Centre for Environmental Sciences, Hasselt University, Agoralaan gebouw D, BE-3590 Hasselt, Belgium; Risk and Health Impact Assessment, Sciensano, Juliette Wytsmanstraat 14, BE-1050 Brussels, Belgium.
Centre for Environmental Sciences, Hasselt University, Agoralaan gebouw D, BE-3590 Hasselt, Belgium; Department of Public Health & Primary Care, University of Leuven (KU Leuven), O&N I Herestraat 49 - bus 706, BE-3000 Leuven, Belgium.
Environ Int. 2021 Feb;147:106332. doi: 10.1016/j.envint.2020.106332. Epub 2020 Dec 31.
Pro-inflammatory conditions such as air pollution might induce biological ageing. However, the available evidence on such an impact in children is still very scarce. We studied in primary schoolchildren the association of ambient residential air pollution exposure with telomere length (TL) and mitochondrial DNA content (mtDNAc), two important targets of the core axis of ageing.
Between 2012 and 2014, buccal TL and mtDNAc were repeatedly assessed using qPCR in 197 Belgian primary schoolchildren (mean age 10.3 years) as part of the COGNAC study. At the child's residence, recent (week), sub-chronic (month) and chronic (year) exposure to nitrogen dioxide (NO), particulate matter ≤ 2.5 µm (PM) and black carbon (BC) were estimated using a high resolution spatiotemporal model. A mixed-effects model with school and subject as random effect was used while adjusting for a priori chosen covariates.
An interquartile range (IQR) increment (1.9 µg/m) in chronic PM exposure was associated with a 8.9% (95% CI: -15.4 to -1.9%) shorter TL. In contrast to PM, chronic exposure to BC and NO was not associated with TL but recent exposure to BC and NO showed significant inverse associations with TL: an IQR increment in recent exposure to BC (0.9 µg/m) and NO (10.2 µg/m) was associated with a 6.2% (95% CI: -10.6 to -1.6%) and 6.4% (95% CI: -11.8 to -0.7%) shorter TL, respectively. Finally, an IQR increment in chronic PM exposure was associated with a 12.7% (95% CI: -21.7 to -2.6%) lower mtDNAc. However, no significant associations were seen for NO and BC or for other exposure windows.
Chronic exposure to PM below the EU threshold was associated with child's shorter buccal TL and lower mtDNAc, while traffic-related pollutants (BC and NO) showed recent effects on telomere biology. Our data add to the literature on air pollution-induced effects of TL and mtDNAc, two measures part of the core axis of cellular ageing, from early life onwards.
炎症状态，如空气污染，可能会诱导生物衰老。然而，目前关于儿童的此类影响的证据仍然非常缺乏。我们研究了小学生的环境居住空气污染暴露与端粒长度（TL）和线粒体 DNA 含量（mtDNAc）之间的关联，这两个是衰老核心轴的重要靶标。
在 2012 年至 2014 年期间，作为 COGNAC 研究的一部分，197 名比利时小学生（平均年龄 10.3 岁）使用 qPCR 重复评估口腔 TL 和 mtDNAc。在儿童居住地，使用高分辨率时空模型估算最近（周）、亚慢性（月）和慢性（年）二氧化氮（NO）、颗粒物≤2.5 µm（PM）和黑碳（BC）的暴露情况。使用混合效应模型，以学校和个体为随机效应，并在调整了预先选择的协变量后进行分析。
慢性 PM 暴露的四分位间距（IQR）增量（1.9 µg/m）与 TL 缩短 8.9%（95%CI：-15.4 至-1.9%）相关。与 PM 相反，慢性 BC 和 NO 暴露与 TL 无关，但最近的 BC 和 NO 暴露与 TL 呈显著负相关：最近暴露于 BC（0.9 µg/m）和 NO（10.2 µg/m）的 IQR 增量与 TL 缩短 6.2%（95%CI：-10.6 至-1.6%）和 6.4%（95%CI：-11.8 至-0.7%）相关。最后，慢性 PM 暴露的 IQR 增量与 mtDNAc 降低 12.7%（95%CI：-21.7 至-2.6%）相关。然而，没有发现 NO 和 BC 或其他暴露窗口的显著关联。
低于欧盟阈值的慢性 PM 暴露与儿童口腔 TL 缩短和 mtDNAc 降低有关，而交通相关污染物（BC 和 NO）对端粒生物学有近期影响。我们的数据增加了关于空气污染诱导 TL 和 mtDNAc 影响的文献，TL 和 mtDNAc 是细胞衰老核心轴的两个组成部分，从生命早期开始。
