Signs of alveolar inflammation in non-smoking Swedish wood trimmers.

Abstract

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

Evaluation of exposure–response relationships for health effects of microbial bioaerosols – A systematic review

“…On the basis of eight studies from the work place wood processing with different effect endpoints no studies for the derivation of exposure limits could be identified mainly due to insufficient exposure data (V1) (Avila and Lacey, 1974;Dahlqvist et al, 1992;Dahlqvist and Ulfvarson, 1994;Johard et al, 1992;Mandryk et al, 1999Mandryk et al, , 2000Schlünssen et al, 2011), no evaluation of dust measurements (V2) (Avila and Lacey, 1974;Dahlqvist et al, 1992) and inconsistent results of statistical analyses (V3) (Mandryk et al, 1999(Mandryk et al, , 2000. Mandryk et al analyzed correlations (Pearson's R) among mean personal exposures.…”

“…Reference 1 2 3 4 5 6 7 8 Avila and Lacey (1974) NV NV (-) NV (-) (-) (-) (-) Johard et al (1992) NV (-) (-) (-) (-) NV (-) (-) Dahlqvist et al (1992) NV NV (-) (-) (-) NV (-) (-) Dahlqvist and Ulfvarson (1994) Roponen et al (2003) NV NV (-) (-) NV NV (-) (-) NV, not valid; V, valid; (-), not assigned. measurement methods for endotoxins and ␤-glucans are not standardized for environmental settings to date these studies were excluded.…”

Terpene exposure and respiratory effects among workers in Swedish joinery shops

“…The occupational exposure limit in Sweden at present is 150 mg/m3 for both total and individual monoterpenes (3, and in sawmills the exposure often exceeds this limit (1,(6)(7). Sawmill workers exposed to monoterpenes and wood dust have been shown to respond with airway symptoms, a decrease in lung function, and airway inflammation, the last-mentioned being reflected by bronchoalveolar lavage (BAL) results (6)(7)(8)(9)(10)(11). After the reduction of sawing fumes in a Swedish sawmill, an 8-year follow-up study was expected to show relative improvement in lung function among the employees working in the saw shed (12).…”

Lung fibrosis and exposure to wood dusts: Two cases report and review of the literature

“…Research studies have pointed out that acute exposure to WDs is associated with an increased blood count of eosinophils whereas bronchoalveolar lavage (BAL) and nasal lavage (NAL) show an increased cellularity, predominantly neutrophils and T cell lymphocytes, with increased expression of inflammatory mediators [29][30][31][32]. At alveolar level, WDs are also able to elicit an intense inflammatory reaction, with highSelected axial slices through the lower lung fields (a-c) show diffuse peripheral reticular opacities in a pattern of distinctive and diffuse honeycombing.…”