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Biomedical subjects

J C Mull

Publications and source records attributed to J C Mull.

26 records · Page 2Linked to original sources

A brief report of gram-negative bacterial endotoxin levels in airborne and settled dusts in animal confinement buildings.

Gram-negative bacterial endotoxins, implicated in adverse worker health responses, were found in settled and airborne dust samples obtained from poultry and swine confinement units. Results of the Limulus amebocyte lysate gel test found endotoxin levels in dust samples ranged from 4.5 to 47.7 micrograms of FDA Klebsiella endotoxin equivalents/gm. Differences in endotoxin levels between dust samples may have been due to variables in time, geographic locations, confined animals, confinement buildings and equipment, and methods of sample collection. Animal confinement workers are potentially exposed to large amounts of gram-negative bacterial endotoxins; however, the respiratory health effects of such exposures to animal confinement workers have yet to be determined.

Agricultural Workers' Diseases↗

Complement activation by commercial allergen extracts of cereal grains.

Commercial allergen extract preparations of whole cereal grains were examined in vitro for their reactivity with the human haemolytic complement cascade. Total haemolytic complement was consumed in a dose-dependent manner which did not correlate with the protein nitrogen content or bacterial endotoxin contamination of the extracts. Alternative pathway activation was shown by C3 conversion in the presence of EGTA while classical complement components C1, C4 and C2 were also much decreased in serum which was free of detectable specific antibody. Very small amounts of allergen extract initiated the formation of complement-dependent factors which were chemotactic for human polymorphonuclear leucocytes. These data suggest a potential for complement activation in vivo by ingestion, inhalation, or injection of cereal grain products.

Allergens↗

Extracts of airborne grain dusts activate alternative and classical complement pathways.

This study investigated the action of aqueous extracts of airborne grain dusts on the human alternative and classical complement pathways. Extracts were shown to consume hemolytic complement in vitro in a dose-dependent manner. No relationship was determined between complement activity ranking and either protein or endotoxin levels. Differential serum chelation with EDTA or EGTA showed that the alternative pathways were activated, while hemolytic titers of the early complement components (C1, C4, C2 and C3) showed that the classical pathway was also involved. Extract-treated sera were chemotactic for human polymorphonuclear leukocytes and complement was required. The in vitro data suggest the potential for the in vivo contribution of the activation of the complement cascade (by either pathway) in eliciting pulmonary pathophysiology after the inhalation of airborne grain dusts.

Chelating Agents↗

In vitro activation of the alternative pathway of complement by settled grain dust.

Settled grain dust was collected from several active grain elevators in the Superior-Duluth areas of the United States. Particle size distribution (47% less than 5 micrometer) and endotoxin contamination (429 ng/gm) of the dust were similar to those reported for the airborne parent dust. Human complement uas activated in vitro in a dose-response manner which could be quantified. This hemolytic consumption was via the alternative pathway as defined by ethylenediaminetertraacetic acid/ethylene-glycol-bis-(beta-amino-ethyl ether) N,N'-tetraacetic acid (EDTA/EGTA) differential serum chelation, factor B conversion, and complement reductions in serum from guinea pigs deficient in C4. It is proposed that continuous low-dose exposure to aerosolized, biologically active rafter dust could contribute to the respiratory insult of grain workers.

Complement Activation↗

Activation of the alternative pathway of complement by grain. I. C3PA conversion and quantification of complement consumption by rye.

Ground whole rye and airborne rye dust of comparable size distribution were tested for their ability to activate the complement cascade via the alternative pathway. Precipitin-negative pooled normal human serum was incubated with increasing amounts of the two rye dusts. Electrophoresis of the resultant supernatant fluids demonstrated the conversion of the proactivator of the third component of complement to the gamma-migrating activator of the third component. This activation was completely prevented by pre-treating the serum with the chelator EDTA, while pre-treatment with EGTA allowed suboptimal arc conversion, strongly implying that complement was activated via the alternative pathway. Quantification of the supernanant fluids showed dose-dependent complement consumption as defined by both CH100 immunodiffusion and CH50 tube haemolytic techniques. Airborne rye dust showed a greater quantitative potential than ground whole rye for activating the alternative pathway. These results indicate the possibility of the direct action of airborne organic dusts on the induction of inflammatory sequelae in the lungs of both sensitized and unsensitized individuals.

Air Pollutants↗

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↗