Measurement of bronchial hyperresponsiveness has been suggested to be a useful test in identifying subjects with asthma in epidemiologic groups. We explored the association between the degree of bronchial hyperresponsiveness, respiratory symptoms suggestive of asthma, chronic bronchitis, and various definitions of asthma based upon information obtained from a questionnaire. We determined bronchial hyperresponsiveness by methacholine inhalation test, administered a standardized respiratory questionnaire, and performed spirometry on 1,392 male workers in various industries: 229 (16.5%) had PC20 less than 8 mg/ml, 66 (4.7%) had PC20 less than 2 mg/ml, and 8 (0.6%) had PC20 less than 0.5 mg/ml. Only 760 workers had no respiratory symptoms; no workers with PC20 less than or equal to 0.5 mg/ml, 31.0% of workers with PC20 greater than 0.5 but less than or equal to 2 mg/ml, and 38.0% of workers with PC20 greater than 2 but less than or equal to 8 mg/ml had no chest symptoms. Those reporting wheeze or breathlessness, and especially those with both symptoms, were significantly more likely to have bronchial hyperresponsiveness with a low PC20. The reporting of chest tightness did not influence this relationship, and there was no difference between the occurrence of "wheeze without a cold" and "persistent wheeze." Although there was a stronger association of PC20 less than or equal to 2 mg/ml with asthma than with chronic bronchitis, the association of PC20 greater than 2 and less than or equal to 8 mg/ml was not different with asthma than with chronic bronchitis. Bronchial hyperresponsiveness was more closely associated with asthma than with any asthmalike symptoms ascertained by a questionnaire developed for the study of chronic bronchitis.(ABSTRACT TRUNCATED AT 250 WORDS)
Two hundred twenty-seven workers in a western red cedar sawmill underwent methacholine bronchoprovocation testing at least 2 times during 3 surveys over a 2-yr period. At the first survey, workers completed a respiratory and occupational questionnaire, performed spirometry, gave serum for measurement of plicatic acid-specific IgE antibodies by radioallergosorbent testing, and had skin prick tests to detect atopy. Bronchial hyperresponsiveness was present initially in 18% of the workers. Approximately 15% of those with initially no hyperresponsiveness developed hyperresponsiveness during the follow-up period; 15% of those with initial hyperresponsiveness also lost it during follow-up. Development of hyperresponsiveness tended to coincide with a decrease in level of pulmonary function, whereas loss of hyperresponsiveness was associated with improvement in pulmonary function. Workers with either persistent bronchial hyperresponsiveness or with varying responsiveness had a higher prevalence of plicatic acid IgE antibodies and lower levels of initial pulmonary function than did workers with persistent nonresponsiveness. Workers with persistent hyperresponsiveness had higher initial estimated total airborne dust exposure than did other workers. Age, duration of sawmill employment, atopy, race, and cigarette smoking did not influence the occurrence of hyperresponsiveness. Levels of plicatic-acid-specific IgE antibodies did not change substantially over the 2 yr. These results indicate that immunologic sensitivity to plicatic acid and change in airway caliber are associated with the occurrence of bronchial hyperresponsiveness in cedar workers.
It has been suggested that the development of bronchial hyperresponsiveness (BHR) in some smokers may be an intermediate event in the progression to chronic obstructive pulmonary disease in this group. If this is true, prevalence data on BHR in a general population should show an independent association between BHR and smoking status. To test this, we analyzed BHR to inhaled methacholine in 654 white men without known asthma, in relation to smoking, skin-test reactivity, type of work (office versus industrial), and indicators of baseline airway caliber (FEV1 % predicted and FEV1/FVC). BHR was measured in the traditional way (PC20) and as the slope of FEV1 versus the methacholine concentration (linear scale). A PC20 of less than 16 mg/ml was considered "responsive" for analyses of this outcome. We found that although a positive skin test, smoking, and being an industrial worker all appeared to be significant predictors of increased BHR (p less than 0.05), once FEV1 (% predicted) and FEV1/FVC% were taken into account, none of these variables alone remained significantly associated with BHR. The strongest predictors of BHR were prechallenge FEV1 and FEV1/FVC (both p less than 0.01). The combination of smoking, atopy, and work groups, which identified a small subgroup of atopic smokers who were office workers, also remained significantly associated with increased BHR. We also used a regression model that allowed for comparison of predictors for BHR between the most responsive subset of the population (n = 84) and the remainder of the study population.(ABSTRACT TRUNCATED AT 250 WORDS)