Effects of chronic organic dust exposure on respiratory function and airway responsiveness in peat moss factory workers.

Fifty-two males and 1 female, who were 19 to 62 y of age (median = 26), were employed at an eastern Quebec peat moss plant and were included in this study. Of these 53 workers, 29 were smokers, 5 were ex-smokers, and 19 had never smoked. The workers were divided by level of exposure into 4 groups: (1) group 1--minimal exposure (N = 7); (2) group 2--light exposure (N = 7); (3) group 3--moderate exposure (N = 17); and (4) group 4--heavy exposure (N = 22). Chest radiographs and physical examinations were normal for all subjects. Only 1 subject had precipitins to Penicillium and Monocillium species isolated from the peat moss plant. Pulmonary function tests were normal and similar in all groups. Thirty-three subjects (20 smokers, 4 ex-smokers, and 9 nonsmokers) had chronic bronchitis; these symptoms were related to work exposure for 28 subjects. Bronchial responsiveness to methacholine was measured in 14 subjects who had persistent cough and sputum. No subject had evidence of airway hyper-responsiveness, i.e., PC20 metacholine less than 8 mg/ml. We concluded that the peat moss workers in our study showed no evidence of extrinsic allergic alveolitis; however, chronic exposure to organic dust leads to chronic cough and sputum production, which is not associated with significant lung impairment nor increase in nonspecific airway responsiveness.

Sequential bronchoalveolar lavage in experimental extrinsic allergic alveolitis. The influence of cigarette smoking.

We studied the alterations induced by acute experimental extrinsic allergic alveolitis (EAA) on bronchoalveolar cell population in smoking and nonsmoking guinea pigs. Sixty-two animals divided into 3 groups were studied: Group 1 (17 animals), controls; Group 2 (21 animals), extrinsic alveolitis; Group 3 (24 animals), cigarette smoking and alveolitis. Bronchoalveolar lavages (BAL) were performed on Days 1, 19, and 44 for all animals. Group 3 animals had a fourth lavage before starting cigarette smoking, that is, 28 days before the beginning of the antigen injections. The other lavages were as for the other groups. BAL results on Day 1 were similar for each group. Cigarette smoking per se did not modify BAL in Group 3. EAA induction resulted in a large increase in all BAL cells, especially neutrophils of recovered fluid, which increased from 38 x 10(3) to 1,474 x 10(3) ml-1 (p less than 0.01) in Group 2 and from 58 x 10(3) to 740 x 10(3) in Group 3 (p less than 0.01). After maintenance, BAL neutrophils.ml-1 decreased to 444 x 10(3) in Group 2 (p less than 0.01), but stayed the same in Group 3: 973 x 10(3). After EAA induction, BAL neutrophils.ml-1 were higher in Group 2 than in Group 3 (p = 0.039); however, Group 2 had less neutrophils.ml-1 than Group 3 (p = 0.035) after EAA maintenance. We conclude that EAA results in a neutrophilic alveolitis and which can be evaluated by sequential BAL, and that cigarette smoking decreases the initial neutrophilic response and retards the eventual recovery during maintenance injections.