Martens Dries S, Cox Bianca, Janssen Bram G, Clemente Diana B P, Gasparrini Antonio, Vanpoucke Charlotte, Lefebvre Wouter, Roels Harry A, Plusquin Michelle, Nawrot Tim S
Centre for Environmental Sciences, Hasselt University, Hasselt, Belgium.
Instituto de Salud Global, Centre for Research in Environmental Epidemiology, Barcelona, Spain.
JAMA Pediatr. 2017 Dec 1;171(12):1160-1167. doi: 10.1001/jamapediatrics.2017.3024.
Telomere length is a marker of biological aging that may provide a cellular memory of exposures to oxidative stress and inflammation. Telomere length at birth has been related to life expectancy. An association between prenatal air pollution exposure and telomere length at birth could provide new insights in the environmental influence on molecular longevity.
To assess the association of prenatal exposure to particulate matter (PM) with newborn telomere length as reflected by cord blood and placental telomere length.
DESIGN, SETTING, AND PARTICIPANTS: In a prospective birth cohort (ENVIRONAGE [Environmental Influence on Ageing in Early Life]), a total of 730 mother-newborn pairs were recruited in Flanders, Belgium between February 2010 and December 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 lengths were included, resulting in a final study sample size of 641.
Maternal residential PM2.5 (particles with an aerodynamic diameter ≤2.5 μm) exposure during pregnancy.
In the newborns, cord blood and placental tissue relative telomere length were measured. Maternal residential PM2.5 exposure during pregnancy was estimated 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 PM2.5 during pregnancy, allowing the identification of critical sensitive exposure windows.
In 641 newborns, cord blood and placental telomere length were significantly and inversely associated with PM2.5 exposure during midgestation (weeks 12-25 for cord blood and weeks 15-27 for placenta). A 5-µg/m3 increment in PM2.5 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. These 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.
Mothers who were exposed to higher levels of PM2.5 gave birth to newborns with shorter telomere length. 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.
端粒长度是生物衰老的一个标志物，它可能提供细胞对氧化应激和炎症暴露的记忆。出生时的端粒长度与预期寿命有关。产前空气污染暴露与出生时端粒长度之间的关联可能为环境对分子寿命的影响提供新的见解。
评估产前暴露于颗粒物（PM）与新生儿端粒长度之间的关联，以脐带血和胎盘端粒长度为指标。
设计、地点和参与者：在一项前瞻性出生队列研究（ENVIRONAGE [早期生活中环境对衰老的影响]）中，2010年2月至2014年12月期间在比利时弗拉芒地区招募了730对母婴，所有婴儿均为单胎足月出生（妊娠≥37周）。为进行统计分析，纳入了脐带血和胎盘端粒长度数据完整的参与者，最终研究样本量为641。
孕期母亲居住地的PM2.5（空气动力学直径≤2.5μm的颗粒物）暴露。
测量新生儿的脐带血和胎盘组织相对端粒长度。使用高分辨率时空插值方法估计孕期母亲居住地的PM2.5暴露情况。在分布滞后模型中，脐带血和胎盘端粒长度均与孕期平均每周PM2.5暴露量相关，从而可以确定关键的敏感暴露窗口。
在641名新生儿中，脐带血和胎盘端粒长度与孕中期（脐带血为第12 - 25周，胎盘为第15 - 27周）的PM2.5暴露显著负相关。整个孕期PM2.5暴露量每增加5μg/m³，脐带血白细胞端粒缩短8.8%（95%CI，-14.1%至-3.1%），胎盘端粒长度缩短13.2%（95%CI，-19.3%至-6.7%）。这些关联在控制了分娩日期、孕周、母亲体重指数、母亲年龄、父亲年龄、新生儿性别、新生儿种族、分娩季节、产次、母亲吸烟状况、母亲教育水平、妊娠并发症和环境温度后依然存在。
暴露于较高水平PM2.5的母亲所生新生儿的端粒长度较短。产前空气污染暴露导致新生儿端粒长度缩短，这表明出生后生活中减少端粒长度的因素对其影响的缓冲能力降低。因此，改善空气质量可能从出生起就促进分子寿命的延长。
