The concentrations of total and respirable airborne endotoxin in the breathing zone of a pony in 3 different management systems, on 8 occasions, are reported. Airborne endotoxin concentrations in all 3 systems were lower than those reported for many other agricultural environments. However, total airborne endotoxin concentrations in many of the conventional stables exceeded those which can induce puImonary inflammation and bronchial hyper-responsiveness in normal human subjects, and exceeded those which can induce bronchoconstriction in humans with pre-existing pulmonary inflammation. Therefore, airborne endotoxin may contribute to the development of airway inflammation and dysfunction in conventionally stabled horses. Potentially detrimental effects of airborne endotoxins on the welfare and exercise performance of stabled horses can be reduced by maintaining horses in 'low dust' stables or at pasture, since these environments had significantly lower airborne dust and endotoxin concentrations.
Most authors consider that long-term inhalation studies represent the most reliable method of obtaining data on the pathogenicity of mineral fibers. However, because of the length of time required and the great cost of inhalation work, other methods of examining the biological effects of mineral fibers have been used. The program of work described here was designed to compare a wide range of techniques, including inhalation, for determining the biological effects of a selection of man-made mineral fibers. Silicon carbide whiskers were examined as a very durable material and also a less durable glass microfiber (code 100/475/ as a relatively soluble man-made vitreous fiber. Amosite asbestos was used as a positive control. long-term inhalation studies with full-life-span follow-up demonstrated that amosite and silicon carbide were both fibrogenic and carcinogenic in rats, while glass microfiber produced very little fibrosis and a few benign pulmonary tumors in numbers similar to those found in controls. Silicon carbide was unusual in that most of the tumors produced were pleural mesotheliomas. Early effects of the fibers were examined after a short period of inhalation, and the pathogenic dusts amosite and silicon carbide were found to produce rapid pulmonary inflammation as determined by the presence of significant numbers of neutrophils in pulmonary lavage fluid. Less pulmonary inflammation followed the inhalation of glass microfiber. Similarly, amosite and silicon carbide inhalation was found to cause a rapid increase in the rate of proliferation of bronchoalveolar lining cells, while the rate of cell division in animals treated with microfiber remained normal. When injected into the peritoneal cavities of rats, all three fiber types produced mesothe liomas, although the glass microfiber produced many fewer and these took much longer to develop. An examination of early inflammation in the peritoneal cavity of mice following injection showed little difference between the fiber types, all of which caused raised numbers of neutrophils in peritoneal fluid. fiber durability was examined both in vivo and in vitro. Following inhalation it was found that fewer very long glass microfibers (>20 pm in length) remained in rats lungs after 12 mo of inhalation than amosite or silicon carbide.Subsequently, however, amosite and microfiber were removed from the lung at similar rates for most fiber dimensions, in contrast to silicon carbide fibers, where clearance was much less. When dust was administered by intratracheal injection, these differences in fiber removal from lung tissue were much less marked. An examination of the in vitro solubility of fibers and their chemical composition after extraction from lung tissue demonstrated that glass microfiber showed significant leaching while amosite showed much less and silicon carbide showed almost no change in chemical composition. The possibility of using short-term in vivo and in vitro tests to provide a screening system to eliminate the need for some of the longer and more expe...
In this article the volumetric overload hypothesis, which predicts the impairment of clearance of particles deposited in the lung in terms of particle volume, is reevaluated. The degree to which simple expressions of retained lung burden explain pulmonary responses to overload was investigated using data from a series of chronic inhalation experiments on rats with two poorly soluble dusts, titanium dioxide and barium sulfate. The results indicated that the difference between the dusts in the level of inflammation and translocation to the lymph nodes could be explained most simply when the lung burden was expressed as total particle surface area. The shape of the statistical relationship for both lung responses indicated the presence of a threshold at approximately 200-300 cm(2) of lung burden. On the basis of this and other similar results, a hypothesis regarding a generic mechanism for the impairment of clearance and associated lung responses is proposed for such "low-toxicity" dusts.
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