RISK FACTORS FOR THE DEVELOPMENT OF CHRONIC OBSTRUCTIVE PULMONARY DISEASE
Section snippets
CIGARETTE SMOKING AND CHRONIC OBSTRUCTIVE PULMONARY DISEASE
In the 1950s, the most widely advanced hypothesis for the cause of COPD linked progressive lung damage to air pollution and recurrent respiratory infections. By 1964, adequate epidemiologic evidence had accumulated for the Advisory Committee to the Surgeon General to conclude that: "Cigarette smoking is the most important of the causes of chronic bronchitis in the United States, and increases the risk of dying from chronic bronchitis and emphysema.74 Nearly all of the studies on which the 1964
AIRWAY RESPONSIVENESS AND CHRONIC OBSTRUCTIVE PULMONARY DISEASE
An increased tendency for bronchial constriction in response to a variety of exogenous stimuli, including methacholine and histamine, is one of the defining features of asthma. Many subjects with COPD, however, also share this feature of airway hyperresponsiveness. The considerable overlap between subjects with asthma and COPD in airway responsiveness; airflow obstruction; and pulmonary symptoms such as cough, phlegm, and wheezing led to the formulation of the Dutch hypothesis in 1961.55 This
Alpha1-Antitrypsin Deficiency and Chronic Obstructive Pulmonary Disease
Alpha1-antitrypsin, specified by the protease inhibitor (PI) locus, is the major serum protease inhibitor of human leukocyte elastase, a serine protease generally considered to be one of the major destructive enzymes in the development of pulmonary emphysema.33, 73 More than 75 different PI alleles have been identified, a few of which result in decreased serum levels of alpha1-antitrypsin.4 The common M allele, with an allele frequency greater than 95% in U.S. populations, is associated with
Respiratory Infections
A variety of other environmental risk factors also have been studied as potential contributors to the development of COPD. Respiratory infections have been studied as a potential risk factor for the development and progression of COPD in adults; childhood respiratory infections also have been assessed as a potential predisposing factor to the eventual development of COPD. A challenging problem in assessing the importance of respiratory infections as a risk factor for COPD is determining whether
SUMMARY
Cigarette smoking clearly has been shown to be the major environmental risk factor predisposing to the development of COPD. Occupational exposures to dust and fumes, air pollution, passive smoke exposure, childhood respiratory infections, and diet may also contribute. Airway hyperresponsiveness is a risk factor for the development of decline in FEV1 but its role in the development of COPD remains uncertain. Alpha1-antitrypsin deficiency is an important genetic risk factor for COPD in the small
ACKNOWLEDGMENTS
The authors appreciate the useful comments provided by Dr. Scott Weiss, Dr. Edward Campbell, and Dr. Ira Tager.
References (76)
- et al.
Molecular basis of alpha-1-antitrypsin deficiency
Am J Med
(1988) - et al.
The alpha 1-antitrypsin gene and its mutations: Clinical consequences and strategies for therapy
Chest
(1989) - et al.
Cadmium fume inhalation and emphysema
Lancet
(1988) - et al.
Risk factors for chronic obstructive lung disease in Saudi Arabia
Respir Med
(1994) - et al.
The urban factor in chronic bronchitis
Lancet
(1965) Alpha 1-antitrypsin Pi types in COPD patients
Chest
(1988)- et al.
Smoking, lung function, and alpha 1-antitrypsin deficiency
Lancet
(1985) - et al.
Variables associated with changes in spirometry in patients with obstructive lung diseases
Am J Med
(1979) - et al.
Familial prevalence of chronic obstructive pulmonary disease in a matched pair study
Am J Med
(1977) - et al.
Alpha 1-antitrypsin Pi-types in 965 COPD patients
Chest
(1986)
Risk factors for ventilatory impairment among middle-aged and elderly men: The Normative Aging Study
Chest
Major genetic mechanisms in pulmonary function
J Clin Epidemiol
Alpha 1-antitrypsin deficiency: The clinical and physiological features of pulmonary emphysema in subjects homozygous for Pi type Z
Br J Dis Chest
Robust inference for variance components models in families ascertained through probands: II. Analysis of spirometric measures
Genet Epidemiol
Excessive airway narrowing in response to bronchoconstrictor stimuli in asthma and chronic obstructive lung disease
Thorax
Alpha 1-antitrypsin deficiency in nonsmokers
Am Rev Respir Dis
Dietary fish oil and airways obstruction
Thorax
Collaborative study to assess risk of lung disease in Pi MZ phenotype subjects
Am Rev Respir Dis
The "horse-racing effect" and predicting decline in forced expiratory volume in one second from screening spirometry
Am Rev Respir Dis
Quantitative relationships between cigarette smoking and ventilatory function
Am Rev Respir Dis
A reexamination of risk factors for ventilatory impairment
Am Rev Respir Dis
The bronchial late response in the pathogenesis of asthma and its modulation by therapy
Ann Allergy
Chronic obstructive pulmonary disease: A challenge in genetic epidemiology
Am J Epidemiol
Risk factors in chronic obstructive pulmonary disease (COPD)
Am J Epidemiol
Changes in risk factors: The epidemiology of cigarette smoking and its impact on chronic obstructive pulmonary disease
Am Rev Respir Dis
The UCLA population studies of chronic obstructive respiratory disease: IV. Respiratory effect of long-term exposure to photochemical oxidants, nitrogen dioxide, and sulfates on current and never smokers
Am Rev Respir Dis
Cumulative and reversible effects of lifetime smoking on simple tests of lung function in adults
Am Rev Respir Dis
Characteristics of bronchial hyperresponsiveness in smokers with chronic air-flow limitation
Am Rev Respir Dis
Trends in COPD morbidity and mortality in the United States
Am Rev Respir Dis
Health effects of involuntary smoking
N Engl J Med
Indoor air pollution and its effect on pulmonary function of adult non-smoking women: II. Associations between nitrogen dioxide and pulmonary function
Int J Epidemiol
The natural history of chronic airflow obstruction
Br Med J
A follow-up study of the natural history of obstructive bronchitis
Factors related to the development of airflow obstruction
Methacholine responsiveness, smoking, and atopy as risk factors for accelerated FEV1 decline in male working populations
Am Rev Respir Dis
Acute lower respiratory illness in childhood as a predictor of lung function and chronic respiratory symptoms
Am Rev Respir Dis
Exposures of older adults with chronic respiratory illness to nitrogen dioxide: A combined laboratory and field study
Am Rev Respir Dis
Passive smoking as a risk factor for development of obstructive respiratory disease and allergic sensitization
Allergy
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Hereditary pulmonary emphysema
2019, Emery and Rimoin's Principles and Practice of Medical Genetics and Genomics: Cardiovascular, Respiratory, and Gastrointestinal DisordersEarly chronic obstructive pulmonary disease: Definition, assessment, and prevention
2015, The LancetCitation Excerpt :Burrows47 suggested three ways for lung function to decrease: gradually, at an accelerated rate throughout adult life (figure 3D); episodically, perhaps related to acute exacerbations (figure 3E); or a phase of rapid progression could develop after a period of so-called normal ageing (figure 3F). Exposures in addition to cigarette smoke can accelerate lung function loss, including air pollution and occupational dusts and fumes.13–15,48,49 Starvation can lead to the development of emphysema.50,51
Hereditary Pulmonary Emphysema
2013, Emery and Rimoin's Principles and Practice of Medical GeneticsGenetic analysis of IREB2, FAM13A and XRCC5 variants in Chinese Han patients with chronic obstructive pulmonary disease
2011, Biochemical and Biophysical Research CommunicationsCitation Excerpt :This disorder is expected to be the third leading cause of worldwide mortality and the fifth leading cause of morbidity by the year 2020 [2]. Cigarette smoking is clearly the major environmental risk factor for the development of COPD [3]. It is well recognized that COPD has a genetic component as well as environmental, and that is may account for these differences in susceptibility.
Address reprint requests to Edwin K. Silverman, MD, PhD, Charming Laboratory, Brigham and Women's Hospital, 180 Longwood Avenue, Boston, MA 02115
This work was supported by Grant No. M01 RR02635 from the National Institutes of Health.