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CAS 107-06-2

1,2-Dichloroethane (Ethylene dichloride)

carcinogenVOCHAPdrinking water contaminantOSHA carcinogen

1,2-Dichloroethane is the industrial chemical intermediate used to make most of the world's vinyl chloride — and PVC production plants have contaminated the air and groundwater in communities from Texas to West Virginia for decades. It is one of the most common organic contaminants in drinking water at Superfund sites.

Where It Comes From

Ethylene dichloride (EDC) has been produced since the 1850s and became one of the highest-volume industrial chemicals in the 20th century primarily as an intermediate in vinyl chloride monomer (VCM) production — over 80% of EDC produced is used to make VCM, which is then polymerized to PVC [1]. Production is concentrated along the Gulf Coast in Louisiana and Texas, where the chemical corridor known as "Cancer Alley" includes numerous EDC/VCM production facilities. Historical contamination from PVC and EDC manufacturing has contaminated soil and groundwater at dozens of locations [2]. EDC was also used as a lead scavenger in leaded gasoline (removing lead deposits from engines), as a fumigant for grain, and as a solvent. Its environmental persistence and widespread production have made it one of the most common Superfund organic contaminants [3].

How You Are Exposed

Occupational inhalation in chemical manufacturing facilities that produce or use EDC is the primary high-dose route [1]. Community air near EDC/PVC production facilities — particularly in industrial corridors — is a significant exposure source. Contaminated groundwater near industrial sites and Superfund sites is a drinking water concern [2]. Historically, EDC was used as a fumigant on stored grain, and residues in grain-based foods were a consumer dietary concern. Vapor intrusion from EDC-contaminated soil into homes is a pathway in affected communities [3].

Why It Matters

EDC is classified as a probable human carcinogen (IARC Group 2A) with evidence for liver cancer, hemangiosarcoma, and possibly lung cancer in occupationally exposed workers [1]. The mechanism involves metabolic activation by cytochrome P450 enzymes to chloroacetaldehyde and chloroethylene oxide — reactive metabolites that form DNA adducts and alkylate proteins. Acute high-level EDC exposure affects the CNS (headache, dizziness, unconsciousness) and causes severe liver and kidney damage [2]. Long-term lower-level exposure is associated with liver function abnormalities, neurological effects, and the elevated cancer risks seen in production worker cohorts. EDC is also a reproductive toxin in animal studies [3].

Who Is at Risk

Workers in EDC and VCM production, PVC manufacturing, and industries using EDC as a solvent carry the highest occupational burdens [1]. Communities in Louisiana's industrial corridor near PVC/EDC facilities have documented elevated cancer rates that have drawn regulatory attention [2]. People who drink groundwater from private wells in areas with EDC contamination from industrial sites face drinking water exposure.

How to Lower Your Exposure

If you live near EDC-producing facilities or in an area with known EDC groundwater contamination, use a certified reverse-osmosis or carbon block filter on your drinking water [1]. Support EPA enforcement of air emissions standards at nearby production facilities and review facility emissions data through EPA's ECHO database [2]. Workers in EDC-using industries: implement engineering controls (local exhaust ventilation, closed systems), use appropriate PPE, and have liver function testing as part of occupational health monitoring [3].

References

  1. [1]IARC. 1,2-Dichloroethane. IARC Monographs Vol 71. 1999. https://monographs.iarc.who.int/
  2. [2]ATSDR. Toxicological Profile for 1,2-Dichloroethane. https://www.atsdr.cdc.gov/toxprofiles/tp38.pdf
  3. [3]EPA. Ethylene Dichloride (1,2-Dichloroethane). https://www.epa.gov/sites/default/files/2016-09/documents/ethylene-dichloride.pdf
  4. [4]Wing S, et al. Environmental justice in North Carolina's hog industry. Environ Health Perspect. 2000;108(3):225-31.

Recovery & Clinical Information

Body Half-Life

1,2-Dichloroethane is metabolized in the liver by CYP2E1 and glutathione S-transferase — blood half-life is approximately 2-4 hours [1]. N-acetyl-S-(2-hydroxyethyl)cysteine and 2-chloroethanol are urinary metabolites detectable for 1-3 days [2].

Testing & Biomarkers

Blood and exhaled air 1,2-DCE for acute exposures; urinary thiodiglycolic acid as occupational biomarker [1]. Liver function tests and kidney function for chronic exposure assessment [2].

Interventions

Activated carbon or reverse osmosis filters remove 1,2-DCE from drinking water [1]. Address vapor intrusion from contaminated sites with sub-slab depressurization [2]. No specific antidote; supportive care for liver effects [1].

Recovery Timeline

Blood levels normalize within 4-8 hours; urine metabolites within 2-3 days [1]. Liver enzyme elevations from chronic exposure resolve within weeks of source removal [2].

Recovery References

  1. [1]ATSDR (2001). Toxicological Profile for 1,2-Dichloroethane. https://www.atsdr.cdc.gov/toxprofiles/tp38.pdf
  2. [2]EPA IRIS (1987). 1,2-Dichloroethane. https://iris.epa.gov/ChemicalLanding/&substance_nmbr=0149

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