Projected effects of tobacco smoking on worldwide tuberculosis control: mathematical modelling analysisBMJ 2011; 343 doi: https://doi.org/10.1136/bmj.d5506 (Published 04 October 2011) Cite this as: BMJ 2011;343:d5506
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Using mathematical modeling, Basu et al. show that cigarette smoking
will increase tuberculosis cases and deaths worldwide in coming years 1.
There are analogous factors which could similarly contribute to the
tuberculosis control which are ignored by the model.
has been defined to be a particle-related injury in which functional
groups at the surface of retained particulate matter (PM) accumulate host
iron 2. The increased iron availability which results with PM exposure
supports proliferation of M. tuberculosis 3 4. This pathway for increased
infection after cigarette smoking is the same as that following numerous
particle exposures (e.g. silica); these similarly increase iron
concentrations to impact the incidence of M. tuberculosis disease 5.
However, the particle which challenges the greatest number of our world's
population is not that associated with cigarette smoking but rather PM
from the burning of biomass. More than two billion people in the world
use biomass as their main source of energy for domestic heating 6. While
such burning is intermittent, it introduces indoor concentrations of PM
which are extraordinarily high. The particle from the burning of biomass
is comparable to that of cigarette smoking in that it is carbonaceous and
a product of combustion. Like all particles, it elevates concentrations
of cell and tissue iron via complexation by surface functional groups and
this will promote microbial growth. Those individuals exposed to the
particles of biomass burning include some of the most vulnerable
populations including newborns and the elderly. The first studies
evaluating for a relationship between burning of biomass and tuberculosis
have suggested an elevation in risk for the infection which can be
approximately equivalent to that reported after cigarette smoking 7.
Accordingly, to reach the goal of halving tuberculosis prevalence in 2015,
attention will have to include not only decreasing cigarette smoking but
public health efforts focused on reducing exposure to PM associated with
the burning of biomass. It is proposed that aggressive measures to
decrease exposure to the burning of biomass will prevent the greatest
number of tuberculosis infections and deaths.
1. Basu S, Stuckler D, Bitton A, Glantz SA. Projected effects of tobacco
smoking on worldwide tuberculosis control: mathematical modelling
analysis. BMJ 2011;343:d5506.
2. Ghio AJ, Hilborn ED, Stonehuerner JG, Dailey LA, Carter JD, Richards
JH, et al. Particulate matter in cigarette smoke alters iron homeostasis
to produce a biological effect. Am J Respir Crit Care Med
3. 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.
4. Sharma AK, Naithani R, Kumar V, Sandhu SS. Iron regulation in
tuberculosis research: promise and challenges. Curr Med Chem
5. Ghio AJ. Disruption of iron homeostasis and lung disease. Biochim
Biophys Acta 2009;1790(7):731-9.
6. Smith KR, Samet JM, Romieu I, Bruce N. Indoor air pollution in
developing countries and acute lower respiratory infections in children.
7. Lin HH, Ezzati M, Murray M. Tobacco smoke, indoor air pollution and
tuberculosis: a systematic review and meta-analysis. PLoS Med
Competing interests: No competing interests
We welcome the paper by Basu and colleagues (1), which highlights the
relationship between smoking and tuberculosis (TB). The projection that
tobacco smoking will produce an excess of 18 million tuberculosis cases
and 40 million deaths from tuberculosis between 2010 and 2050, if smoking
trends continue, is certainly worrying. But after studying smoking habit
among TB patients it is not altogether surprising.
There is good evidence that smokers with TB have generally more
severe disease and increased mortality, largely due to the
immunosuppressive effect of tobacco smoking. (2, 3). Furthermore, smokers
are more likely to take risks than non-smokers, suffering more accidents
and injury, more likely to take excessive alcohol and recreational drugs,
and undertake risky sexual practices (4).
As part of a recent study evaluating adherence to isoniazid
medication in the management of active TB disease and latent infection, we
examined a range of factors that may influence the drug's metabolism,
including smoking habit. We verified smoking behaviour with the
SmokeScreen test, a colorimetric assay for cotinine and other nicotinic
metabolites, based on the Konig reaction (5). This test incorporates the
assay into a sealed plastic tube, the SafeTube, as described by Whitfield
and Cope, 2004 (6), making it suitable for point of care testing.
Furthermore, it will detect tobacco use from sources other than
conventional cigarettes, such as bidis, a cheap and popular medium common
in the Indian Subcontinent with a high nicotine and tar content. A study
from a deprived area of Delhi suggested an even greater risk of TB
associated with bidi smoking (7).
Our recent study involved 100 patients attending two inner-city TB
out-patients clinics. The majority were being treated for active TB
disease, with a minority treated with chemoprophylaxis for latent
infection. The majority of patients were recent immigrants, the largest
groups coming from the Indian subcontinent (52%) or Sub-Saharan Africa
(26%); only 9% were residents of the UK.
We found 25% of patients admitted to smoking but a further 12% were
current smokers, as identified by the cotinine test. This is approaching a
32% rate of denial. This results in 37% of patients being smokers, much
higher than the 21% expected in a normal population. Furthermore, most
cigarette smoking was found among people from countries with a high
prevalence of TB, as previously noted by Basu and colleagues (1).
These are alarming figures. Clearly, many patients with tuberculosis
feel the need to deny smoking when questioned by a specialist healthcare
professional. It is a theory that smokers, because of their risk-taking
personalities, may be more likely to be non-adherent to their treatment
This data provides evidence that smoking may be more prevalent among
TB patients than previously assumed and regular biochemical tests,
preferably at point of care, should be carried out so that smokers can be
identified and the appropriate steps taken to help them to quit.
Dr Graham F. Cope, Honorary Senior Research Fellow, University of
Mr. Roshan Soobratty, TB Specialist Nurse, Croydon University Hospital,
Dr Ruth Whitfield, formally Associate Specialist in Respiratory Medicine,
Croydon University Hospital, Croydon, UK.
Dr. Heather Milburn, Consultant Respiratory Physician, Honorary Senior
Lecturer, Guy' and Thomas's NHS Foundation Trust and King's College,
University of London, London, UK.
1. Basu S, Stuckler D, Bitton A, Glantz SA. Projected effects of
tobacco smoking on worldwide tuberculosis control: mathematical modelling
analysis. BMJ 2011: 343: d5506.
2. Huttunen R, Heikkinen T, Syrjanen J. Smoking and the outcome of
infection (review). Int Med 2011; 269: 258-269.
3. Kulkarni R, Rampersaud R, Aguilar JL, Randis TM, Kreindler JL,
Ratner AJ. Cigarette smoke inhibits airway epithelial cell innate immune
responses to bacteria. Infect Immun 2010; 78: 2146-2152.
4. Hansen BT, Kjaer SK, Munk C, Tryggvadottir L Spar?n P, Hagerup-
Jenssen M, et al. Early smoking initiation, sexual behavior and
reproductive health -- a large population-based study of Nordic women.
Prev Med 2010; 51: 68-72
5. Cope G; Nayyar P; Holder R; et al. A simple near-patient test for
nicotine and its metabolites in urine to assess smoking habit. Clin Chim
Acta 1996; 256: 135-149.
6. Whitfield R, Cope GF. Point of care test to monitor treatment
adherence to anti-tuberculous therapy. Ann Clin Biochem 2004; 41: 411-413.
7. Cullum N, Tregay N, Milburn HJ. Increased risk of tuberculosis
(TB) amongst Bidi smokers. Eur Respir J 2007; 30(suppl 51): 412s.
8. Shuter J, Bernstein SL. Cigarette smoking is an independent
predictor of nonadherence in HIV-infected individuals receiving highly
active antiretroviral therapy. Nic Tob Res 2008; 10: 731-736.
Principle author: Graham Cope email: firstname.lastname@example.org
Competing interests: GFC invented the SmokeScreen test and is a director of GFC Diagnostics, which manufactures and distributes the test.