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Biomedical subjects

S A Olenchock

Publications and source records attributed to S A Olenchock.

77 records · Page 5Linked to original sources
PubMed1976

The role of precipitins and complement activation in the etiology of allergic lung disease.

An experimental model of allergic lung disease has been described that is monitored by analysis of arterial oxygen tension following aerosol challenge with antigen. Rabbits immunized to a classical soluble antigen, human serum albumin (HSA), to the point where severe Arthus skin reactivity was demonstrable, were aerosol-challenged with antigen. Arterial oxygen tension measurements made on pre- and post-challenge samples yielded early, late, and continuous response patterns, reminiscent of those obtained in humans following provocation testing. Aerosol challenge of unimmunized animals with HSA resulted in no change from baseline conditions. Unimmunized rabbits exposed to small and massive (10X) aerosols of Aspergillus spores also demonstrated various postchallenge depressions in arterial oxygen tension as well as decreased levels in hemolytic complement activity, depending on the species of fungus and dose of spores used. Unimmunized animals pretreated with cobra venom factor in a manner known to achieve complement depletion failed to respond with altered arterial oxygen tensions following similar aerosol challenge. It is postulated that although precipitins may play a role in artificial disease initiated by soluble antigens, nonspecific complement activation may be more important in understanding the etiology of spontaneous disease in humans brought about by inhalation of moldy particulate matter.

Administration, Intranasal↗
PubMedDate not supplied

Acute experimental pulmonary responses to cardroom cotton dust.

Laboratory rabbits were exposed for 60 min to aerosols of dry cardroom cotton dust 4 days/wk (Tuesday through Friday) for 15 consecutive weeks. As a parameter of pulmonary pathophysiology, arterial blood gases were monitored with time after challenge. Post-exposure blood gas analyses at 1 hr showed progressive decreases in arterial oxygen tension, with concommitant increases in arterial carbon dioxide tension and the alveolar-arterial oxygen gradient. These responses appeared to result from acute reversible airway obstruction which caused unequal gas distribution and ventilation-perfusion inequalities. When a group of proven responder rabbits was challenged with cardroom cotton dust which was first treated in a manner which paralleled the preparation of medical grade cotton, only minor decreases in arterial oxygen tension were observed. The data suggest that some, as yet undefined, agent(s) which was removed by the treatment was responsible for inciting the observed pathophysiology.

Animals↗
PubMedDate not supplied

Aflatoxin in respirable corn dust particles.

Samples of airborne grain dust representing a variety of grains were examined for the presence of aflatoxins. Although aflatoxins could not be detected in most of the samples, one corn sample contained 130 ppb aflatoxin B1. When the components of this sample were separated according to aerodynamic diameter and analyzed for aflatoxins, it was found that particles with diameters 7-11 micrometers and less than 7 micrometers had much higher levels of aflatoxins than the sample as a whole. These findings suggest that measurements of aflatoxin in whole corn might underestimate aflatoxin levels in corn dust aerosols.

Aflatoxins↗
PubMedDate not supplied

Immunological studies of grain dust.

Epidemiological investigations of grain workers have suggested the presence of biological hazards in terminal grain elevators. Immunological assessments of the involved individuals, however, have produced inconclusive results. We have recently demonstrated in vitro a potential biological mechanism which could occur in vivo upon inhaling airborne graon dust, thereby constituting a potential inflammatory insult to the respiratory tracts of grain workers. Airborne dusts of similar size distributions generated by transporting grain in terminal grain elevators have been shown to activate the alternative pathway of complement in precipitin-negative pooled normal human serum. These dusts consumed hemolytic complement in a dose-response manner as quantified by both CH100 immunodiffusion and CH50 tube methods. The proactivator of C3 was converted to the activator form in the presence of the chelator EGTA, but conversion was prevented by EDTA. Likewise, serum from guinea pigs genetically deficient in C4, thereby lacking a functional classical complement pathway, showed complement consumption by grain dusts via the alternative pathway. Relative CH50 toxicity ranking of the various dusts was found to be unrelated to the amount of endotoxin present. Of interest, aged settled dust (20-30 years) remained relatively active against the alternative complement pathway as did 15 min aqueous extracts of ground whole rye.

Air Pollutants, Occupational↗