Pulmonary toxicity of an atmospheric particulate sample is due to the soluble fraction.

Adverse health effects have been associated with the inhalation of a variety of atmospheric particles. The potential toxicity of a recently collected urban air particulate sample (EHC-93, mean diameter < 1 microm) was assessed after instilling 1 mg to mouse lung. A soluble fraction (15% of total) and an insoluble fraction of the original dust were also instilled at 1 and 0.15 mg doses and the lung reaction was followed for up to 8 weeks. The complete dust sample induced an inflammatory response in the first week with increased cell numbers and protein levels in lavage fluid. There was also ultrastructural evidence of epithelial necrosis followed by increased thymidine labeling during repair. The insoluble fraction induced only mild inflammation with no evidence of cell injury or repair at either dose. The soluble fraction produced similar early inflammatory changes but also produced the greatest lung injury. Type 1 cell necrosis was observed, followed by increased tritiated thymidine uptake mainly by Type 2 epithelial cells. This was found after 0.15 mg soluble fraction and was greatly increased in the 1.0 mg group, which subsequently developed fibrosis. The results indicate that while all particle samples induce some inflammation, the lung toxicity produced by the total dust sample EHC-93 can be accounted for by the reaction to its 15% soluble component. This suggests that the pulmonary response and cell injury following exposure to this urban dust is related to soluble material, probably metal ions, rather than to the number or composition of the insoluble particles.