Testing of the permeation resistance of eight glove and suit barriers against commercially available substituted silanes and siloxanes was performed using the ASTM F739-96 standard test method. In addition to barrier performance to the pure organosilanes, the permeation rates of the hydrolysis product (usually ethanol or methanol) were investigated. The silanes and siloxanes used as the challenge agents were N-2-(aminoethyl)-3-aminopropyltrimethoxysilane; 3-aminopropyltriethoxysilane; 3-chloropropyltrimethoxysilane; ethyltriacetoxysilane; 3-glycidoxypropyltrimethoxysilane; 1,1,1,3,3,3-hexamethyldisilazane; hexamethyldisiloxane; 3-methacryloxypropyltrimethoxysilane; methyltriacetoxysilane (50%)/ethyltriacetoxysilane (50%); methyltrimethoxysilane; methyltris(methylethylketoxime)silane; phenyltrimethoxysilane; polydimethyl siloxanes (PS 340); octamethylcyclotetrasiloxane (D4); tetraethoxysilane; tetramethoxysilane; 1,1,3,3-tetramethyl disiloxane; triethoxysilane; trimethoxysilane; vinyltrimethoxysilane; and vinyltris(methylethylketoxime)silane. Protective gloves tested were nitrile rubber, neoprene rubber, butyl rubber, 4H laminate, and polyvinyl chloride. Garments tested included Tyvek/Saranex 23P, CPF 2, and Responder, all made by Kappler Safety Group. In all cases the protective suit materials lasted 8 hours or more. The only glove that lasted 8 hours against all chemicals was the 4H laminate. The polyvinyl chloride glove lasted 10 min to 8 hours or more depending on the chemical. The nitrile, neoprene, and butyl rubber gloves lasted from 53 min to 8 hours or more depending on the chemical. The alcohol permeation was similar to the organosilicon compounds. The suit materials and the butyl glove all lasted more than 8 hours for both methanol and ethanol.

Ethanol↗

PubMedDate not supplied

Potentiation of inhaled staphylococcal enterotoxin B-induced toxicity by lipopolysaccharide in mice.

Nonhuman primates are the established model for evaluating toxic responses to staphylococcal enterotoxins (SEs), as they react similarly to humans. Rodents are generally considered unresponsive to SEs. Binding affinities and T-cell reactivity suggest that SE binds more efficiently to primate major histocompatability complex class II receptors than to mouse receptors. We investigated the potentiation of staphylococcal enterotoxin B (SEB) inhalation toxicity by lipopolysaccharide (LPS) in BALB/c mice. Lethality occurred only when SEB was potentiated by LPS. Neither SEB nor LPS produced lethal effects alone. Temporal responses of interleukin 1 alpha, tumor necrosis factor alpha, interleukin 2, and interferon-gamma evoked by inhaled SEB were enhanced by LPS. By 24 hr after intoxication, serum cytokines decreased to baseline levels, and consistent pulmonary perivascular leukocytic infiltrates were evident histologically. Histologic lesions induced by inhalation exposure to SEB by mice, with or without potentiation by LPS, were similar to those in the rhesus monkey. Predominant pulmonary lesions included severe, diffuse interstitial and alveolar pulmonary edema, leukocytic infiltrates, mild perivascular edema, and alveolar fibrin deposition. Although the mechanism of aerosolized SEB-induced toxicity has not been completely resolved, similarities in histologic lesions, cytokine responses, and acute dose-response suggest the LPS-potentiated mouse model may be a credible alternative to the nonhuman primate model.

Animals↗