Background: Visual impairment among children and adolescents is a major public health concern. However, evidence regarding the associations of PM 2.5 and its chemical constituents with incident visual impairment remains limited, particularly in highly polluted regions. We aimed to investigate these associations in northern China. Methods: This study included 12,433,993 school students from a dynamic cohort in Shandong Province, China, followed from 2012 to 2024. Annual concentrations of PM 2.5 and its five major chemical constituents were estimated using data from the Tracking Air Pollution in China database. Visual impairment was defined as visual acuity below 4.9 in either eye. Cox proportional hazards models were used to estimate associations, with penalized splines characterizing exposure–response relationships. Quantile g-computation assessed the joint association of the five constituents. Results: During 35,156,004 person-years of follow-up, 8,036,370 participants (64.6%) developed visual impairment. Each IQR increase in PM 2.5 concentration was associated with a 58% higher risk of incident visual impairment ( HR , 1.58; 95% CI , 1.53–1.63), while the five constituents were also positively associated with incident visual impairment ( HR s: 1.53–1.57). PM 2.5 and all five chemical constituents showed predominantly non-threshold linear or supra-linear exposure–response relationships. A simultaneous one-quartile increase in all five constituents was associated with a 26% higher risk of incident visual impairment ( HR , 1.26; 95% CI, 1.24–1.28). Stronger associations were consistently observed among students in higher grades. Conclusions: Our findings provide evidence of the adverse associations of PM 2.5 and its chemical constituents with visual impairment risk and emphasize the need for more rigorous regulations targeting these pollutants in China.
Chronic exposure to polycyclic aromatic hydrocarbons (PAHs) is associated with increased risk of cancer through a mutagenic mode of action. We investigated how exposure duration influences mutagenicity in bone marrow (BM) and liver of MutaMouse males orally exposed to increasing doses of benzo[ b ]fluoranthene (BbF), a priority PAH, for 28, 90, or 180 days. We applied Duplex Sequencing (DS) across 20 endogenous loci to assess dose- and time-dependent effects on mutation frequency, clonal expansion of mutant cells, mutation distribution, and spectra. Mutation frequencies increased with BbF dose and exposure duration in both tissues. After 90 and 180 days of exposure to 25 mg/kg/day BbF, mutation frequency was 1.7x and 2.1x higher in BM, and 3.8x and 8.6x higher in liver, than 28-day exposures. Clonally derived mutations increased significantly with exposure duration in BM but not liver. Intergenic loci incurred more mutations than genic regions in both tissues across all exposure durations. Mutation spectra were dominated by C:G > A:T transversions and were enriched in SBS4, the mutation signature associated with tobacco-induced human lung cancer. Benchmark dose (BMD 50 ) modeling showed increasing BbF potency with longer exposures. BMD 50 decreased from 8.2 (28d) to 3.7 (90d) and 3.0 (180d) mg/kg/day in BM; in liver, BMD 50 shifted from 14.3 (28d) to 4.3 (90d) and 3.9 (180d) mg/kg/day. The observed tissue-specific responses may be attributed to differences in proliferation rate, metabolic activity, and cellular lifespan. Our findings provide insights into the mutagenic impacts of prolonged PAH exposure and highlight tissue-specific differences in mutation susceptibility.
