Managing the Risk of Occupational Allergy in the Enzyme Detergent Industry.

Enzyme proteins have potential to cause occupational allergy/asthma. Consequently, as users of enzymes in formulated products, detergents manufacturers have implemented a number of control measures to ensure that the hazard does not translate into health effects in the workforce. To that end, trade associations have developed best practice guidelines which emphasize occupational hygiene and medical monitoring as part of an effective risk management strategy.

The safety of ethyl oleate is supported by a 91-day feeding study in rats.

The purpose of this study was to determine the safety of ethyl oleate (EO) in a 91-day feeding study in Sprague-Dawley rats. EO was mixed into AIN-93G purified diet at levels of 0, 3.3, 6.

The safety of the use of ethyl oleate in food is supported by metabolism data in rats and clinical safety data in humans.

The absorption, distribution, and excretion of radiolabeled ethyl oleate (EO) was studied in Sprague-Dawley rats after a single, peroral dose of 1.7 or 3.4 g/kg body weight and was compared with a radiolabeled triacylglycerol (TG) containing only oleic acid as the fatty acid (triolein).

Effects of doxylamine succinate on thyroid hormone balance and enzyme induction in mice.

The effects of doxylamine (as the succinate salt) on microsomal enzyme activity and serum thyroid hormone levels were examined in B6C3F1 mice following dietary exposure for 7 or 15 days (0, 40, 375, 750, or 1500 ppm in diet, expressed as free base doxylamine). In addition, the hepatic P450 enzyme inducer sodium phenobarbital (375 ppm, expressed as free acid phenobarbital) was used as a positive control for CYP2B induction. Exposure of mice to doxylamine produced dose-related increases in liver weight at both time points.

Altered regulation of pituitary gonadotropin-releasing hormone (GnRH) receptor number and pituitary responsiveness to GnRH in 2,3,7,8-tetrachlorodibenzo-p-dioxin-treated male rats.

2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) increases the potency of androgens as feedback inhibitors of luteinizing hormone (LH) secretion. Our objectives were to determine if this increase is due to pituitary or hypothalamic dysfunction (or both), and to investigate the mechanism by which TCDD produces this effect. Seven days after dosing, TCDD inhibited the compensatory increases in (i) pituitary gonadotropin-releasing hormone (GnRH) receptor number, (ii) LH secretory responsiveness of the pituitary to GnRH, and (iii) plasma LH concentrations which should have occurred in response to TCDD-induced decreases in plasma testosterone concentrations.

Androgenic deficiency in male rats treated with perfluorodecanoic acid.

Effects of perfluorodecanoic acid (PFDA, 20-80 mg/kg, ip) on the androgenic status of sexually mature male rats were investigated 7 days after treatment. PFDA decreased plasma androgen concentrations in a dose-dependent fashion with an ED50 of approximately 30 mg/kg. The highest dose of PFDA decreased plasma testosterone and 5 alpha-dihydrotestosterone concentrations to 12 and 18%, respectively, of ad libitum-fed control (ALC) values.

2,3,7,8-tetrachlorodibenzo-p-dioxin increases the potency of androgens and estrogens as feedback inhibitors of luteinizing hormone secretion in male rats.

Tetrachlorodibenzo-p-dioxin (TCDD) decreases plasma androgen concentrations in male rats, without increasing plasma luteinizing hormone (LH) concentrations. If plasma LH concentrations had increased appropriately, plasma androgen concentrations in these animals would have returned to normal. The mechanism by which TCDD prevents the compensatory increase in plasma LH concentrations was therefore investigated.

Plasma concentrations of pituitary hormones in 2,3,7,8-tetrachlorodibenzo-p-dioxin-treated male rats.

Experiments were conducted to test the hypothesis that acute TCDD toxicity is associated with pituitary hypofunction. Sexually mature male Sprague-Dawley rats were given graded doses of TCDD (0-100 micrograms/kg) and evaluated 7 days later. Despite pronounced hypophagia and body weight loss, plasma concentrations of growth hormone (GH), follicle-stimulating hormone (FSH), and luteinizing hormone (LH) were not significantly affected by any dose of TCDD.

Characterization of the enhanced paw edema response to carrageenan and dextran in 2,3,7,8-tetrachlorodibenzo-p-dioxin-treated rats.

Rats pretreated with 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD, 10 micrograms/kg) are supersensitive to the edemagenic effects of carrageenan and dextran as indicated by the increased potency of these irritants in TCDD-treated animals compared to controls. This effect of TCDD was characterized using indomethacin, dexamethasone and a combination of cyproheptadine and pyrilamine as inhibitors of edema formation. Because TCDD increases the potency of carrageenan and dextran, it was necessary to select appropriate doses of the edemagenic irritants in order to evaluate the effect of edema inhibitors properly.