Abstract
Particulate matter with an aerodynamic diameter of 2.5 μm or less (PM2.5) is a ubiquitous air pollutant that is increasingly threatening the health of adults and children worldwide. One health impact of elevated PM2.5 exposure is alterations in telomere length (TL)—protective caps on chromosome ends that shorten with each cell division. Few analyses involve prenatal PM2.5 exposure, and paired maternal and cord TL measurements. Here, we analyzed the association between average and trimester-specific prenatal PM2.5 exposure, and maternal and newborn relative leukocyte TL measured at birth among 193 mothers and their newborns enrolled in a New-York-City-based birth cohort. Results indicated an overall negative relationship between prenatal PM2.5 and maternal TL at delivery, with a significant association observed in the second trimester (β = −0.039, 95% CI: −0.074, −0.003). PM2.5 exposure in trimester two was also inversely related to cord TL; however, this result did not reach statistical significance (β = −0.037, 95% CI: −0.114, 0.039), and no clear pattern emerged between PM2.5 and cord TL across the different exposure periods. Our analysis contributes to a limited body of research on ambient air pollution and human telomeres, and emphasizes the need for continued investigation into how PM2.5 exposure during pregnancy influences maternal and newborn health.
Highlights
Numerous studies have shown an association between high levels of air pollution and adverse human health outcomes, including in children
We examined the relationship between prenatal PM2.5 exposure and maternal and cord rLTL, adjusting for several sociodemographic and obstetric characteristics, including: gestational age at birth, child sex, ethnicity (Dominican vs. African American), maternal age, and maternal education (
We found that exposure to PM2.5 during pregnancy was inversely associated with maternal rLTL at delivery, with the strongest associations identified for exposure occurring during the second trimester (Table 2)
Summary
Numerous studies have shown an association between high levels of air pollution and adverse human health outcomes, including in children. In a recent study for the Global Burden of Disease, ambient particulate matter (PM) was listed as the sixth most influential risk factor affecting public health worldwide [1], with fine particles smaller than 2.5 μm in aerodynamic diameter (PM2.5 ) linked to an estimated 4.2 million deaths globally [2]. Prenatal exposure to PM2.5 has been associated with a range of adverse birth outcomes, including preterm birth, reduced birthweight, and stillbirth [5–9], as well as diseases associated with aging [10]. Environmental influences on telomere length (TL) may be one intermediate step linking exposure to air pollutants with adverse health outcomes [11,12]. Increasing evidence has documented that a range of pro-oxidant environmental exposures, including particulate air pollutants, may be associated with enhanced telomere attrition. Longitudinal studies of telomere dynamics in adults have demonstrated a fixed ranking and tracking of TL across age, suggesting that the early life period may be a critical window for the establishment of inter-individual differences in TL
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