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ABSTRACT |
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The objective of this study was to determine if the weight gain that accompanies smoking cessation is independently associated with reductions in FEV1 and FVC, using a multicenter randomized intervention trial of smoking cessation in 10 communities in the United States and Canada. Enrollees were currently smoking women and men 35 to 60 yr of age with mild-to-moderate airway obstruction. Participants were randomized to one of three study groups: an intensive smoking cessation program with an inhaled bronchodilator (or a placebo), and usual care. Changes in absolute and percent predicted FEV1 and FVC between baseline and fifth annual follow-up visit were monitored in relation to changes in body weight during the interval. At the baseline examination, percent predicted FEV1 was maximal at 90 to 100% ideal body weight (IBW) and was lower as body weight deviated from this range. The FVC decreased linearly when IBW exceeded 100%. Weight gain was greatest during the first 12 mo after smoking cessation. Weight gain was associated with lower fifth-year FEV1 and FVC in all smoking categories: continuous smokers, intermittent smokers, and sustained quitters. The FVC was affected by weight gain more than was the FEV1, and the FEV1 was affected by smoking cessation more than FVC. Men showed more impairment of FVC with weight gain than did women, possibly because of differential patterns of fat deposition. In sustained quitters, after adjustment for baseline factors, the estimated reduction of FVC was 17.4 ml/kg weight gain for men and 10.6 ml/kg for women. The estimated loss of FEV1 was 11.1 ml/kg weight gain for men and 5.6 ml/kg for women. Lung function after smoking cessation is significantly influenced by weight gain and affects men more than women. The deleterious effects of weight gain are small, however, in comparison with the beneficial effects of smoking cessation.
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INTRODUCTION |
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INTRODUCTION
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Cessation of tobacco smoking, although generally accepted as beneficial to health and pulmonary function, is associated with weight gain (1). Weight gain, particularly if it is excessive, may detract from the beneficial effects of smoking cessation.
The Lung Health Study (LHS) was a clinical trial to evaluate the effects of smoking cessation intervention and an inhaled bronchodilator on pulmonary function in smokers with mild-to-moderate chronic obstructive pulmonary disease (COPD). The main results of the trial showed that the smoking cessation intervention slowed the decline in lung function, and that the bronchodilator had a small beneficial effect that was not sustained after the medication was discontinued (2). Smoking cessation was associated with an increase in weight (P. O'Hara, J. E. Connett, M. Nides, R. Murray, and W. Lee. Excessive weight gain after smoking cessation among lung health study participants [submitted article]). The mean weight gain over 5 yr in participants who quit smoking and remained abstinent (sustained quitters) was 8.8 kg for women and 7.6 kg for men. Among sustained quitters, 10.7% of men and 12.8% of women gained more than 10 kg during the first 12 mo after smoking cessation. At the end of 5 yr, 33.9% of the male and 37.0% of the female sustained quitters had gained more than 10 kg, in comparison with the continuing male and female smokers of whom only 5.2% and 1.4%, respectively, gained this much weight.
Cross-sectional studies have shown that extreme levels of obesity are associated with abnormal lung function, but that most otherwise healthy, nonsmoking obese persons have normal spirometry (3). However, several longitudinal studies have shown that increases or decreases in body weight can lead to worsening or improvement, respectively, of pulmonary function (3). Previous studies have not, however, directly addressed whether weight gain after smoking cessation has a detrimental affect on lung function, nor have they focused on the population at greatest risk, i.e., those with abnormal lung function. It is thus a concern whether smoking cessation in those with abnormal lung function who experience large weight gains causes a net benefit or decrement in lung function. Therefore, we analyzed the data from the Lung Health Study to answer the following questions:
- What are the effects of weight gain after smoking cessation on pulmonary function (FEV1 and FVC)?
- Is the effect of weight gain on pulmonary function different in sustained quitters, intermittent smokers, and continuing smokers?
- Is the effect of weight gain associated with smoking cessation different in men and women?
The Lung Health Study (LHS) provides an excellent data set to conduct this analysis because of the large numbers of participants in a prospective study with a relatively high rate of intervention-related smoking cessation and carefully assessed smoking status, lung function, and weight before and during a 5-hr period after smoking cessation intervention.
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Patient Selection for the Lung Health Study
LHS study design and procedures have been described previously (2,
9). Briefly, at 10 clinical centers in North America, community volunteers underwent a three-stage screening process on three separate
days prior to randomization. The screening procedures were as follows. Screen 1: initial spirometry; Screen 2: a brief general health
questionnaire and spirometry before and after inhaled isoproterenol;
Screen 3: a respiratory questionnaire and methacholine-inhalation challenge testing (10, 11). Eligible subjects were 35 to 60 yr of age, had
smoked 10 or more cigarettes a day within the 30 d before Screen 1, and had a ratio of FEV1/FVC of 
70% at Screen 2 and 75% at
Screens 1 and 3, and an FEV1 of 55 to 90 percent predicted at Screen 2 and 50 to 90 percent predicted at Screen 3 (12). Candidates for the
study were excluded if they had a serious illness, were pregnant, used
physician-prescribed bronchodilators, beta-adrenergic antagonists, or
systemic corticosteroids, reported alcohol use in excess of 25 drinks
per week, if their body weight was over 150% of ideal body weight, or
refused consent to participate (13). A total of 5,887 participants were
entered into the trial.
LHS Protocol
Eligible participants were randomly assigned to three groups: Usual Care (UC); Special Intervention-Placebo Inhaler (SIP); or Special Intervention-AtroventTM (ipratropium bromide) Inhaler (SIA). UC participants were advised to stop smoking at the outset of the study and were followed for 5 yr. They visited the clinic annually for completion of a health and respiratory questionnaire and had spirometry before and after 200 µg isoproterenol by metered-dose inhaler. SIA and SIP participants were all offered a 4-mo intensive smoking cessation program emphasizing behavior modification and nicotine replacement therapy (nicotine gum, 2 mg) (14). Self-reported smoking status was verified by measurement of end-expired carbon monoxide and salivary cotinine (2). At each of the five annual visits, SIA and SIP participants were also administered a respiratory questionnaire, had their weight measured, and underwent spirometry before and after isoproterenol.
Outcome Measures
Forced expiratory spirometry was performed and body weight and height were measured at each annual visit. Body weight and height were measured while participants were wearing light indoor clothing but without shoes. Scales were of the balance-beam type (DetectoTM Model 439, or equivalent) and were calibrated with a 20-kg test weight. Height was measured with the stadiometer integrated into the scale. Participants who were assigned to the smoking intervention group had their weight measured at 4-mo intervals in addition to the annual visit. Body mass index (BMI) was calculated as the participant's body weight in kilograms divided by his or her standing height in meters squared. Ideal body weight was calculated from population norms (13).
Details of the spirometry testing have been reported previously (15). Spirometry was performed with a rolling dry-seal spirometer with the participant in the standing position. The procedures for conduct of the spirometry sessions met or exceeded the ATS recommendations (16). All spirometry data were included in the present analysis whether or not they met the protocol standards for acceptability and reproducibility. Values were expressed as absolute FEV1 and FVC (liters BTPS) and as percent of predicted (12). The predicted values were adjusted for African-Americans and Asians by multiplying the predicted value by 0.88 (17). The largest postbronchodilator FEV1 and postbronchodilator FVC from the baseline S2 visit and from the fifth annual visit were used as the study values for the present analysis. The rationale for using the postbronchodilator value is that it is less subject to transient bronchoconstriction, and has been shown to be more predictive of mortality in patients with COPD than the prebronchodilator value (18).
Drugs used in this study were supplied by the following pharmaceutical companies. Atrovent and placebo inhalers, Boehringer Ingelheim Pharmaceutical, Inc. (Ridgefield, CT); Nicorette, Marion Merrell Dow Inc. (Kansas City, MO).
Data Analysis
The analysis included the 5,346 participants who completed pulmonary function testing at both the baseline and the fifth annual visits (93.7% of living participants). Male and female participants were categorized by assignment group (UC, SIP, and SIA). In addition, subjects were categorized by smoking status as either "sustained quitters," "intermittent smokers," or "continuing smokers" (2). Sustained quitters were defined as participants who succeeded in stopping smoking during the initial smoking cessation program and subsequently reported not smoking at each annual visit, as verified by salivary cotinine or expired carbon monoxide. "Intermittent smokers" were those who were smoking at one or more, but not at all annual visits. "Continuing smokers" were people who were smoking at all annual visits. Visit nonattendees were conservatively assumed to be smokers for that visit.
Standard descriptive statistics based on counts (for categorical data) or means and standard deviations (for quantitative variables) were used throughout. Graphic presentations of data were based on computations of the mean value of the outcome variable (e.g., change in FEV1 or FVC) on the vertical axis versus means within quintiles of the predictor variable on the horizontal axis.
In order to assess the independent and interactive predictors of change in FEV1 and FVC during the 5 yr of follow-up, multivariate models were constructed. The following variables were used: sex, intervention group, percentage weight change (along with a sex interaction term), age, height, percent predicted FEV1 or FVC at baseline, cigarettes smoked per day at baseline, and smoking status during follow-up (along with sex and weight change interaction terms). Computations were made using SAS PROC GLM (19). The general linear model was used to estimate the mean effect size for weight gain on lung function, adjusted for smoking status as well as for the other possible influential factors.
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Baseline characteristics of the study participants (all of whom were smokers initially) during their baseline examination are shown in Table 1. Their mean sex specific BMI was similar to that of the population of the United States (20). The relationship between baseline lung function and ideal body weight at study entry is shown in Figure 1. Percent predicted FEV1 was maximal at 90% of ideal body weight for women and 100% of ideal body weight for men (Figure 1, top panel). The cross-sectional relationship of BMI with baseline FVC percent predicted showed a linear decline with increasing body weight above 90 to 95% ideal body weight for both men and women (Figure 1, bottom panel). These patterns were similar for both men and women. The effect of body weight on FVC was greater than the effect of body weight on FEV1.
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In the smoking intervention groups (SIA and SIP), 1 yr after randomization, 35% of the men and 33% of the women were biochemically validated nonsmokers. At the end of the 5-yr trial, 23% of the SIA and SIP men and 20% of the SIA and SIP women were biochemically validated sustained quitters. In contrast, only 9% of the usual care (UC) participants quit during the first year and only 5% were sustained quitters at the end of the 5 yr.
Mean weight increased approximately 5 kg during the first year in both men and women who had quit smoking. Thereafter, the weight gain was slower, approximately 0.5 kg/yr and was similar in all smoking categories (P. O'Hara et al., submitted article). Women who quit smoking gained more weight than did men who quit smoking, both as absolute weight gain and as percent of baseline weight (Figure 2).
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Within smoking categories, mean annual FEV1 declines were greater in those who gained the most weight during the follow-up period (Figure 3). This association of weight gain with decline in FEV1 occurred in all three smoking categories, and it was stronger in men than in women. The effect of continuing smoking was associated with a greater decline in FEV1 than was seen among continuous quitters with the most weight gain. For example, the continuing male smokers in the lowest quintile of weight gain lost approximately twice as much lung function as continuous quitters who were in the highest quintile of weight gain.
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FVC showed a response to changes in weight that was similar to FEV1, but the beneficial effect of smoking cessation was less pronounced and the effect of weight gain was more pronounced for FVC than for FEV1 (Figure 4).
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In order to asses the independent correlates of change in percent predicted FEV1 and FVC over 5 yr, multivariate models were constructed. The following variables were entered into the model: sex, intervention group, percentage weight change (along with a sex interaction term), age, height, percent predicted FEV1 and FVC at baseline, cigarettes smoked per day at baseline, and smoking classification (along with sex and weight change interaction terms). The multivariate analysis showed that there was a significant interaction between weight change and sex for both FEV1 and FVC (p < 0.001). This model estimated that a 10% increase in weight was associated with a 0.83% predicted fall in FEV1 (p < 0.002) and a 1.11% predicted fall in FVC (p < 0.001). Men lost 1.14% predicted FEV1 and 1.08% predicted FVC more than did women for each 10% increase in weight. Although statistically significant, this effect of weight gain was small in comparison with the effect of smoking cessation for which the model estimated that continuing smokers lost 9.18% predicted FEV1 (p < 0.001) and 7.43% predicted FVC (p < 0.001) compared with sustained quitters.
Using similar statistical models, we estimated the effect of a 10-kg increase in body weight on 5-yr changes in FEV1 and FVC. The adjusted effect of weight gain on lung function for each of the sex-smoking categories separately is shown in Table 2. For the same absolute change in weight, men showed a significantly greater loss of FEV1 and FVC than did women for each of the smoking categories (p < 0.001 for interaction of sex and weight gain). Again, this effect was small compared with that of smoking status, which accounted for a 5-yr loss of 254.0 ml in FEV1 (p < 0.001) and 264.6 ml in FVC (p < 0.001) for continuing smokers compared with sustained quitters. Thus, on average, a person who quit smoking would have to gain about 60-kg of weight to have the same effect on FEV1 as continuing to smoke; she or he would have to gain about 38-kg to have the same effect on FVC from continuation of smoking.
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INTRODUCTION
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The major finding of this study is that the weight gain that occurs with smoking cessation, as well as normal aging, is associated with a reduction in both FEV1 and FVC. The magnitude of the changes are significant, but these changes do not outweigh the benefit of stopping smoking. Weight gain caused greater impairment in FVC than in FEV1, whereas continuing to smoke caused greater decline in FEV1 than in FVC. Gaining weight has a similar effect on FEV1 and FVC whether subjects continued to smoke or stopped smoking. We found no apparent threshold below which increasing weight did not affect lung function. The effect of weight gain after smoking cessation on FVC was greater in men than in women.
These findings have important implications for smoking cessation programs, particularly those directed toward persons with impairment of lung function such as those in the Lung Health Study. The net benefit of smoking cessation on lung function clearly overrides the deleterious effects of the weight gain that frequently accompanies quitting. Because excessive weight gain occurs in the first year after cessation, it tends to have a "one-time" effect on lung function. In contrast, continuing to smoke causes persistently greater decline in lung function, which leads to progressively worse pulmonary function over time.
The magnitude of the weight gain after smoking cessation is certainly of clinical importance in those persons who gain large amounts of weight, and it may contribute to ill health through worsening of hypertension or glucose intolerance. The mean effect on lung function, however, is small for the overall population. Some men, however, show substantial reductions in lung function following weight gain, and the combination of increased weight and diminished lung function may combine to impair exercise tolerance. For example, complaints of breathlessness were present in about the same percentage of men in the highest quintile of weight gain as in continuing smokers. Thus, although the overall benefit of smoking cessation is clear, there is a subgroup of men who gain excessive weight after smoking cessation who do not enjoy the full health benefits of smoking cessation. Smoking cessation programs can optimize the benefit to persons with impaired lung function by using strategies to limit weight gain.
The Lung Health Study used an educational/behavioral approach to smoking intervention that included monitoring of weight and nutrition counseling. Despite these efforts, weight gain after smoking cessation occurred in three-quarters of our participants and was often substantial. More than one third of people who quit smoking gained more than 10 kg during the 5 yr of the study, with the most dramatic weight gain in the year after smoking cessation. Among sustained quitters, 4.1% of men and 4.7% of women gained 20 kg or more, compared with 0.2 and 0.4% in the continuing smokers, respectively (P. O'Hara et al., submitted article). Nicotine gum use can delay or diminish weight gain after smoking cessation, but it does not prevent it once the nicotine replacement is stopped (21). Similarly, transdermal nicotine replacement may initially diminish weight gain, but does not affect long-term weight gain after smoking cessation (22, 23).
The mechanism of weight gain after smoking cessation is thought to be the consequence of reduced energy expenditure and increased caloric intake (24, 25). For this reason, it is difficult to control body weight after smoking cessation. In the LHS, only 35% of male and 29% of female participants who quit smoking were able to maintain body weight within 5 kg of their baseline level over a 5-yr interval (P. O'Hara et al., submitted article).
Obesity can impair lung function in several ways. Mechanisms that can be involved include: alterations in the pressure-volume characteristics of the thorax (26), microatelectasis from decreased depth of inspiration (27), or increased pulmonary blood volume from increased plasma volume (8).
Similar to that found in other studies, we found somewhat different relationships between weight and lung function in the cross-sectional baseline analysis and the longitudinal follow-up study. In the cross-sectional analysis, the FEV1 was greatest in those persons near ideal body-weight, and declined for body weights that were either lower or higher than ideal. Further, the male and female relationships were similar in the cross-sectional analysis. In the longitudinal analysis, there was a decrease in FEV1 with weight gain at all levels, and the patterns of men and women differed. We did not find, in the longitudinal analysis, any clear threshold of weight gain below which there was no loss of lung function.
We interpret the cross-sectional pattern of weight on FEV1 to reflect the competing effects of COPD and obesity on pulmonary function. The association of low body weight with poorer lung function might be the result of either heavier smoking and a greater nicotine effect in this group, or the adverse effects of COPD on nutrition. In support of this, a previous cross-sectional study of middle-aged steelworkers by Nemery and colleagues (28) found that the lower weight of smokers could be entirely accounted for by the group of smokers with airflow obstruction defined as a FEV1/FVC ratio less than 66%. Smokers with airflow obstruction weighed 4.8 kg less than did smokers with normal lung function. Two general population studies have shown a similar relationship of FVC to body weight, with an optimal value near ideal body weight (29, 30). These studies have been interpreted as showing the competing effects of "muscularity" and "obesity," and this phenomenon may contribute to our findings (31). Bande and colleagues (30) found that age had an important effect on the relationship of both FVC and FEV1 with body weight. In young nonsmokers (mean age, 20 yr), increasing weight was associated with increases in FEV1 and FVC, presumably because of increased respiratory muscle strength. In middle-aged nonsmokers (age > 30 yr), however, increasing weight showed relationships similar to those found in this study. A recent case-control study of steelworkers showed that those who had rapid declines in lung function averaging 95 ml/yr FEV1 gained 4.3 kg over 6 yr, whereas those with stable lung function gained only 1.0 kg during the interval (32).
In the longitudinal analysis, there were clear differences between men and women in the effect of weight gain on lung function. For any smoking classification (sustained quitter, intermittent smoker, or continuing smoker), men lost more lung function than did women when they gained weight. This was more notable in FVC than in FEV1, presumably because the benefits of smoking cessation had greater influence on airflow obstruction as reflected by the FEV1. A previous general population study by Chen and colleagues (31) also found that women showed less impairment of lung function when they gained weight. Our study extends that finding to weight gain after smoking cessation in a population of people with mild-moderate airflow limitation. The finding that women have less impairment of lung function from weight gain after smoking cessation may explain why women who quit smoking have greater pulmonary function benefit from smoking cessation than do men (33).
One mechanism for the sex difference in lung function impairment from weight gain may be that men who gain weight tend to preferentially increase abdominal fat compared with women (34). Women who quit smoking tend to gain proportionally more weight than men, but they do not develop as much abdominal fat as would be expected from the magnitude of the weight gain (35, 36). Our data would be consistent with the notion that men do have more abdominal fat deposition than women after smoking cessation, and that this phenomenon leads to the greater reduction in FEV1 and FVC with weight gain. Abdominal fat, or the associated increase in visceral fat, may impair lung function directly through alteration of thoracic mechanics. Unfortunately, we did not measure waist-hip ratios (WHR) in the LHS participants, so that we are not able to directly address this issue. Our findings do lead us to speculate, however, that WHR or the distribution of visceral fat may be the link between impairment in spirometry and coronary heart disease risk, which cannot be explained by body weight or smoking status alone (37). Elevation of WHR is a strong predictor of serum lipids, hypertension, glucose intolerance, and coronary artery disease (34). Furthermore, smoking, per se also is associated with more abdominal fat deposition for a given body weight (36). Thus, it is conceivable that spirometric measures may serve to some extent as a surrogate measure of increased WHR and the multiple associated cardiovascular risk factors, partially explaining the link between spirometry and cardiac mortality.
In summary, we have found that the weight gain that occurs with smoking cessation in persons with early COPD leads to a relative reduction in FVC and FEV1, with a greater effect on men than on women. The effect of weight gain is small in comparison with the effect of continued smoking on pulmonary function, and it would not justify continuing smoking as a means of weight control. Smoking cessation programs should develop and emphasize strategies to minimize weight gain after smoking cessation.
APPENDIX
CREDIT ROSTER: LUNG HEALTH STUDY RESEARCH GROUP
The principal investigators and senior staff of the clinical and coordinating centers, the NHLBI, members of the Safety and Data Monitoring Board, and the Morbidity and Mortality Review Board are as follows.
CASE WESTERN RESERVE UNIVERSITY, Cleveland, OH
M. D. Altose, M.D. (Principal Investigator)
A. F. Connors, M.D. (Co-Principal Investigator)
S. Redline, M.D. (Co-Principal Investigator)
C. D. Deitz, Ph.D.
R. F. Rakos, Ph.D.
HENRY FORD HOPSITAL, Detroit, MI
W. A. Conway, Jr., M.D. (Principal Investigator)
A. DeHorn, Ph.D. (Co-Principal Investigator)
J. C. Ward, M.D. (former Co-Principal Investigator)
C. S. Hoppe-Ryan, C.S.W.
R. L. Jentons, M.A.
J. A. Reddick, R.N.
C. Sawicki, R.N., M.P.H.
JOHNS HOPKINS UNIVERSITY SCHOOL OF MEDICINE, Baltimore, MD
R. A. Wise, M.D. (Principal Investigator)
S. Permutt, M.D. (Co-Principal Investigator)
C. S. Rand, Ph.D. (Co-Principal Investigator)
MAYO CLINIC, Rochester, MN
P. D. Scanlon, M.D. (Principal Investigator)
L. J. Davis, Ph.D. (Co-Principal Investigator)
R. D. Hurt, M.D. (Co-Principal Investigator)
R. D. Miller, M.D. (Co-Principal Investigator)
D. E. Williams, M.D. (Co-Principal Investigator)
G. M. Caron
G. G. Lauger, M.S.
S. M. Toogood (Pulmonary Function Quality Control Manager)
OREGON HEALTH SCIENCES UNIVERSITY, Portland, OR
A. S. Buist, M.D. (Principal Investigator)
W. M. Bjornson, M.P.H. (Co-Principal Investigator)
L. R. Johnson, Ph.D. (LHS Pulmonary Function Coordinator)
UNIVERSITY OF ALABAMA AT BIRMINGHAM, Birmingham, AL
W. C. Bailey, M.D. (Principal Investigator and Associate Chief of Staff for Education, Department of Veterans Affairs Medical Center, Birmingham)
C. M. Brooks, Ed.D. (Co-Principal Investigator)
J. J. Dolce, Ph.D.
D. M. Higgins
M. A. Johnson
B. A. Martin
UNIVERSITY OF CALIFORNIA AT LOS ANGELES, Los Angeles, CA
D. P. Tashkin, M.D. (Principal Investigator)
A. H. Coulson, Ph.D. (Co-Principal Investigator)
H. Gong, M.D. (former Co-Principal Investigator)
P. I. Harber, M.D. (Co-Principal Investigator)
V. C. Li, Ph.D., M.P.H. (Co-Principal Investigator)
M. Roth, M.D. (Co-Principal Investigator)
M. A. Nides, Ph.D.
M. S. Simmons
I. P. Zuniga
UNIVERSITY OF MANITOBA, Winnipeg, MAN
N. R. Anthonisen, M.D. (Principal Investigator, Steering Committee Chair)
J. Manfreda, M.D. (Co-Principal Investigator)
R. P. Murray, Ph.D. (Co-Principal Investigator)
S. C. Rempel-Rossum
J. M. Stoyko
UNIVERSITY OF MINNESOTA COORDINATING CENTER, Minneapolis, MN
J. E. Connett, Ph.D. (Principal Investigator)
M. O. Kjelsberg, Ph.D. (Co-Principal Investigator)
M. K. Cowles, Ph.D.
D. A. Durkin
P. L. Enright, M.D.
K. J. Kurnow, M.S.
W. W. Lee, M.S.
P. G. Lindgren, M.S.
S. Mongin, M.S.
P. O'Hara, Ph.D. (LHS Intervention Coordinator)
H. T. Voelker
L. Waller, Ph.D.
UNIVERSITY OF PITTSBURGH, Pittsburgh, PA
G. R. Owens, M.D. (Principal Investigator)
R. M. Rogers, M.D. (Co-Principal Investigator)
J. J. Johnston, Ph.D.
F. P. Pope, M.S.W.
F. M. Vitale, M.A.
UNIVERSITY OF UTAH, Salt Lake City, UT
R. E. Kanner, M.D. (Principal Investigator)
M. A. Rigdon, Ph.D. (Co-Principal Investigator)
K. C. Benton
P. M. Grant
The Salt Lake City Center has been assisted by the Clinical Research Center, Public Health Research Grant M01-RR00064 from the National Center for Research Resources.
SAFETY AND DATA MONITORING BOARD
M. Becklake, M.D.
B. Burrows, M.D.
P. Cleary, Ph.D.
P. Kimbel, M.D. (Chairperson; deceased October 2, 1990)
L. Nett, R.N., R.R.T. (former member)
J. K. Ockene, Ph.D.
R. M. Senior, M.D. (Chairperson)
G. L. Snider, M.D.
W. Spitzer, M.D. (former member)
O. D. Williams, Ph.D.
NATIONAL HEART, LUNG, and BLOOD INSTITUTE, Bethesda, MD
S. S. Hurd, Ph.D. (Director, Division of Lung Diseases)
J. P. Kiley, Ph.D. (Project Officer)
M. C. Wu, Ph.D. (Div. of Epidemiology & Clinical Applications)
MORTALITY AND MORBIDITY REVIEW BOARD
S. M. Ayres, M.D.
R. E. Hyatt, M.D.
B. A. Mason, M.D.
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Footnotes |
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Correspondence and requests for reprints should be addressed to Robert A. Wise, M.D., Johns Hopkins Asthma & Allergy Center, 5501 Hopkins Bayview Circle, Room 4B.72, Baltimore, MD 21224.
(Received in original form October 8, 1997 and in revised form November 17, 1997).
Acknowledgments: Supported by Contract NO1-HR46002 from the Division of Lung Diseases, National Heart, Lung, and Blood Institute, National Institutes of Health.
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References |
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ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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1. U.S. Public Health Service. Centers for Disease Control. Office on Smoking and Health. 1990. The health benefits of smoking cessation: a report of the Surgeon General. Centers for Disease Control, Atlanta, GA. DHHS Publication No. (CDC) 90-8416, 373-383.
2.
Anthonisen, N. R.,
J. E. Connett,
J. Kiley,
M. D. Altose,
W. C. Bailey,
A. S. Buist,
W. A. Conway,
P. A. Enright,
R. E. Kanner,
P. O'Hara,
G. R. Owens,
P. D. Scanlon,
D. P. Tashkin,
R. A. Wise, and
for the
Lung Health Study Research Group.
1994.
Effects of smoking intervention and the use of an anticholinergic bronchodilator on the rate of
decline in FEV1: The Lung Health Study.
J.A.M.A.
272:
1497-1505
3. Ray, C. S., D. Y. Sue, G. Bray, J. E. Hansen, and K. Wasserman. 1983. Effects of obesity on respiratory function. Am. Rev. Respir. Dis. 128: 501-506 [Medline].
4. Refsum, H. E., P. H. Holter, T. Lovig, J. F. Haffner, and J. O. Stadaas. 1990. Pulmonary function and energy expenditure after marked weight loss in obese women: observations before and one year after gastric banding. Int. J. Obes. 14: 175-183 [Medline].
5.
Thomas, P. S.,
E. R. Cowen,
G. Hulands, and
J. S. Milledge.
1989.
Respiratory function in the morbidly obese before and after weight loss.
Thorax
44:
382-386
6.
Dontas, A. S.,
D. R. Jacbos,
A. Corcondilas,
A. Keys, and
P. Hannan.
1984.
Longitudinal versus cross-sectional vital capacity changes and
affecting factors.
J. Geront.
39:
430-438
7.
Luce, J. M..
1980.
Respiratory complications of obesity.
Chest
78:
626-631
8.
Borkan, G. A.,
D. Sparrow,
C. Wisniewski, and
P. S. Vokonas.
1986.
Body weight and coronary artery disease risk: patterns of risk factor
change associated with long-term weight change: The Normative Aging Study.
Am. J. Epidemiol.
124:
410-419
9. Connett, J., J. Kusek, W. Bailey, P. O'Hara, and M. Wu. 1993. Design of the Lung Health Study: a randomized clinical trial of early intervention for chronic obstructive pulmonary disease. Control. Clin. Trials 14: 3S-19S [Medline].
10. Ferris, B. G. 1978. Epidemiologic standardization project. Am. Rev. Respir. Dis. 118(6, Part 2):1-88.
11. Tashkin, D. P., M. D. Altose, J. E. Connett, R. E. Kanner, W. W. Lee, R. A. Wise, and the Lung Health Study Research Group. 1992. Airway responsiveness to inhaled methacholine in smokers with early chronic obstructive pulmonary disease. Am. Rev. Respir. Dis. 145: 301-310 [Medline].
12. Crapo, R. D., A. H. Morris, and R. M. Gardner. 1981. Reference spirometric values using techniques and equipment that meet ATS recommendations. Am. Rev. Respir. Dis. 123: 659-664 [Medline].
13. National Center for Health Statistics. Weight by height and age for adults 18-74 years. National Center for Health Statistics, Hyattsville, MD. Vital and health statistics. Series 11, No. 208. DHEW Publication No. (PHS) 79-1656.
14. O'Hara, P., J. Grill, M. A. Rigdon, J. E. Connett, G. A. Lauger, and J. J. Johnston. 1993. Design and results of the initial intervention program for the Lung Health Study. Prev. Med. 22: 304-315 [Medline].
15. Enright, P. L., L. R. Johnson, J. E. Connett, H. Voelker, and A. S. Buist. 1991. Spirometry in the Lung Health Study. 1: Methods and quality control. Am. Rev. Respir. Dis. 143: 1215-1223 [Medline].
16. American Thoracic Society. 1995. Standardization of spirometry: 1994 update (ATS Statement). Am. J. Respir. Crit. Care Med. 152: 1107-1136 [Medline].
17. American Thoracic Society. 1991. Lung function testing: selection of reference values and interpretative strategies. Am. Rev. Respir. Dis. 144: 1202-1218 [Medline].
18. Anthonisen, N. R., E. C. Wright, J. E. Hodgkin, and the IPPB Trial Group. 1986. Prognosis in obstructive pulmonary disease. Am. Rev. Respir. Dis. 133: 14 [Medline].
19. SAS Institute. 1993. SAS/STAT User's Guide, Ver. 6, 4th ed. 1990. SAS Institute Inc., Cary, NC.
20. Abraham, S., M. Carroll, M. Najjar, and R. Fulwood. 1983. Obese and overweight adults in the United States. National Center for Health Statistics, Hyattsville, MD. Vital and health statistics. Series 11, no. 230. DHHS Publication No. (PHS) 83-1680.
21. Nides, M., C. Rand, J. Dolce, R. Murray, P. O'Hara, H. Voelker, and J. Connett. 1994. Weight gain as a function of smoking cessation and 2-mg nicotine gum use among middle-aged smokers with mild lung impairment in the first 2 years of the Lung Health Study. Health Psychol. 13: 354-361 [Medline].
22.
Fiore, M. C.,
D. E. Jorenby,
T. B. Baker, and
S. L. Kenford.
1992.
Tobacco dependence and the nicotine patch: clinical guidelines for effective use.
J.A.M.A.
268:
2687-2694
23. Allen, S. S., D. Hatsukami, and J. Gorsline. 1994. Cholesterol changes in smoking cessation using the transdermal nicotine system. Prev. Med. 23: 190-196 [Medline].
24.
Perkins, K. A.,
L. H. Epstein,
R. L. Stiller,
B. L. Marks, and
R. G. Jacob.
1989.
Acute effects of nicotine on resting metabolic rate in cigarette
smokers.
Am. J. Clin. Nutr.
50:
545-550
25.
Klesges, R. C.,
L. H. Eck,
T. R. Isbell,
W. Fulliton, and
C. L. Hanson.
1990.
Smoking status: effects on the dietary intake, physical activity,
and body fat of adult men.
Am. J. Clin. Nutri.
51:
784-789
26.
Naimark, A., and
R. M. Cherniack.
1960.
Compliance of the respiratory
system and its components in health and obesity.
J. Appl. Physiol.
15:
377-382
27. Caro, C. G., J. Butler, and A. B. Dubois. 1960. Some effects of restriction of chest cage expansion on pulmonary function in man: an experimental study. J. Clin. Invest. 39: 573-583 .
28. Nemery, B., N. E. Moavero, L. Brasseur, and D. C. Stanescu. 1983. Smoking, lung function, and body weight. B.M.J. 286: 249-251 .
29. Dockery, D. W., J. H. Ware, B. G. Ferris Jr., D. S. Glicksberg, M. E. Fay, and A. Spiro. 1985. Distribution of forced expiratory volume in one second and forced vital capacity in healthy, white, adult never-smokers in six U.S. cities. Am. Rev. Respir. Dis. 131: 511-520 [Medline].
30. Bande, J., J. Clement, and K. P. van de Woestijne. 1980. The influence of smoking habits and body weight on vital capacity and FEV1 in male Air Force personnel: a longitudinal and cross-sectional analysis. Am. Rev. Respir. Dis. 122: 781-790 [Medline].
31.
Chen, Y.,
S. L. Horne, and
J. A. Dosman.
1993.
Body weight and weight gain related to pulmonary function decline in adults: a six year follow
up study.
Thorax
48:
375-380
32.
Wang, M.,
L. McCabe,
E. L. Petsonk,
J. L. Hankinson, and
D. E. Banks.
1997.
Weight gain and longitudinal changes in lung function in steel
workers.
Chest
111:
1526-1532
33. Chen, Y., S. L. Horne, and J. A. Dosman. 1991. Increased susceptibility to lung dysfunction in female smokers. Am. Rev. Respir. Dis. 143: 1224-1230 [Medline].
34. Shimokata, H., J. D. Tobin, D. C. Muller, P. J. Elahi, and R. Andres. 1989. Studies in the distribution of body fat: I. Effects of age, sex and obesity. J. Gerontol. 44: M66-M73 [Abstract].
35.
Lissner, L.,
C. Bengtsson,
L. Lapidus, and
C. Bjorkelund.
1992.
Smoking initiation and cessation in relation to body fat distribution based on
data from a study of Swedish women.
Am. J. Public Health
82:
273-275
36. den Tonkelaar, I., J. C. Seidell, P. A. vanNoord, E. A. Baanders-van Halewijn, and I. J. Ouwehand. 1990. Fat distribution in relation to age, degree of obesity, smoking habits, parity and estrogen use: a cross-sectional study in 11,825 Dutch women participating in the DOM-project. Int. J. Obes. 14: 753-761 [Medline].
37. Tockman, M. S., J. D. Pearson, J. L. Fleg, E. J. Metter, S. Y. Kao, K. G. Rampal, L. J. Cruise, and J. L. Fozard. 1995. Rapid decline in FEV1: a new risk factor for coronary heart disease mortality. Am. J Respir. Crit. Care Med. 151: 390-398 [Abstract].
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