Lack of mutagenic activity of 1,6-hexamethylene diisocyanate.

1,6-Hexamethylene diisocyanate (HDI) is an aliphatic diisocyanate used in the manufacture of higher molecular weight biuret and trimer polyisocyanate resins. These resins are commonly used in polyurethane paints, resulting in potential occupational, and to a lesser extent consumer exposures. Because some isocyanates have been reported to be mutagenic, HDI was tested in the bacterial reverse mutation assay (Ames test), CHO/HGPRT gene mutation assay, and in the mouse micronucleus test, using vapor-phase exposures.

Thirteen-week subchronic rat inhalation toxicity study with a recovery phase of trivalent chromium compounds, chromic oxide, and basic chromium sulfate.

The toxicity of trivalent chromium compounds; chromic oxide and basic chromium sulfate, was investigated in rats in a 13-week nose-only inhalation study that included a 13-week recovery period. Nose-only exposures to insoluble chromic oxide dust at 4.4, 15, or 44 mg/m3 or soluble basic chromium sulfate dust at 17, 54, or 168 mg/m3 (trivalent chromium equivalent concentrations of 3, 10, and 30 mg/m3) were carried out for 6 h/day, 5 days/week.

A 2-year inhalation study of phosphine in rats.

Phosphine is a highly toxic gas used as a fumigant, a dopant in semiconductor manufacturing, and in the production of organophosphines. In a chronic toxicity and oncogenicity study of phosphine, 60 male and female F344 rats per group were exposed via whole-body inhalation for 6 h/day, 5 days/wk for up to 104 wk to mean concentrations of 0, 0.3, 1, or 3 ppm phosphine.

Fluticasone propionate attenuates ozone-induced rhinitis and mucous cell metaplasia in rat nasal airway epithelium.

Ozone (O3) is the principal oxidant pollutant in photochemical smog. Repeated exposures to O3 induces inflammation and mucous cell metaplasia in the nasal airways of laboratory animals. Our study was designed to determine the efficacy of a topical anti-inflammatory corticosteroid in preventing O3-induced rhinitis and mucous cell metaplasia in rat nasal epithelium.

Acute inhalation toxicology of oxalyl chloride.

The acute inhalation LC50 of oxalyl chloride was determined in rats following a one-hour exposure. Four groups of 10 animals per group were exposed to a concentration range of 462-2233 ppm. One set of six animals was exposed to a concentration of oxalyl chloride of 1232 ppm for one hour to evaluate the histopathological change to the lungs.

Inhalation toxicity of chromium from Whetlerite dust in rats.

The acute inhalation toxicity and metabolic fate of chromium and copper from Whetlerite dust in rats were investigated. Groups of male and female, Sprague-Dawley rats were exposed to Whetlerite dust and base carbon dust as outlined in the OECD Limit Test guidelines. At 14, 28 and 180 days post-exposure, rats were evaluated for gross pathological changes and tissues were collected for chromium and copper determination.

Sequence of cardiorespiratory effects of soman altered by route of administration.

Dilute soman was administered to anesthetized guinea-pigs by slow infusion (30 micrograms/kg/10 min); intravenous (IV), subcutaneous (SC), intraperitoneal (IP), intratracheal (IT), and upper-airway (UAW) routes were used. Times to ventilatory failure were 8.8 +/- 1.