Qu Rongrong, Sun Beibei, Jiang Jing, An Zhen, Li Juan, Wu Hui, Wu Weidong, Song Jie
Henan International Collaborative Laboratory for Health Effects and Intervention of Air Pollution, School of Public Health, Xinxiang Medical University, Xinxiang, Henan Province 453003, China.
Henan International Collaborative Laboratory for Health Effects and Intervention of Air Pollution, School of Public Health, Xinxiang Medical University, Xinxiang, Henan Province 453003, China.
Sci Total Environ. 2023 Dec 20;905:167209. doi: 10.1016/j.scitotenv.2023.167209. Epub 2023 Sep 18.
Although converging lines of research have pointed to the adverse neural effects of air pollution, evidence linking ozone (O) and neural damage remains limited.
To investigate the subclinical neural effects of short-term ozone (O) exposure in elderly adults.
A panel of healthy elderly individuals was recruited, and five repeated measurements were conducted from December 2018 to April 2019 in Xinxiang, China. Serum neural damage biomarkers, including brain-derived neurotrophic factor (BDNF), neurofilament light chain (NfL), neuron-specific enolase (NSE), protein gene product 9.5 (PGP9.5), and S100 calcium-binding protein B (S100B) were measured at each follow-up session. Personal O exposure levels were calculated based on outdoor monitoring and sampling times. A linear mixed-effects model was adopted to quantify the acute effect of O on serum neural damage biomarkers. Stratification analysis based on sex, education level, physical activity, and glutathione S-transferases (GST) gene polymorphism analysis was performed to explore their potential modifying effects.
A total of 34 healthy volunteers aged 63.7 ± 5.7 y were enlisted and completed the study. The concentration of the daily maximum 8-h average O (O-8h) ranged from 19.5 to 160.5 μg/m during the study period. Regression analysis showed that short-term O exposure was associated positively with serum concentrations of neural damage biomarkers. A 10 μg/m increase in O-8h exposure was associated with an increment of 74 % (95 % CI:1 %-146 %) and 197 % (95 % CI:39 %-356 %) in BDNF (lag 2 d) and NfL (lag 1 d), respectively. The stratification results suggest that males, people with lower education levels, lower physical activity, and GST theta 1 (GSTT1)-sufficient genotype might be marginally more vulnerable.
This study provides new evidence for the neural damage risk posed by O exposure, even at relatively low concentrations, which, therefore, requires that stringent air quality standards be developed and implemented.
尽管越来越多的研究表明空气污染对神经有不良影响,但将臭氧(O₃)与神经损伤联系起来的证据仍然有限。
研究老年人短期暴露于臭氧(O₃)下的亚临床神经效应。
招募一组健康的老年人,于2018年12月至2019年4月在中国新乡进行了五次重复测量。在每次随访时测量血清神经损伤生物标志物,包括脑源性神经营养因子(BDNF)、神经丝轻链(NfL)、神经元特异性烯醇化酶(NSE)、蛋白基因产物9.5(PGP9.5)和S100钙结合蛋白B(S100B)。根据室外监测和采样时间计算个人O₃暴露水平。采用线性混合效应模型量化O₃对血清神经损伤生物标志物的急性影响。进行基于性别、教育水平、身体活动和谷胱甘肽S-转移酶(GST)基因多态性分析的分层分析,以探讨它们的潜在修饰作用。
共招募了34名年龄为63.7±5.7岁的健康志愿者并完成了研究。研究期间,每日最大8小时平均O₃(O₃-8h)浓度范围为19.5至160.5μg/m³。回归分析表明,短期O₃暴露与血清神经损伤生物标志物浓度呈正相关。O₃-8h暴露每增加10μg/m³,BDNF(滞后2天)和NfL(滞后1天)分别增加74%(95%CI:1%-146%)和197%(95%CI:39%-356%)。分层结果表明,男性、教育水平较低、身体活动较少以及谷胱甘肽S-转移酶θ1(GSTT1)基因足够型的人可能略更易受影响。
本研究为O₃暴露(即使在相对较低浓度下)带来的神经损伤风险提供了新证据,因此需要制定和实施严格的空气质量标准。