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A method has been developed which allows the incubation of alveolar macrophages as weakly affixed monolayers in siliconized glass dishes. Without vigorous mechanical agitation and without using proteolytic enzymes, these cells were subsequently transferred to cuvettes where the zymosan-stimulated chemiluminescence of the suspended cells was measured. In vitro incubations of activated rabbit alveolar macrophage monolayers with airborne dusts from four West German sites (1 to 200 micrograms/10(6) cells), fly ash fractions of a special waste incinerator at Hamburg (50 to 1,000 micrograms/10(6) cells), and quartz dust DQ 12 (5 to 200 micrograms/10(6) cells) resulted in a dose- dependent depression of the zymosan-stimulated chemiluminescence. The depression of chemiluminescence was correlated with particle numbers, estimated dust surface, and antimony and lead masses of the dusts to which the cells were exposed. Cytotoxicity was better correlated with these parameters than with dust mass.

Elastase release from cultured, activated and nonactivated rabbit alveolar macrophages (AM) was investigated after stimulation by different environmentally related mineral dusts (50-1000 micrograms/10(6) cells). Eight different dusts were analyzed for element contents and grain size: one rural and three urban airborne dusts, a coarse and a fine fraction of a sieved waste incinerator fly ash, a sonicated coarse fly ash fraction, and the standard quartz dust DQ 12. The fine fly ash fraction, the sonicated coarse fly ash fraction, and the quartz dust DQ 12 enhanced elastase release by activated AM. Only one of the tested airborne dusts effected a comparable elastase release. The untreated coarse fraction of the fly ash did not cause a significant increase of extracellular elastase activities. Elastase release was dependent on particle numbers and chemical composition and correlated best with barium and tin contents. Nonactivated AM released higher elastase activities than activated AM at low-dose levels. The possible role of dust-induced elastase secretion in the pathogenesis of emphysema is discussed.