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Maternal exposure to PM(2.5) during pregnancy and asthma risk in early childhood: Consideration of phases of fetal lung development

Increasingly studies suggest prenatal exposure to air pollution may increase risk of childhood asthma. Few studies have investigated exposure during specific fetal pulmonary developmental windows. OBJECTIVE: To assess associations between prenatal fine particulate matter exposure and asthma at age 4...

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Detalles Bibliográficos
Autores principales: Hazlehurst, Marnie F., Carroll, Kecia N., Loftus, Christine T., Szpiro, Adam A., Moore, Paul E., Kaufman, Joel D., Kirwa, Kipruto, LeWinn, Kaja Z., Bush, Nicole R., Sathyanarayana, Sheela, Tylavsky, Frances A., Barrett, Emily S., Nguyen, Ruby H. N., Karr, Catherine J.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Lippincott Williams & Wilkins 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7943175/
https://www.ncbi.nlm.nih.gov/pubmed/33709049
http://dx.doi.org/10.1097/EE9.0000000000000130
Descripción
Sumario:Increasingly studies suggest prenatal exposure to air pollution may increase risk of childhood asthma. Few studies have investigated exposure during specific fetal pulmonary developmental windows. OBJECTIVE: To assess associations between prenatal fine particulate matter exposure and asthma at age 4. METHODS: This study included mother–child dyads from two pregnancy cohorts—CANDLE and TIDES—within the ECHO-PATHWAYS consortium (births in 2007–2013). Three child asthma outcomes were parent-reported: ever asthma, current asthma, and current wheeze. Fine particulate matter (PM(2.5)) exposures during the pseudoglandular (5–16 weeks gestation), canalicular (16–24 weeks gestation), saccular (24–36 weeks gestation), and alveolar (36+ weeks gestation) phases of fetal lung development were estimated using a national spatiotemporal model. We estimated associations with Poisson regression with robust standard errors, and adjusted for child, maternal, and neighborhood factors. RESULTS: Children (n = 1,469) were on average 4.3 (SD 0.5) years old, 49% were male, and 11.7% had ever asthma; 46% of women identified as black and 53% had at least a college/technical school degree. A 2 μg/m(3) higher PM(2.5) exposure during the saccular phase was associated with 1.29 times higher risk of ever asthma [95% confidence interval (CI): 1.06, 1.58]. A similar association was observed with current asthma (risk ratio 1.27, 95% CI: 1.04, 1.54), but not current wheeze (risk ratio 1.11, 95% CI: 0.92, 1.33). Effect estimates for associations during other developmental windows had CIs that included the null. CONCLUSIONS: Later phases of prenatal lung development may be particularly sensitive to the developmental toxicity of PM(2.5).