The methyl, ethyl, and butyl ethers of triethylene glycol (TM, TE, and TB, respectively) were evaluated in three screening studies to assess their potential hazards to humans. The assessment!; included (1) an in vitro procedure to determine the ability of the materials to penetrate human skin, (2) a 21-day dermal limit test in rabbits to determine potential systemic toxicities, and (3) a screening procedure to evaluate the chemicals' potentials to induce developmental toxicity. In the in vitro dermal absorption procedure, the three test materials crossed human epidermis at molar rates 170-330 times more slowly than the lower molecular weight homolog ethylene glycol methyl ether (EM), a chemical known to induce systemic effects following skin application. In the 21-day dermal study, daily applications of 1000 mglkg TM, TE, or TB did not produce systemic toxicity in male or female rabbits, including hematologic or testicular effects. The low dermal penetration rate of the triethylene glycol ethers may have played a role in this outcome. In the developmental toxicity screening test, oral doses of 1000 mg/kg given on Days 6-15 of gestatiorn did not produce maternal toxicity in rats and had no effect on viability or growth of offspring,, pre-or postnatally, indicating low developmental toxic potential for these compounds. The results of these studies indicate that triethylene glycol methyl, ethyl, and butyl ethers have ver,y low capacities to be absorbed through the skin of exposed individuals, low potentials to produce systemic toxicity following oral or dermal exposures, and do not appear to be selectively toxic to the developing conceptus. The data clearly indicate that triethylene glycol ethers do not exhibit toxicologic profiles comparable to those of the methyl and ethyl ethers of ethylene glycol.

No abstract

The mutagenic activity of vinyl chloride (VC) and vinylidene dichloride (VDC) at three exposure levels was assessed in fertile male CD-1 mice with the dominant lethal test. Each compound was assessed in a separate study. Male mice were exposed by inhalation to VC at 3000, 10,000, and 30,000 ppm and to VDC at 10, 30, and 50 ppm for 6 hr/day for 5 days. By comparison with control males exposed to air, no mutagenic effects on any maturation stage of spermatogenesis in treated males were detected. There was no significant increase in the number of postimplantational early fetal deaths as shown by the number of females with one or more early deaths or the number of early deaths/pregnancy or the number of early deaths/total implants/pregnancy. There was no evidence of pre-implantational egg losses as indicated by the total implants/pregnant female. There was also no reduction in fertility. (The reduction in fertility at 50 ppm VDC was unproven). The lack of effect was not due to the insensitivity of the system used, since both the VC and VDC study a mutagenic effect was clearly demonstrated in male mice dosed IP with the positive control compounds cyclophosphamide (CTX) and/or ethylmethane sulfonate (EMS). During dosing these animals were housed under similar exposure conditions to those animals exposed to the test substances but with a flow of air through the exposure chambers. Thus, neither VC nor VDC is mutagenic in the mouse at the stated exposure levels as measured by the dominant lethal test.

No abstract

JSTOR is a not-for-profit service that helps scholars, researchers, and students discover, use, and build upon a wide range of content in a trusted digital archive. We use information technology and tools to increase productivity and facilitate new forms of scholarship. For more information about JSTOR, please contact support@jstor.org.. The National Institute of Environmental Health Sciences (NIEHS) and Brogan & Partners are collaborating with JSTOR to digitize, preserve and extend access to Environmental Health Perspectives. The mutagenic activity of vinyl chloride (VC) and vinylidene dichloride (VDC) at three exposure levels was assessed in ferti}e male CD-1 mice with the dominant lethal test. Each compound was assessed in a separate study.Male mice were exposed by inhalation to YC at 3000 10,000, and 30s00Q ppm and to VDC at 10, 30, and 50 ppm for 6 hr/day for 5 days. By comparison with control males exposed to air, no mutagenic effects on any maturation stage of spermatogenesis in treated males were detected. There was no significant inerease in the number of postimplantational early fetal deaths as shown by the number of females with one or more early deaths or the number of early deathslpregnancy or the number of early deaths/total implants/pregnancy. There was no evidence of pre-implantational egg losses as indicated by the total implants/pregnant female. There was also no reduction in fertility. (The reduction in fertility at 50 ppm VDC was unproven).The lack of effect was not due to the insensitivity of the system used, since both the VC and VDC study a mutagenic effect was clearly demonstrated in male mice dosed IP with the positive control compounds cyclophosphamide (CTX) and/or ethylmethane sultonate (EMS). During dosing these animals were housed under similar exposure conditions to those animals exposed to the test substances but with a flow of air through the exposure chambers.Thus neither VC nor VDC is mutagenic in the mouse at the stated exposure levels as measured by the dominant lethal test. this type in mice after VC and VDC exposure at three levels. At the same time negative control animals exposed to air and positive control animals also exposed to air and given EMS andXor CTX were assayed.