Lung Health Study (LHS) I and III

This study has been completed.
Sponsor:
Information provided by:
National Heart, Lung, and Blood Institute (NHLBI)
ClinicalTrials.gov Identifier:
NCT00000568
First received: October 27, 1999
Last updated: August 17, 2005
Last verified: August 2005
  Purpose

In the Lung Health Study I, to determine the effects of Special Care, compared to Usual Care, on rate of decline in pulmonary function in a group of cigarette smokers identified as having mild abnormalities in pulmonary function.

In the Lung Health Study III, to determine the long-term effects of smoking cessation and continued smoking, on cardiopulmonary morbidity, mortality, and the rate of decline in the one second forced expiratory volume (FEV1) in men and women with early chronic obstructive lung disease who have been followed prospectively for 12 to 15 years.


Condition Intervention Phase
Lung Diseases
Lung Diseases, Obstructive
Chronic Obstructive Pulmonary Disease
Behavioral: smoking cessation
Drug: ipratropium
Phase 3

Study Type: Interventional
Study Design: Allocation: Randomized
Masking: Double-Blind
Primary Purpose: Prevention

Resource links provided by NLM:


Further study details as provided by National Heart, Lung, and Blood Institute (NHLBI):

Study Start Date: September 1984
Estimated Study Completion Date: January 2005
  Hide Detailed Description

Detailed Description:

BACKGROUND:

Chronic obstructive pulmonary disease (COPD) is a major cause of mortality and morbidity in the United States, affecting nearly 10 million persons. COPD accounts for 60,000 deaths yearly and ranks as the fourth leading cause of death. If current trends continue, it may become the nation's fourth or even third leading cause of death by the year 2000.

Epidemiological studies consistently indicated that smoking was the over-whelming risk factor for accelerated decline in pulmonary function and subsequent development of COPD. Furthermore, evidence from several studies indicated that the rate of decline in pulmonary function approached a more normal rate of decline upon cessation of cigarette smoking.

Another presumed risk factor for accelerated decline in pulmonary function was the presence of hyperreactive airways, although it was not clear whether the mere presence of hyperreactive airways contributed to the accelerated decline, or whether the decline resulted from the reaction of the airways to various irritants over a long period of time. It is possible that if the hyperreactive airway was kept non-reactive by pharmacological means over a period of years, the expected abnormal decline might be lessened. This effect might be enhanced by the cessation of cigarette smoking.

Although the evidence was strong that smoking and hyperreactive airways were risk factors for COPD, it had not been demonstrated whether removal of risk factors at a stage when mild dysfunction had already occurred would effectively modify the course of COPD.

DESIGN NARRATIVE:

Lung Health Study I

Randomized and controlled. Cigarette smokers with evidence of airways obstruction underwent baseline testing that included spirometric responses to isoproterenol and methacholine and were then randomly assigned to one of three groups: a no intervention or usual care group; a group receiving a smoking cessation program and bronchodilator therapy; a group receiving a smoking cessation program and a placebo bronchodilator. The placebo/bronchodilator therapy was double-blind. The smoking intervention consisted of an intensive 12-session smoking cessation program combining behavior modification and use of nicotine gum, with a continuing five-year maintenance program to minimize relapse. The bronchodilator consisted of ipratropium bromide prescribed three times daily, two puffs per time, from a metered-dose inhaler. All groups were followed yearly for five years. The primary endpoint was the rate of change of FEV1. Respiratory morbidity was a secondary endpoint. Recruitment began in November 1986 and was completed in January 1989. The clinical phase of the trial ended in April 1994. The study continues under contract N01-HR-46002 through September, 2004 for data analysis and dissemination of research results.

Lung Health Study III

Beginning in fiscal year 1998, all surviving participants of LHS I are invited to participate in the long-term followup. The study will determine, using an intent-to-treat analysis, whether the LHS I smoking intervention significantly reduces the incidence of clinically important respiratory and cardiovascular disease over a 12- to 15-year period following study enrollment. The study will also estimate the magnitude of the effects of FEV1 and FVC on the risks of cardiovascular and respiratory morbidity and mortality, after controlling for smoking history. Studies will be conducted on the role of other factors such as gender, airways reactivity, weight gain, and co-morbidities in determining the rate of decline in pulmonary function and the risks of cardiovascular and respiratory morbidity and mortality. A determination will also be made as to whether the improvement in lung function and reduction in respiratory symptoms associated with smoking cessation result in improved health-related quality of life (HRQL) and less depression over an extended follow-up period. The LHS III, an investigator initiated long-term follow-up study, is not an NIH- defined clinical trial.

  Eligibility

Ages Eligible for Study:   35 Years to 60 Years
Genders Eligible for Study:   Both
Accepts Healthy Volunteers:   No
Criteria

Men and women who were cigarette smokers and between the ages of 35 and 60.

  Contacts and Locations
Choosing to participate in a study is an important personal decision. Talk with your doctor and family members or friends about deciding to join a study. To learn more about this study, you or your doctor may contact the study research staff using the Contacts provided below. For general information, see Learn About Clinical Studies.

Please refer to this study by its ClinicalTrials.gov identifier: NCT00000568

Sponsors and Collaborators
Investigators
Investigator: John Connett University of Minnesota - Clinical and Translational Science Institute
  More Information

Publications:
The Lung Health Study: Design of the Trial and Recruitment of Participants. Controlled Clin Trials, 14(2):1S-83S, 1993.
Owens GR: Lung Health Study: Assessing the Impact of Early Intervention. Monograph. Chronic Bronchitis: Time to Act, Strategies for Prevention and Intervention. From the Proceedings of the Boehringer Ingelheim Ireland Symposium. Killarney, Ireland, July 1988.
Owens GR: Pulmonary Function Tests as Guides in the Differential Physiologic Comparisons of Obstructive Pulmonary Diseases. J Respir Dis, II(6):S23-S29, 1990.
Tashkin DP, Altose MD, Connett JE, et al and the Lung Health Study Research Group: Airway Hyperresponsiveness in "Irreversible" Chronic Obstructive Pulmonary Disease. In: Spector SL, (Ed). Provocation Testing in Clinical Practice. New York, Marcel Dekker, Inc. ,575-598, 1995.
Owens G. Editorial: Obstructive, Occupational, and Environmental Diseases: Editorial Overview. Current Opinion in Pul Med, 1:73-75, 1995.
Cowles MK, Carlin BP, Conett JE: Bayesian Tobit Modeling of Longitudinal Ordinal Clinical Trial Compliance Data with Nonignorable Missingness. J Am Stat Assoc, 92(433):86-98, 1996.
Bjornson W: Early Chronic Obstructive Pulmonary Disease: Results from the Lung Health Study. Am J Health Behav, 20(5):270-278, 1996.

ClinicalTrials.gov Identifier: NCT00000568     History of Changes
Other Study ID Numbers: 206
Study First Received: October 27, 1999
Last Updated: August 17, 2005
Health Authority: United States: Federal Government

Additional relevant MeSH terms:
Lung Diseases
Lung Diseases, Obstructive
Pulmonary Disease, Chronic Obstructive
Respiratory Tract Diseases

ClinicalTrials.gov processed this record on September 18, 2014