TY - JOUR
T1 - Prenatal nitrate exposure and childhood asthma. Influence of maternal prenatal stress and fetal sex
AU - Bose, Sonali
AU - Chiu, Yueh Hsiu Mathilda
AU - Hsu, Hsiao Hsien Leon
AU - Di, Qian
AU - Rosa, Maria José
AU - Lee, Alison
AU - Kloog, Itai
AU - Wilson, Ander
AU - Schwartz, Joel
AU - Wright, Robert O.
AU - Cohen, Sheldon
AU - Coull, Brent A.
AU - Wright, Rosalind J.
N1 - Publisher Copyright:
Copyright © 2017 by the American Thoracic Society.
PY - 2017/12/1
Y1 - 2017/12/1
N2 - Rationale: Impact of ambient pollution upon children’s asthma may differ by sex, and exposure dose and timing. Psychosocial stress can also modify pollutant effects. These associations have not been examined for in utero ambient nitrate exposure. Objectives: We implemented Bayesian-distributed lag interaction models to identify sensitive prenatal windows for the influence of nitrate (NO32) on child asthma, accounting for effect modification by sex and stress. Methods: Analyses included 752 mother–child dyads. Daily ambient NO32 exposure during pregnancy was derived using a hybrid chemical transport (Geos-Chem)/land-use regression model and natural log transformed. Prenatal maternal stress was indexed by a negative life events score (high [.2] vs. low [<2]). The outcome was clinician-diagnosed asthma by age 6 years. Measurements and Main Results: Most mothers were Hispanic (54%) or black (29%), had a high school education or less (66%), never smoked (80%), and reported low prenatal stress (58%); 15% of children developed asthma. BDILMs adjusted for maternal age, race, education, prepregnancy obesity, atopy, and smoking status identified two sensitive windows (7–19 and 33–40 wk gestation), during which increased NO32 was associated with greater odds of asthma, specifically among boys born to mothers reporting high prenatal stress. Cumulative effects of NO32 across pregnancy were also significant in this subgroup (odds ratio = 2.64, 95% confidence interval = 1.27–5.39; per interquartile range increase in ln NO32). Conclusions: Prenatal NO32 exposure during distinct sensitive windows was associated with incident asthma in boys concurrently exposed to high prenatal stress.
AB - Rationale: Impact of ambient pollution upon children’s asthma may differ by sex, and exposure dose and timing. Psychosocial stress can also modify pollutant effects. These associations have not been examined for in utero ambient nitrate exposure. Objectives: We implemented Bayesian-distributed lag interaction models to identify sensitive prenatal windows for the influence of nitrate (NO32) on child asthma, accounting for effect modification by sex and stress. Methods: Analyses included 752 mother–child dyads. Daily ambient NO32 exposure during pregnancy was derived using a hybrid chemical transport (Geos-Chem)/land-use regression model and natural log transformed. Prenatal maternal stress was indexed by a negative life events score (high [.2] vs. low [<2]). The outcome was clinician-diagnosed asthma by age 6 years. Measurements and Main Results: Most mothers were Hispanic (54%) or black (29%), had a high school education or less (66%), never smoked (80%), and reported low prenatal stress (58%); 15% of children developed asthma. BDILMs adjusted for maternal age, race, education, prepregnancy obesity, atopy, and smoking status identified two sensitive windows (7–19 and 33–40 wk gestation), during which increased NO32 was associated with greater odds of asthma, specifically among boys born to mothers reporting high prenatal stress. Cumulative effects of NO32 across pregnancy were also significant in this subgroup (odds ratio = 2.64, 95% confidence interval = 1.27–5.39; per interquartile range increase in ln NO32). Conclusions: Prenatal NO32 exposure during distinct sensitive windows was associated with incident asthma in boys concurrently exposed to high prenatal stress.
KW - Air pollution
KW - Asthma
KW - Nitrate
KW - Prenatal
KW - Sensitive window
UR - http://www.scopus.com/inward/record.url?scp=85038124461&partnerID=8YFLogxK
U2 - 10.1164/rccm.201702-0421OC
DO - 10.1164/rccm.201702-0421OC
M3 - Article
AN - SCOPUS:85038124461
SN - 1073-449X
VL - 196
SP - 1396
EP - 1403
JO - American Journal of Respiratory and Critical Care Medicine
JF - American Journal of Respiratory and Critical Care Medicine
IS - 11
ER -