Abstract
This study assessed the tobacco smoking-associated risk for tuberculous pleural effusion (TPE) in India. Ninety-two patients with TPE and 184 controls were randomly selected and assessed regarding their tobacco-smoking status and type, quantity and duration of tobacco used. Odds ratios (ORs) for the association of smoking cigarette, beedi and cigarette or beedi with TPE were 19.22 (p < 0.0001), 2.89 (p = 0.0006) and 4.57 (p < 0.0001) respectively. ORs for developing TPE increased with an increase in beedi/cigarette consumption, duration and pack years of smoking (p < 0.001 each). TPE was significantly associated with confounding risk factors viz., regular alcohol use (OR = 1.89, p = 0.019), history of contact with tuberculosis (TB) patient (OR = 8.07, p < 0.0001), past history of TB (OR = 22.31, p < 0.0001), family history of TB (OR = 9.05, p = 0.0002) and underweight (OR = 3.73, p = 0.0009). Smoking (OR = 3.07, p < 0.001), regular alcohol use (OR = 2.10, p = 0.018), history of contact with TB patient (OR = 4.01, p = 0.040), family history of TB (OR = 10.80, p = 0.001) and underweight (OR = 5.04, p < 0.001) were independently associated with TPE. Thus, both cigarette- and beedi-smoking have a significant association with TPE. The risk for TPE in tobacco smokers is dose- and duration-dependent.
Highlights
Tuberculosis (TB) is the leading cause of mortality by an infectious disease [1]
As such cigarette smoke may impair the macrophage and dendritic cell function leading to persistence and/or replication of ingested mycobacteria [6,7,8,9]
The χ2 test of association was used for testing the association between Tuberculous pleural effusion (TPE) and various variables about which information was recorded from subjects at the time of their entry into the study
Summary
Tuberculous pleural effusion (TPE) is a frequently seen clinical condition and is regarded as a form of extra-pulmonary tuberculosis (EPTB) [3]. Increased risk of TB in smokers may be due to various factors like reduction in natural killer cytotoxic activity, suppression of T cell function in both lung and blood, impairment of mucociliary clearance of particles and increase in the number of alveolar macrophages in the lower respiratory tract. Immediate or innate immunity is affected by cells of the macrophagephagocytic group as they handle and eliminate mycobacteria. As such cigarette smoke may impair the macrophage and dendritic cell function leading to persistence and/or replication of ingested mycobacteria [6,7,8,9]
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