CIGARETTE SMOKING AND HEALTH
AMERICANTHORACIC SOCIETY.
MEDICAL SECTION OF AMERICAN LUNGASSOC~AT~ON
THISOFFlClAL STATEMENT OF THE AMERICANTHORACIC
SOCIETY
OF DIRECTORS. NOVEMBER 1984
Putpose of the Statement
In I W,the first Surgeon General's Report
on Smoking and Wealrh stared that cigarette
smoking was a causal risk factor for Iung can-
cer and a contributing factor for other dis-
eases. Over the nex t Ewenty years, the evidence
tin king smoking and many diseases became
increasingly certain so that the 1983 Surgeon
GenernI's Report on Smoking and Health con-
cluded that cigarette smoking is the largest
avoidable cause of death and disabiiity in the
United States. Because the adverse effects of
cigarette smoking continue to be major health
probtems, a committee of the Scientific As-
sembly an Environmentat and Occupational
Health of the American Thoracic Society has
prepared thisstatement on cigarette smoking
and health.
This statement summarizes the adverse
health effects of cigarette smoking, addresses
t h e addictive nature o f the habit, and reviews
aspects of smoking cessa~ionand pmvenrion.
Emphasis is placed on information that has
accumulated since the 1 !W Surgeon General's
Report. We racognize that lherearernanynon-
pulmonary health effects o f cigarette srnok-
ing and discuss some or them in this report,
but we wilt address adverse putmonary health
effects in more detail. We are stating a con-
sensus point of view and not an in-depth re-
view and wilt provide only a limited number
of references because of space limitations and
the availability of detailed documents such
as the Surgeon General Reports.
Because we conclude that srnaking causes
many adverse effects, we need to state how
a judgment of a causal relationship is made.
Extensive evidence has been published on the
effects of cigarette smoking and health. The
evidence includes laboratory investigations of
smoke characteristics And biological activity,
short-term clinical investigations, and epide-
miological studies that exanline the prevalence
of disease in populations in relation to ciga-
rette use Direct experiments with humans.
regarded by some a5 scienrifically necessary
for establishing causality, are neither ethical
nor feasible and have not been considered
necessary for many other deleterious agents
such as ionizing radiation and asbestos. The
judgments concerning causality of assacia-
tions between tobacco smoking and diseases
stated jn this document are based on all avail-
able evidence, both from the laboratory and
fmm human popuPations. Associations have
been judged as causal on the basis of biologi-
cal plausibiIity, reproducibility, an appropri-
ate temporal relationship between exposure
WAS ADOPTED BY THE ATS BOARD
and disease, and sufficient strength of the as- bons. Theaddiaive properties of nicotine and
sociation with evidence of a dose-response the myriad of chemica! compounds in tobacco
rcIationship. Specificityof the association o f smoke make it unIikeIy that a "safe"cigarette
exposure and disease strengthens the argu- can be produced. Thc low tar and low nico-
ment for causality. tine cigarettes now being marketed may be
marginally safer in terms of lung cancer rhan
Prevalence of Qgarette Smoking their predecessors on a unit basis. However,
Although the prevalence of cigarette smok- there is concern that smokers of thcse prod-
ing has decreased since the publication ofthe ucts adjust their consumption and smoking
first Surgeon GeneraSVsReport on Smoking pattern to achieve the nicotine blood concen-
and Health in 1964, millions of Americans trations reached with the regular typcs of cig-
still smoke. I n 1964, SZ@o of men and 34% arettes and thus inhale more total smoke.
of women wer age 20 rvere cigarette smokers. The pathophysiologic mechanisms undtr-
By 1980, these percentages had decreased to lying the health effects of cigarette smoking
38% for men and 30To for women. A Gallup are complex because of the myriad smoke
survqr in 1984 indicated that the rate of smok- components and their many direct and in-
ing among adults dedined to 29%. The per direct interactions with environmental and
capita consumption of cigaretta in the United genetic factors. Because cigarette smoking IS
States aIso decreased from 4,345 cigarettes per known to be an independent risk factor for
adult wer 18 in 1%3 to 3,494 in 1983, a 20% chronic obstructive pulmonary disease, lung
decline over the 20-year period. Smoking cancer, and coronary heart disease, patients
among younger individuals, especially young with other recognized genetic. metabolic, or
women, remains a major public health con- occupational risk factors for these diseases
cern. Several studies indicate that smoking must be strongly advised not to smoke, Un-
is now more prevalent among teenage women fortunately, we do not know why some
than men. In spite of the recognized adverse smokers develop severe chronic obstructive
health effects of cigarette smoking, about pulmonary disease, lung cancer, or coronary
35% of adolescenrs (age 12 through I f ) cur- heart disease, whereas other individuals are
sently smoke cigarettes. minimally affected. We do know that, as a
group, smokers have a higher risk of develop-
ing chronic obstructive lung disease, Iung can-
Cost of Smoking cer, and coronary heart disease than those
The enormous economic costs of smoking whodonot smoke. Currently, thereis no way
must bcconsidcred in addition to rhe adverse of predicting which individuals will develop
health effects and the concomitant reduction severe disease and which individuals will not.
jn qualily o f life. I n terms of health care. the Disease can be most effectively prevented by
costs attributable ta cigarette smoking exceed avoiding smoking all together.
$17 billion pcr year. When tost work and
productivity arcadded to direct medical costs,
General Heath Effects and Mortality
the total cost to soclet y is estimated to exceed Since the first Surgeon General's Reporl was
541 billion per year or $180 per capita. If' these
costs were borne by smokers in the Form of published in 1944, compelling epidemiologic,
clinical, and experimental evidence has ac-
cigarette taxes, the price of cigarettes would
rise to over 53 per pack. For the individual cumulated to strengthen the association be-
tween cigarette smoking and both morrality
under 50 who smokes over 2 packs per day,
and morbidity from awide rangeof diseases.
thesumof rifetime loss in earnings and med-
The overall mortality ratio for adult cigarette
ical expenses is estimated to excced %34,00n
smokers versus adutt nonsmokers is about 1 -7.
The rnorraliry ratio is the ratio or the number
How Cigarettes Work of observed deaths in smokersto the number
The burning cigarette is a chemical factory expected from nonsmokers. The mortality ra-
that generates thousands of different corn- tio in smokers increases with the amount
pounds. The precise chemical composition OF smoked and is directly proportional to the
smoke depends on the type of cigarette and duration of cigarette smoking. Mortality rae
the way in which it is smoked. Major toxic tios are also higher for those who start smok-
constituents of cigarette smoke include but ing at younger ages. While it is hard to calcu-
are not limited to carbon monoxide, nicotint,
and particulates that contain most of the car- Inks fmm AMERICANR ~ V I BOP
WR ~ S P I U ADfSEASE
~Y
cinogenic polvnuclear aromatic hydrmar- 2 1 3 2 . No. 5 , Nwcrnber 1985, pp 1133-1136
late exactly the effects of smoking on life ex-
pectancy, all estimates lead to the conclusion
that life expectancy at any age is significantly
shortened by cigarette smoking. For exam-
ple. a 30- to 35-year-old, two-pack-a-day
smoker has a life expectancy R to 9 years
shorter than a nonsmoker of the same age.
The excess morlality noted in smokers is
greatest for the 45- to 54-year-old age groups
for both men and women. Cigarette smoking
is the largest preventable cause of premature
death in the United States today.
In addition to its e f k t a n mortality, ciga-
rette smoking causm substantial morbidity.
Both men and women who smoke report more
acute and chronic symptoms and illnesses
than people who have never smoked.
General Pulmonary Effects
Cigarerte smoking produces structural and
functional changes in both the conducting air-
ways and the pulmonary parenchyma. The
structural changes in the large airways con-
sist of hypertrophy and hyperplasia of the mu-
cous glands. These changes are rcsponsibIe
for the increase in mucus production that
leads to the increased cough and sputum
production. Structural changes in smaller air-
ways range from relatively mild inflamma-
tion to narrowing and closure of airways due
to inflatnmation,goblet cell hyperplasia, and
intraluminal mucus. Changes in the paren-
chyma include increased nurnkrs of inflam-
matory cells and ultimately destruction of the
alveolar walls, most commonly in the central
pa-t of the lobule, and therefore termed cen-
trilobular emphysema.
Airway disease attributable to cigaret~e
smoking withour coexistingemphysema is not
usuallv associated with severe irnvairrnent of
pulmonary function. Smokers with sewre
functional impairment usually have an ap-
preciable amount of emphysema. Thus, it is
IikeIy that the lOto 15% of cigarette smokers
who develop appreciabIeimpairment of their
lung function are the ones who have devel-
oped emphysema in addition to bronchitis.
Atthough an explanation for the failure of
alf smokers to develop emphysema remains
to be established, new hypotheses on the
pathogenesis of emphysema provide insight.
In the lung, there is a balance between fac-
tors causing proteolysis and factors protect-
ing the lung from proteolysis. Neutrophil:
elastase is thought to be responsible for pro-
teolysis, whereas alpha-1-antiprorease Is con-
sidered to k the major protective factor. Cig-
arette smoke can both increase the influx of
neutwphils, and thereby the burden of neu-
trophil eiastase, and inaetirateaIpha-1-anti-
protease. Thus, smoking cigarettes increases
the potential for prore01ysis. However,the bio-
logic interactions between cigarette smoke and
tkc lung are undoubtedly much more com-
plex and furthw research is needed in n his area.
The structuraI changes associated with cig-
arette smoking are associated wish functional
impairment. Mild fr~nctiona!impairment,
which i s almost certainly caused by disease
at the level of the small peripheral airways,
can be detected with very sensitive tests in
many cigarette smokers after 10 to 15 years
of smoking. Hm'ver, small airways disease
is no1 necessarily a forerunner of the severe
functional impairment seen with emphysema.
The I-second forced expimtory volume, the
E V , , is the most predictive and reproduci-
ble purrnonary Function test for both epidemi-
ologic and clinical studies. In nonsmokers,
the FEV,declines with age during adult life
at the rate of about 20 to 30 rnl per year. I n
most smokers, the rate of decline js increased
ro about 30 to 45 ml per year. In the EO to
15% of smokers who develop clinically sig-
nificant impairment, the rate of decline is
about 80 to 100 mE per year. The two pul-
monary function characteristics, which are
helpful in identifying the smoker who is likely
to develop sewre pulmonary impairment, are
a relatively low PEV, by middle-age and a
faster than expected fall in FEY, from year
to year. Patients with emphysema associated
with smoking cigarettes have a reduced sin-
gle breath diffusing capacity, but a low diffus-
ing capacity is nor specific for emphysema.
Lung Cancer
Of the many adverse consequences OF ciga-
rette smoking, lung cancer was the first to be
causally linked to tobacco smoke exposure.
T h e 1961Surgeon GeneraI's report concluded
that cigarette smoking was causally d a t e d
to lung cancer in men and was probably of
similar importance in women. Since that re-
view, abundant additional data have w n -
firmed that cigarette smoking is the major
cause of Eung cancer in the United States in
both men and wmen.
The risk for individual smokers varies with
smoking praaices, Dose-response relation-
ships have been demonstrated with duration
and amount of smoking. Deeper inhalation
and earlier age of starting increase Iung can-
cer risk. I n some studies, modifications of
the cigarette to reduce the yield of far have
been associated with modest reductions of
lung cancer risk. However, the current low
tar products have not been evaluated in epi-
demiologic studies.
In the United States, lungcancer incidence
and mortali t y have been lower in women than
in men. The difference refleasternpod trends
o f smoking in the two groups, Cigarette use
became widespread among men early in this
century, whereas large numbtrs of women did
not smoke untiE the 1940s. As a result, the
pattern of increasing lung cancer in women
has paralleled that seen earlier in men but has
lagged by about 25 years. In 1985, Iung can-
cer will become the leading cause of cancer
deaths in women,a preeminence that i s largely
attributable to cigarette smoking.
Other Cancers
Ma!ignanciesotkerthan lung cancer havealso
been linked to cigarette smoking. Nurnwous
reports of the Surgeon General have applied
the criteria for causality on a sire-specific ba-
sh. In the 19% Surgeon GenemE's report on
cancer, cigarette smoking was designated as
a "major cause" for cancer of the lung, lar-
nyx, oral cavity, and esophagus in the United
States. Cigarette smoking was also identified
as a "contributory factor" for cancers of the
bladder, kidney, and pancreas. Reduction o f
smoking should have direct and demonstra-
ble benefits far those sites where cigarette
smoking is a major cause.
Cardiwaseular Effects
Cigarette smokers experience a 70% greater
death rate due 10 coronary heart disease than
nonsmokers. The first Surgeon General's Re-
pon concluded that there was an assmiat ion
between smoking and coronary heart disease,
but that evidence was jnsufficient to make
the judgment of a causaI reIationship. By
1979, however, it w a s recognized that ciga-
rette smokingwas a major risk factor far corn-
nary heart disease among both men and
women in the United Stater In 1980, cardio-
vascular disease accounted for nearly half of
all U.S. deaths (960,000of 1,980,000 total
deaths), and nearly 60% of these deat hs were
due to coronary heart disease. Investigators
estimate that JO to 40To of deaths due to coro-
nary heart d i w s e art attributabbeto cigarette
smoking.
P~gnancyand Smoking
Cigarette smoking by pregnant women leads
to a variety of adverse consequences for the
unborn child. The mortality rate of babies
of mothers who smoke is higher than the mor-
tality rate of babies whose mothers do not
smoke Babies born to women who smoke
during pregnancy are 200 grams lighter on
the average rhan babies born to nonsmokers.
The more a woman smokes, the greater the
reduction En the birth weight of her baby. Be-
cause the duration of fetal gestation does not
appear to be shortened by maternal cigarette
smoking, thelower birth weights seen in ba-
bies of smokers appear to be due to retarda-
tion of fetal growth. In multiplestudies, preg-
nant w m e n who smoke have a 10 ro 20%
increased risk of spontaneous abortion. This
correlation continues to hold when other risk
factors - age, parity, ducation, race, and so-
cioeconomic status-are controlled, Other
complica~ionsofpregnancy that are seen sig-
nificantly more often in smoking mothers in-
clude placenta previa, abruptio placenta,
bleeding during pregnancy, and premature
rupture of membranes. Theseconditions also
contributeto increased fetal death. Those who
provide prenatal a r e should counsel,pregnant
women about theadwrse effects of smoking
on pregnancy and infant health.
Occupatisn and Smoking
Smoking is a major risk factor in certain oc-
cupational lung diseases. Ajnvays obstruction
is the most common occupationally as-
sociated classof lung disease in which srnok-
ing plays a major role Smoking and occupa-
tional exposure to coal mine dust or grain or
cotton dust appear to act in an additive fash-
ion to produce bronchitis and airways obstruc-