By National Research Council, Board on Environmental Studies and Toxicology, Committee on Toxicology, Committee on Acute Exposure Guideline Levels
This booklet is the 6th quantity within the sequence Acute publicity guide degrees for Selected Airborne Chemicals, and comprises AEGLs for chemical substances resembling ammonia, nickel carbonyl and phosphine, between others.
At the request of the dept of security, the nationwide learn Council has reviewed the proper clinical literature compiled by means of knowledgeable panel and confirmed Acute publicity guide degrees (AEGLs) for 12 new chemical compounds. AEGLs characterize publicity degrees less than which hostile future health results aren't prone to ensue and are necessary in responding to emergencies reminiscent of unintentional or intentional chemical releases locally, the place of work, transportation, the army, and for the remediation of infected sites.
Three AEGLs are licensed for every chemical, representing publicity degrees that lead to: 1) extraordinary yet reversible ache; 2) long-lasting overall healthiness results; and three) life-threatening overall healthiness impacts.
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Extra info for Acute Exposure Guideline Levels for Selected Airborne Chemicals: Volume 6
1. Metabolism and Disposition No information was located regarding allylamine metabolism after inhalation exposure, but some animal toxicokinetic data were found for oral and intravenous administration. In a toxicokinetics study conducted by Boor (1985), allylamine was absorbed by male Sprague-Dawley rats within minutes of gavage administration of 150 mg/kg radiolabeled allylamine. Radioactivity was found in numerous organs, the greatest amount being in the aorta and coronary arteries, where levels were about 5- to 10-fold greater than in most other organs, including the myocardium.
Consistent with this, the benzylamine oxidase inhibitor, semicarbazide, protected myocytes from toxic effects of allylamine in vitro, whereas the monoamine oxidase inhibitors clorgyline and pargyline were ineffective (Ramos et al. 1988). Copyright © National Academy of Sciences. All rights reserved. 2. Mechanism of Toxicity Allylamine has been shown to cause severe myocardial damage and vascular smooth muscle lesions in a variety of animal species upon acute exposure (Boor and Hysmith 1987). It has been used to cause lesions (proliferation of smooth muscle cells and fibrosis) that mimic human atherosclerosis by the oral, parenteral, inhalation, and intravenous routes (Boor et al.
Concentration of allylamine causing a 50% decrease in the breathing rate; Gagnaire et al. 1989) of male OF1 Swiss mice was determined to be 9 ppm in two oronasal exposure studies. In one study, exposure was for a total of 15 min to 3-12 ppm (Gagnaire et al. 3 ppm (Gagnaire et al. 1993). Mice were exposed by enclosing the head in a 200-L stainless steel exposure chamber into which allylamine vapor was delivered by bubbling air through the liquid amine. The effect on breathing rate was maximal 10-15 min after exposure in both studies; recovery after the 15-min exposure occurred within 1 min; recovery after the 60-min exposure was slower.