title: Fungal spores as such do not cause nasal inflammation in mold exposure.
abstract: The increased frequency of respiratory symptoms and diseases among sawmill workers has been linked to occupational exposure to airborne contaminants, especially to different fungi. Similar adverse health effects, together with elevated levels of inflammatory mediators in the nasal lavage (NAL) fluid, have been detected in people working in mold-damaged buildings. However, the indoor fungal spore concentrations in moldy houses are much lower than those in sawmills. To study the effect of fungal spores as such on the inflammatory markers in the NAL fluid, we conducted a similar study in sawmill workers who had an intense exposure to fungal spores. NAL was performed in 11 sawmill workers both during high occupational microbial exposure and during their vacation. Concentrations of nitric oxide (NO), tumor necrosis factor-alpha (TNFalpha), interleukin (IL)-4, IL-5, and IL-6 in NAL fluid were analyzed, and occupational exposure to inhalable dust, fungal spores, endotoxins and terpenes was confirmed by personal monitoring during the day of sampling. In addition, health data were collected with a questionnaire. Personal exposures to fungal spores varied from 2 x 10(5) spores/m(3) to 1.5 x 10(6) spores/m(3) (mean 7 x 10(5) spores/m(3)). Concentrations of inhalable dust, endotoxins, and terpenes were relatively low. There were no differences between work and vacation in the concentrations of NO and proinflammatory cytokines in NAL fluid or in the reporting of symptoms, and the levels were lower than in workers at a moldy school building. However, the concentration of TNFalpha in the NAL fluid was positively correlated with the concentration of terpenes in the working environment (r =.768; p =.006). These results show that microbial exposure as such does not invariably result in inflammatory changes detectable with the NAL method. We suggest that the type of microbial flora or microbial products in the occupational environment determines the proinflammatory potency of microbial exposure.
authors.affiliation: Laboratory of Toxicology, National Public Health Institute, PO Box 95, FIN-70701 Kuopio, Finland. Marjut.Roponen@ktl.fi
authors.forename: Marjut
authors.initials: M
authors.lastname: Roponen
authors.forename: M
authors.initials: M
authors.lastname: Seuri
authors.forename: A
authors.initials: A
authors.lastname: Nevalainen
authors.forename: M-R
authors.initials: MR
authors.lastname: Hirvonen
mesh_terms: D000328:Adult; D016902:Air Pollution, Indoor; D004391:Dust; D005658:Fungi / Q000276:immunology*; D006801:Humans; D007249:Inflammation / Q000473:pathology*; D019570:Inhalation Exposure; D008297:Male; D008875:Middle Aged; D009296:Nasal Cavity / Q000276:immunology / Q000473:pathology; D016273:Occupational Exposure; D011998:Recreation; D013170:Spores / Q000276:immunology
chemical_list: D004391:Dust