Prenatal fine particulate exposure associated with reduced childhood lung function and nasal epithelia GSTP1 hypermethylation: Sex-specific effects
Author
Lee, Alison G.Le Grand, Blake
Hsu, Hsiao-Hsien Leon
Chiu, Yueh-Hsiu Mathilda
Brennan, Kasey J.
Bose, Sonali
Rosa, Maria José
Brunst, Kelly J.
Kloog, Itai
Wilson, Ander
Schwartz, Joel C.

Morgan, Wayne
Coull, Brent A.
Wright, Robert O.
Baccarelli, Andrea A.
Wright, Rosalind J.
Affiliation
Univ Arizona, Dept PediatIssue Date
2018-04-27
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BIOMED CENTRAL LTDCitation
Lee, A. G., Le Grand, B., Hsu, H. H. L., Chiu, Y. H. M., Brennan, K. J., Bose, S., ... & Schwartz, J. (2018). Prenatal fine particulate exposure associated with reduced childhood lung function and nasal epithelia GSTP1 hypermethylation: Sex-specific effects. Respiratory research, 19(1), 76.Journal
RESPIRATORY RESEARCHRights
© The Author(s). 2018. Open Access. This article is distributed under the terms of the Creative Commons Attribution 4.0 International License.Collection Information
This item from the UA Faculty Publications collection is made available by the University of Arizona with support from the University of Arizona Libraries. If you have questions, please contact us at repository@u.library.arizona.edu.Abstract
Background: In utero exposure to particulate matter with an aerodynamic diameter of less than 2.5 mu m (PM2.5) has been linked to child lung function. Overlapping evidence suggests that child sex and exposure timing may modify effects and associations may be mediated through glutathione S-transferase P1 (GSTP1) methylation. Methods: We prospectively examined associations among prenatal PM2.5 exposure and child lung function and GSTP1 methylation in an urban pregnancy cohort study. We employed a validated satellite-based spatiotemporally resolved prediction model to estimate daily prenatal PM2.5 exposure over gestation. We used Baysian distributed lag interaction models (BDLIMs) to identify sensitive windows for prenatal PM2.5 exposure on child lung function and nasal epithelia GSTP1 methylation at age 7 years, and to examine effect modification by child sex. Results: BDLIMs identified a sensitive window for prenatal PM2.5 exposure at 35-40 weeks gestation [cumulative effect estimate (CEE) = -0.10, 95% CI = -0.19 to -0.01, per mu g/m(3) increase in PM2.5] and at 36-40 weeks (CEE = -0. 12, 95% CI = -0.20 to -0.01) on FEV1 and FVC, respectively, in boys. BDLIMs also identified a sensitive window of exposure at 37-40 weeks gestation between higher prenatal PM2.5 exposure and increased GSTP1 percent methylation. The association between higher GSTP1 percent methylation and decreased FEV1 was borderline significant in the sample as a whole (ss = -0.37, SE = 0.20, p = 0.06) and in boys in stratified analyses (ss = -0.56, SE = 0.29, p = 0.05). Conclusions: Prenatal PM2.5 exposure in late pregnancy was associated with impaired early childhood lung function and hypermethylation of GSTPI in DNA isolated from nasal epithelial cells. There was a trend towards higher GSTP1 percent methylation being associated with reduced FEV1. All findings were most evident among boys.Note
Open Access Journal.ISSN
1465-993XPubMed ID
29703190Version
Final published versionSponsors
National Institutes of Health (NIH) [R01 ES010932, U01 HL072494, R01 MD006086, R01 HL080674]; NIH [P30 ES023515, P30 ES000002, P30 ES009089, T32 ES007142, K23 HL135349, K99 ES027496]ae974a485f413a2113503eed53cd6c53
10.1186/s12931-018-0774-3
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Except where otherwise noted, this item's license is described as © The Author(s). 2018. Open Access. This article is distributed under the terms of the Creative Commons Attribution 4.0 International License.
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