Associations between exposure to ambient air pollution and changes in blood telomeres in young people: A repeated-measure study

端粒 污染物 臭氧 微粒 二氧化氮 空气污染物 端粒酶 化学 空气污染 环境化学 生物化学 DNA 基因 有机化学
作者
Xiaojing Zhu,Zhigang Li,Ziye Wang,Guo Chen,Yan Qian,Zhanshan Wang,Xiaoqian Li,Yongjie Wei
出处
期刊:Chemosphere [Elsevier BV]
卷期号:336: 139053-139053 被引量:3
标识
DOI:10.1016/j.chemosphere.2023.139053
摘要

Telomere length (TL) is one of the early biomarkers of aging. Air pollutants play an important role in promoting the aging process. However, few studies have explored how they adversely affect human health by altering telomeres. This study aims to investigate the associations between telomere alterations and exposure to ambient air pollutants, thereby shedding light on the intrinsic and profound link between these pollutants and aging. We recruited 26 healthy young people and conducted 7 repeated measure studies from 2019 to 2021, and TL and telomerase (TA) in the blood samples. We analyzed the associations between air pollutants, including ozone (O3), particulate matter in diameter smaller than 2.5 μm (PM2.5) and 10 μm (PM10), nitrogen dioxide (NO2), sulfur dioxide (SO2), and carbon monoxide (CO) and telomere variability, and explored the lagged effects by linear mixed-effects model. The result showed that short-term exposure to O3 was negatively associated with TL, and this effect in the lag days went up to around 0. In contrast, the associations between O3 and TA presented positive tendency and gradually decreased to around 0 in the lag days. The association between PM2.5 and TL showed positive tendency and gradually decreased to negative. There was no statistically significant association between PM2.5 and TA. Other pollutants (PM10, NO2, SO2, CO) showed similar patterns of variation to that of PM2.5. Our findings suggest that short-term exposure to O3 shortens TL, which can be gradually recovered through activating TA activity, while exposure to PM2.5, PM10, NO2, SO2 and CO lengthens TL and then becomes shorter over time. This implies that the human body has some ability to self-repair telomere changes after exposure to air pollutants, and predictably, when this exposure exceeds a certain threshold, it cannot be repaired, leading to aging of the body.
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