Associations of Short-Term Exposure to Fine Particulate Matter with Neural Damage Biomarkers: A Panel Study of Healthy Retired Adults
Jie Song, Rongrong Qu, Beibei Sun, Renjie Chen, Haidong Kan, Zhen An, Jing Jiang, Juan Li, Yange Zhang, Weidong Wu
Abstract
Exposure to fine particulate matter (PM2.5) is associated with various adverse health effects, such as respiratory and cardiovascular diseases. This study aimed to evaluate the association of PM2.5 with neural damage biomarkers. A total of 34 healthy retirees were recruited from Xinxiang Medical University from December 2018 to April 2019. Concentrations of PM2.5 constituents including 24 metals and nonmetallic elements and 6 ions, and 5 biomarkers of neural damage 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) in serum were measured. A linear mixed-effect model was employed to estimate the association of PM2.5 and its constituents with neural damage biomarkers. Modification effects of glutathione S-transferase theta 1 gene (GSTT1) polymorphism, sex, education, and physical activity on PM2.5 exposure with neural damage were explored. PM2.5 and its key constituents were significantly associated with neural damage biomarkers. A 10 μg/m3 increase in PM2.5 concentration was associated with 2.09% (95% CI, 39.3–76.5%), 100% (95% CI, 1.73–198%), and 122% (95% CI, 20.7–222%) increments in BDNF, NfL, and PGP9.5, respectively. Several constituents such as Cu, Zn, Ni, Mn, Sn, V, Rb, Pb, Al, Be, Cs, Co, Th, U, Cl–, and F– were significantly associated with NfL. The estimated association of PM2.5 with NSE in GSTT1-sufficient volunteers was significantly higher than that in GSTT1-null volunteers. Therefore, short-term PM2.5 exposure was associated with neural damage, and GSTT1 expression levels modified the PM2.5-induced adverse neural effects.