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1. Ethylene Dichloride
2. Ethylene Dichloride, 14c-labeled
3. Ethylene Dichloride, 14c2-labeled
4. Ethylene Dichloride, 36cl-labeled
5. Ethylene Dichloride, 38cl-labeled
6. Ethylene Dichloride, Ion (1+)
1. Ethylene Dichloride
2. 107-06-2
3. Ethylene Chloride
4. Ethane, 1,2-dichloro-
5. Glycol Dichloride
6. Dichloroethylene
7. Dutch Liquid
8. Dutch Oil
9. Ethane Dichloride
10. Aethylenchlorid
11. Dichloro-1,2-ethane
12. Sym-dichloroethane
13. Dichloremulsion
14. 1,2-dichlorethane
15. Brocide
16. 1,2-bichloroethane
17. Dichlor-mulsion
18. Bichlorure D'ethylene
19. Borer Sol
20. Di-chlor-mulsion
21. 1,2-dce
22. Freon 150
23. Alpha,beta-dichloroethane
24. Edc (halocarbon)
25. 1,2-ethylene Dichloride
26. Destruxol Borer-sol
27. Ethyleendichloride
28. Cloruro Di Ethene
29. Rcra Waste Number U077
30. 1,2-dicloroetano
31. 1,2-ethylidene Dichloride
32. Chlorure D'ethylene
33. 1,2-dichloorethaan
34. Dce
35. 1,2-dichlor-aethan
36. 1, 2-dichloroethane
37. Aethylendichlorid
38. S-dichloroethane
39. Hcc 150
40. Ethylenedichloride
41. Nci-c00511
42. Edc
43. Ent 1,656
44. 1,2-dichloraethan
45. 1.2-dichloroethane
46. .alpha.,.beta.-dichloroethane
47. 1,2-dichloro-ethane
48. Mfcd00000963
49. Chebi:27789
50. Ethane, 1,2-dichloro-, Homopolymer
51. 55163iji47
52. Caswell No. 440
53. Aethylenchlorid [german]
54. Ry Dichloro-1,2-ethane
55. Ethyleendichloride [dutch]
56. 1,2-dichloroethane, Analytical Standard
57. Cloruro Di Ethene [italian]
58. 29561-65-7
59. 52399-93-6
60. Hsdb 65
61. 1,2-dichloorethaan [dutch]
62. 1,2-dicloroetano [italian]
63. Ccris 225
64. Chlorure D'ethylene [french]
65. 1,2 Dichloroethane
66. 1,2-dichlor-aethan [german]
67. Bichlorure D'ethylene [french]
68. Dichlorure D'ethylene
69. Dichloro-1,2-ethane [french]
70. Clch2ch2cl
71. Ethylene Dichloride [bsi:iso]
72. 1,2-dichloroethane 100 Microg/ml In Methanol
73. Dichlorure D'ethylene [iso-french]
74. Einecs 203-458-1
75. Un1184
76. Rcra Waste No. U077
77. Epa Pesticide Chemical Code 042003
78. Ethylenechloride
79. Ethylendichloride
80. Ai3-01656
81. Alpha,bet
82. Dichloro Ethylene
83. Ethylene-chloride
84. Unii-55163iji47
85. Ethylene Dichoride
86. 1,2-dichloroethane, Acs
87. 1,2dichlorethane
88. 1,2dichloroethane
89. Ehtylene Dichloride
90. 1,2 Dichlorethane
91. 1,2 Dichoroethane
92. 1,2-dichloroetane
93. 1,2-dichloroethan
94. 1,2-dichoroethane
95. 1,2-dicloroethane
96. 1,2-dichioroethane
97. 1,2-dichloroetharie
98. 1 ,2-dichloroethane
99. 1, 2 Dichloroethane
100. 1,2 -dichloroethane
101. 1,2 Dichloro Ethane
102. 1,2,-dichloroethane
103. 1,2- Dichloroethane
104. 1,2-di-chloroethane
105. 1,2-dichloro Ethane
106. 1.2-di-chloroethane
107. Ch2clch2cl
108. 1,2-ethylenedichloride
109. Clch2-ch2cl
110. Dichloro-1, 2-ethane
111. C1ch2ch2cl
112. Clch2ch2c1
113. Edc, Jmaf
114. Cl(ch2)2cl
115. Dsstox_cid_438
116. 12-dichloroethane
117. Bmse000568
118. Ec 203-458-1
119. Dsstox_rid_75587
120. Dsstox_gsid_20438
121. Chembl16370
122. 1,2-dichloroethane Acs Grade
123. 1,2-dichloroethane, For Hplc
124. Ethylene Dichloride, Bsi, Iso
125. Dtxsid6020438
126. Ethylene Dichloride [mi]
127. Dichloroethane Reagent Grade Acs
128. Ethylene Dichloride [fcc]
129. Ethylene Dichloride [iso]
130. 1,2-dichloroethane, Acs Reagent
131. 1,2-dichloroethane, Hplc Grade
132. Ethylene Dichloride [hsdb]
133. Ethylene Dichloride [inci]
134. 1,2-dichloroethane [iarc]
135. Amy33455
136. Ethylene Dichloride [mart.]
137. Zinc8220695
138. Tox21_202466
139. 1,2-dichloroethane, Lr, >=99%
140. Ethylene Dichloride [who-dd]
141. Stl264187
142. 1,2-dichloroethane [usp-rs]
143. Akos000120021
144. 1,2-dichloroethane, P.a., 99.5%
145. Db03733
146. Un 1184
147. 1,2-dichloroethane, Ar, >=99.5%
148. 1,2-dichloroethane, Anhydrous, 99.8%
149. Ncgc00091763-01
150. Ncgc00091763-02
151. Ncgc00091763-03
152. Ncgc00260015-01
153. Cas-107-06-2
154. 1,2-dichloroethane, For Hplc, 99.8%
155. 1,2-dichloroethane, Acs Reagent, >=99%
156. 1,2-dichloroethane, Reagentplus(r), 99%
157. 1,2-dichloroethane, For Hplc, >=99.8%
158. 1,2-dichloroethane, Spectrophotometric Grade
159. D0310
160. D0364
161. E0289
162. Ft-0626325
163. Ft-0771283
164. R 150
165. 1,2-dichloroethane 10 Microg/ml In Methanol
166. 1,2-dichloroethane, Acs Reagent, >=99.0%
167. C06752
168. 1,2-dichloroethane 1000 Microg/ml In Methanol
169. 1,2-dichloroethane, Saj First Grade, >=99.0%
170. Q161480
171. 1,2-dichloroethane, Jis Special Grade, >=99.5%
172. Ethylene Dichloride [un1184] [flammable Liquid]
173. J-503815
174. 1,2-dichloroethane, Anhydrous, Zero2(tm), 99.8%
175. 1,2-dichloroethane, Spectrophotometric Grade, >=99%
176. Ethambutol Hydrochloride Impurity D [ep Impurity]
177. 1,2-dichloroethane, Puriss., Absolute, Over Molecular Sieve (h2o <=0.005%), >=99.5% (gc)
| Molecular Weight | 98.96 g/mol |
|---|---|
| Molecular Formula | C2H4Cl2 |
| XLogP3 | 1.5 |
| Hydrogen Bond Donor Count | 0 |
| Hydrogen Bond Acceptor Count | 0 |
| Rotatable Bond Count | 1 |
| Exact Mass | 97.9690055 g/mol |
| Monoisotopic Mass | 97.9690055 g/mol |
| Topological Polar Surface Area | 0 Ų |
| Heavy Atom Count | 4 |
| Formal Charge | 0 |
| Complexity | 6 |
| Isotope Atom Count | 0 |
| Defined Atom Stereocenter Count | 0 |
| Undefined Atom Stereocenter Count | 0 |
| Defined Bond Stereocenter Count | 0 |
| Undefined Bond Stereocenter Count | 0 |
| Covalently Bonded Unit Count | 1 |
A case /was reported/ of an 18-yr old man who becamee drowsy, cyanotic, and exhibited bradycardia after drinking approx 50 mL of Marament which is equivalent to 50 g of 1,2-dichloroethane (714 mg/kg/day); he died 17 hr later in a state of circulatory shock.
DHHS/ATSDR; Toxicological Profile for 1,2-Dichloroethane p. 33 TP-93/06 (1994)
Ingestion of 1 or 2 oz, 400-800 mg/kg body weight, by an adult male is fatal, deaths caused by circulatory or respiratory failure.
USEPA; Intermedia Priority Pollutant Guidance Doc p.2-1 (1982)
The compound 1,2-dichloroethane (DCE) is a ubiquitous environmental contaminant. The primary route of exposure of humans to DCE is inhalation of its vapor. The present investigation was undertaken to determine the distribution and accumulation of DCE in the blood, lung, liver, brain, kidney and abdominal fat of rats during and after inhalation exposure. Male rats were exposed to 160 ppm (v/v) of DCE vapor for 360 min and the concentrations of DCE in the blood and tissues during the inhalation exposure period and after the end of the exposure period were measured. DCE accumulation in the abdominal fat was much greater than that in the blood and other tissues. The information we obtained in this study is useful basic data pertaining to the pharmacokinetics of DCE and DCE-mediated carcinogenicity: Our results suggest that one of the factors involved in the induction of peritoneal tumors in rats exposed to DCE vapor by inhalation is DCE accumulation in the abdominal fat.
PMID:23573923 Take M et al; J Environ Sci Health A Tox Hazard Subst Environ Eng 48 (9): 1031-6 (2013)
The effect of the pretreatment of male Sprague-Dawley rats with phenobarbital (PB), butylated hydroxyanisole (BHA) and disulfiram (DSF) on the inhalation kinetics of 1,2-dichloroethane [ethylene dichloride (EDC)] was studied by the gas uptake method. A closed recirculating system was constructed and characterized. The rate curves in all the pretreatment regimens showed saturable dependence on EDC concentration. These saturable dependencies (Michaelis-Menten) appeared to be associated with enzymatic metabolism. In general, a two-compartment, steady-state pharmacokinetic model described the uptake data. Data were transformed by Hanes plots to calculate the inhalational Km, the ambient EDC concentration at which uptake proceeded at half maximum rate, and Vmax, the maximum rate of uptake (i.e., maximum rate of metabolism). Although PB and BHA pretreatments did not affect the Km of EDC, PB pretreatment increased the Vmax while DSF pretreatment decreased both the Km and Vmax.
PMID:3813877 Igwe OJ et al; Arch Toxicol 59 (3): 127-34 (1986)
The levels of 1,2-dichloroethane (1,2-EDC), and its metabolites 2-chloroethanol, monochloroacetic acid, and 2-chloroacetaldehyde were determined by gas chromatography in the organs of human cadavers in cases of acute poisoning. The highest 1,2-dichloroethane levels were observed in the stomach and omentum; lower levels in the kidney, spleen, brain, heart, large and small intestines, and blood, and no detectable amounts in the liver. 2-Chloroethanol and monochloroacetic acid, minor metabolites of 1,2-dichloroethane, were detected in small amounts in the myocardium, brain, stomach, and small intestine. 2-Chloroacetaldehyde, because it is a reactive intermediate in the biotransformation of 1,2-dichloroethane was not detectable in the organs. The administration of acetylcysteine to acutely intoxicated humans showed no positive clinical effect. ...
Luzhnikov EA et al; Sud Med Ekspert 28 (2): 47-9 (1985)
Urinary excretion of thiodiglycolic acid and thioethers after 1,2-dichloroethane dosing was studied in rats. Male Sprague-Dawley rats were administered 0, 0.12, 0.25, 0.50, 1.01, 2.02, 4.04 or 8.08 umol/kg (14)C labeled 1,2-dichloroethane orally. Urine samples were collected for 24 hours and analyzed for thiodiglycolic acid and thioethers before and after alkaline hydrolysis by gas chromatography and the Ellman reagent/absorption spectrophotometry (thioether assay), respectively. The amounts of 1,2-dichloroethane derived radioactivity excreted decreased as a logarithmic function of increasing 1,2-dichloroethane dose ranging from 62.1% of the dose for 0.12 and 0.25 umol/kg 1,2-dichloroethane to 7.4% of the 8.08 umol/kg dose. The concentrations of urinary thiodiglycolic acid were well correlated with 1,2-dichloroethane dose up to 2.02 umol/kg. When expressed as a percentage of the dose urinary excretion of thiodiglycolic acid was not dependent on the dose over the range 0.12 to 1.01 umol/kg 1,2-dichloroethane and amounted to 21.8% of the dose. Before alkaline hydrolysis no thioethers could be detected. After alkaline hydrolysis, urinary excretion of thioethers by rats dosed with 0.12 and 0.25 umol/kg did not differ significantly from the control value. Between 0.25 and 4.04 umol/kg 1,2-dichloroethane, thioether excretion increased linearly with dose. The highest thioether/thiodiglycolic ratio 0.17 occurred in rats given 8.08 umol/kg 1,2-dichloroethane. Urinary thiodiglycolic acid concentrations were not altered by alkaline hydrolysis. The /results suggest/ that urinary thiodiglycolic acid excretion correlates well with the oral dose of 1,2-dichloroethane in rats. Urinary thiodiglycolic acid excretion may be a useful marker of 1,2-dichloroethane exposure. Thiodiglycolic acid is hydrolyzed under alkaline conditions. The thioether assay is not appropriate for estimating urinary thiodiglycolic acid excretion.
Payan JP et al J Appl Toxicol 13 (6): 417-22 (1993)
For more Absorption, Distribution and Excretion (Complete) data for 1,2-Dichloroethane (11 total), please visit the HSDB record page.
In rats, radiolabeled ethylene dichloride was excreted primarily in the urine, and the major urinary metabolites were chloroacetic acid, 5-carboxymethyl cysteine, and thiodiacetic acid.
Gosselin, R.E., R.P. Smith, H.C. Hodge. Clinical Toxicology of Commercial Products. 5th ed. Baltimore: Williams and Wilkins, 1984., p. II-164
The metabolism and binding of (14)C-labelled 1,2-dichloroethane in female C57BL mice were studied. As shown by whole-body autoradiography of iv injected mice, a selective localization of non-volatile and bound 1,2-dichloroethane metabolites occurred in the nasal olfactory mucosa and the tracheo-bronchial epithelium. Low levels of metabolites were also present in the epithelia of the upper alimentary tract, vagina and eyelid, and in the liver and kidney. A decreased mucosal and epithelial binding was observed after pretreatment with metyrapone, indicating that the binding might be due to an oxidative metab of 1,2-dichloroethane. The levels of in vivo binding were considerably lower in mice injected ip with 1,2-dichloroethane as compared to mice given equimolar doses of (14)C-labelled 1,2-dibromoethane. In vitro experiments with 1000 g supernatants from various tissues showed that nasal mucosa has a marked ability to activate 1,2-dichloroethane into products that become irreversibly bound to the tissue. The nasal olfactory mucosa is a target tissue for toxicity of 1,2-dichloroethane.
Brittebo EB et al; Toxicol 56 (1): 35-45 (1989)
... Using isolated rat hepatocytes as a model system, and electron spin resonance spectroscopy coupled to the spin trapping technique as a detection technique, the formation of free radical derivatives was demonstrated, both under normoxic as well as under hypoxic conditions from carbon tetrachloride (CCl4), chloroform (CHCl3), 1,1,1-tetrachloroethane, and 1,1,2,2-tetrachloroethane. In contrast, free radical production was only detectable under hypoxic conditions when 1,2-dibromoethane, 1,1-dichloroethane, 1,2-dichloroethane, and 1,1,2-trichloroethane were added to the hepatocyte suspensions....
PMID:6393297 Tomasi A et al; Toxicol Pathol 12 (3): 240-6 (1984)
Chlorinated hydrocarbons found in a bioassay to be carcinogenic to both B6C3F1 mice and Osborne-Mendel rats (1,2-dichloroethane), carcinogenic only to mice (1,1,2-trichloroethane, 1,1,2,2-tetrachloroethane, hexachloroethane, trichloroethylene, and tetrachloroethylene), and noncarcinogenic to either species (1,1-dichloroethane and 1,1,1-trichloroethane) were used to investigate the biochemical bases for tumorigenesis. Studies were conducted after chronic oral dosing of adult mice and rats with the MTD and 1/4 MTD of each compound. The extent to which the compounds were metabolized in 48 hr, hepatic protein binding, and urinary metabolite patterns were examined. Metabolism of the compounds (mmoles per kg body weight) was 1.7 to 10 times greater in mice than in rats. Hepatic protein binding (nanomole equivalents bound to 1 mg of liver protein) was 1.2 to 8.3 times higher in mice than in rats except for 1,2-dichloroethane and 1,1,1-trichloroethane. The noncarcinogens 1,1-dichloroethane and 1,1,1-trichloroethane exhibited 2 to 18 times more binding in mice than did the carcinogens 1,2-dichloroethane and 1,1,2-trichloroethane. Urinary metabolite patterns of the compounds were similar in both species. The biochemical parameters measured provided no clue to differentiate the carcinogens from the noncarcinogens.
PMID:4054011 Mitoma C et al; Drug Chem Toxicol 8 (3): 183-94 (1985)
For more Metabolism/Metabolites (Complete) data for 1,2-Dichloroethane (16 total), please visit the HSDB record page.
Whole body (animal studies): complete elimination within 48 hours; [TDR, p. 649]
TDR - Ryan RP, Terry CE, Leffingwell SS (eds). Toxicology Desk Reference: The Toxic Exposure and Medical Monitoring Index, 5th Ed. Washington DC: Taylor & Francis, 1999., p. 649
The mechanism of the hepatocellular toxicity of l,2-dichloroethane ... was examined in vitro. Hepatocytes from male Wistar rats were preloaded with tritium (3)H labeled sodium palmitate and (14)C labeled glucosamine. They were incubated with 0 to 6.5 uM 1,2-dichloroethane for 5 to 60 min. Cytotoxicity was assessed by measuring changes in cellular exclusion of trypan blue dye leakage of intracellular lactate dehydrogenase (LDH) into the medium and depletion of intracellular reduced glutathione (GSH). The cells were separated into the cytosolic microsome total Golgi apparatus and secreted lipoglycoprotein fractions which were assayed for changes in the distribution of (3)H and (14)C activity. 1,2-Dichloroethane did not significantly affect cellular trypan blue exclusion and LDH leakage until after 30 and 15 min incubation respectively. Hepatocellular GSH concentrations were significantly decreased after 5 min. Incubation with 4.4 uM 1,2-dichloroethane. 1,2-Dichloroethane large decrease in lipoglycoprotein secretion which was accompanied by significant accumulations of (3)H and (14)C activity in the cells. The levels of (3)H and (14)C activity were significantly increased in the microsomes and Golgi apparatus after 5 and 15 min of 1,2-dichloroethane treatment. Within the lipoglycoprotein fraction 1,2-dichloroethane significantly decreased the amounts of radiolabel in the lipid and sugar moieties. ...
Cottalasso D et al; Occupat Environ Med 51 (4): 281-85 (1994)
DNA sequence changes produced by 1,2-dibromoethane, 1,2-dichloroethane and 1-bromo-2-chloroethane were analyzed using the vermilion locus of Drosophila melanogaster. Under excision repair proficient (exr+) conditions (mutagenized exr+ males mated with exr+ females) all mutants isolated from the first generation (Fl) after 1,2-dibromoethane and 1,2-dichloroethane exposure represented rearrangements (multi-locus deletions, small deletions with tandem repeats, duplicate insertions). By contrast mutants expressing a vermilion phenotype only in the F2 (Fl mosaics) all carried single bp changes. When exr+ males after exposure to 1,2-dibromoethane were mated to excision repair deficient (exr-) mus 201 females 11 of 14 mutational events isolated from either Fl or F2 progeny were single bp changes. In general the mutation spectra for the three dihaloalkanes were similar to the spectrum obtained at the same locus for the direct acting monofunctional agent methylmethanesulfonate. The data lend support to the conclusions that these 1,2-dihaloalkanes are genotoxic through modification at ring nitrogens in DNA primarily at the N7 of guanine and, lesser extent, at the N1 of adenine. These N-adducts could be directly miscoding. However, more important for the mutagenic action of chemicals seems to be the formation of non-coding lesions and/or misrepair.
PMID:8200089 Ballering LA et al; Carcinogenesis 15 (5): 869-75 (1994)
The mechanism of action for 1,2-dichloroethane-induced toxicity is not known. However, studies in rats and mice indicate that 1,2-dichloroethane may be metabolized to 2-chloroacetaldehyde, S-(2-chloroethyl)glutathione, and other putative reactive intermediates capable of binding covalently to cellular macromolecules ... . The ability of a chemical to bind covalently to cellular macromolecules is often correlated with the induction of toxic effects ... . In addition, 1,2-dichloroethane has been shown to promote lipid peroxidation in vitro ... . Lipid peroxidation is also assoc with production of tissue damage. The lag time between inhalation exposure and onset of effects ... in an occupationally exposed 51-yr old male may have been a reflection, in part, of the time required to metabolize 1,2-dichloroethane to active intermediates.
DHHS/ATSDR; Toxicological Profile for 1,2-Dichloroethane p. 71 TP-93/06 (1994)
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