Impact of cigarette smoking and cumulative exposure on serum lipid profile: A cross-sectional study

Cigarette smoking is a major modifiable risk factor for cardiovascular disease and has been associated with adverse changes in lipid metabolism. However, evidence regarding the relationship between cumulative smoking exposure and lipid profiles in Syrian populations remains limited.

To evaluate the association between cigarette smoking, smoking duration, and cumulative exposure expressed as pack-years with serum lipid parameters among Syrian adults.

A cross-sectional observational study was conducted among 70 adult participants recruited from the laboratory of Al-Nabek Hospital, Deir Atiyah, Syria. Participants included 50 smokers and 20 non-smokers. Serum total cholesterol (TC), triglycerides (TG), low-density lipoprotein cholesterol (LDL-C), and high-density lipoprotein cholesterol (HDL-C) were measured using standard enzymatic methods. Smoking duration and cigarettes smoked per day were recorded, and cumulative exposure was estimated using pack-years. Initial comparisons between smokers and non-smokers were performed using independent-samples t-tests. Multivariable linear regression models were subsequently used to examine the association between smoking status and each lipid parameter while adjusting for age and body mass index (BMI).

Compared with non-smokers, smokers had higher mean TG (180.58 ± 70.89 vs 128.16 ± 16.00 mg/dL; p = 0.002), LDL-C (101.92 ± 39.10 vs 70.08 ± 10.52 mg/dL; p < 0.001), and TC (186.77 ± 50.10 vs 135.99 ± 12.16 mg/dL; p < 0.001), and lower HDL-C (43.24 ± 4.13 vs 47.54 ± 9.42 mg/dL; p = 0.010). Longer smoking duration was accompanied by progressively higher mean TG, LDL-C, and TC across smoking-duration categories. In multivariable regression adjusted for age and BMI, smoking was independently associated with higher TC (β = 41.47, 95% CI 16.29-66.65; p = 0.002) and LDL-C (β = 24.24, 95% CI 4.60-43.88; p = 0.016), and lower HDL-C (β = -5.51, 95% CI -10.53 to -0.50; p = 0.032). The association with TG was positive but borderline and did not reach conventional statistical significance (β = 35.00, 95% CI -0.41-70.41; p = 0.053).

Smoking was associated with an adverse lipid profile characterized by higher TC, LDL-C, and TG and lower HDL-C. The associations with TC, LDL-C, and HDL-C remained statistically significant after adjustment for age and BMI. Longer smoking duration was accompanied by less favorable lipid values; however, these findings should be interpreted cautiously because of the exploratory sample size, unequal group sizes, incomplete information on some potential confounders, and the cross-sectional design. The observed pattern across smoking-duration and pack-year categories should not be interpreted as definitive evidence of a causal dose-response relationship.