Objective  To explore the association of smoking with insulin resistance and islet β-cell function among healthy workmen in a large chemical plant in Nanjing city and to provide evidences for diabetes prevention and control in occupational populations.

  Methods  We recruited 3 366 male workers without cardiovascular and cerebrovascular diseases, kidney disease, tumor, and diabetes and hazardous occupational exposures in two workshops of a large chemical plant and assigned the workers into a non-smoking, light, moderate, and heavy smoking groups based on their packets of cigarettes smoked per year. Questionnaire interviews, physical examination and laboratory detections were conducted among the workers during June – December 2018. The indexes of homeostasis model assessment-insulin resistance (HOMA-IR) and homeostasis model assessment-β cell function (HOMA-β) were calculated for all the workers. Binary logistic regression was adopted to assess the impact of smoking on HOMA-IR/β.

  Results  For the 3 135 workmen (mean age: 43.45 ± 10.95 years) with valid information, the detection rate of diabetes (fasting plasma glucose FPG ≥ 7.0 mmol/L or/and hemoglobin A1c HbA1c ≥ 6.5%) was 6.35%. With the increment of number of cigarettes smoked per day, the FPG and HbA1c increased but the fasting blood insulin and HOMA-β decreased gradually in a dose-response manner. The HOMA-IR increased significantly in light smokers but decreased in moderate and heavy smokers. Compared to the non-smokers, the heavy smokers were at a higher risk for HOMA-IR decline, with an odds ratio (OR) of 3.57 (95% confidence interval 95% CI = 2.77 – 4.59) and an adjusted OR of 1.64 (95% CI = 1.22 – 2.22); in comparison with the non-smokers, the smokers with > 15 cigarettes smoked per day had a higher risk of HOMA-IR decline, with an OR of 1.62 (95% CI = 1.33 – 1.99) and an adjusted OR of 1.10 (95% CI = 0.87 – 1.40).

  Conclusion  Smoking could induce a dose-dependent decrease in islet β-cell function and cause insulin resistance in some extent.