TY - JOUR
T1 - Prenatal fine particulate exposure and early childhood asthma
T2 - Effect of maternal stress and fetal sex
AU - Lee, Alison
AU - Leon Hsu, Hsiao Hsien
AU - Mathilda Chiu, Yueh Hsiu
AU - Bose, Sonali
AU - Rosa, Maria José
AU - Kloog, Itai
AU - Wilson, Ander
AU - Schwartz, Joel
AU - Cohen, Sheldon
AU - Coull, Brent A.
AU - Wright, Robert O.
AU - Wright, Rosalind J.
N1 - Publisher Copyright:
© 2017 American Academy of Allergy, Asthma & Immunology
PY - 2018/5
Y1 - 2018/5
N2 - 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 (PM 2.5 ) and maternal stress and childhood asthma (n = 736). Methods: Daily PM 2.5 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 PM 2.5 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/m 3 ] increase in prenatal PM 2.5 level) during which children concomitantly exposed to prenatal PM 2.5 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 PM 2.5 ). Conclusions: Prenatal PM 2.5 exposure during sensitive windows is associated with increased risk of child asthma, especially in boys concurrently exposed to elevated maternal stress.
AB - 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 (PM 2.5 ) and maternal stress and childhood asthma (n = 736). Methods: Daily PM 2.5 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 PM 2.5 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/m 3 ] increase in prenatal PM 2.5 level) during which children concomitantly exposed to prenatal PM 2.5 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 PM 2.5 ). Conclusions: Prenatal PM 2.5 exposure during sensitive windows is associated with increased risk of child asthma, especially in boys concurrently exposed to elevated maternal stress.
KW - Particulate matter
KW - ambient air pollution
KW - childhood asthma
KW - negative life events
KW - prenatal stress
KW - sex- and temporal-specific effects
UR - http://www.scopus.com/inward/record.url?scp=85032199967&partnerID=8YFLogxK
U2 - 10.1016/j.jaci.2017.07.017
DO - 10.1016/j.jaci.2017.07.017
M3 - Article
C2 - 28801196
AN - SCOPUS:85032199967
SN - 0091-6749
VL - 141
SP - 1880
EP - 1886
JO - Journal of Allergy and Clinical Immunology
JF - Journal of Allergy and Clinical Immunology
IS - 5
ER -