Prenatal Pollution Exposure Shortens Babies' Telomeres, Speeds Up Aging

Mothers exposed to higher levels of air pollution during pregnancy gave birth to newborns with shorter telomere length, according to a new study published in JAMA Pediatrics, suggesting that these babies are more likely to experience accelerated aging because of their exposure.

Telomeres are nucleoprotein structures that cap the end of chromosomes and shorten with each cellular division. In previous studies, shorter telomere length has been associated with increased age-related diseases, mortality, and accelerated biological aging.

To determine the effect of prenatal pollution exposure on telomere length, Dries S Martens, MSc (pictured), of the Center for Environmental Sciences at Hasselt University in Belgium, and colleagues studied a cohort of 641 mother-newborn pairs, and found that mothers with higher residential exposure to PM_2.5 (particulate matter with an aerodynamic diameter ≤2.5 μm air pollution) gave birth to newborns with significantly lower telomere length that could not be explained by other known influencers of telomere length like smoking, obesity, or socioeconomic class.

The associations were controlled for date of delivery, gestational age, maternal body mass index, maternal age, paternal age, newborn sex, newborn ethnicity, season of delivery, parity, maternal smoking status, maternal educational level, pregnancy complications, and ambient temperature.

“This study adds to the growing body of evidence that even relatively low levels of pre-natal exposure to air pollution contributes to fetal programming at the molecular level and more precisely at the level of telomere biological features,” the authors wrote. “Adequate reduction of environmental fine-particle air pollution levels may promote longevity as from birth onwards and may enhance overall quality of life.”

According to the study, for every 5-μg/m3 increase in residential PM_2.5 exposure during pregnancy, cord blood telomeres shortened by 9% and placental telomeres shortened by 13%.

“To our knowledge, this study is the first to report an association between prenatal exposure to PM_2.5 air pollution and TL at birth, both in cord blood and placental tissue. We theorize that biological aging is associated with PM_2.5 air pollution exposure, even before birth, which may underlie potential adverse health consequences later in life,” the authors wrote.

In a prospective birth cohort (ENVIRONAGE [Environmental Influence on Aging in Early Life]), 730 mother-newborn pairs were recruited in Flanders, Belgium between 2010 and 2014, all with a singleton full-term birth (≥37 weeks of gestation). For statistical analysis, participants with full data on both cord blood and placental telomere length were included, resulting in a final study sample size of 641 mother-newborn pairs.

Researchers measured cord blood and placental tissue relative to telomere length in the newborns, and estimated maternal residential PM_2.5 exposure during pregnancy using a high-resolution spatial-temporal interpolation method. In distributed lag models, both cord blood and placental telomere length were associated with average weekly exposures to PM_2.5 during pregnancy, allowing for the identification of critical sensitive exposure windows.

In the 641 newborns studied, cord blood and placental telomere length were significantly and inversely associated with PM_2.5 exposure during midgestation (weeks 12-25 for cord blood and weeks 15-27 for placenta). A 5-µg/m3 increment in PM_2.5 exposure during the entire pregnancy was associated with 8.8% (95% CI, −14.1% to −3.1%) shorter cord blood leukocyte telomeres and 13.2% (95% CI, −19.3% to −6.7%) shorter placental telomere length.

“Mothers who were exposed to higher levels of PM_2.5 gave birth to newborns with shorter telomere length,” authors concluded. “The observed telomere loss in newborns by prenatal air pollution exposure indicates less buffer for postnatal influences of factors decreasing telomere length during life. Therefore, improvements in air quality may promote molecular longevity from birth onward.”