Background: Low-grade systemic inflammation is commonly observed in conditions associated with reduced FEV1. Active cigarette smoking, which is a leading risk factor for decreased FEV1, can also independently induce systemic inflammation.
Study objectives: To determine the independent contributions of active cigarette smoking and reduced FEV1 (as well as their potential interactions) on systemic inflammation.
Design: Cross-sectional survey.
Setting: The US general population.
Participants: A total of 7,685 adult participants, ≥ 40 years of age, in the Third National Health and Nutrition Examination Survey, who had acceptable data on spirometry and laboratory measurements such as serum C-reactive protein (CRP).
Measurements: The participants were stratified into four equal groups (quartiles) based on the percent predicted FEV1 values. Each group was further categorized as active smokers or nonsmokers according to serum cotinine level (ie, ≥ 10 or < 10 ng/mL). Serum levels of CRP, plasma fibrinogen, blood leukocytes, and platelets were compared across the predicted FEV1 quartile groups and across smoking status using multiple logistic regression models.
Results: We found that active smoking by itself increased the odds of having elevated CRP levels by 63% (adjusted odds ratio [OR], 1.63; 95% confidence interval, 1.28 to 2.09). The adjusted OR for reduced FEV1 was 2.27 (95% confidence interval, 1.92 to 2.70). Having both risk factors increased the OR to 3.31 (95% confidence interval, 2.73 to 4.02). Similar findings were observed for blood leukocytes and plasma fibrinogen.
Conclusion: These findings suggest an additive effect of active smoking and reduced FEV1 on markers of systemic inflammation and suggest their potential interactions in the pathogenesis of systemic complications observed in patients with poor lung function.