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Long-term ozone exposure and lung function in middle childhood

Ozone (O3) exposure interrupts normal lung development in animal models. Epidemiologic evidence further suggests impairment with higher long-term O3 exposure across early and middle childhood, although study findings to date are mixed and few have investigated vulnerable subgroups. Participants from...

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Published in:Environmental research 2024-01, Vol.241, p.117632-117632, Article 117632
Main Authors: Hazlehurst, Marnie F., Dearborn, Logan C., Sherris, Allison R., Loftus, Christine T., Adgent, Margaret A., Szpiro, Adam A., Ni, Yu, Day, Drew B., Kaufman, Joel D., Thakur, Neeta, Wright, Rosalind J., Sathyanarayana, Sheela, Carroll, Kecia N., Moore, Paul E., Karr, Catherine J.
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Language:English
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Summary:Ozone (O3) exposure interrupts normal lung development in animal models. Epidemiologic evidence further suggests impairment with higher long-term O3 exposure across early and middle childhood, although study findings to date are mixed and few have investigated vulnerable subgroups. Participants from the CANDLE study, a pregnancy cohort in Shelby County, TN, in the ECHO-PATHWAYS Consortium, were included if children were born at gestational age >32 weeks, completed a spirometry exam at age 8–9, and had a valid residential history from birth to age 8. We estimated lifetime average ambient O3 exposure based on each child's residential history from birth to age 8, using a validated fine-resolution spatiotemporal model. Spirometry was performed at the age 8–9 year study visit to assess Forced Expiratory Volume in the first second (FEV1) and Forced Vital Capacity (FVC) as primary outcomes; z-scores were calculated using sex-and-age-specific reference equations. Linear regression with robust variance estimators was used to examine associations between O3 exposure and continuous lung function z-scores, adjusted for child, sociodemographic, and home environmental factors. Potential susceptible subgroups were explored using a product term in the regression model to assess effect modification by child sex, history of bronchiolitis in infancy, and allergic sensitization. In our sample (n = 648), O3 exposure averaged from birth to age 8 was modest (mean 26.6 [SD 1.1] ppb). No adverse associations between long-term postnatal O3 exposure were observed with either FEV1 (β = 0.12, 95% CI: −0.04, 0.29) or FVC (β = 0.03, 95% CI: −0.13, 0.19). No effect modification by child sex, history of bronchiolitis in infancy, or allergic sensitization was detected for associations with 8-year average O3. In this sample with low O3 concentrations, we did not observe adverse associations between O3 exposures averaged from birth to age 8 and lung function in middle childhood. •Child FEV1 and FVC were ascertained via spirometry at age 8–9 in the CANDLE cohort.•We used a point-based spatiotemporal model to assess lifetime O3 exposure, age 0–8.•O3 exposures in this sample were modest with limited variability.•No adverse associations were observed between long-term O3 and lung function.•No effect modification found by bronchiolitis, allergic sensitization, or child sex.
ISSN:0013-9351
1096-0953
DOI:10.1016/j.envres.2023.117632