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Short-term ozone exposure and serum neural damage biomarkers in healthy elderly adults: Evidence from a panel study
Rongrong Qu1, Beibei Sun1, Jing Jiang1
1Henan International Collaborative Laboratory for Health Effects and Intervention of Air Pollution, School of Public Health, Xinxiang Medical University, Xinxiang, Henan Province 453003, China.
Background:
Although converging lines of research have pointed to the adverse neural effects of air pollution, evidence linking ozone (O3) and neural damage remains limited.
Objectives:
To investigate the subclinical neural effects of short-term ozone (O3) exposure in elderly adults.
Methods:
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 O3 exposure levels were calculated based on outdoor monitoring and sampling times. A linear mixed-effects model was adopted to quantify the acute effect of O3 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.
Results:
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 O3 (O3-8h) ranged from 19.5 to 160.5 μg/m3 during the study period. Regression analysis showed that short-term O3 exposure was associated positively with serum concentrations of neural damage biomarkers. A 10 μg/m3 increase in O3-8h 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.
Conclusions:
This study provides new evidence for the neural damage risk posed by O3 exposure, even at relatively low concentrations, which, therefore, requires that stringent air quality standards be developed and implemented.
