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1) had elevated serum aspartate aminotransferase and lactic dehydrogenase, indicating severe hepatic damage. These enzymes were elevated 5 hours after exposure in one man who died 12 hours after exposure and 24 hours after exposure in the second patient who died 64 hours following exposure. Liver from the patient dying first had intrasinusoidal nuclear fragmentation consistent with Kupffer cell damage; autolysis precluded examination of the second patient’s liver. No studies were located regarding hepatic effects in animals after dermal exposure to 1,2-dibromoethane.

Animal studies also identify the upper respiratory tract as a site for 1,2-dibromoethane binding and metabolism. These animal studies are relevant to humans because they suggest a possibility for adverse effects in the human respiratory system following low-level exposure to 1,2-dibromoethane by inhalation. Cardiovascular Effects. Cardiovascular effects as terminal events were reported in patients dying after dermal and inhalation exposure to 1,2-dibromoethane. One individual also had acute myocardial lesions (Letz et al.

Although the size of the group studied was too small to analyze mortality rates on a year-by-year basis, a comparison of rates was done by grouping person-years of follow-up into four age ranges over the period of the study (23 years). No increase in mortality from any cause, including neoplasia, was identified in the 1,2-dibromoethane workers. Chronic inhalation exposure of rodents to 1,2-dibromoethane has been associated with neoplasms in the respiratory tract, as well as in other organ systems.

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