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• W2011013045 abstract "Why do only 20 percent of cigarette smokers develop chronic obstructive lung disease (COLD)? Competing risks may be part of the answer. Smokers may die of conditions such as coronary artery disease and lung cancer prior to developing COLD. However, susceptibility also may be an important part of the problem. Early investigators formulated two theories about the origins of COLD. The first, which we call the British hypothesis, held that cigarette smoking led to inflammation and phlegm production. This mucus hypersecretion led to abnormalities in airway clearance and in certain persons susceptible to repeated infections. These infections destroyed lung tissue and led to a more rapid decline in lung function and to airflow obstruction.1Fletcher CM Peto R Tinker C Speizer FE The natural history of chronic bronchitis and emphysema. Oxford University Press, New York1976Google Scholar An alternative hypothesis, first proposed by the Dutch, held that in susceptible individuals, cigarette smoking led to increased levels of bronchial responsiveness which, through repeated acute increases in airflow obstruction, led to a more rapid decline in pulmonary function.2Orie NG Shuster HJ DeVries K Tammeling SJ Wittop J The host factor in bronchiolitis.in: Orie NGM Shuster HJ Bronchitis, an international symposium. Royal Vangorcum, Assen, Netherlands1961: 43-59Google Scholar Fletcher and others tested the British hypothesis in a landmark study of British transport and postal workers.1Fletcher CM Peto R Tinker C Speizer FE The natural history of chronic bronchitis and emphysema. Oxford University Press, New York1976Google Scholar This study demonstrated that respiratory infections bore no relationship to rate of decline in lung function, thus raising serious doubt about infection as a risk factor for the development of COLD. Another major contribution of this study was an exposition of the methodologic issues in the longitudinal assessment of changes in adult lung function. The Transport and Postal Workers Study suggested that initial levels of lung function at study onset was an important determinant of future rate of decline in lung function. This was due to two factors: the statistical concept of regression to the mean, and their finding that those subjects with low levels of lung function had greater rates of decline of lung function (the so-called horseracing effect). Normally attained maximal level of lung function in early adult life may also serve as a surrogate for past history of environmental exposures in childhood and, thus, provides an important correlate of rate of decline in lung function. Existing data bearing on the Dutch hypothesis are relatively sparse, but recently have been well reviewed.3Fanta CH Ingram Jr., RH Airways responsiveness and chronic airway obstruction.Med Clin N Am. 1981; 65: 473-487Crossref PubMed Scopus (4) Google Scholar, 4Fish JE Mankes HA Airway reactivity: role in acute and chronic disease.Current Pulmonology. 1984; 5: 169-199Google Scholar In cross-sectional data, increased levels of airways responsiveness have been associated with lower levels of pulmonary function in normal subjects5Lorber DB Kattenborn W Burrows B Response to isoproterenol in a general population sample.Am Rev Respir Dis. 1978; 118: 855-861PubMed Google Scholar and in subjects with chronic bronchitis.6Pride NB Taylor RG Joyce H Gross E Holland F Relation between bronchial reactivity to inhaled histamine and annual decline in FEV1, in male smokers and ex-smokers.. 1984; 85: 22SGoogle Scholar, 7Ramsdale E Morris M Hargreave F The diagnostic significance of increased bronchial responsiveness to methacholine in patients with chronic airflow obstruction.Chest. 1984; 85: 22S-23SAbstract Full Text Full Text PDF Google Scholar Several investigators have also reported that chronic cigarette smoking is associated with increased levels of airways responsiveness.6Pride NB Taylor RG Joyce H Gross E Holland F Relation between bronchial reactivity to inhaled histamine and annual decline in FEV1, in male smokers and ex-smokers.. 1984; 85: 22SGoogle Scholar, 7Ramsdale E Morris M Hargreave F The diagnostic significance of increased bronchial responsiveness to methacholine in patients with chronic airflow obstruction.Chest. 1984; 85: 22S-23SAbstract Full Text Full Text PDF Google Scholar, 8Woolcock A Yen K Anderson S Stuckey M Bronchial responsiveness to histamine—a population study.in: Presented at the 26th Aspen Lung Conference. 1983Google Scholar, 9Buczko GB Day A Vanderdoelen JL Boucher R Zamel N Effects of cigarette smoking and short-term smoking cessation on airway responsiveness to inhaled methacholine.Am Rev Respir Dis. 1984; 129: 12-14PubMed Google Scholar, 10Gerrard JW Cockroft DW Mink JT Cotton DJ Poonarvale R Dosman JA Increased nonspecific bronchial reactivity in cigarette smokers with normal lung function.Am Rev Respir Dis. 1980; 122: 577-581PubMed Google Scholar Data from the Tucson group lend additional support for the Dutch hypothesis. These investigators have found that cigarette smoking in adults is associated with elevated serum IgE levels11Burrows B Halonen M Lebowitz MD Knudson RJ Barbee RA The relationship of serum immunoglobulin E allergy skin tests and smoking to respiratory disorders.J Allergy Clin Immunol. 1982; 70: 199-204Abstract Full Text PDF PubMed Scopus (72) Google Scholar and the subsequent development of doctor-diagnosed asthma.12Dodge RR Burrows B The prevalence and incidence of asthma like symptoms in a general population sample.Am Rev Respir Dis. 1980; 122: 567-571PubMed Google Scholar Burrows et al13Burrows B Lebowitz MD Barbee BA Knudson RJ Halonen M Interactions of smoking and immunologic factors in relation to airways obstruction.Chest. 1983; 84: 657-661Abstract Full Text Full Text PDF PubMed Scopus (23) Google Scholar have even suggested that the serum IgE measured in cigarette smokers may be related to microorganisms in the respiratory tract, thus possibly linking the British and the Dutch hypotheses. The methodologic issues raised in the British Transport and Postal Workers Study provide an important context for considering existing longitudinal data about airways responsiveness. Since both level of pulmonary function and cigarette smoking are major determinants of rate of decline in lung function, one would need to control for the effects of these (and possibly other) variables to establish that increased levels of airways responsiveness are truly an independent risk factor for decline in lung function. The work of Barter and Campbell,14Barter CE Campbell AH Relationship of constitutional factors and cigarette smoking to decrease in 1-second forced expiratory volume.Am Rev Respir Dis. 1976; 113: 305-310PubMed Google Scholar and the earlier work of Kanner et al15Kanner RE Renzetti Jr, AD Klauber MR Smith CB Golden CA Variables associated with changes in spirometry in patients with obstructive lung diseases.Am J Med. 1979; 67: 44-50Abstract Full Text PDF PubMed Scopus (70) Google Scholar, 16Kanner RE Renzetti Jr, AD Standish WM Barkman Jr, HW Klauber MR Predictors of survival in subjects with chronic airflow obstruction.Am J Med. 1983; 74: 249-255Abstract Full Text PDF PubMed Scopus (49) Google Scholar support the Dutch hypothesis, showing increased levels of airways responsiveness in COLD patients with more rapid rates of decline in lung function. However, both studies failed to control for the initial level of pulmonary function. The major contribution of the article by Kanner and associates in this issue of Chest (see page 54) is that airways responsiveness remains a predictor of rate of decline in lung function in patients with COLD even when controlled for initial level of lung function. The authors state that they think the increase in responsiveness observed in their patients was simply the result of cigarette smoking, but they do not examine this question. Thus, the origin of the increase in responsiveness and its relationship to atopy and cigarette smoking are not clarified by their investigation. The major problem with all existing longitudinal work published on increased responsiveness is that only subjects who already have COLD have been examined. At best, the Barter and Campbell and Kanner data can identify increased levels of responsiveness as a correlate of disease. At worst, their findings may simply be the result of selection bias. Although it is important to know that those subjects with COLD who have increased levels of airways responsiveness will fare poorly, a far more important question is whether one can identify the causes of increased levels of responsiveness, and its relationship to other putative risk factors, and whether such responsiveness is an independent risk factor for the development of COLD. This is a central question in adult COLD epidemiology at the present time for two reasons. First, if smoking causes increased levels of airways responsiveness, this will provide important insight into the pathogenesis of COLD. Secondly, it may target a group of subjects at high risk in whom therapeutic trials of bronchodilators might be used to attempt to intervene in the disease process. To determine whether increased level of airways responsiveness is a risk factor for COLD, one would have to follow prospectively a large cohort of subjects randomly selected from a community, some of whom smoked and some of whom did not, and assess respiratory symptoms, atopy, airways responsiveness and pulmonary function longitudinally over several years. Whether existing data are currently available with sufficient power to answer this question, or whether new studies carried out over several years will be required, the issue is of enough importance that a variety of methodologic approaches should be considered." @default.
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• W2011013045 title "Increased Levels of Airways Responsiveness as a Risk Factor for Development of Chronic Obstructive Lung Disease" @default.
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