Maria José Rosa1, Hsiao-Hsien Leon Hsu2, Allan C Just3, Kasey J Brennan4, Tessa Bloomquist5, Itai Kloog6, Ivan Pantic7, Adriana Mercado García8, Ander Wilson9, Brent A Coull10, Robert O Wright11, Martha María Téllez Rojo12, Andrea A Baccarelli13, Rosalind J Wright14. 1. Department of Environmental Medicine and Public Health, Icahn School of Medicine at Mount Sinai, New York, NY, USA. Electronic address: maria.rosa@mssm.edu. 2. Department of Environmental Medicine and Public Health, Icahn School of Medicine at Mount Sinai, New York, NY, USA. Electronic address: leon.hsu@mssm.edu. 3. Department of Environmental Medicine and Public Health, Icahn School of Medicine at Mount Sinai, New York, NY, USA. Electronic address: allan.just@mssm.edu. 4. Department of Environmental Health Sciences, Columbia University Mailman School of Public Health, New York, NY, USA. Electronic address: kb2891@cumc.columbia.edu. 5. Department of Environmental Health Sciences, Columbia University Mailman School of Public Health, New York, NY, USA. Electronic address: tb2715@cumc.columbia.edu. 6. Department of Geography and Environmental Development, Ben-Gurion University of the Negev, P.O.B. 653, Beer Sheva, Israel. Electronic address: ikloog@bgu.ac.il. 7. Department of Developmental Neurobiology, National Institute of Perinatology, Mexico City, Mexico. 8. Center for Nutrition and Health Research, National Institute of Public Health, Ministry of Health, Cuernavaca, Morelos, Mexico. Electronic address: adrianam@insp.mx. 9. Department of Statistics, Colorado State University, Fort Collins, CO, USA. Electronic address: ander.wilson@colostate.edu. 10. Department of Environmental Health, Harvard T.H. Chan School of Public Health, Boston, MA, USA. Electronic address: bcoull@hsph.harvard.edu. 11. Department of Environmental Medicine and Public Health, Icahn School of Medicine at Mount Sinai, New York, NY, USA; Institute for Exposomic Research, Icahn School of Medicine at Mount Sinai, New York, NY, USA. Electronic address: robert.wright@mssm.edu. 12. Center for Nutrition and Health Research, National Institute of Public Health, Ministry of Health, Cuernavaca, Morelos, Mexico. Electronic address: mmtellez@insp.mx. 13. Department of Environmental Health Sciences, Columbia University Mailman School of Public Health, New York, NY, USA. Electronic address: ab4303@cumc.columbia.edu. 14. Department of Environmental Medicine and Public Health, Icahn School of Medicine at Mount Sinai, New York, NY, USA; Institute for Exposomic Research, Icahn School of Medicine at Mount Sinai, New York, NY, USA; Kravis Children's Hospital, Department of Pediatrics, Icahn School of Medicine at Mount Sinai, New York, NY, USA. Electronic address: rosalind.wright@mssm.edu.
Abstract
INTRODUCTION: In utero particulate matter exposure produces oxidative stress that impacts cellular processes that include telomere biology. Newborn telomere length is likely critical to an individual's telomere biology; reduction in this initial telomere setting may signal increased susceptibility to adverse outcomes later in life. We examined associations between prenatal particulate matter with diameter ≤2.5 µm (PM2.5) and relative leukocyte telomere length (LTL) measured in cord blood using a data-driven approach to characterize sensitive windows of prenatal PM2.5 effects and explore sex differences. METHODS: Women who were residents of Mexico City and affiliated with the Mexican Social Security System were recruited during pregnancy (n = 423 for analyses). Mothers' prenatal exposure to PM2.5 was estimated based on residence during pregnancy using a validated satellite-based spatio-temporally resolved prediction model. Leukocyte DNA was extracted from cord blood obtained at delivery. Duplex quantitative polymerase chain reaction was used to compare the relative amplification of the telomere repeat copy number to single gene (albumin) copy number. A distributed lag model incorporating weekly averages for PM2.5 over gestation was used in order to explore sensitive windows. Sex-specific associations were examined using Bayesian distributed lag interaction models. RESULTS: In models that included child's sex, mother's age at delivery, prenatal environmental tobacco smoke exposure, pre-pregnancy BMI, gestational age, birth season and assay batch, we found significant associations between higher PM2.5 exposure during early pregnancy (4-9 weeks) and shorter LTL in cord blood. We also identified two more windows at 14-19 and 34-36 weeks in which increased PM2.5 exposure was associated with longer LTL. In stratified analyses, the mean and cumulative associations between PM2.5 and shortened LTL were stronger in girls when compared to boys. CONCLUSIONS: Increased PM2.5 during specific prenatal windows was associated with shorter LTL and longer LTL. PM2.5 was more strongly associated with shortened LTL in girls when compared to boys. Understanding sex and temporal differences in response to air pollution may provide unique insight into mechanisms.
INTRODUCTION: In utero particulate matter exposure produces oxidative stress that impacts cellular processes that include telomere biology. Newborn telomere length is likely critical to an individual's telomere biology; reduction in this initial telomere setting may signal increased susceptibility to adverse outcomes later in life. We examined associations between prenatal particulate matter with diameter ≤2.5 µm (PM2.5) and relative leukocyte telomere length (LTL) measured in cord blood using a data-driven approach to characterize sensitive windows of prenatal PM2.5 effects and explore sex differences. METHODS:Women who were residents of Mexico City and affiliated with the Mexican Social Security System were recruited during pregnancy (n = 423 for analyses). Mothers' prenatal exposure to PM2.5 was estimated based on residence during pregnancy using a validated satellite-based spatio-temporally resolved prediction model. Leukocyte DNA was extracted from cord blood obtained at delivery. Duplex quantitative polymerase chain reaction was used to compare the relative amplification of the telomere repeat copy number to single gene (albumin) copy number. A distributed lag model incorporating weekly averages for PM2.5 over gestation was used in order to explore sensitive windows. Sex-specific associations were examined using Bayesian distributed lag interaction models. RESULTS: In models that included child's sex, mother's age at delivery, prenatal environmental tobacco smoke exposure, pre-pregnancy BMI, gestational age, birth season and assay batch, we found significant associations between higher PM2.5 exposure during early pregnancy (4-9 weeks) and shorter LTL in cord blood. We also identified two more windows at 14-19 and 34-36 weeks in which increased PM2.5 exposure was associated with longer LTL. In stratified analyses, the mean and cumulative associations between PM2.5 and shortened LTL were stronger in girls when compared to boys. CONCLUSIONS: Increased PM2.5 during specific prenatal windows was associated with shorter LTL and longer LTL. PM2.5 was more strongly associated with shortened LTL in girls when compared to boys. Understanding sex and temporal differences in response to air pollution may provide unique insight into mechanisms.
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