Acute inflammatory reaction in rats after intratracheal instillation of material collected from a nylon flocking plant

Several cases of interstitial lung disease have been diagnosed among worker s at a nylon flock plant, but the etiologic agent for the disease outbreak was unknown. The results of a medical survey and industrial hygiene study i ndicated that the dust present in the plant may be responsible. Thus, airbo rne dust collected at the plant was examined for its inflammatory potential in rat lungs. The endpoints measured were: (1) breathing rates, (2) differ ential cell counts of bronchoalveolar lavage cells, (3) alveolar macrophage (AM) chemiluminescence, (4) albumin concentration and matrix metalloprotea se activities in the acellular fluid from the initial bronchoalveolar lavag e, and (5) pulmonary histopathology. In the first study, rats received a si ngle dose of the airborne dust sample (10 mg/kg body weight) by intratrache al (IT) instillation. Al 1 d post-IT, all inflammatory endpoints were signi ficantly increased versus controls, but by 29 d post-IT they did not differ significantly from controls. Histopathology demonstrated mild to moderate, multifocal, suppurative pneumonia, usually centered around bronchioles, at 1 d post-IT. At 29 d post-IT, pulmonary inflammation was minimal to mild a nd characterized by alveolar histocytosis usually restricted to the immedia te area of retained birefringent fibers. In subsequent experiments, airborn e dust was extracted with water and the dust (washed airborne dust) and wat er extract (soluble fraction) were separated by centrifugation for further study. Nylon tow dust was prepared in the laboratory by milling uncut nylon strands (called tow) that had not been treated with the finish or dyes tha t are commonly used in the flock plants. Rats were administered a single do se of a dust sample (10 mg/kg body weight) or the soluble fraction (1.3 ml/ kg body weight) by IT administration and the same endpoints were measured a t 1 d post-IT. The dust samples caused significant increases in all of the inflammatory endpoints; however, the soluble fraction was much less active. Histological analysis of the lungs 1 d post-IT confirmed lung inflammation was occurring and tended to center around bronchioles. The results suggest that: (1) nylon flocking generates particles of respirable size that can i nteract with AM in the lung and fan be detected in the lung 29 d after expo sure, (2) the dust samples examined cause an inflammatory response, (3) wat er-extractable agent(s) from airborne dust contribute only minimally to the inflammatory response, and (4) the acute inflammatory response to these du sts is substantial when compared to other pathologic occupational dusts pre viously examined in our laboratory.