cigarette smoking and lower respiratory tract infection

7/25/2019 Cigarette Smoking and Lower Respiratory Tract Infection

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Cigarette Smoking and Lower Respiratory Tract Infection

1. Introduction

Acute bronchitis, one of the most common diagnoses in ambulatory care medicine, accounted for

approximately 2.5 million visits to U.S. physicians in 199 !Slusarcic" # $c%aig, 2&&&'. (his

condition consistently ran"s as one of the top ten diagnoses for )hich patients see" medical care,

)ith cough being the most fre*uently mentioned symptom necessitating office evaluation!+nutson # raun, 2&&2- Saldas et al., 2&&/'. (he diagnosis is based on clinical findings,

)ithout standardi0ed diagnostic signs and sensitive or specific confirmation laboratory tests

!effinger et al., 199/'.

Acute bronchitis is usually caused by a viral infection, especially by influen0a, parainfluen0a andrespiratory syncytial virus, it is also caused by adenovirus, coronavirus and rhinovirus !$arrie,

199'. hen microbiological studies are performed, less than 1&32&4 of patients )ill haveevidence of acute bacterial infection !$acfarlane et al., 2&&1'. (hus,Bordetella pertussis,Mycoplasma pneumoniaeand Chlamydia pneumoniaehave been clearly established as causes of

acute bronchitis. ut there is no clear evidence that Streptococcus pneumoniae,Haemophilus

influenzaeorMoraxella catarrhaliscause acute bronchitis in adults )ithout underlying lungdisease- studies have failed to distinguish bet)een coloni0ation and acute infection !amire03

onda et al., 191- (reanor # 6ayden, 2&&&'. 6o)ever, these bacteria are important causes of

superinfections after acute viral respiratory illnesses !6ament et al., 1999- 7eltola # $c%ullers,2&&8'.

(he devastating health impact of cigarette smo"ing is )ell "no)n !+uper et al., 2&&2- Ste)art et

al., 2&&'. espite ongoing efforts to reduce smo"ing prevalence, over 1.1 billion peoplecontinue to smo"e, representing one3sixth of the )orld:s population !;ha et al., 2&&2'. %igarettesmo"ing is a ma


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defenses !Sopori et al., 1998- Sopori et al., 199'. e revie)ed the epidemiology of smo"ing3

related lung infections and the mechanisms by )hich smo"ing increases the ris" of infection.

2. Mechanisms by which cigarette smoking may predispose

to respiratory infections(he specific mechanisms by )hich cigarette smo"ing increases the ris" of respiratory infections

are incompletely understood !Saldas et al., 2&&/- omagala3+ula)i", 2&&'. (hey aremultifactorial and probably interactive in their effects. $echanisms by )hich smo"ing increases

the ris" of infections include structural changes in the respiratory tract !ye # Adler, 1998' and a

decrease in immune response !Sopori et al., 199'.

2.1. Structural changes caused by smoking

(he ciliated respiratory epithelium, the main target of most respiratory viruses, is the first line of

defense against harmful environmental agents and protects by s)eeping particles a)ay in theoverlying mucus gel layer, phagocytosing and "illing some pathogens, maintaining a barrier

through tight induced lung inflammation. A number of components of cigarette smo"e, including

acrolein, acetaldehyde, formaldehyde, free radicals produced from chemical reactions )ithin the

cigarette smo"e, and nitric oxide, may contribute to the observed structural alterations in the

air)ay epithelial cells !$arcy # $errill, 19/'.

Smo"e directly compromises the integrity of this physical barrier, increases the permeability of

the respiratory epithelium and impairs mucociliary clearance !ye # Adler, 1998- ;ones et al.,

19&- urns et al., 199'. Although cigarette smo"e has been sho)n to activate epithelial cells toproduce pro3inflammatory mediators !$io et al., 199/', it attenuates the in vitroproduction of

pro3inflammatory mediators by epithelial cells follo)ing stimulation )ith pathogen3associated

molecular patterns !7A$7s', such as lipopolysaccharide or double3stranded BA !Caan et al.,2&&8- auer et al., 2&&'. Smo"e also induces direct oxidative damage to membrane lipids and

causes extensive single3strand BA brea"s, triggering repair and apoptotic cascades !+im et al.,

2&&8'. (hus, cigarette smo"e acutely suppresses the respiratory epithelium and chronically can

cause damage, inflammation and may ultimately transform it.

2.2. Effect of cigarette smoke on the lung and systemic immunity

%igarette smo"e has been sho)n to affect a )ide range of host defense mechanisms !Sopori etal., 1998'. 6o)ever, findings bet)een studies can be controversial and sometimes contradictory,

probably because of differences in smo"ing history, genetic susceptibility and socioeconomic

status !such as exercise, nutrition, occupation and ambient air *uality, )hich can modify
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disease'. Similar issues apply to animal models and in vitrosystems, in )hich parameters of

smo"e exposure, such as duration, fre*uency and mode vary mar"edly bet)een studies

!omagala3+ula)i", 2&&- StDmpfli # Anderson, 2&&9'. Accordingly, as the patterns of smo"eexposure are so varied individually and geographically, no single experimental smo"e exposure

system can replicate the diversity of human smo"ing patterns, and each experimental system

probably reflects only facets of the overall picture.

2.2.1. Cell-mediated immune responses

White blood cell count and distribution in peripheral blood. Smo"ers usually exhibit an elevated

peripheral )hite blood cell count, around &4 higher than that of nonsmo"ers !=riedman et al.,

19/- Eeung # uncio, 198-(ollerud et al., 199- $ili et al., 1991'. Ft has been sho)n asignificant relationship bet)een the )hite blood cell count in smo"ers and the plasma

concentration of nicotine !(aylor et al., 19@'. Ft has been suggested that nicotine induced

catecholamine release might be the mechanism for this effect !=riedman et al., 19/'. ther

studies support the hypothesis that cigarette smo"ing causes bone marro) stimulation !Gan

?eden # 6ogg, 2&&&'. Ft has been suggested that proinflammatory factors released from alveolarmacrophages, such as tumor necrosis factor H, interleu"in !FC' 1, FC3, and granulocyte3

macrophage colony3stimulating factor, are probably responsible for the stimulation of bonemarro) by cigarette smo"ing. Ft has been reported the same relationship bet)een cigarette

smo"ing and increased leu"ocyte count in adolescents, indicating that there appears to be a rapid

effect of cigarette smo"ing on )hite blood cell count that is unli"ely to be due to smo"inginduced chronic disease conditions as seen in adult smo"ers !(ell et al., 195'.

eports of the effects of smo"ing on the different subsets of lymphocyte ( cells are conflicting.

Cight to moderate smo"ers )ere reported to have a significant increase in %I and %8I

counts and a trend to)ard increased %I lymphocyte count !$iller et al., 192- 6ughes et al.,

195- (ollerud et al., 199-$ili et al., 1991'. y contrast, studies of heavy smo"ers !over 5&pac"3years' reported a decrease in %8I and a significant increase in %I cell counts. (hus,

the decrease observed in the ratio of %8I to %I lymphocytes in heavy smo"ers )as duepredominantly to an increase of %I cells !Jinns et al., 192'. (hese effects appeared to be

reversible as soon as @ )ee"s after smo"ing cessation !$iller et al., 192'. ther studies have

reported no difference in the %8I and %I lymphocyte counts among moderate smo"ers

!%ostabel et al., 19@'. Since %8I cells facilitate 3cell proliferation and differentiation andimmunoglobulin synthesis, the decrease in this subset observed in heavy smo"ers might

contribute to the increased susceptibility to infections in this population.

Airways and lun parenchyma. ronchoalveolar lavage studies have demonstrated a mar"ed

decrease in the absolute number of %8I cells, and an increase in %I cells )ith a lo)er%8IK%I cell ratio in moderate smo"ers vs nonsmo"ers !Ceatherman et al., 198- %ostabel et

al., 19@- e)ers et al., 199'. Bo significant changes in these variables in the peripheral blood

)ere found in this population of moderate smo"ers, in contrast )ith the findings in heavysmo"ers discussed previously. (hus, changes in lymphocyte population in the bronchoalveolar

lavage in smo"ers may disclose pathologic changes earlier than in blood. $oreover, these

findings suggest that smo"ers have a deficit in cell3mediated immunity in the lung alveolus, asite critical in the first3line defense against infection.
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(he retention of %I ( cells in the lungs of chronic smo"ers )arrants particular attention as it

is a hallmar" of %7 and it is "no)n that these cells can activate alveolar macrophages to

produce matrix metalloproteinase 12, a potent elastin3degrading en0yme that has been lin"ed toemphysema !6autama"i et al., 199/-Jrumelli et al., 2&&8'. =urthermore, %I ( cells are

re*uired for inflammation and tissue destruction in smo"e3induced emphysema in mice !$aeno

et al., 2&&/'. %igarette smo"e has also been found to promote the retention of virus3specific%I memory effector ( cells, but to )ea"en their defensive ability !Jualano et al., 2&&'.

Smo"ing is also associated )ith significant increases in the percentage of macrophages in

bronchoalveolar lavage fluid !e)ers et al., 199'. )ing to their strategic positioning )ithin

the alveolar space, alveolar macrophages have a "ey role in sensing and eliminating microbialagents early in the course of an infection. %igarette smo"ing increases the number of alveolar

macrophages !Sopori et al., 199' and activates them to produce pro3inflammatory mediators,

reactive oxygen species and proteolytic en0ymes !de oer et al., 2&&&-ussell et al., 2&&2',thereby providing a cellular mechanism that lin"s smo"ing )ith inflammation and tissue

damage. Similar to its effects on the respiratory epithelium, cigarette smo"e compromises the

ability of alveolar macrophages to phagocytose bacteria !+ing et al., 19-erenson et al., 2&&@'and apoptotic cells !6odge et al., 2&&/' and to sense 7A$7s !ranni" et al., 2&&8- %hen et al.,

2&&/- Jaschler et al., 2&&'. Fmportantly, cigarette smo"e may not simply suppress the function

of alveolar macrophages as previously suggested, but instead might s"e) their inflammatory

mediator profile. (he nature of the s"e)ing may be a determinant of disease susceptibility.Accordingly, one study reported a distinctive state of activation of alveolar macrophages in

smo"ers that distinguished them from those in non3smo"ers !oodruff et al., 2&&5'. (his

highlights a "ey emerging concept L smo"e may induce partial $1 deactivation or partial $2activation of macrophages. (he balance and intensity of this s"e)ing has direct implications for

the immune system and its response to disease because effective host defense re*uires a

macrophage activation programme that is appropriate for the particular type of pathogen and

because $13type macrophages can cause mar"ed lung damage !emphysema', )hereas $23typemacrophages are lin"ed to tumour progression. (he molecular mechanisms of altered alveolar

macrophage responsiveness and s"e)ing are not presently understood but they are at least

partially reversible by exposure to the reduced form of glutathione, )hich implicates oxidativedamage of effector path)ays. (he infection ris" is compounded by host deficiencies or

polymorphisms in innate and adaptive immune response genes, in particular those encoding

pattern recognition receptors, such as mannose3binding lectin, and their signal transductionintermediates !ec"er # :Beill, 2&&/'.

Fn the lungs, dendritic cells !%s', )hich are the most potent antigen3presenting cells and are

indispensable for the initiation of ( cell3mediated immune responses !$ellman # Steinman,

2&&1', are probably highly susceptible to smo"e3induced effects because of their anatomicalposition !in the lumen and directly beneath the epithelium of the lung' !$c%omb et al., 2&&'.

Although it is "no)n that the %3directed chemo"ine %M%C1 is upregulated in emphysema

!$c%omb et al., 2&&', there are only a fe) studies assessing the effects of smo"ing on lung%s in humans and animal models !(souma"idou et al., 2&&'. %linical studies suggest that the

number of mature %s is reduced in the large air)ays of patients )ith %7 )ho smo"e

!;ahnsen et al., 2&&@'. =ollo)ing smo"ing cessation, the numbers of mature %s increase and aresimilar to non3smo"ing healthy controls. y contrast, the number of immature %s is increased
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in the small air)ays of patients )ith %7 compared )ith individuals )ho have never smo"ed

and individuals )ho smo"e but do not have %7 !$c%omb et al., 2&&'. (hese data indicate

that smo"ing behavior may affect % numbers and maturity state.

!eu"ocytes function. 7olymorphonuclear leu"ocytes from the peripheral blood of smo"ers

exhibit depressed migration and chemotaxis compared )ith 7$Bs from nonsmo"ers !Boble #7enny, 19/5-%orberand et al., 19/9'. (he motility and chemotaxis of 7$Bs are depressed in the

oral cavity of smo"ers compared )ith nonsmo"ers !?ichel # Shahri", 19@9-Boble # 7enny,19/5'. (he )hole cigarette smo"e, its gas phase and the )ater3soluble fraction are potent

inhibitors of 7$B chemotaxis !ridges et al., 19//'. f the )ater3soluble fraction of cigarette

smo"ing, the unsaturated aldehydes !acrolein and crotonaldehyde' )ere the ma


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$urphy, 2&&1- ed0icha, 2&&8-7api et al., 2&&@' and to microbial coloni0ation of the air)ays,

)hich occurs in approximately one third of patients )ith %7 !7atel et al., 2&&2'.

!.1. "iral infections

?nvironmental tobacco smo"e exposure increases significantly the ris" of lo)er respiratory tractinfections in children, especially maternal smo"ing !(able 1'. Using mouse models, it has been

investigated the effects of cigarette smo"e on inflammatory processes, viral clearance andsecondary immune protection follo)ing influen0a virus infection !obbins et al., 2&&@- Jualano

et al., 2&&- +ang et al., 2&&'. %igarette smo"e exposure )as found to be associated )ith

exacerbated pro3inflammatory responses to influen0a virus, although neither the rate of viralclearance nor the development of influen0a virus3specific memory responses )ere compromised.

6ence, cigarette smo"e mainly affects primary antiviral inflammatory processes, )hereas

secondary immune protection remains intact !obbins et al., 2&&@'. (he heightenedinflammatory response )as associated )ith increased production of pro3inflammatory mediators

and mortality. =urthermore, one study !+ang et al., 2&&' sho)ed that increased inflammation

led to accelerated emphysema formation and air)ay fibrosis, providing evidence that alteredresponsiveness to viral agents may contribute to the pathogenesis of emphysema.

Common cold$Several epidemiological studies support the association bet)een smo"ing and the

prevalence of colds and lo)er respiratory tract symptoms. Fn a prospective cohort study that

examined a large group of US Army recruits found an increased ris" of upper respiratory tractinfection in smo"ers !relative ris"N 1.5- 954 confidence interval O%FP, 1.131.' !la"e et al.,

19'. Ft has been reported that smo"ing status is predictive of the development of clinical colds

)hen healthy volunteers are exposed intranasally to a lo) dose of respiratory viruses !%ohen et

al., 199'. Giral suspensions )ere installed into the nares and infections )ere diagnosed on thebasis of viral isolation, virus3specific antibody, and clinical findings. Smo"ers had a significantly

higher incidence of acute infection !clinical cold' than nonsmo"ers !N 2.2- 954 %F, 1.&38.2'. Among virologically confirmed infected individuals, smo"ing )as associated )ith ahigher li"elihood of symptoms leading to a clinical diagnosis !N 1.- 954 %F, 1.&&3.@'.

(he relationship bet)een smo"ing and increased symptoms from viral respiratory infections

could be explained by impairment of immune processes that limit viral replication orenhancement of inflammatory processes involved in the production of symptoms.

%nfluenza$Several studies have confirmed the relationship bet)een cigarette smo"ing and the

ris" of influen0a infections !=in"lea et al., 19@9'. Fnfluen0a infections are more severe, )ith more

cough, acute and chronic phlegm production, breathlessness, and )hee0ing in smo"ers. =emalesmo"ers in the Fsraeli Army had increased ris" of influen0a !N 1.88- 954 %F, 1.&32.&1' and

complications associated to influen0a infection compared )ith nonsmo"ers !+ar" # Cebiush,191'. Fn another study, the incidence of influen0a in healthy young male recruits )as higheramong smo"ers !N 2.82- 954 %F, 1.53.' !+ar" et al., 192'. Fnfluen0a )as more severe

among smo"ers, )ith a dose3related increase in rateN &4 in nonsmo"ers, 84 in light smo"ers,

and 584 in heavy smo"ers !pQ&.&&1'. verall, 1.24 !954 %F, [email protected]' of influen0a cases

)ere attributed to cigarette smo"ing.
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?nhanced bacterial adherence has been documented for respiratory cells infected, )ith influen0a

A virus being responsible for viral3bacterial combination pneumonia !6ament et al., 1999'.

Studies have suggested that inflammatory activation of platelet3activating factor is an importantfactor in the attachment and invasion of cells by pneumococcal strains. %igarette smo"ing alters

platelet3activating factor metabolism and may contribute to the increased incidence of bacterial

superinfection in people )ho develop influen0a !$iyaura et al., 1992-Fchimaru # (ai, 1992'.
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#eferences$1'&nviron Health #rospect199/-1&5N&23@- 2'#ediatr #ulmonol1999-2/N531.- '

&ur ' &pidemiol2&&&-1@N8@53- 8'' #ediatr2&&&-1/N@53/&- 5'An &sp #ediatr2&&&-5N9385- @'(ev Saude#ublica2&&-/N8539- /'Acta #aediatr2&&-92N118321- '&ur '

&pidemiol2&&5-2&N/1932/- 9' )obControl2&&@-15N2983&1- 1&'&nviron Health #erspect

2&&@-118N112@32- 11'&ur ' #ediatr2&&/-1@@N85539- 12'%ndian ' #ediatr2&&-/5N538&- 1'

Arch Bronconeumol2&&9-85N5539&.

%able 1.

(he environmental tobacco smo"e !?(S' exposure increases the ris" of lo)er respiratory tract

infections !C(F' in children.

Although influen0a )as more severe in smo"ers, antibody levels to A!61B1' antigen )ere notsignificantly higher than those of nonsmo"ers. $oreover, influen0a antibodies )ane more

rapidly in smo"ers than in nonsmo"ers !=in"lea et al., 19/1'. (his finding suggests that smo"ers

are not only at a high ris" of influen0a, but have an increased susceptibility to ne) attac"s

after)ard !+ar" et al., 192'. Fnfluen0a rates are similar in vaccinated smo"ers and nonsmo"ers.6o)ever, influen0a vaccination can be considered to be more efficacious in smo"ers than

nonsmo"ers because the infection rates are higher in unvaccinated smo"ers !%rui


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systematic revie) !Strachan # %oo", 199/' of around 5& studies in children up to years,

including studies used for *uantitative analysis, has confirmed these findings. (here )as

consistency in the findings bet)een the community and hospital studies. 7ooled ratios )erefound to be 1.5/ for smo"ing by either parent and 1./2 for maternal smo"ing. (he revie)ers also

found that there )as a significantly increased ris" from smo"ing by other household members in

families )here the mother did not smo"e !odds ratio 1.29'. Fn most of the studies also a dose3response relationship )as evident, and the associations )ith paternal smo"ing )ere still present

after ad


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A population based case3control study !Buorti et al., 2&&&' sho)ed that smo"ing )as the

strongest independent ris" factor for invasive pneumococcal disease among immunocompetent

adults. (he )as 8.1 !954 %F, 2.83/.' for active smo"ing and 2.5 !954 %F, 1.235.1' forpassive smo"e exposure in nonsmo"ers compared )ith nonexposed nonsmo"ers. (he attributable

ris" in this population )as 514 for cigarette smo"ing and 1/4 for passive smo"ing. (he ris" of

pneumococcal disease declined to nonsmo"er levels 1& years after cessation. Fn another case3control study, current smo"ing )as associated )ith a nearly 23fold ris" of community3ac*uired

pneumonia !N 1.- 954 %F, 1.113.19', )here 24 of the ris" )as attributable to cigarette

smo"ing !Almirall et al, 1999'. (here )as a trend to)ard a dose3response relationshipN A 5&4reduction in the )as reported 5 years after cessation of smo"ing.

Fn vitro adherence of Streptococcus pneumoniaeto buccal epithelial cells has been sho)n to be

increased in cigarette smo"ers !aman et al., 19'. (his increased adherence may persist for up

to three years after smo"ing cessation. Since increased adherence of bacteria to surface cells is anestablished pathogenic step for bacterial coloni0ation and infection in the lung, this may

contribute to the increased ris" of respiratory infection that exists in cigarette smo"ers.

!eionnaires disease$Cegionnaires disease is a life3threatening lo)er respiratory tract infection

responsible for 14 to 4 of community3ac*uired pneumonia. iverse environmental factorshave been identified, and cigarette smo"ing appears to be an independent ris" factor !oebbeling

# en0el, 19/- Straus et al., 199@'. (he ris" of legionnaires disease )as significantly increased

for smo"ing !N .8- 954 %F, 2.&935./9', specially for persons )ithout an underlying disease!N /.89- 954 %F, .231/.1' !Straus et al., 199@'.

*titis media and exposure to secondhand tobacco smo"e$Cong term tobacco smo"e exposure is

a ris" factor for otitis media and bronchitis in children !ichardson, 19'. Fn a case3control

study, children )ith recurrent otitis media more commonly had exposure to secondhand smo"e

!N 1.- 954 %F, 1.&23.89- pT&.&8'. A prospective follo)3up of the case group sho)ed nosignificant difference in the clinical course of the children )ho )ere exposed to secondhand

smo"e !+itchens, 1995'. Fn other study, passive smo"ing )as a significant ris" factor for otitismedia )ith effusion and recurrent otitis media !Flicali et al, 1999'. ut only maternal smo"ing

)as a significant factor !pQ&.&&1'. $oreover, in utero exposure to cigarette smo"e )as

associated )ith an increased ris" of otitis media. Fn a study !Stathis et al, 1999', acute ear

infections )ere associated )ith the mother:s consumption of 1 to 9 cigarettes !N 1.@- 954 %F,1.132.5', 1& to 19 cigarettes !N 2.@, 954 %F, [email protected]', and 2& or more cigarettes !N .- 954

%F, 1.935.9' per day during pregnancy. =or subacute ear infections, an association )as present

)ith the mother:s consumption of 1& to 19 cigarettes !N 2.@- 954 %F, 1.835.&' and 2& or morecigarettes !N 2.- 954 %F, 1.3@.&'. Fn utero exposure to 2& or more cigarettes per day )as also

associated )ith an increased ris" of ear surgery by 5 years after delivery !N 2.9- 954 %F, 1.3

@.@'.

)uberculosis$eveloping tuberculosis disease involves t)o distinct transitions, )ith theircorresponding ris" factorsN the transition from being exposed to being infected and the transition

from being infected to developing disease. Several studies have sho)n that smo"ing is a ris"

factor for tuberculin s"in test reactivity, s"in test conversion, and the development of activetuberculosis !(able 2'. Ft has been reported an increased relative ris" of development of
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tuberculosis for heavy smo"ers compared )ith nonsmo"ers !N 2.1/- 954%F, 1.293.@' !Eu et

al., 19'. After ad


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14/14

#eferences$1' )ubercle19-@9N1&5312 - 2'Am ' #ub Health1998-8N1/5&3@- ' )uber !un

+is199@- //N1123@- 8')uber !un +is199@-//N5/388- 5'&ur (espir '2&&1-1N9593@8- @'

)horax2&&2-5/N9@83@- /'%nt ' )uberc !un +is2&&2-@N/398- '%nt ' )uberc !un +is2&&-/N9&3@- 9'Addict Biol2&&-N938- 1&' Southeast Asian ' )rop Med #ublic Health

2&&8-5N21932/- 11'%nt ' )uberc !un +is2&&8-N19832&- 12'Am ' (espir Crit Care Med

2&&8-1/&N1&2/3- 1'%nt ' &pidemiol2&&5-8N91832- 18' Southeast Asian ' )rop Med #ublicHealth2&&5-@N18535&.

%able 2.

(obacco smo"ing and active tuberculosis !('.

(he biological basis by )hich tobacco smo"ing increases tuberculosis ris" may be through adecrease in immune response, mechanical disruption of cilia function, defects in macrophage

immune responses, andKor %8I lymphopenia, increasing the susceptibility to pulmonary

tuberculosis !ich # ?llner, 1998- n)ubalili et al., 19/'.

'. Conclusion

Smo"ing appears to be an important ris" factor for the ac*uisition of a lo)er respiratory tract

infection !bronchitis, influen0a, pneumonia, tuberculosis'. (his lin" is li"ely mediated by

smo"ing:s adverse effects on respiratory defenses !structural and immune system changesinduced by smo"ing'. %onsidering the high rates of morbidity and mortality from pneumonia,

tuberculosis and influen0a, as )ell as the economic conse*uences of )or" days lost from lesser

respiratory infections, the merits of smo"ing cessation are clear. (he fact that smo"ers have beensho)n to be less li"ely than nonsmo"ers to undergo vaccination and yet are probably at higher

ris" for influen0a and pneumococcal infections highlights the importance of targeting this group

for vaccination. (he available epidemiological evidence, from studies )orld)ide, indicates adose3response relationship bet)een smo"ing and tuberculosis and that the association is li"ely to

be a causal one. (his provides a compelling reason for smo"ing cessation measures to be

underta"en to combat the scourge of tuberculosis, particularly in developing countries.

7hysicians should educate their smo"ing patients about their increased ris" of respiratoryinfections, the importance of appropriate vaccinations, and the benefits of smo"ing cessation.
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cigarette smoking and lower respiratory tract infection

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