| Literature DB >> 33508628 |
Tuanwei Wang1, Yuting Tu1, Kan Wang1, Shiyang Gong1, Guanghui Zhang2, Yunxia Zhang1, Yu Meng1, Tongshuai Wang1, Anqi Li1, Junpeng Cui2, Huan Liu2, Weifeng Tang3, Jing Xi3, Yiyi Cao3, Yang Luan3, David C Christiani4, William Au5, Zhao-Lin Xia6.
Abstract
Carcinogenic effects from low doses of lead (Pb) exposure to populations have been suspected but not concluded. Therefore, a large-scale cross-sectional study was conducted by us to investigate genotoxic effects from Pb exposure during 2016-2018 in North China. Blood lead levels (BLLs) and cumulative blood lead levels (CBLLs) were measured. Multiple relevant biomarkers were used to assess genotoxicity of Pb: mitochondrial DNA copy number (mtDNAcn, n = 871), Comet Tail Intensity (n = 872), γ-H2AX (n = 345), relative telomere length (rTL, n = 757), micronuclei (MN, n = 934) and phosphatidylinositol glycan class A mutation (PIG-A, n = 362). The BLL data show right-skewed distribution, with increase of the median (P25, P75) from 17.4 (8.9, 26.4) μg/dl in 2016 to 18.5 (10.5, 27.2) μg/dl in 2017, and to 20.8 (11.3, 31.0) μg/dl in 2018. Multivariate regression analyses show that mtDNAcn was non-linearly associated with BLLs or CBLLs, i.e. decreased at low levels but increased at the higher levels. Comet and Micronuclei data show positive dose-response relationships with BLLs as well as CBLLs. γ-H2AX data show an overall increased trend with BLLs while rTL data show a shortening trend. No associations were found for PIG-A mutation with Pb exposure. Our findings indicate that current low dose exposure to Pb can still cause health hazards to occupational populations, and the mechanism may be via the induction of DNA & chromosome damage rather than via the mutagenesis pathway.Entities:
Keywords: Comet; Lead exposure; Micronuclei; PIG-A mutation; Relative telomere length; mtDNAcn
Year: 2020 PMID: 33508628 DOI: 10.1016/j.envpol.2020.116181
Source DB: PubMed Journal: Environ Pollut ISSN: 0269-7491 Impact factor: 8.071