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Wood trimmers are exposed to molds that periodically grow on timber that may induce alveolitis and obstructive lung disease. We have evaluated respiratory symptoms, bronchial reactivity, and lung function in 28 wood trimmers at a Swedish sawmill and in 19 unexposed office workers. Eleven (sero-positive) of the wood trimmers had precipitating antibodies in peripheral blood against one or several molds. The exposure to dust (median 0.26 mg/m3), viable mold spores (median 2950 cfu/m3), viable bacteria (median 370 cfu/m3), airborne endotoxins (range 0.0015-0.0025 microgram/m3), and terpenes (range 0.4-23 mg/m3) was lower than levels that earlier have been reported to affect lung function. The wood trimmers reported an increased prevalence of cough and breathlessness. They also showed signs of a mild obstructive impairment with a tendency to increase bronchial sensitivity to metacholine and decreased FEV1 after 2 days free from exposure. FEV1 decreased more during the working week in the sero-positive workers than among the sero-negative workers, and for the whole group the decrease in FEV1 and MEF25 was correlated to the degree of mold exposure.

Wood trimmers are periodically exposed to mould and may develop extrinsic allergic alveolitis (EAA). To investigate if there were any signs of EAA in wood trimmers with low exposure, 19 non-smoking wood trimmers underwent bronchoalveolar lavage (BAL), spirometry, and measurement of diffusion capacity (TLco). The group was subdivided into those with (n = 9) and without serological antibodies against mould. In 14 workers the TL,0 was measured both at the beginning and at the end of a week at work. Twenty five healthy non-smokers served as BAL controls and 19 healthy non-smokers as lung function controls. The median exposure of total dust was well below the Swedish threshold value, and the exposure of mould and bacteria was also low. The cell concentrations and the proportions of the various alveolar cells did not differ between the groups. The concentrations of the soluble components albumin, fibronectin, and hyaluronan were, however, significantly increased (p < 0.001 for all) in the workers. No difference was found in lung function between the workers and the controls, and the TLco was not impaired during a week at work. The groups of seropositive and seronegative workers did not differ in any of these parameters. The results are interpreted as a low intensity alveolar inflammation. The presence of precipitating antibodies against mould did not predict any greater risk of developing a more intense inflammation. Analysis of soluble non-cellular BAL components seems to reflect a discrete ongoing