1. TOBACCO AND TUBERCULOSIS
Mini Lecture 1
Module: Effects of Tobacco on the Respiratory System
Key References:
Bates MN, Khalakdina A, Pai M, Chang L, Lessa F, Smith KR. Risk of tuberculosis from exposure to tobacco smoke: a systematic review and meta-analysis. Arch Intern Med. 2007; 167(4):335–42.
Arcavi L, Benowitz NL. Cigarette smoking and infection. Arch Intern Med. 2004;164(20):2206–16.
Siddiqi K, Lee AC. An integrated approach to treat tobacco addiction in countries with high tuberculosis incidence. Trop Med Int Health 2009 Apr;14(4):420–8.
Ng N, Padmawati RS, Prabandari YS, Nichter M. Smoking behaviour among former tuberculosis patients in Indonesia: Intervention Is needed. The International Journal of Tuberculosis and Lung Disease. 2008;12(5):567–72.
World Health Organization, International Union against Tuberculosis and Lung Disease. A WHO/The Union monograph on TB and tobacco control: joining efforts to control two related global epidemics. WHO/HTM/TB/ Geneva, World Health Organization, 2007.
Leung CC, Lam TH, Ho KS, Yew WW, Tam CM, Chan WM. Passive smoking and tuberculosis. Arch Intern Med. 2010; 170(3):287–92.

2. Objectives of the Mini Lecture
GOAL OF MINI LECTURE: Provide students with knowledge about the harmful effects of tobacco on tuberculosis, and skills to provide smoking cessation counseling for TB patients.
LEARNING OBJECTIVES:
Students will be able to:
Understand the burden of smoking among TB patients.
Understand the association between smoking and TB, and impact of smoking on TB.
Conduct counseling to encourage TB patients to quit smoking.
Module Description:
This module is intended to provide students with knowledge about the burden of tuberculosis (TB) and smoking among TB patients . The association between smoking and TB as well as the how smoking can worsen TB will be presented. This module will providean example of smoking cessation counseling for TB patients.

3. Contents Core Slides Optional Slides Global Burden of TB TB in India
Smoking: A Risk Factor for TB
Smoking Interferes with TB Treatment and Places Household Members at Risk
Secondhand Smoking and TB
Smoking and Respiratory Infections: Mechanisms
Smoking Cessation: TB Patients
DOTS Providers and Smoking Cessation
Burden of TB in Five Countries
Smoking, TB Clinical Manifestation, Conversion, and Relapse
Smoking and TB: Immunopathogenesis
Iron, Smoking, and TB
Cessation Messages: TB Patients
WHO, TB, and Tobacco: Key Messages

4. CORE SLIDES Tobacco and Tuberculosis Mini Lecture 1
Module: Effects of Tobacco on the
Respiratory System

5. Global Burden of TB
DOTS programmes (1995–2006): 31.8 million new and relapse cases, and 15.5 million new smear-positive cases.
In 2006: 9.2 million new cases (139 per ), including 4.1 million new smear-positive cases and 0.7 million HIV-positive cases.
Major burden was in Africa (23%), South-East Asia (35%), and Western Pacific (25%).
Notes:
Most of the new TB cases reported in 2006 were identified in India, China, Indonesia, South Africa, and Nigeria. Most of this TB burden is in low-and middle-income countries in Africa and Asia, with the highest incidence per capita reported in Africa (363 per 100,000 population). About 3% of the estimated 14.4 million prevalent cases of TB in 2006 were multidrug resistant TB (MDR-TB) cases. A total of 1.7 million deaths from TB was estimated in 2006, with about 12% deaths among people infected with HIV.
The WHO launched its Stop TB strategy in 2006 in order to achieve case detection and treatment success in The strategy includes six major components: (i) DOTS expansion and enhancement; (ii) addressing TB/HIV, MDR-TB, and other challenges; (iii) contributing to health system strengthening; (iv) engaging all care providers; (v) empowering patients and communities; and (vi) enabling and promoting research.
In 2006, DOTS has been implemented in 184 countries worldwide, and accounted for 99% of all estimated TB cases. The DOTS programmes has reached the highest treatment success rate in 2005 (84.7%, which is close to the target of 85%). The treatment success varies from 71% in the European region, 76% in the African region, 78% in the American region, 83% in the Eastern Mediterranean region, and over 85% in the South-East Asia and Western Pacific regions.
Reference:
World Health Organization. Global tuberculosis control: surveillance, planning, financing. Geneva: World Health Organization; 2007.
World Health Organization 2007

6. TB in India
Highest tuberculosis (TB) burden in the world, with an annual case load of 1.8 million, representing one fifth of total global cases and two thirds of cases in South Asia.
Implemented DOTS strategy under the Revised National TB Control Program (RNTCP), covering the entire country by March 2006.
Achieved a DOTS treatment success rate of 87% in 2004 against a target of 85%.
Notes:
India has the highest tuberculosis (TB) burden in the world, with an annual case load of 1.8 million; this represents one fifth of total global cases and two thirds of cases in South Asia. The DOTS strategy, which is based on directly observed short-course treatment, uninterrupted drug supplies, an adequate recording and reporting system, a national network of laboratories, and governmental commitment to tuberculosis control, is the internationally recommended approach to TB control, and is at the heart of the World Health Organization (WHO) Stop TB strategy. India has implemented this strategy in a phased manner, under the Revised National TB Control Program (RNTCP). In March 2006, the coverage of the DOTS strategy reached the entire country. To its credit, India achieved a DOTS treatment success rate of 87% in 2004 against a target of 85%.
References:
Agarwal SP, Vijay S, Kumar P, Chauhan LS. The history of tuberculosis control in India: glimpses through decades. In Agarwal SP, Chauhan LS (eds.), Tuberculosis control in India. New Delhi: Directorate General of Health Services, Ministry of Health and Family Welfare: Elsevier; Pp. 15–22.
Pradeepkumar AS, Thankappan KR, Nichter M. Smoking among tuberculosis patients in Kerala, India: proactive cessation efforts are urgently needed. Int J Tuberc Lung Dis. 2008; 12:1139–45.
Pradeepkumar et al. 2008

7. Smoking: A Risk Factor for TB
Smoking increases risk for TB infection, disease and mortality:
Increases risk of TB infection by 1.73 times as compared to non-smokers.
Increases risk of TB disease by 2.3 to 2.7 times compared to non-smokers.
Increases risk of TB mortality by 1.60 times compared to non-smokers.
Notes:
There is now sufficient evidence to link smoking to TB infection, TB diseases, and TB mortality. The meta-analysis conducted by Bates et al. showed no evidence of heterogeneity among studies conducted to assess the association between smoking and TB infection and TB diseases. There were more heterogeneities among studies to assess smoking and TB mortality, mainly due to different methods to derive cause-of-death data in developing countries (death certificates which is more unreliable and verbal autopsy).1
With a higher risk of smokers getting TB infection (defined as a minimum tuberculin skin test indurations diameter of 10 mm), the proportion of smokers who are infected and are at risk for TB disease will increase. If smoking increases the risk of TB disease in those already infected, this will increase the proportion of smokers at risk for TB mortality. The independent RR for TB disease can be estimated by dividing the study derived RR for TB disease (2.3–2.7) by the RR for TB infection (1.7). This gives an estimated RR for development of TB disease in an infected population of 1.4 to 1.6. Ex-patients are more than three times more likely to relapse if they smoke following short course TB treatment.
Smoking, which increases the incidence of clinical tuberculosis, is a cause of half the male tuberculosis deaths in India, and of a quarter of all male deaths in middle age (plus smaller fractions of the deaths at other ages). At current death rates, about a quarter of cigarette or beedie smokers would be killed by tobacco at ages 25–69 years, with those killed at these ages losing about 20 years of life expectancy. Overall, smoking currently causes about deaths per year in India, chiefly from respiratory or vascular disease: about men aged 25–69 years, about older men, and much smaller numbers of women (since few women smoke).
The relative risk for death from tuberculosis was 4.5 (95% CI 4.0–5.0). Of the 1840 deaths from tuberculosis among men aged 25–69 years, 79% involved smokers. For other respiratory diseases, chief among which was chronic obstructive lung disease, the relative risk was 2.9 and the smoking-associated proportion was 45%. Overall, tuberculosis and other respiratory diseases accounted for a substantial proportion of all smoking associated mortality.
References:
Bates MN, Khalakdina A, Pai M, Chang L, Lessa F, Smith KR. Risk of tuberculosis from exposure to tobacco smoke: a systematic review and meta-analysis. Arch Intern Med. 2007; 167(4):335–42.
Gajalakshmi V, Peto R, Kanaka TS, Jha P. Smoking and mortality from tuberculosis and other diseases in India: retrospective study of adult male deaths and controls. Lancet. 2003; 362:507–15.
Shang S, Ordway D, Henao-Tamayo M, Bai X, Oberley-Deegan R, Shanley C. Cigarette smoke increases susceptibility to tuberculosis--evidence from in vivo and in vitro models. J Infect Dis. 2011; 203(9):1240–8. Epub 2011 Feb 28.
van ZylSmit RN, Pai M, Yew WW, Leung CC, Zumla A, Bateman ED, et al. Global lung health: the colliding epidemics of tuberculosis, tobacco smoking, HIV, and COPD. Eur Respir J. 2010; 35:27–33.
Slama K, Chiang C Y, Enarson D A, Hassmiller K, Fanning A, Gupta P, et al. Tobacco and tuberculosis: a qualitative systematic review and meta-analysis. Int J Tuberc Lung Dis. 2007; 11(10):1049–61.
Bates et al. 2007

8. Smoking Interferes with TB Treatment and Places Household Members at Risk
Smoking is a risk factor for delayed sputum conversion time.1
The risk of Isoniazid resistance has been found to be over 3 times as great for smokers compared with nonsmokers.2
1. Guler et al 2007; 2. Ruddy et al. 2005
Notes:
Several epidemiological studies have been published on the relationship between smoking and adverse health outcomes among TB-infected persons. Several of these reports of these reports were presented at the 2009 World Conference on Smoking and Health ( Smoking delays sputum conversion, increases chances of drug resistance, and increases chances that family members will become infected.
References:
Guler M, Unsal E, Dursun B, Aydln O, Capan N. Factors influencing sputum smear and culture conversion time among patients with new case pulmonary tuberculosis. Int J Clin Pract. 2007; 61(2):231–5.
Ruddy M, Balabanova Y, Graham C, Fedorin I, Malomanova N, Elisarova E, et al. Rates of drug resistance and risk factor analysis in civilian and prison patients with tuberculosis in Samara Region, Russia. Thorax. 2005; 60:130–135. doi: /thx

9. Secondhand Smoking and TB
Exposure to secondhand smoke (SHS) increases the risk of getting TB infection by 3.3 times compared withthe non-smokers.
The risk of TB infection due to SHS exposure is significantly higher among children than adults.
The dose-response relationship between exposure intensity and risk of TB infection  depends on number of cigarettes consumed by family members & proximity of contact with smoking members.
Notes:
There is mounting evidence of a dose-response relationships between intensity of exposure to passive smoking and the risk of TB infection. The meta-analysis conducted by Lin et al. showed that the risk of getting pulmonary TB was 3.3 times (95% CI = 1.93–5.72) that of non-smoker. The risk of getting TB from second-hand smoking exposure was higher among children than adults, with a case-control study in Thailand reporting ORs as high as 9.3, and another case-control study in Spain reporting an OR of 5.4 (95% CI = 2.44–11.9).1
This meta-analysis also confirms a dose-response relationship between passive smoking and the risk of TB infection. The probability of TB infection increases with the number of daily cigarettes smoked by family member, as well as with the proximity of contact with smoking household member. The adjusted OR for those who were in close contact was 9.3 (95% CI = 3.14–27.6). 1
Leung et al. followed a cohort of female never-smokers aged 65 to 74 in Hong Kong for five years. They found that passive exposure to secondhand tobacco smoke in the household was independently associated with obstructive lung disease (OR 1.43; 95% CI = 1.16–1.77) and diabetes mellitus (OR 1.13; 95% CI = 1.02–1.26) at baseline and with the development of both active TB (hazard ratio [HR], 1.49; 95% CI = 1.01–2.19) and culture-confirmed TB (HR, 1.70; 95% CI = ) on prospective follow-up after potentially confounding background variables were controlled for. Passive smoking accounted for 13.7% of active TB and for 18.5% of culture-positive TB in this cohort. Based on these findings they have called for increased emphasis to be placed on exposure to second hand smoke in national TB programs.2
Reference:
Lin HH, Ezzati M, Murray M. Tobacco smoke, indoor air pollution and tuberculosis: a systematic review and meta-analysis. PLoS Med. 2007; 4(1):e20.
Leung CC, Lam TH, Ho KS, Yew WW, Tam CM, Chan WM. Passive smoking and tuberculosis. Arch Intern Med. 2010; 170(3):287–92.
Lin et al. 2007

10. Smoking and Respiratory Infection: Mechanisms
Structural changes:
Peri-bronchiolar inflammation and fibrosis
Mucosal permeability increases and changes in pathogen adherence
Impairment of mucociliary clearance
Disruption of the respiratory epithelium
Immunologic mechanisms:
Decreased immune response & circulating immunoglobulins
Impaired cellular immunity
Notes:
Although the exact pathogenesis mechanism is unclear, cigarette smoking is suggested to increase the risk of systemic infection through its effect on airway structural changes and immunologic systems.
Cigarette smoking can lead to structural changes in the respiratory tract, which include peribronchiolar inflammation and fibrosis, increased mucosal permeability, changes in pathogen adherence, impairment of mucociliary clearance, and disruption of the respiratory epithelium. Toxic agents in cigarette smoke, including acrolein, acetaldehyde, formaldehyde, free radicals produced from chemical reactions within the cigarette smoke, and nitric oxide, may contribute to the observed structural alterations in the airway epithelial cells.
Cigarette smoking alters cellular and humoral immune system functions, through as yet unclear pathogenesis mechanisms. These alterations include a decreased level of circulating immunoglobulins, a depression of antibody responses to certain antigens, a decrease in CD4+ lymphocyte counts, an increase in CD8+ lymphocyte counts, depressed phagocyte activity, and decreased release of proinflammatory cytokines.
Reference:
Arcavi L, Benowitz NL. Cigarette smoking and infection. Arch Intern Med. 2004; 164(20):2206–16.
Arcavi 2004

11. Smoking Cessation: TB Patients
The clinical encounter is a teachable moment during which the patient may be more receptive to cessation messages.1
The physicians should take advantage of the clinical encounter to deliver cessation messages to all TB patients who smoke.2
Patients need to be made aware that returning to smoking after completing DOTS therapy will increase their odds of TB relapse two to three fold.3
Notes:
Health professionals should be encouraged to provide smoking cessation messages to TB patients during each clinical encounter, as the illness can be a teachable moment for TB patients. Patient counseling needs to increase both patients’ awareness of the harmful effect of tobacco for general health and for the well being of TB patients in particular.1 TB patients must be made aware of the increased chances of them relapsing to TB if they return to smoking after finishing TB therapy. This message needs to be repeated at each point of patient contact and especially toward the end of treatment when smoking relapse is most likely to occur. In countries like India where chewing of tobacco is as common as smoking, the message must be delivered that chewing is not a safe alternative to smoking. TB patients should neither smoke nor chew tobacco.
References:
McBride CM, Emmons KM, Lipkus IM. Understanding the potential of teachable moments: the case of smoking cessation. Health Educ Res. 2003; 18(2):156–70.
Slama K, Chiang CY, Enarson DA. Tobacco cessation and brief advice. Int J Tuberc Lung Dis. 2007; 11(6):612–6.
Batista JAL, Militão de Albuquerque MFP, de Alencar Ximenes RA, Rodrigues LC. Smoking increases the risk of relapse after successful tuberculosis treatment. Int J Epidemiol. 2008; 37(4):841–51.
1. McBride et al. 2003; 2. Slama et al. 2007; 3. Batista et al. 2008

12. DOTS Providers and Smoking Cessation
In many countries with high TB and smoking prevalence rates, smoking cessation is not yet integrated into the national TB control program.1
The WHO recognizes the need to do so and to involve both practitioners and DOTS providers in tobacco cessation.2
Smoking cessation needs to be integrated in TB management programs and guidelines. Health professionals should be provided appropriate knowledge and skills to provide cessation counseling to TB patients.3
Notes:
Integration of tobacco control into TB control programs seems feasible and essential. However, questions about the cost effectiveness of this initiative are yet to be explored.1 DOTS providers can be important people to support cessation among TB patients during treatment and post-treatment. Encounters with DOTS providers, who are mainly family members, are more common than with health professionals, particularly after the treatment cycle has been concluded. DOTS providers need to be trained and provided with appropriate skills to support cessation among TB and ex-TB patients.3
Integration of smoking cessation into a well-established TB control program will potentially leverage the success of both TB and cessation treatment. Any cessation counseling effort provided to TB patients needs to be recorded into TB program monitoring, and this will enable assessment of the effectiveness of this intervention in the future.2
References:
Siddiqi K, Lee AC. An integrated approach to treat tobacco addiction in countries with high tuberculosis incidence. Trop Med Int Health 2009 Apr;14(4):420-8.
Slama K, Chiang CY, Enarson DA. Tobacco cessation and brief advice. Int J Tuberc Lung Dis 2007 Jun;11(6):612-6.
Pradeepkumar AS, Thankappan KR, Nichter M: Smoking among tuberculosis patients in Kerala, India: proactive cessation efforts are urgently needed. Int J Tuberc Lung Dis 2008;12:
A WHO/The Union Monograph on TB and Tobacco Control: Joining efforts to control two related epidemics. Geneva: World Health Organization; 2007.
1. Siddiqi and Lee 2008; 2. Slama et al. 2007; 3. Pradeepkumar et al

13. OPTIONAL SLIDES Tobacco and Tuberculosis Mini Lecture 1
Module: Effects of Tobacco on the
Respiratory System

14. Burden of TB in Five Countries
TB Estimates (2006)
India
China
Indonesia
South Africa
Nigeria
Incidence / 100,000
168 99
234
940
311
Prevalence / 100,000
299
201
253
998
615
Death / 100,000 28 15 38
218 81
Case Detection Rate (%) 64 79 73 71 20
DOTS treatment success (%) 86 94 91 75
Notes:
In 2006, five countries had the highest absolute total number of TB patients, i.e. India, China, Indonesia, South Africa, and Nigeria. Despite its lower total number of cases compared to India, China, and Indonesia, South Africa has the highest incidence and prevalence rates, up to 940 and 998 per 100,000 population.
The case detection rate, which is the number of new smear-positive cases detected by DOTS programmes divided by the estimated number of incident smear-positive cases, was estimated at about 61% in 2006 (about 2.5 new smear-positive cases out of an estimated 4.1 million new smear-positive cases). The Western Pacific is the only WHO region that achieved the case detection rate target, which was set at 70%. The case detection rate was lowest in the African region (46%) and the European region (52%).
The treatment success ratea were high, over 85% in many countries in the South-East Asia and Western Pacific regions, but in the African region, the treatment rate was less than expected (85%), mainly due to high rates of HIV infection, the increasing problem of multi-drug resistance, and weak health services.
Reference:
World Health Organization. Global tuberculosis control: surveillance, planning, financing. Geneva: World Health Organization; 2007.
World Health Organization 2007

15. Smoking, TB Clinical Manifestation, Conversion, and Relapse
TB smokers have higher possibility of experiencing pulmonary TB, clinical manifestations, having cavitary lesions, and being smear-positive.
Smoking is not associated with sputum conversion two months after treatment, but smoking prolongs the conversion time among smokers compared with non-smokers.
Smoking is an independent predictor of TB relapse, in addition to irregular treatment and drug resistance.
Notes:
A study in Hong Kong found out that smokers have less possibility of experiencing extra-pulmonary TB. Most TB patients who smoked have pulmonary TB, with a more severe clinical and radiological appearance (more cough, dyspnea, cavitary lesions), and are more likely to have positive sputum-smears.
Smoking is proven not related to sputum conversion two months after treatment; however, it prolongs the sputum conversion time among smokers more than among non-smokers.
A study in South India that followed-up cured TB patients for up to 18 months identified that TB relapse was associated with irregular treatment, drug-resistance, and smoking. The relapse rate among smokers is higher compared to non-smokers who comply to the treatment.
Reference:
Chiang CY, Slama K, Enarson DA. Associations between tobacco and tuberculosis. Int J Tuberc Lung Dis. 2007; 11(3):258–62.
Chiang et al. 2007

16. Smoking and TB: Immunopathogenesis
Notes:
Mycobacterium tuberculosis can be found not only in healed primary lesion in lungs, but also in histopathologically normal lungs. Haematogenous dissemination occurs during 2-3 weeks following TB infection, and the TB bacteria can be disseminated to any part of the lungs. M. tuberculosis is mainly found in a dormant state in bronchoalveoral macrophages of an infected host. In macrophages, M. tuberculosis can decrease host defense by preventing phagosome acidification and lysosome fusion. The dormant state of M. tuberculosis in macrophages is maintained by sequences of metabolism chains involving nitric oxide (NO), inducible nitric oxide synthase (iNOS) and TNF-α. The TNF-α activates iNOS, which produces NO from the imino nitrogen of arginine. NO competes with oxygen for the regulation of a 48-gene regulon in M. tuberculosis, which leads to the dormant state.
This equilibrium will be influenced by: (i) neutralization of TNF-α by therapeutic antibodies used in chronic inflammatory diseases; or (ii) down-regulation of TNF-α by nicotine binding (as agonist) to α-7 subunit of the nicotinic acetylcholine receptors on alveolar macrophages. This will lead to the development of progressive disease from latent M. tuberculosis infection.
Reference:
Davies PD, Yew WW, Ganguly D, Davidow AL, Reichman LB, Dheda K, et al. Smoking and tuberculosis: the epidemiological association and immunopathogenesis. Trans R Soc Trop Med Hyg. 2006; 100(4):291–8.
Nicotine can reactivate latent mycobacterium tuberculosis by down-regulation of TNF-α by the macrophages in the lungs  lack of nitric oxide  switch off the latent TB state.
Davies et al. 2006

17. Iron, Smoking, and TB
A smoker inhales 1.1 g of iron from smoking 1 pack of cigarettes.
Iron levels in alveolar macrophages are higher in asymptomatic TB smokers (2 fold) and symptomatic TB smokers (4.6-7 fold) than in nonsmokers.
Iron loading promotes overgrowth of M. tuberculosis in bronchoalveoral macrophages and decreases the phagocytosis ability of macrophages.
Notes:
Living M. tuberculosis captured in macrophages prevents phagosome acidification and lysosome fusion, thus it decreases the phagocytosis ability of macrophages. The bacilli can acquire iron from host endosomal holotransferin, and can utilize the host lipid trafficking for the delivery of additional iron by mycobactin. Tobacco contains an iron load that can reach up to 1.1 g in each pack of cigarettes. The exact mechanism of how the increase of iron load by smoking can influence the risk of tuberculosis is currently lacking.
Reference:
Boelaert JR, Vandecasteele SJ, Appelberg R, Gordeuk VR. The effect of the host's iron status on tuberculosis. J Infect Dis. 2007; 195(12):1745–53.
Boelaert et al. 2007

18. Cessation Messages: TB Patients
66% of TB patients in Kerala (India ) received a general or TB specific message about quitting 4 or more times during treatment:
98% received advice at the beginning of treatment.
69% received advice at the end of treatment.
1.3% of TB patients were never advised about quitting.
50% of TB patients who received messages were only given general advice to quit smoking.
Notes:
All patients in this study conducted in Kerala, India were asked if any health professional had inquired about their smoking habits at any of their TB-related clinic visits since diagnosis. All of those who smoked in the months before diagnosis were then asked whether they had received any cessation advice from any health professional. Those who reported receiving smoking cessation advice were asked what messages they had received. All 153 study patients except one reported that they had been asked about tobacco use by health staff.
A content analysis of messages received by smokers at the time of diagnosis revealed that only about half contained TB-specific messages—messages that smoking aggravates TB, smoking reduces the effectiveness of TB treatment and smoking can cause relapse of TB. The five most common TB-specific messages reported were: 1) “Smoking is bad for this disease. Stop it”; 2) “Because you have TB, give up smoking”; 3) “Smoking will prevent cure, so stop it”; 4) “This disease is due to smoking, so stop it”; 5) “Smoking will reduce the effect of drugs, so give up smoking.” Fifty per cent of study patients who received messages stated that they were only given general advice to quit smoking without any explanation. The four most common general messages were: 1) “You should quit smoking”; 2) “Don’t smoke again”; 3) “Give up smoking”; 4) “Stopping smoking is good for your health.”
Most patients reported receiving only one brief message from a doctor at the time of diagnosis, a time when they were quite ill, and being told many things about their medication. Two fifths of DOTS providers were health staff and three fifths were non-health staff (mostly anganwadi workers, grass root workers in the integrated child development services scheme). When the DOTS provider was a health staff member, only 30% of TB patients received a cessation message. When non-health staff were the DOTS providers, more than three quarters of TB patients reported being told to quit smoking while taking treatment.
Reference:
Pradeepkumar AS, Thankappan KR, Nichter M: Smoking among tuberculosis patients in Kerala, India: proactive cessation efforts are urgently needed. Int J Tuberc Lung Dis. 2008; 12:
Pradeepkumar et al. 2008

19. WHO,TB, and Tobacco: Key Messages
Smoking substantially increases the risk of tuberculosis (TB) and death from TB.
More than 20% of global TB incidence may be attributable to smoking.
Controlling the tobacco epidemic will help control the TB epidemic.
Smoking is a risk factor for TB, independent of alcohol use and other socioeconomic risk factors.
Smoking increases the risk of TB disease by more than two-and-a-half times.
References:
World Health Organization Tobacco Free Initiative. Fact sheet on tuberculosis and tobacco. September Available at:
A WHO/The Union Monograph on Tb and Tobacco Control: Joining efforts to control two related epidemics. Geneva: World Health Organization; 2007.

20. The most important health message a doctor can give to patients is to quit smoking.