| 摘 要： |
Background:Limited evidence suggests the association of air pollutants with a series of diabetic cascades including inflammatory pathways, glucose homeostasis disorder, and prediabetes and diabetes. Subclinical strategies for preventing such pollutants-induced effects remain unknown. Methods:We conducted a cross-sectional study in two typically air-polluted Chinese cities in 2018-2020. One-year average PM1, PM2.5, PM10, SO2, NO2, and O-3 were calculated according to participants' residence. GAM multinomial logistic regression was performed to investigate the association of air pollutants with diabetes status. GAM and quantile g-computation were respectively performed to investigate individual and joint effects of air pollutants on glucose homeostasis markers (glucose, insulin, HbA1c, HOMA-IR, HOMA-B and HOMA-S). Complement C3 and hsCRP were analyzed as potential mediators. The ABCS criteria and hemoglobin glycation index (HGI) were examined for their potential in preventive strategy. Results:Long-term air pollutants exposure was associated with the risk of prediabetes [Prevalence ratio for O-3 (PR_O-3) = 1.96 (95% CI: 1.24, 3.03)] and diabetes [PR_PM1 = 1.18 (95% CI: 1.05, 1.32); PR_PM2.5 = 1.08 (95% CI: 1.00, 1.16); PR_O-3 = 1.35 (95% CI: 1.03, 1.74)]. PM1, PM10, SO2 or O-3 exposure was associated with glucose -homeostasis disorder. For example, O-3 exposure was associated with increased levels of glucose [7.67% (95% CI: 1.75, 13.92)], insulin [19.98% (95% CI: 4.53, 37.72)], HOMA-IR [34.88% (95% CI: 13.81, 59.84)], and decreased levels of HOMA-S [-25.88% (95% CI:-37.46,-12.16)]. Complement C3 and hsCRP played mediating roles in these relationships with proportion mediated ranging from 6.95% to 60.64%. Participants with HGI <=-0.53 were protected from the adverse effects of air pollutants. Conclusion:Our study provides comprehensive insights into air pollutant-associated diabetic cascade and suggests subclinical preventive strategies. |
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