Association of long-term air pollution exposure with the risk of prediabetes and diabetes: Systematic perspective from inflammatory mechanisms, glucose homeostasis pathway to preventive strategies

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. 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 O3 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. Long-term air pollutants exposure was associated with the risk of prediabetes [Prevalence ratio for O3 (PR_O3) = 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_O3 = 1.35 (95% CI: 1.03, 1.74)]. PM1, PM10, SO2 or O3 exposure was associated with glucose-homeostasis disorder. For example, O3 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. Our study provides comprehensive insights into air pollutant–associated diabetic cascade and suggests subclinical preventive strategies.