title: Heating of indoor dust causes reduction in its ability to stimulate release of IL-8 and TNFalpha in vitro compared to non-heated dust.
abstract: Dust is a major contaminant of the indoor air environment and may affect human health. Indoor dust accumulates on surfaces including heaters and light fixtures, and will be heated when these devices are used. Heat treatment of the dust may change its biologic properties and in this study we simulated the heat treatment with a dust-heating model (50-250 degrees C). The residual and the non-heated dust from seven samples were tested in cultures of fresh peripheral blood mononuclear cells and in A549 cell culture using the release of TNFalpha and IL-8, respectively, as effect indicators. The endotoxin-content and the particle size distribution of the residual and the non-heated dust suspensions were determined for some of the samples. We found that the residual dust had less ability to induce the release of TNFalpha and IL-8. The cytokine decline pattern was similar for all the dust tested and could partly be explained by the reduction in endotoxin content or possibly by inhibitory decomposition products. No correlation was found between the measured particle size distribution and the decreased cytokine levels. The results in this study suggest that the residual dust promotes reduced cytokine response and thereby a possibly lower inflammation reaction in the airways if suspended and inhaled compared with the non-heated dust.
  
  
  CONCLUSIONS
  Accumulation of indoor dust on electric heaters and light fixtures may produce a bad odor when switched on in the cold season and some people claim respiratory distress during such events. To investigate to what extent the residuals of heated indoor dust represent a health hazard, we measured the effect in cell cultures before and after heat treatment of the dust. The in vitro results imply that the residual dust will cause a lower proinflammatory response in the airways if suspended and inhaled compared with non-heated dust. This is partly explained by heat destruction of inflammatory components in the dust.
authors.affiliation: Department of Neuroscience, Norwegian University of Science and Technology, Trondheim, Norway.
authors.forename: M
authors.initials: M
authors.lastname: Mathiesen
authors.forename: E K
authors.initials: EK
authors.lastname: Pedersen
authors.forename: O
authors.initials: O
authors.lastname: Bjørseth
authors.forename: K W
authors.initials: KW
authors.lastname: Egeberg
authors.forename: T
authors.initials: T
authors.lastname: Syversen
mesh_terms: D000393:Air Pollutants; D016902:Air Pollution, Indoor / Q000009:adverse effects; D004391:Dust; D004847:Epithelial Cells / Q000187:drug effects / Q000276:immunology; D005434:Flow Cytometry; D006358:Hot Temperature; D006801:Humans; D016209:Interleukin-8 / Q000096:biosynthesis* / Q000276:immunology; D007963:Leukocytes, Mononuclear / Q000187:drug effects / Q000276:immunology; D008168:Lung / Q000187:drug effects / Q000276:immunology*; D014409:Tumor Necrosis Factor-alpha / Q000096:biosynthesis* / Q000276:immunology
chemical_list: D000393:Air Pollutants; D004391:Dust; D016209:Interleukin-8; D014409:Tumor Necrosis Factor-alpha