maternal stress, child sex, and exposure dose and timing.

Objective

We prospectively examined associations between coexposure to prenatal particulate matter with an aerodynamic diameter of less than 2.5 microns (PM2.5) and maternal stress and childhood asthma (n = 736).

Methods

Daily PM2.5 exposure during pregnancy was estimated using a validated satellite-based spatiotemporally resolved prediction model. Prenatal maternal negative life events (NLEs) were dichotomized around the median (high: NLE ≥ 3; low: NLE < 3). We used Bayesian distributed lag interaction models to identify sensitive windows for prenatal PM2.5 exposure on children's asthma by age 6 years, and determine effect modification by maternal stress and child sex.

Results

Bayesian distributed lag interaction models identified a critical window of exposure (19-23 weeks' gestation, cumulative odds ratio, 1.15; 95% CI, 1.03-1.26; per interquartile range [1.7 μg/m3] increase in prenatal PM2.5 level) during which children concomitantly exposed to prenatal PM2.5 and maternal stress had increased risk of asthma. No significant association was seen in children born to women reporting low prenatal stress. When examining modifying effects of prenatal stress and fetal sex, we found that boys born to mothers with higher prenatal stress were most vulnerable (19-21 weeks' gestation; cumulative odds ratio, 1.28; 95% CI, 1.15-1.41; per interquartile range increase in PM2.5).

Conclusions

Prenatal PM2.5 exposure during sensitive windows is associated with increased risk of child asthma, especially in boys concurrently exposed to elevated maternal stress.

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Key words : Particulate matter, ambient air pollution, negative life events, prenatal stress, childhood asthma, sex- and temporal-specific effects

Abbreviations used : AOD, BDLIM, DLM, IQR, NLEs, PM2.5


Plan


 The Asthma Coalition on Community, Environment, and Social Stress (ACCESS) project has been funded by the National Institutes of Health (NIH; grant nos. R01 ES010932, U01 HL072494, and R01 HL080674 to R.J.W., principal investigator), and phenotyping and biostatistical support was funded by NIH grant numbers P30 ES023515, P30 ES000002, and T32 ES007142. During the preparation of this manuscript, A.L. was supported by NIH grant number K23 HL135349 and M.J.R. was supported by NIH grant number T32 HD049311-09.
 Disclosure of potential conflict of interest: A. Lee, S. Bose, J. Schwartz, B. A. Coull, and R. O. Wright received grants from the National Institutes of Health for this work. The rest of the authors declare that they have no relevant conflicts of interest.


© 2017  American Academy of Allergy, Asthma & Immunology. Publié par Elsevier Masson SAS. Tous droits réservés.
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