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Tabacco Smoking and Pulmonary Tuberculosis : A Case-control Study

T M Dhamgaye*

Key words : Tuberculosis, tobacco smoking.

Tuberculosis is one of the main causes of mortality due to communicable disease. Every year, tobacco causes an estimated 4 million deaths globally. By the early 2030, tobaco related death would increase to about 10 millions a year1. Tobacco smoking rates have decreased in industrialised countries since 1975, but there has been a corresponding 50% increase in smoking rates in low- income countries2. Tuberculosis and tobacco together consitute a considerable threat to global health. They interact in many ways. Tuberculosis infection, incidence and severity are related to tobacco use1.
The incidence of new cases of tuberculosis has increased in many countires of the world. Resurgence in tuberculosis has been mainly due to human immunodeficiency virus (HIV) epidemic3. Besides HIV, other factors include poverty, illicit drug use, homelessness, migration, inadequate healthcare resources, etc4,5. There are many factors that increase the risk of progression from tuberculosis infection to development of tuberculosis disease. Active smoking is one of the factors that have been implicated in increased risk of development of active pulmonary tuberculosis. In India, tobacco is consumed mainly in the form of bidis (54%) , followed by smokeless tobacco (27%) and cigarettes (9%)6. ‘Bidi’ is a traditional tobacco product made from a mixture of granulated tobacco and specially prepared tobacco stems rolled into a dried tendu (Diospyrus melanoxylon) leaf and bound with string.
The association between cigarette smoking, and pulmonary tuberculosis has been assessed in few studies7-12. In contrast to the information on cigarette smoking, no data are available on the relation between bidi smoking and pulmonary tuberculosis. A case-control study was carried out to determine whether there is an association between bidi tobacco smoking and pulmonary tuberculosis.

Material and Method

A case-control study was undertaken at a district tuberculosis hospital, a public population-based hospital from April 1997 to December 1998. Eligible case patients were male, residents of Yavatmal district and older than 20 years of age seeking care at the hospital. A case was defined as patient with clinical, radiological evidence of active pulmonary tuberculosis with sputum smear positive for acid-fast bacilli. A control was defined as person who had no clinical radiological or bacteriological evidence of active pulmonary tuberculosis. Women were not included in this study because the bidi or cigarette smoking among women was not reported. Patients with radiological evidence of tuberculosis with sputum- negative for acid- fast bacilli were excluded. Other exclusion criteria included previous antituberculosis medication and patients with other associated conditions identified as risk factors for other associated conditions identified as risk factors for tuberculosis. Control group consisted of 160 healthy individuals who were accompanying other patients to the hospital. The subjects in the control group were individually matched with the patients for their age, sex, and socio-economic status and geographical area. Exclusion criteria from control group included previous antituberculosis medication and subjects with associated conditions such as asthma and chronic obstructive pulmonary disease (COPD) for which smoke exposure is considered as a risk factor.
Eligible patients were briefed about the study and informed consent was obtained from every person enrolled in the study. All participating cases and control were subjected to the same diagnostic procedures. Assessment was done by clinical history, physical examination, chest x- ray and sputum smear for acid- fast bacilli.
A semi-structured interview schedule was developed based on the antitobacco action plan. The information was collected through interview schedule and comprised socio-economic and demographic factors based on particulars of occupation, family income, housing condition and years of education. The data collected included details regarding smoking habits as well as the history of the other underlying medical conditions.
Tobacco smoking is a common habit amont men in India. Smokers consume tobacco in various forms eg, bidi (tobacco rolled in tendu leaves), chillum, hookah, cigarette and tobaccoo chewing. Bidi smoking is predominantly common among the rural population. All the study population came from rural villages predominately tribal and underprivileged classes. The prevalence rate of cigarettee smoking in the study population was less than 2%. The information on tobacco smoking collected from the cases and control at the time of interviews comprised smoking status, age of onset of smoking, type of tobacco smoking and quantity of bidis smoked per day. Tobacco smokers were classified according to whether they smoked fewer than 10 bidis per day, 10-20 bidis per day or more than 20 bidis per day. Heavy smokers were current smokers smoking 20 bidis or more daily or persons with a 20 or more years smoking history.
Tobacco smoking was the study variable in the study as risk factor of developing tuberculosis in infected persons. Age, education and income were controlled variables. The odd's ratio (OR) were estimated by the Mantel- Haenszel method and the 95% confidence interval (CI) of the OR were calculated.

Observations

Of the 313 patients in the study, 153 were cases and 160 patients were control. The demographic and social characteristics of the study population are depicted in Table 1. The mean age was 37.9 ± 13.7 years among cases and 35.0 ± 12.4 years among controls. Differences in the variables between cases and controls were not statistically significant. Since all the cases and control patients were predominantly from the rural village in the district, which were homogeneous with respect to demographic and social characteristics, all the cases as a group did not differ from the controls. Thirty-three per cent of cases and 23% of controls were active smokers (Table 2). The crude OR was 1.66 (95% CI : 1.01-2.73) in active smoker (p<0.05.) The age adjusted OR was 1.70 (95%CI: 1.01-2.88) Of the 51 bidi smokers in cases, 12 smoked fewer than ten bidis per day, and 22 smoked twenty or more per day.
There was clear dose- response relationship between the number of bidis smoked daily and risk of tuberculosis. The risks associated with bidi smoking were greater among those who smoked 20 or more bidies a day as compared with those who smoked fewer (Table 2). The adjusted OR for mild (1-10 bidis/ day), moderate (11-20/ day) and heavy smokers (>20/ day) was 0.86, 2.42 and 2.72 respectively. Table 3 shows the cumulative effect of smoking and the risk of active pulmonary tuberculosis. The risk associated with smoking was largest for persons who had smoked for 20 years or more (adjusted OR 3.07; 95%CI: 1.37-6.86, p<0.01).

Discussion

The study has shown that bidi smoking was associated with moderate increase in the risk of pulmonary tuberculosis. Persons who have smoked for more than 20 bidis per day have a significantly increased rise of tuberculosis with a relative risk of 2.72. This study has shown that there is a strong dose- response relationship between the number of bidi smoked daily and the risk of pulmonary tuberculosis. Also smoking has been significantly associated with increased risk of pulmonary tuberculosis in heavy smokers with smoking duration of 20 years or more (adjusted OR 3.07; 95% CI: 1.37-6.86). The study suggests that smoking increases the risk for the development of pulmonary tuberculosis. As age is a possible confounder, the crude OR was adjusted for age. Male patients from rural district area were included in the study to minimise the effect of other confounders.
Studies reporting association between smoking and pulmonary tuberculosis with adjustment of confounders are limited. Yu et al8 in Shanghai study reported a relative risk of tuberculosis of 2.17 amongst smokers consuming 400 or more cigarettes per year independently of age, gender, contact with a patient of tuberculosis. However, Brown and campbell9 demonstrated a clear association between alcohol and tuberculosis and no independent association between tobacco used and tuberculosis. In Barcelona, Alcaide et al10 reported that active smoking was independently associated with pulmonary tuberculosis with a relative risk of 3.8 (95% CI : 1.5 to 9.8). The data showed a dose-response relationship between the number of cigarettes smoked daily and risk of active pulmonary tuberculosis. Kolappan and Gopi11 using a case-control method reported OR of 2.48 (95% CI : 1.42 to 4.37) for smokers. The age adjusted OR was 2.24 (95% CI : 1.27 to 3.94).
Case-control studies for tuberculosis are complex, as the number of possible confounders is potentially large. Therefore, the results from prospective studies on the causes of tuberculosis are important. Hnizdo and Murray13 from South Africa studies gold miners; they were regularly exmined. The study followed cohorts to death. The main exposure of interest was silica. However, tobacco use in addition to silica emerged as an independent factor associated with pulmonary tuberculosis at autopsy.
Worldwide tobacco consumption was estimated to be increasing by 2% a year, with the biggest rise occurring in the developing countries. A major concern in the India is the widespread consumption of tobacco products in the form of bidis, since these have extermely high level of tar, nicotine and other toxic agents. A bidi delivers as much as 40-50 mg of tar as compared to 18-28 mg in Indian cigarettes, and 1.74-2.05 mg nicotine as compared to 1.55-1.92 mg in cigarettes14.
All men in the present study are bidi smokers. Bidi smoke may be more injurious because bidi contains unrefined form of tobacco as compared to cigarettes15. A bidi is also required to be puffed more frequently per minute to keep it burning. In the experimental study15, it has been shown that bidi smoke at 2 puffs / minute produces similar amounts of steam-volatile phenols, hydrogen cyanide and benzo(a)pyrene as unfiltered cigarette at 1 puff/ minute.
The biological mechanism for the association between tobacco smoke and pulmonary tuberculosis may be due to the decrease in immune response16 and other mechanisms such as mechanical disruption of cilia function. It is possible that the nicotine in tobacco smoke might interfere with the immune response of the host to Mycobacterium tuberculosis11. In smokers, the chemotactic, microbicidal and secretory functions of leucocytes appear to be normal but monocytes may partially lack the ability to kill an intracellular organisms. In light to moderate smokers, an increase in total T- cells and T- helper cells is seen, whereas in heavy smokers there is a fall in T- helper cells count but increase in T-suppressor cells17. Exposure to tobacco smoke causes morphological and functional changes in the alveolar macrophages18.
Smoke induced oxidative cellular damage along with inflammation leads to recruitment of inflammatory mediators from serum, resulting in damage to the respiratory passages. Lung defence mechanism is affected by impairment of mucociliary clearance of Mycobacterium tuberculosis and other potential pathogens19.
Smoking has been associated with pulmonary tuberculosis particularly in heavy smokes8,10. It appears that smokes have an increased risk of progressing from infection to disease. At present it is not clear whether smoking also increases the risk of infection, but higher prevalence rates of tuberculous infection were found among the smokers20,21.
In summary, there is an association between bidi smoking and the development of pulmonary tuberculosis with a dose-response relationship with the number of bidis consumed daily. Further large prospective studies are warranted to support the evidence for association between tobacco smoking and pulmonary tuberculosis.

Acknowledgment

The author is greateful to Mr LR Kulkarni, Associate Professor in Statistics, Indira Gandhi Medical College, Nagpur for statistical assistance.

References

1 Yach D — Partnering for better lung health: improving tobacco and tuberculosis control. Int J Tuberc Lung Dis 2000; 4: 693-7.
2 Yu JJ, Shopland DR — Cigarette smoking behavior and consumption characteristics for the Asia- Pacific region. World Smoking Health 1989; 14: 7-9.
3 Sudre P, ten Dam G, Kochi A — Tuberculosis– a global overview of the situation today. Bull World Health Organ 1992; 70: 149-59.
4 Reichman LB — The U shaped curve of concern. Am Rev Respir Dis 1991; 148: 741-2.
5 Brudney K, Dobkin J — Resurgent tuberculosis in New York city : human immunodeficiency virus, homelessness, and the decline of tuberculosis control programs. Am Rev Respir Dis 1991; 144: 745-9.
6 Anonymous — IUALTD: the world tobacco situation. IUALTD News Bull Tobacco Health 1998; 11: 19-21.
7 Adelstein AM, Rimingston J — Smoking and pulmonary tuberculosis: an analysis based on a study of volunteers of mass miniature radiography. Tuber Lung Dis 1967; 48: 219-26.
8 Yu GP, Hsieh CC, Peng J — Risk factors associated with the prevalence of pulmonary tuberculosis among sanitary workers in Shanghai. Tuber Lung Dis 1988; 69: 105-12.
9 Brown KE, Campell AH — Tobacco, alcohol and tuberculosis. Br J Dis Chest 1961; 55: 150-8.
10 Alcaide I, Altet MN, Plans P, Parron I, Folguera L, Salto E, et al — Cigarette smoking as a risk factor for tuberculosis in young adults: a case- control study. Tuber Lung Dis 1996; 77: 112-6.
11 Kolappan C, Gopi PG — Tobacco smoking and pulmonary tuberculosis. Thorax 2002; 57: 964-6.
12 Lewis JG, Chamberlain DA — Alcohol consumption and smoking habits in male patients with pulmonary tuberculosis. Br J Prev Soc Med 1963; 17: 149-52.
13 Hnizdo E, Murray J — Risk of pulmonary tuberculosis relative to silicosis and exposure to silica dust in South African gold miners. Occup Enviorn Med 1998; 55: 496-502.
14 World Health Organisation — Health Situation in the South East Asia region 1994-1997. New Delhi: WHO, 1999.
15 Pakhale SS, Jayant K, Bhide SV — Chemical analysis of smoke of Indian cigarettes, bidis and other indigenous forms of smoking – levels of steam-voltatile phenol, hydrogen cyanide and benzo(a)pyrene. Indian J Chest Dis Allied Sci 1990; 32: 75-81.
16 Johnson JD, Houchens DP, Kluwe WM, Craig DK, Fisher GL — Effects of mainstream and environmental tobacco smoke on the immune system in animals and humans: a review. Crit Rev Toxicol 1990; 20: 369-95.
17 Sherman CB — The health consequences of cigarette smoking: pulmonary diseases. Med Clin North Am 1992; 76: 355-75.
18 Sibille Y, Renolds HY — Macrophages and polymorphonuclear neutrophils in lung defense and injury. Am Rev Respir Dis 1990; 141: 471-501.
19 Stophen J, David MD — Cigarette smoking and disease. In: Fishman AP, Elias JA, Grippi MA, Kaiser LV, Senior RM, editors. Fishman’s Pulmonary Diseases and Disorders. 3rd ed. New York: McGraw-Hill, 1998: 687-99.
20 Center for Disease Control — Prevalence of tuberculous infection among US residents of Cuban descent– Dade County, Florida, 1982-84. MMWR Morb Mortal Wkly Rep1992; 41: 74-81.
21 Nisar M, Williams CS, Ashby D, Davies PD — Tuberculin testing in residential homes for the elderly. Thorax 1993; 48: 1257-60.

*DTCD, MD (Obstet Gynaecol), MD (Chest), Professor and Head of the Department of Tuberculosis and Chest Diseases, Government Medical College, Aurangabad 431001
Accepted January 14, 2006

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