Smoking and liver enzymes in older Chinese men : the Guangzhou biobank cohort study (GBCS)

Abstract

Objective: To examine the association between smoking and common liver enzymes (Alanine aminotransferase (ALT), aspartate aminotransferase (AST) and γ-glutamyl transferase (GGT)) among older Chinese men aged 50 or above.

Design: Cross-sectional study based on Guangzhou Biobank Cohort Study

Setting: Guangzhou, China.

Subjects: 2049 Guangzhou older men in the Guangzhou Biobank Cohort Study who were free of clinical indications of liver diseases.

Methods: Information on cigarette smoking and potential confounding variables were collected by standardized interviews and laboratory assays. Elevation of liver enzymes was defined as >40 U/L for ALT, >40 U/L for AST and >50 U/L for GGT. Both logistic regression and linear regression modeling were used to estimate the association of cigarette smoking with liver enzymes, adjusted for age, education, personal income, body mass index (BMI), physical activity and alcohol drinking.

Results: Current smoking was positively associated with elevated GGT. Compared to never smokers, the adjusted odds ratios (OR) [95% confidence interval] of elevated GGT was 1.58 [1.06-2.35] and 1.68 [1.18-2.41] for those who smoked ≥20 cigarettes/day and ≥20 pack-years, respectively, while the adjusted OR for those who smoked <40 years and those who smoked ≥40 years was 1.57 [1.06-2.33] and 1.38 [0.92-2.08], respectively. The interaction effect of smoking and BMI was significant for elevated ALT and GGT (both P<0.001). The risk of elevated ALT increased with increasing BMI. Compared to never smokers with normal weight, the adjusted OR of elevated ALT was 3.76 [2.14-6.60] for never smokers with obesity. The risks of elevated GGT increased with increasing smoking intensity (daily smoking amount, duration or pack-years) and BMI. Compared to never smokers with normal weight, the adjusted OR of elevated GGT was 3.48 [1.76-6.87] for heavy smokers who also had obesity. The interaction effect of smoking and drinking was significant for elevated AST and GGT (both P<0.001) but not for ALT. However, no association of daily smoking amount, duration or pack-years with elevated AST by drinking status was found (all P>0.05). The risk of elevated GGT was significantly increased by increasing smoking intensity, duration or pack-years in moderate or excessive drinkers. The adjusted OR of elevated GGT was 5.29 [3.03-9.23] for heavy smokers who drank excessively, compared to those who never smoked and drank.

Conclusion: Cigarette smoking was positively associated with elevation of GGT concentrations. The significant interactions between smoking and BMI or drinking on elevation of GGT suggest smoking cessation is urgently needed especially for alcohol drinker or obese individuals. The use of elevated GGT could be an early signal of liver cell damage for smokers.