Investigation of the cytotoxic and proinflammatory effects of cement dusts in rat alveolar macrophages.

Exposure to cement dust, a specifically alkaline and irritant dust, is one of the most common occupational dust exposures worldwide. Although several adverse respiratory health effects have been associated with cement dust exposure, the evidence is not conclusive. In the current study, cytotoxic and pro-inflammatory effects as well as oxidative stress elicited by a number of cement dusts, including a limestone and cement clinker sample, were tested using the NR8383 rat alveolar macrophage cell line and primary rat alveolar macrophages. DQ12 quartz and TiO(2) were included as positive and negative controls, respectively. Cytotoxicity was determined by the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazoliumbromide assay and the lactate dehydrogenase assay, oxidative stress was determined by measurement of the depletion of total cellular glutathione, and electron spin resonance was applied to determine reactive oxygen species (ROS) generation. The release of the cytokines tumor necrosis factor-alpha (TNFalpha), interleukin-1 beta (IL-1 beta), and macrophage inflammatory protein-2 (MIP-2) was determined by enzyme-linked immunosorbent assay. None of the dust samples were found to cause toxicity to the macrophages or notable glutathione depletion when compared to DQ12. The cement samples also failed to activate macrophages for the generation of ROS and the production of inflammatory cytokines IL-1 beta and MIP-2. In contrast, however, most of the cement dusts were found to activate macrophage TNFalpha production, and this was significantly associated with their content of CaO. Further research is needed to determine the relevance of these in vitro observations for occupational cement dust exposure settings.