Download Acute Exposure Guideline Levels for Selected Airborne by National Research Council, Board on Environmental Studies PDF

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 comparable to ammonia, nickel carbonyl and phosphine, between others.

At the request of the dep. of protection, the nationwide examine Council has reviewed the correct medical literature compiled by way of a professional panel and proven Acute publicity instruction degrees (AEGLs) for 12 new chemical substances. AEGLs signify publicity degrees less than which adversarial future health results aren't prone to take place and are beneficial in responding to emergencies corresponding to unintended or intentional chemical releases locally, the office, transportation, the army, and for the remediation of infected sites.

Three AEGLs are licensed for every chemical, representing publicity degrees that bring about: 1) remarkable yet reversible soreness; 2) long-lasting healthiness results; and three) life-threatening healthiness impacts.

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Extra info for Acute Exposure Guideline Levels for Selected Airborne Chemicals: Volume 6

Sample text

Orally administered allylamine was shown to be metabolized to acrolein and hydrogen peroxide, which may both be responsible for the observed toxic effects (Boor et al. 1987). The metabolite acrolein has been detected in both rat and human aorta, myocardium, and liver homogenates incubated with allylamine (Boor and Nelson 1982). The acrolein is believed to be subsequently conjugated with glutathione to form 3-hydroxypropylmercapturic acid, which was the sole metabolite in the urine of Sprague-Dawley rats collected 24 and 48 h after gavage with 150 mg/kg radiolabeled allylamine (2 µCi/kg 14C-labeled; Boor et al.

An intraspecies uncertainty factor of 10 was used because the variability of the cardiotoxic response to allylamine among humans is undefined, and potentially sensitive populations exist (diabetics, persons with congestive heart failure). 2 ppm, respectively, indicating that for these longer exposure durations, cardiotoxicity is a more sensitive end point than eye and respiratory irritation. Copyright © National Academy of Sciences. All rights reserved. Acute Exposure Guideline Levels for Selected Airborne Chemicals: Volume 6 16 Acute Exposure Guideline Levels AEGL-3 values were derived from a study on rat inhalation with a lethal concentration in 50% of the sample (LC50) in which exposures were for 1, 4, or 8 h (Hine et al.

1989). Consistent with glutathione involvement in allylamine metabolism, a depletion of reduced glutathione in the aorta, blood, and lungs was shown to occur and be maximal 1-6 h after gavage treatment with allylamine (Awasthi and Boor 1994). It is proposed that the metabolism of allylamine to acrolein and hydrogen peroxide occurs via benzylamine oxidase, which is a form of amine oxidase with high activity in vascular tissue, especially the aorta (Boor et al. 1987). 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.

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