Effects of Coal Dust on the Development of Acute and Chronic Infections in the Respiratory Tract.
An adverse effect of mineral particles on the viral induction of interferon, an important nonimmunological defense entity capable of mediating cell resistance against respiratory infections, was observed. Assays of virus infectivity and interferon potency were developed. Cell monolayers were treated with coal dust (of different ranks and different sources), or asbestos fibers of serpentine (Rhodesian and Canadian chrysotiles) (12001295) and amphibole (1318098) (amosite (12172735), anthophyllite (17068789), crocidolite (12001284)) varieties, and the effect was partial or complete interferon synthesis depression. The decrease in interferon production was related to a decrease in mineral particle size. The adverse effect of these particles on interferon production resulted in higher levels of influenza virus multiplication. Pretreating cell monolayers, coal dust, or asbestos fibers with a nonionic polymer, poly(4-vinylpyridine-N-oxide) (PVPNO) (NOCAS), produced marked reductions in the depressive activity of dust or fiber on interferon induction. Maximal adverse activity of the polymer was time and concentration dependent. The pretreatment of asbestos fibers with polymer was more rapid and effective than the pretreatment of cell monolayers. The enzyme neuraminidase is thought to cause the antagonistic activity of asbestos fibers or cell monolayers on interferon production to be partially negated. It is suggested that sialic acid, which is cleaved by the enzyme from mucroproteins, may be the principal anionic material with which magnesium containing forms of asbestos react with cells to depress interferon production.
Air-contamination; Aerosols; Dusts; Pulmonary-system-disorders; Polymers; Minerals; Lung-disorders; Particulates; Enzymes; Pyridines;
12001-29-5; 1318-09-8; 12172-73-5; 17068-78-9; 12001-28-4;
Appalachian Laboratory for Occupational Safety and Health, NIOSH, Morgantown, West Virginia