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.