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Director of Thoracic Medicine, The Royal Melbourne Hospital, and Professorial Associate in Medicine, The University of Melbourne.
Correspondence to: Michael C. Pain, MD, FCCP, Thoracic Medicine, Royal Melbourne Hospital, Grattan Street, Parkville Victoria 3050, Australia
Chronic airway disease is a major cost to the community and, as a matter of some urgency, the causes of this group of conditions need to be defined. Most physicians would be able to point to a multifactorial situation with airway inflammation, loss of pulmonary elastic supporting tissue, bronchial muscular dysfunction, and accumulation of secretions due to mucociliary impairment all having the potential to explain the pathogenesis. The further superimposition of variables such as the hypoxic polycythemic response, central sensitivity to carbon dioxide, and hypoxic pulmonary vasoconstriction add to the spectrum of clinical syndromes. As to the reason why an individual develops chronic airway disease, current thinking would suggest that this is the tobacco-smoking-induced illness par excellence. Yet, this is too simplistic. All physicians will have seen elderly patients with impeccable pulmonary function who have been heavy cigarette smokers for their entire adult lives and, perhaps more unusually, lifetime nonsmokers with chronic airflow disease. Early studies examining tobacco smoking and ventilatory capacity suggested that there was more to it than simply the amount of tobacco consumed, and the operation of some other risk factor was suggested.1 About 25% of male cigarette smokers proceed to develop significant airway abnormality2 and the role of nonspecific bronchial reactivity in defining this subgroup at special risk has been examined but remains inconclusive.3 ,4 Variation between individuals in the efficiency of protective mechanisms such as the antielastase systems may also be a factor determining the likelihood for emphysema.
Epidemiological studies can contribute to an unraveling of etiological factors, provided that sufficiently heterogeneous populations can be studied. It is sobering to realize that if cigarette smoking were a universal habit, recognition of the role it plays in the incidence of lung cancer would have been long delayed. To quote Geoffrey Rose, "the cause that is universally present has no influence at all on the distribution of disease, and it may be quite unfindable by the traditional methods of clinical impression and case-control and cohort studies; for all of these depend on heterogeneity of exposure.5
With this background, the article by Berglund and colleagues in this issue of CHEST (see page 49) is of considerable interest. The group from Loma Linda University has had the opportunity to study over 1,300 subjects as part of the Adventist Health Study of Smog. These subjects were a geographically stable, nonsmoking population whose general exposure to particulate air pollution was reasonably documented over 20 years. Respiratory-orientated questionnaires were completed on four occasions over 16 years. At the end of the observational period, spirometry with bronchodilator reversibility was performed in 98% of subjects. Categorization into diagnostic subgroups (asthma, chronic bronchitis, emphysema) was based on patient-reported symptoms and a history of diagnosis by a physician. The study was designed to weigh the importance of factors other than direct cigarette smoking in the genesis of chronic airway disease.
What were the findings? Significant airflow obstruction was demonstrated in 10.6% and chronic airway disease in 15% of the population. The prevalence was higher in males and increased with advancing age, past smoking history, parental airway disease, environmental tobacco smoke exposure, and a history of childhood respiratory illness. Interestingly, ambient dust exposure was a barely significant risk factor in males only. An earlier study from this group6 in a larger cohort of similar subjects and using estimates of levels of mean particle size of < 10 mg indirect (PM10) from total suspended particulate measurements suggested a relative risk of 1.17 for developing symptoms of airway obstruction if ambient PM10 levels exceeded 100 µg/m3 for 1,000 h/yr.
Comparing the spirometric data with symptoms reported with the questionnaire established some important points. Spirometric airflow obstruction (FEV1/vital capacity < 65%) was present in 7.5% of asymptomatic subjects. Subjects with definite symptoms showed obstructive spirometry in 25% of cases, although chronic cough alone (unlike cough with sputum) was not significantly associated with airflow obstruction. Patients considered to have asthma on the questionnaire reassuringly showed greater acute reversibility on spirometry.
Does this study have clinical messages? It confirms previous findings, which indicate that respiratory illness in early life is a determinant of airway disease in adulthood. It suggests that tobacco smoke, even in nonsmokers, appears as a risk factor in terms of past smoking and environmental tobacco smoke exposure. Ambient dust exposure (in contrast to occupational exposure)7 ,8 seems of minor importance, highlighting the need for further studies on the role of fine particulate inhalation in producing increased general mortality.9 ,10 In terms of the possible use of questionnaires to screen adult populations considered at risk of developing significant chronic airway disease, it suggests that productive cough and breathlessness are robust but late markers and that an asymptomatic population will still require objective testing for detection. Finally, the study emphasizes the large amount of subject cooperation, data collection, and collaborative multidisciplinary skill required in respiratory epidemiology.
References
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