Smoking and Lung Function of Lung Health Study
Participants after 11 Years
Nicholas R. Anthonisen, John E. Connett, and Robert P. Murray for the Lung Health Study Research Group
University of Manitoba, Winnipeg, Manitoba, Canada; and University of Minnesota, Minneapolis, Minnesota
Eleven years after Lung Health Study (LHS) entry, we performed
spirometry in 77.4% of surviving participants who enrolled in a
long-term follow-up study. Those not enrolling tended to be
younger male heavy smokers who continued to smoke during the
LHS. Their initial LHS lung function, after adjustment for these
factors, did not differ from that of enrollees. Smoking habits by
original LHS treatment groups (smoking intervention vs. usual care)
tended to converge, but 93% of participants who were abstinent
throughout the LHS were still abstinent at 11 years. Differences in
lung function between treatment groups persisted; smoking inter-
vention participants had less decline in FEV1 than usual care partici-
pants. Men who quit at the beginning of the LHS had an FEV1 rate
of decline of 30.2 ml/year, whereas women who quit declined at
21.5 ml/year. Men continuing to smoke throughout the 11 years
declined by 66.1 ml/year, and women continuing to smoke declined
by 54.2 ml/year. When decline in FEV1 was expressed as a percent-
age of predicted normal value, no significant sex-based difference
was apparent among continuing smokers. At 11 years, 38% of con-
tinuing smokers had an FEV1 less than 60% of the predicted normal
value compared with 10% of sustained quitters.
Keywords: clinical trial; COPD; lung function; smoking intervention
The original Lung Health Study (LHS 1) was a randomized
clinical trial of smoking cessation and regular administration
of an inhaled bronchodilator (ipratropium bromide) in 5,887
middle-aged smokers (35–60 years old at study entry) who
had airway obstruction, but who did not regard themselves
as having lung disease, and who did not have other serious
illnesses. The main outcome variables were annual change
in lung function in the form of the FEV1, and morbidity and
mortality (1). Intent-to-treat analysis showed that smoking
cessation reduced the rate of decline of lung function,
whereas inhaled bronchodilator did not (2).
Follow-up rates in LHS 1 were unusually high, with more
than 90% of participants attending each of five annual visits
for assessment of pulmonary function (2). Further, at the end
of LHS 1, 5,003 participants were enrolled in a lung cancer
substudy designed to ascertain the incidence of cancer. These
participants were contacted at 6-month intervals, usually by
telephone, and questioned in regard to their health and smok-
ing habits. This follow-up was also successful, with direct
contact rates exceeding 94% at all 6-month intervals. Because
of this success, an extension of LHS 1 (LHS 3) was thought
(Received in original form December 31, 2001; accepted in final form May 22, 2002)
Supported by a cooperative agreement with the National Institutes of Health
(NHLBI-1U10-HL59275).
Correspondence and requests for reprints should be addressed to John E. Connett,
Ph.D., Biostatistics/CCBR, 2221 University Avenue SE, Suite 200, Minneapolis,
MN 55414-3080. E-mail: john-c@ccbr.umn.edu
This article has an online data supplement, which is accessible from this issue’s
table of contents online at www.atsjournals.org
Am J Respir Crit Care Med Vol 166. pp 675–679, 2002
DOI: 10.1164/rccm.2112096
Internet address: www.atsjournals.org
feasible, asking the original participants to return to the origi-
nal clinical centers for reassessment approximately 11 years
after their enrollment. This report details the results of pul-
monary function measurements as related to smoking habits
of people who participated in LHS 3. The objectives of LHS
3 were as follows: to ascertain whether differences in lung
function between randomly assigned treatment groups per-
sisted, to assess whether differences in smoking habit persist
between treatment groups, and to determine whether the
profound impact of smoking cessation on lung function de-
cline noted in LHS 1 persisted or increased.
Protocols were approved by the institutional review board
for human studies at each clinical center, and written in-
formed consent was obtained from each participant.
METHODS
All LHS 1 participants who were not known to be deceased were
deemed eligible for LHS 3. Those who could be contacted were asked
to return for spirometry and to answer smoking questionnaires. Remote
participants were visited to obtain data. Some participants refused spi-
rometry, and insofar as lung function is concerned, this report is confined
to those who did not.
Questionnaires included the same ones administered as part of LHS
1, including a modified American Thoracic Society–Division of Lung
Diseases questionnaire (1). A detailed smoking history was obtained,
and smoking status was checked by measuring expired carbon monoxide
with a Vitalograph EC50 (Vitalograph, Buckingham, UK), as in LHS
1. Results of 10 ppm or higher were considered indicative of smoking.
Spirometry was performed with a rolling seal spirometer, exactly
as it had been in LHS 1 (3). The same spirometers were used (Spirotech
500; Spirotech, Atlanta, GA), and the same quality control program.
Measurements of FEV1 and FVC were made before and at least 20
minutes after two puffs (200 ␮g) of albuterol from a metered dosed
inhaler. The largest single FEV1 and FVC were reported, and were
converted to percentages of the predicted normal value by using the
formulas of Crapo and coworkers (4).
Results were analyzed according to the original LHS 1 treatment
assignment: usual care (UC) and smoking intervention (SI). The latter
was a combination of groups that were assigned either to active bron-
chodilator or placebo therapy; both received the smoking cessation
program, and were similar, including rates of smoking cessation. Partici-
pants were also divided into three groups based on smoking history.
Sustained quitters (SQs) were biochemically validated ex-smokers at
each of the follow-up visits of LHS 1, who gave a history of abstinence
(no month with as much as one cigarette per day) between the end of
LHS 1 and enrollment in LHS 3, and who also had a carbon monoxide
reading at the LHS 3 visit that was less than 10 ppm. Continuing smokers
(CSs) were those who reported smoking at all scheduled follow-up
visits, and throughout the time between the end of LHS 1 and LHS 3.
Intermittent quitters (IQs) were smoking at some but not all of their
LHS 1 and LHS 3 visits, or in the interval of time between the two
studies. Because of uncertainties regarding dose of cigarettes, the IQ
group was not considered in some analyses.
Comparisons between LHS 3 participants and nonparticipants were
performed using t tests for quantitative variables, and ␹2 tests for cate-
gorical variables. Comparisons adjusted for other covariates were based
on analysis of covariance (for quantitative variables) or logistic regres-
sion (for dichotomous variables). Comparisons of changes in lung func-
tion variables between the SI and UC groups were based on t tests.
The average interval between the baseline visit for LHS 1 and the
676 AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE VOL 166 2002

TABLE 1. GENERAL CHARACTERISTICS OF LUNG HEALTH STUDY 3 PARTICIPANTS COMPARED

WITH THOSE WHO REFUSED
LHS 3 Refused p Value

Number 4,517 896

SI, % 67.3 64.6 0.119
Age as of LHS 3 61.3 (6.8) 59.7 (6.8) ⬍ 0.001
Sex, % male 61.9 66.0 0.021
Cigarettes/d, baseline LHS 1 30.9 (12.7) 32.7 (13.2) ⬍ 0.001
Smoking status at end of LHS 1
Sustained quitter, % 18.8 6.6 ⬍ 0.001
Intermittent quitter, % 29.0 21.5 ⬍ 0.001
Continuing smoker, % 52.2 71.9 ⬍ 0.001
Attended last LHS 1 visit, % 99.2 85.6 0.001
Symptoms at end of LHS 1, %
Cough 32.6 39.7 0.001
Phlegm 33.1 39.2 0.001
Wheeze 59.5 62.9 0.053
Dyspnea 33.6 32.5 0.532
FEV1 % predicted post-BD, baseline LHS 1 78.4 78.4 0.966
FEV1 % predicted post-BD, end of LHS 1 75.3 74.9 0.362
BD response (%), baseline LHS 1 4.3 4.3 0.844
Change in FEV1% predicted/yr in LHS 1 ⫺0.62 ⫺0.81 0.005
Methacholine reactivity
Reaction to ⭐ 5 mg/ml, % 33.6 31.9 0.334
No reaction to 25 mg/ml, % 28.2 30.0 0.414

Definition of abbreviation: BD ⫽ bronchodilator; LHS ⫽ Lung Health Study; SI ⫽ smoking intervention.

LHS 3 visit was 10.99 years (SD, 0.63) for SI participants and 11.03
years (SD, 0.62) for UC participants.
RESULTS
Of the original 5,887 participants in LHS 1, 5,413 were eligible
for LHS 3 in that they were not known to be dead. Of those
eligible, 4,517 (83.4%) were enrolled in LHS 3, whereas 896 did
not enter. Enrollment ranged from 77.1 to 91.0% at the various
clinical centers. Of those enrolled, 4,194, or 92.8%, underwent
spirometry testing. As indicated in Table 1, there were differ-
ences between LHS 1 participants who entered LHS 3 and those
who did not. People who did not attend the LHS 3 visit were
younger and more likely to be male. They were heavier smokers
on entry into LHS 1 and less likely to have quit smoking during
the initial 5 years of the study. They were also less compliant,
in that fewer returned for spirometry at the end of LHS 1 than
participants who entered LHS 3. LHS 1 group assignment did
not differ significantly between participants who enrolled in LHS
3 and those who did not. People who did not enter LHS 3 were
more likely to have reported cough or phlegm at the end of
LHS 1 than those who did (Table 1). Cough and phlegm were
strongly associated with contemporary smoking habit, and when
smoking was taken into account by logistic regression, differ-
ences in cough and phlegm between LHS 3 participants and
nonparticipants became nonsignificant. There was no significant
difference between the two groups in terms of wheeze or dys-
pnea. Lung function is also shown in Table 1. FEV1, expressed
as a percentage of the predicted normal value, and FEV1/FVC
at both entry and end of LHS 1, were similar in those who
entered LHS 3 and those who did not. Rates of decline of FEV1
were significantly greater in those who did not enter LHS 3 than
in those who did enter, but after adjustment for smoking status,
rates of decline in the two groups were not significantly different.
There was no difference in bronchodilator response or in metha-
choline reactivity.
Table 1 does not show all comparisons between enrollees
and those who did not enter LHS 3. The nonenrollees were
significantly less likely to have been married at the end of LHS
1 than LHS 3 enrollees, but differences in employment rates,
alcohol consumption, and years of education were not significant.
Doctor visits or days in bed due to lower respiratory tract ill-
nesses did not differ significantly between these groups. LHS 3
entrants were more likely to have been hospitalized during LHS
1 than those who did not enter, although there were no significant
differences in hospitalizations for respiratory illnesses, coronary
artery disease, or other cardiovascular disease, the most com-
monly encountered individual causes of hospitalization. Finally,
there were no differences in body mass index or blood pressure
measured at the end of LHS 1 between the two groups.
At the LHS 3 visit, 16.7% of the participants were sustained
quitters, 57.4% were intermittent smokers, and 25.9% had
smoked continuously since the beginning of LHS 1. There were
major differences between treatment groups in smoking habit
(p ⫽ 0.001), with 21.9% of the SI group being sustained quitters
compared with 6.0% of the UC group, and 23.4% of the SI
group being continuing smokers, in contrast to 31.3% of the UC
group. On the other hand, changes in smoking status between
LHS 1 and LHS 3 were not greatly different between groups
(Table 2). In both, approximately 93% of sustained quitters at
the end of LHS 1 were abstinent at the LHS 3 visit, whereas
about a quarter of continuing smokers at the end of LHS 1 had
TABLE 2. CHANGE IN SMOKING STATUS BETWEEN END OF
LUNG HEALTH STUDY 1 AND LUNG HEALTH STUDY 3
% Quit (CO Validated) at LHS 3
Total SI UC
Status at End of LHS 1 (n ⫽ 4,517) (n ⫽ 3,040) (n ⫽ 1,477)
Sustained quitter 92.9 92.7 94.7
Intermittent quitter
Not smoking 79.9 76.2 87.3
Smoking 43.3 42.8 45.1
Continuous smoker 24.1 22.4 26.3
Definition of abbreviations: CO ⫽ carbon monoxide; LHS ⫽ Lung Health Study;
SI ⫽ special intervention; UC ⫽ usual care.
Anthonisen, Connett, and Murray: Smoking and Lung Function 677

Figure 2. Loss of lung

Figure 1. Loss of lung
function over the years of
function among LHS 3 en-
study among sustained
rollees over the 11 years of
quitters (open symbols),
study of the SI group
continuing smokers (closed
(closed symbols) and the
symbols), and intermittent
UC group (open symbols).
smokers (gray symbols).
Average values of post-
Average values of post-
bronchodilator FEV1 are
bronchodilator FEV1 are
shown, expressed in abso-
shown, expressed in abso-
lute terms in (A ) and as a
lute terms in (A ) and as a
percentage of the pre-
percentage of the pre-
dicted normal value in (B ).
dicted normal value in (B ).

quit by the time of LHS 3. Between studies, there was a tendency
for intermittent quitters in the UC group to quit at a higher rate
than those in the SI group (Table 2), accounting for the more
rapid increase in abstinence in the UC group in the interstudy
period (see Figure E1 in the online data supplement). At the
LHS 3 visit, 48.8% of all participants were not smoking, with
51.7% of the SI group and 42.9% of the UC group in this
category.
Figure 1 shows the decline in FEV1 in LHS 3 enrollees ac-
cording to treatment group. The difference between the SI and
UC groups observed among LHS 3 enrollees in LHS 1 was
maintained over the 6 years between LHS 1 and LHS 3 and was
significant (p ⫽ 0.001), whether the FEV1 was considered in
absolute terms or as a percentage of the predicted normal value.
The intergroup differences at the LHS 3 visit were slightly but
not significantly larger than those measured after the fifth year
of LHS 1. Over the 11 years of the combined studies, the FEV1
of the UC group declined by 587 ml, or 12.3% of the predicted
normal value, whereas that of the SI group declined by 502 ml,
or 9.3% of the predicted normal value.
Figure 2 shows lung function decline of the LHS 3 participants
according to smoking habit. The data diverge sharply, with sus-
tained quitters losing function at a considerably slower rate than
continuing smokers, with intermittent quitters’ data lying in be-
tween. Table 3 shows the average annual loss of FEV1 in each
treatment group according to smoking status. For SI and UC
participants combined, SQs lost less than 27 ml/year, approxi-
mately 0.22% of the predicted normal value. IQs lost approxi-
mately 48 ml/year, or approximately 0.91% of the predicted
normal. CSs lost 60 ml/year, or 1.3% of the predicted normal
value. In each smoking category lung function losses were slightly
smaller in the SI group than in the UC group, but differences
between SI and UC groups reached statistical significance only
for losses expressed as a percentage of predicted normal values
in intermittent quitters and in continuing smokers.
Absolute rates of decline of FEV1 differed between men and
women. Female SQs lost an average of 21.5 ml/year (SEM, 1.2),
whereas male SQs lost an average of 30.2 ml/year (SEM, 1.4).
In the CS category, women lost an average of 54.3 ml/year (SEM,
1.3), whereas men lost an average of 66.1 ml/year (SEM, 1.4).
When expressed as percentages of the predicted normal value,
declines were still less for females among SQs but similar be-
tween women and men in the CS category. Among SQ partici-
pants, women averaged a loss of 0.11%/year (SEM, 0.06), which
was significantly (p ⬍ 0.01) less than for the men, who lost an
average of 0.31%/year (SEM, 0.05). In the CS category, women
averaged a decline of 1.41%/year (SEM, 0.06), and men averaged
a decline of 1.31%/year (SEM, 0.04), figures that were not sig-
nificantly different.
DISCUSSION
The main findings of this study were that differences in smoking
habit established during the first year of LHS 1 were remarkably

TABLE 3. ANNUAL CHANGE IN FEV1 AND FEV1 % PREDICTED-BASELINE LUNG HEALTH STUDY 1
TO LUNG HEALTH STUDY 3 ACCORDING TO LUNG HEALTH STUDY 3 SMOKING HISTORY
(CARBON MONOXIDE VALIDATED)

SI Participants UC Participants

Status at LHS 3 n FEV1/ml/yr n FEV1/ml/yr p Value

Sustained quitter 637 ⫺26.7 (26.5) 85 ⫺30.3 (26.5) 0.250

Intermittent quitter 1,521 ⫺47.5 (31.7) 848 ⫺50.0 (34.5) 0.079
Continuing smoker 630 ⫺60.0 (33.7) 424 ⫺63.8 (32.2) 0.070
FEV1 % pred/yr FEV1 % pred/yr

Sustained quitter 637 ⫺0.23 (1.03) 85 ⫺0.40 (1.11) 0.109

Intermittent quitter 1,521 ⫺0.91 (1.21) 848 ⫺1.02 (1.28) 0.041
Continuing smoker 630 ⫺1.29 (1.16) 424 ⫺1.44 (1.26) 0.043

Definition of abbreviations: SI ⫽ special intervention; UC ⫽ usual care.

678 AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE VOL 166 2002
stable, so that there were significant differences in lung function
between randomly assigned treatment groups after 11 years.
Further, differences in lung function between participants who
quit smoking and those who did not increased progressively over
11 years, resulting in substantial differences in the prevalence
of FEV1 values that are associated with disabling illness.
The original Lung Health Study was remarkable for the com-
pleteness of its follow-up, and LHS 3 was a similar success; of
the original participants who were not known to be dead, more
than 77% were enrolled and underwent spirometry 11 years
after study entry. There were differences between those who
were enrolled in LHS 3 and those who were not (Table 1), and
these differences were not surprising. People who did not enter
LHS 3 tended to be younger, male, and single at the end of LHS
1. They had been heavier smokers on study entry, were less
likely to have quit, and had been less compliant in terms of
follow-up than those who were enrolled. Although significant,
these differences were relatively small. Although LHS 3 enroll-
ees had less cough and phlegm at the end of LHS 1 than did
those who did not enter, the differences were accounted for by
differences in smoking habits, and there were no differences in
wheeze, dyspnea, body mass index, or blood pressure. During
LHS 1, people who did not enroll in LHS 3 lost lung function
more rapidly than those who entered, but not more rapidly than
enrollees of the same age, sex, and smoking habit. We are unable
to explain the increased tendency of LHS 3 participants to have
been hospitalized during LHS 1, but this may have related to
their greater compliance and concern regarding their health sta-
tus, indicated by their higher rate of quitting smoking. In sum-
mary, LHS 3 participants were a biased sample of the original
LHS 1 population, but the biases among surviving participants
were relatively minor, and more than 80% of living LHS 1
participants was enrolled.
Cross-sectional smoking quit rates tended to converge when
treatment groups were compared (see Figure E1 in the online
data supplement); quitting was more common in the UC group
than in the SI group in the interval between LHS 1 and LHS 3.
This tendency has been noted in other follow-up studies of clini-
cal trials involving smoking cessation (5), and indeed a similar
trend was observed during LHS 1 in that cross-sectional quit
rates in the UC group after the first year increased faster than
in the SI group (2). This was presumably due to the much higher
quit rate being obtained in the SI group at the onset of LHS 1,
so that relapse occurred in this group more often than in the
UC group. However, the convergence of cross-sectional quit
rates was in some ways misleading, in that changes in smoking
habit occurred largely among intermittent smokers and not
among either sustained quitters or continuing smokers (Table 2).
Indeed, some 93% of those who quit for the 5 years of LHS 1
were able to maintain abstinence in the subsequent 6 years. Five
years of abstinence would seem to be a “cure” of the smoking
habit.
The stability of smoking habit, especially among those who
quit at the onset of LHS 1, was the major reason that differences
in lung function between the SI and UC groups established
during LHS 1 persisted essentially unchanged for the additional
6 years between LHS 1 and LHS 3. This is supported by the
data of Table 3, which shows that SI–UC differences in rate
of decline of FEV1 were small in groups with similar smoking
histories. The major SI–UC difference was that the SI group
was composed of a larger fraction of SQs and a smaller fraction
of CSs than was the UC group. When lung function was examined
as a function of smoking history, LHS 3 results were essentially
a linear extrapolation of the LHS 1 data, showing a continuing
sharp divergence between the SQ and CS groups.
The cumulative impacts of smoking cessation are illustrated
Figure 3. Distribution of
values of postbronchodila-
tor FEV1 among enrollees in
LHS 3 who were sustained
quitters and continuing
smokers. The ordinate rep-
resents the percentage of
either sustained quitters or
continuing smokers; the
abscissa shows categories
of FEV1, expressed as a per-
centage of the predicted
normal value.
in Figure 3, which shows the frequency distribution of FEV1
measured at LHS 3 in the CS and SQ groups. The distributions
are strikingly different, especially at low values of FEV1. Among
CSs, 18.1% had FEV1 less than 50% of the predicted normal,
as compared with only 3.3% of the SQ group; 38.0% of the
CS group had FEV1 less than 60% of the predicted normal as
compared with 10.0% of the SQ group. Thus, a substantial frac-
tion of participants who continued to smoke had levels of lung
function thought to represent “moderate” or “severe” chronic
obstructive pulmonary disease, whereas this was true of few
sustained quitters. Over the 11 years of observation, the mean
difference in FEV1 between CSs and SQs was approximately
0.5 L, or 14% of the predicted normal value. Although these
differences may not seem large, they were associated with a
large difference in the fraction of each group that would be
considered disabled. Obviously, if trajectories of lung function
continue to diverge in the future as they have over the past 11
years, many more continuing smokers will develop low levels of
FEV1, and this will be much less common in sustained quitters.
The LHS was one of a limited number of studies with a group
of female smokers large enough to examine sex differences in
the effects of smoking on lung function. Rates of decline of FEV1
were assessed in terms of change expressed as a percentage
of the predicted normal value, which should account for sex
differences in stature and lung size. There was a small sex differ-
ence among SQs favoring the women, but none among CSs,
apparently indicating that the effects of smoking and smoking
cessation were similar for the two sexes. Two previous cross-
sectional studies of smokers in Beijing and Copenhagen (6, 7)
indicated that lung function in women might be more affected
by smoking than in men, but longitudinal data from the Tucson
group (8) showed that women smokers lost lung function more
slowly than did men, and an Australian longitudinal study
showed a similar rate of loss between the sexes (9). At LHS 3
enrollment, male continuing smokers consumed 25.2 cigarettes
per day as compared with 22.1 per day by female continuing
smokers. It could therefore be argued that the women were
slightly more sensitive than the men, but the important point
is probably that among people with mild to moderate airway
obstruction, loss of lung function in continuing smokers is similar
between the sexes.
There have been many other studies comparing decline in
FEV1 between smokers and ex-smokers (8–19). All found, like
the LHS, that smoking cessation was associated with a rate of
decline that did not differ from that noted in never smokers and
was considerably less than that of continuing smokers. Quantita-
tive comparisons among studies are difficult because of varying
age of the subjects and differing classifications of smoking habit.
Nevertheless, for ex-smokers, our SQ group, figures of 21.5 ml/
year for women and 30.2 ml/year for men agree well with those
Anthonisen, Connett, and Murray: Smoking and Lung Function
of most others (8–11, 14, 15). However, the mean rate of loss
observed in our female continuing smokers was substantially
higher at 54.2 ml/year than in other studies of women (8, 9, 14,
15, 18, 19), and the mean decline of 66.1 ml/year among our
male continuing smokers was higher than most comparable data
(8–10, 13, 15, 19), and most of the studies that showed rates of
decline similar to ours among male smokers also had relatively
high rates of decline among nonsmokers (12, 16–18). Thus, loss
of lung function among the continuing smokers of the LHS was
more rapid compared with most previous observations. This is
likely due to the original selection criteria for the LHS, which
sought to identify smokers at high risk for the development
of clinical chronic obstructive pulmonary disease and therefore
recruited people with evidence of airway obstruction, defined
as having FEV1/FVC less than 0.70. Burrows and coworkers (20)
had previously found that obstruction defined in this way was
a predictor of rapid decline in a group of 13 men, and argued
that spirometry might identify high-risk smokers. The LHS data
support this argument. The data also indicate the crucial and
sustained benefit of smoking cessation by high-risk smokers.
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APPENDIX
Principal investigators and senior staff of the clinical and coordinating
centers, the NHLBI, and members of the Data Monitoring Board and
the Morbidity and Mortality Review Board:
Case Western Reserve University, Cleveland, OH: M. D. Altose,
M.D. (Principal Investigator), S. Redline, M.D. (Co-Principal Investiga-
tor), C. D. Deitz, Ph.D.; Henry Ford Hospital, Detroit, MI: M. S.
Eichenhorn, M.D. (Principal Investigator), W. A. Conway, M.D. (Co-
Principal Investigator), R. L. Jentons, M.A., K. Braden; Johns Hopkins
University School of Medicine, Baltimore, MD: R. A. Wise, M.D. (Prin-
cipal Investigator), S. Permutt, M.D. (Co-Principal Investigator), C. S.
Rand, Ph.D. (Co-Principal Investigator), M. Daniel, V. Santopietro,
K. A. Schiller; Mayo Clinic, Rochester, MN: P. D. Scanlon, M.D. (Princi-
pal Investigator), J. P. Utz, M.D. (Co-Principal Investigator), G. M.
Caron, K. S. Mieras, L. Walters; Oregon Health Sciences University,
Portland: A. S. Buist, M.D. (Principal Investigator), V. J. Bortz, D. J.
Youtsey; University of Alabama at Birmingham: W. C. Bailey, M.D.
(Principal Investigator), C. M. Brooks, Ed.D. (Co-Principal Investiga-
tor), L. B. Gerald, Ph.D., M.S.P.H. (Co-Principal Investigator), S. Er-
win, D. Gardner, M. Johnson, J. Mangan; University of California, Los
Angeles: D. P. Tashkin, M.D. (Principal Investigator), A. H. Coulson,
Ph.D. (Co-Principal Investigator), E. C. Kleerup, M.D. (Co-Principal
Investigator), I. P. Zuniga; University of Manitoba, Winnipeg: N. R.
Anthonisen, M.D. (Principal Investigator), J. Manfreda, M.D. (Co-
Principal Investigator), R. P. Murray, Ph.D. (Co-Principal Investigator),
S. C. Rempel-Rossum; University of Minnesota Coordinating Center,
Minneapolis: J. E. Connett, Ph.D. (Principal Investigator), P. G. Lind-
gren, M.S., M. A. Skeans, M.S., H. T. Voelker; University of Pittsburgh,
Pittsburgh, PA: R. M. Rogers, M.D. (Principal Investigator), G. R.
Owens, M.D. (Co-Principal Investigator), M. E. Pusateri; University of
Utah, Salt Lake City: R. E. Kanner, M.D. (Principal Investigator),
G. M. Villegas, A. Sharp; Safety and Data Monitoring Board: C. Furb-
erg, M.D., Ph.D., J. R. Landis, Ph.D., E. Mauger, Ph.D., J. R. Maurer,
M.D., Y. Phillips, M.D., J. K. Stoller, M.D., I. Tager, M.D., A. Thomas,
Jr., M.D.; Morbidity and Mortality Review Board: T. Cuddy, M.D., R.
Fontana, M.D., R. E. Hyatt, M.D., C. T. Lambrew, M.D., B. A. Mason,
M.D., D. Mintzer, M.D., R. Wray, M.D.; National Heart, Lung, and
Blood Institute, Bethesda, MD: S. S. Hurd, Ph.D. (Former Director,
Division of Lung Diseases), J. P. Kiley, Ph.D. (Director, Division of
Lung Diseases), G. Weinmann, M.D. (Project Officer, Director, Airway
Biology and Disease Program), T. Croxton, Ph.D. (Project Officer),
M. C. Wu, Ph.D. (Division of Epidemiology and Clinical Applications).