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DEVELOPMENTAL TOXICITY OF DI- AND TETRACHLOROETHANE AND DICHLOROPROPANE IN EMBRYO CULTURE
Citation:
Andrews, J E., H P. Nichols, AND E S. Hunter III. DEVELOPMENTAL TOXICITY OF DI- AND TETRACHLOROETHANE AND DICHLOROPROPANE IN EMBRYO CULTURE. Presented at Society of Toxicology, Nashville, TN, March 17-21, 2002.
Description:
DEVELOPMENTAL TOXICITY OF DI- AND TETRACHLOROETHANE AND DICHLOROPROPANE IN EMBRYO CULTURE. JE Andrews, H Nichols, and ES Hunter. Reproductive Toxicology Division, NHEERL, USEPA, RTP, NC.
Disinfection of drinking water with chlorine results in numerous chlorinated byproducts (DBPs). Among these are the di-substituted propanes and the di-and tetra- substituted ethanes. We chose to evaluate the developmetal toxicity of 1,3-dichloropropane (1,3DP), 2,2-dichloropropane (2,2DP), 1,1-dichloroethane (1,1DE) and 1,1,2,2-tetrachloroethane (TCE) in rat whole embryo culture (WEC) due to their presence in drinking water and a lack of developmental toxicity data available for these compounds. Gestational day (GD) 9 rat embryos were exposed to 2.5-7.6 mM 1,3 DP, 8.7-19.4 mM 2,2 DP, 8.9-23.8 mM 1,1DE, or 0.5-2.9 mM TCE for 48 hours and then evaluated for dysmorphology, developmental score (DEVSC), head length (HL), somite number (SN), crown rump length (CRL) and embryo lethality. All four compounds were dysmorphogenic in rat WEC. 1,3 DP was dysmorphogenic at all concentrations >3.8 mM and embryolethal at concentrations 5.1 mM. Anomalies consisted primarily of opened neural tube, rotational and eye defects. DEVSC, HL, SN and CRL were significantly reduced at concentrations > 3.8 mM. 2,2DP was dysmorphogenic in rat WEC at concentrations 11.6 mM and embryolethal at concentrations 14.5 mM. Anomalies were predominantly open neural tube, heart defects and rotational defects. DEVSC was significantly reduced at concentrations 11.6 mM. 1,1DE was significantly dysmorphogenic following exposure to 17.9 mM but was also significantly embryolethal (35%). The predominant anomalies were eye defects but there was overall delayed embryonic development at the higher exposure concentrations. Concentrations of 23.8 mM were 100% embryolethal. TCE was dysmorphogenic at concentrations 1.4 mM and embryolethal at concentrations 2.4 mM. Anomalies were primarily heart, eye and rotational defects. The relative developmental toxicity for the four compounds based on molar concentrations was TCE>1,3DP>2,2DP>1,1DE. The pattern of anomalies was inconsistent between the 4 compounds suggesting that their toxicity is probably expressed through different mechanisms. The concentrations of these DBPs required to induce dysmorphology are much higher than those for the haloacetic acids, another class of DBPs that we have studied extensively. This abstract does not reflect EPA Policy.