Logan C Dearborn, Marnie F Hazlehurst, Melissa M Melough, Adam A Szpiro, Allison R Sherris, Margaret A Adgent, Yu Ni, Rosalind J Wright, Neeta Thakur, Nicole R Bush, Paul E Moore, Christine T Loftus, Catherine J Karr, Kecia N Carroll
{"title":"Prenatal ozone exposure and child lung function: Exploring effect modification by oxidative balance score.","authors":"Logan C Dearborn, Marnie F Hazlehurst, Melissa M Melough, Adam A Szpiro, Allison R Sherris, Margaret A Adgent, Yu Ni, Rosalind J Wright, Neeta Thakur, Nicole R Bush, Paul E Moore, Christine T Loftus, Catherine J Karr, Kecia N Carroll","doi":"10.1016/j.ijheh.2024.114491","DOIUrl":null,"url":null,"abstract":"<p><strong>Background: </strong>Prenatal exposures to ozone (O<sub>3</sub>) may impact child lung function, including through oxidative stress pathways, contributing to lifelong morbidity. Diet, reflected in oxidative balance scores (OBS), may modify these pathways and is a potential target for interventions to mitigate O<sub>3</sub> effects.</p><p><strong>Methods: </strong>We examined associations between prenatal exposure to O<sub>3</sub> and child lung function at age 8-9 years via spirometry in the CANDLE cohort within the ECHO-PATHWAYS Consortium. O<sub>3</sub> was estimated using a point-based spatiotemporal model and averaged over fetal morphological lung development phases: pseudoglandular, canalicular, and saccular. Lung function z-scores were calculated for FEV<sub>1</sub>, FVC, FEV<sub>1</sub>/FVC, and FEF<sub>25-75</sub>. OBS during pregnancy was derived using maternal diet and lifestyle factors. Linear regression models adjusted for child, maternal, and neighborhood characteristics and exposure in other prenatal windows. Using two and three-way multiplicative interaction terms, we explored effect modification by OBS and maternal race.</p><p><strong>Results: </strong>Women (N = 661) self-identified as Black (61%), White (33%), or another race (6%); 40.7% attended some college/technical school. Mean O<sub>3</sub> concentrations ranged from 26.1 to 29.5 ppb across exposure windows. No associations between prenatal O<sub>3</sub> exposure and lung function were observed in primary models, although there was a suggestive adverse association of 10 ppb higher O<sub>3</sub> in the saccular window (24-35 weeks) with lower z-scores for FEV<sub>1</sub>/FVC (-0.23, 95% CI: -0.52, 0.05) and FEF<sub>25-75</sub> (-0.17, 95% CI: -0.43, 0.09). No effect modification by OBS or maternal race was found in two-way models. In three-way interaction models, higher O<sub>3</sub> was associated with lower child FEV<sub>1</sub> among Black women with lower OBS and among White women with higher OBS although data was sparse for those with the highest OBS.</p><p><strong>Conclusions: </strong>In a large, well-characterized pregnancy cohort, we did not find robust evidence of an effect of prenatal O<sub>3</sub> on lung function. There was suggestion of enhanced vulnerability for some subgroups in exploratory analyses.</p>","PeriodicalId":94049,"journal":{"name":"International journal of hygiene and environmental health","volume":"264 ","pages":"114491"},"PeriodicalIF":0.0000,"publicationDate":"2024-12-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"International journal of hygiene and environmental health","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.1016/j.ijheh.2024.114491","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
Prenatal ozone exposure and child lung function: Exploring effect modification by oxidative balance score.
Background: Prenatal exposures to ozone (O3) may impact child lung function, including through oxidative stress pathways, contributing to lifelong morbidity. Diet, reflected in oxidative balance scores (OBS), may modify these pathways and is a potential target for interventions to mitigate O3 effects.
Methods: We examined associations between prenatal exposure to O3 and child lung function at age 8-9 years via spirometry in the CANDLE cohort within the ECHO-PATHWAYS Consortium. O3 was estimated using a point-based spatiotemporal model and averaged over fetal morphological lung development phases: pseudoglandular, canalicular, and saccular. Lung function z-scores were calculated for FEV1, FVC, FEV1/FVC, and FEF25-75. OBS during pregnancy was derived using maternal diet and lifestyle factors. Linear regression models adjusted for child, maternal, and neighborhood characteristics and exposure in other prenatal windows. Using two and three-way multiplicative interaction terms, we explored effect modification by OBS and maternal race.
Results: Women (N = 661) self-identified as Black (61%), White (33%), or another race (6%); 40.7% attended some college/technical school. Mean O3 concentrations ranged from 26.1 to 29.5 ppb across exposure windows. No associations between prenatal O3 exposure and lung function were observed in primary models, although there was a suggestive adverse association of 10 ppb higher O3 in the saccular window (24-35 weeks) with lower z-scores for FEV1/FVC (-0.23, 95% CI: -0.52, 0.05) and FEF25-75 (-0.17, 95% CI: -0.43, 0.09). No effect modification by OBS or maternal race was found in two-way models. In three-way interaction models, higher O3 was associated with lower child FEV1 among Black women with lower OBS and among White women with higher OBS although data was sparse for those with the highest OBS.
Conclusions: In a large, well-characterized pregnancy cohort, we did not find robust evidence of an effect of prenatal O3 on lung function. There was suggestion of enhanced vulnerability for some subgroups in exploratory analyses.
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