Associations of blood lead levels with multiple genotoxic biomarkers among workers in China: A population-based study

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. [Display omitted] •Multiple relevant genotoxic biomarkers were evaluated in a large group of lead (Pb)-exposed workers.•Pb induced changes of mitochondrial DNA copy number, DNA & chromosome damage and telomere erosion, but not PIG-A mutation.•Mechanisms for Pb-induction of health hazards may be via the clastogenesis but not the mutagenesis pathway. From a large-scale population study, Pb exposure was associated with alteration of mitochondrial DNA copy number, damage in DNA & chromosome and erosion of telomere, but not PIG-A mutation. Our results suggest that clastogenesis but not the mutagenesis is likely the pathway for Pb-induced health hazards.