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There were no toxicokinetic studies that directly addressed absorption, distribution, metabolism, or excretion of 1,2-dibromoethane. However, sufficient information is available from existing dossier studies to infer toxicokinetic properties.

Systemic availability of 1,2-dibromoethane is dependent on absorption across body surfaces, which is increased by lipophilicity and small molecular weight. The partition coefficient (Log Pow) for dibromoethane is approximately 2; lipophilicity is generally regarded as a log Powof greater than 3.0, so dibromoethane is weakly hydrophilic, but close to the transition point that would allow presence in either medium. Water solubility was approximately 4000 mg/L, which is within the range defined as water soluble. The molecular weight of dibromoethane is 188, well below the size for exclusion by skin (about 500). Based on its known physical properties, dibromoethane would be expected to cross all body surfaces, although the proportion of the dose that penetrates the skin may be affected by time of contact and occlusion. Rowe et al, 1952, concluded that the substance crossed the dermal membranes in rabbits, however the study did not quantify the dermal absorption rate. Based upon this information it can be concluded that the substance will pass the dermal barrier in humans. The importance of time for dermal penetration in humans is explicitly stated as a criteria for systemic effects by Pflesser (1938).

All acute and subchronic studies in this dossier indicate that systemic effects are seen after oral, dermal, and inhalation exposure, indicating absorption across all these body surfaces and full systemic distribution. These in vivo reports are consistent with the prediction of penetration into the body according to the physical parameters. Rowe et al (1952) tested the acute effects of dibromoethane in six species (rat, guinea pig, rabbit, mouse, chicken, and monkey) and found LD50values to be within 10 fold of each other, ranging from 55 mg/kg in rabbits to 420 mg/kg in mice. Humans can therefore be assumed to have an acute toxicity close to this range. Monkeys were not tested for an LD50value, but appeared to be a sensitive species based on clinical signs after 49 days of inhalation exposure at 50 ppm whereas rabbits tolerated 59 days of exposure without apparent adverse effect. Rats exposed to 63 days of 50 ppm showed 50% mortality due to pneumonia and lung infections in the males that the authors did not attribute to treatment, but only 20% of females died (no report of cause of death), indicating a possible gender difference in metabolism or excretion. There was also a gender effect in rats when determining LD50values; the LD50in males was 150 mg/kg while the females were 120 mg/kg. No other species was tested for LD50in both genders. Pathology reports across species and both genders in rats indicated effects in liver, kidney, and lung, verifying systemic exposure by the inhalation route. Additionally, after both dermal and inhalation exposure, signs of central nervous system effects were noted, indicating the ability of dibromoethane to pass the blood brain barrier and penetrate a lipophilic tissue. 

Bioaccumulation is not expected for dibromoethane, despite its ability to penetrate lipophilic tissues as evidenced by effects in the central nervous system reported directly by Rowe et al (1952) and inferentially by Nitschke et al (1980; this report contained a reference for St George, 1937, of vertigo, nausea, giddiness, vomiting, and drowsiness that is likely to have come from human exposure reports). Nitschke et al, 1980, conducted a repeat dose study that observed effects in liver and nasal epithelium that largely resolved during a 90 day recovery period. If the dibromoethane bioaccumulated, nearly complete recovery would not be likely in this time frame.

There is little direct data to address metabolism. Genetic studiesin vitroindicate that dibromoethane is mutagenic regardless of the presence of S9 fraction, so it is not clear whether the parent compound is not metabolized or whether its metabolites are also mutagenic. One mechanism of action for the mutagenicity appears to be single strand DNA breakage from alkylation (White et al, 1981); its chemical structure indicates that dibromoethane would not require enzymatic modification to alkylate a nucleophilic center like DNA, bromine is a good leaving group. Nonetheless, evidence of fatty liver and other hepatic effects appear at lower doses than effects on other tissues, indicating a strong possibility that the liver P450s that are known to metabolize other halogenated alkanes and produce these liver effects are also metabolizing dibromoethane. Male and female rats both developed tumors in a carcinogenesis study, but the pattern of tissue tumors was different between the genders, reinforcing the possibility of a gender-specific effect that could reflect a different metabolic profile (Fielding-Douglas et al, 1982). Also, epithelial cells appear to be more susceptible to the hyperplasia and ultimate production of tumors than other cell types, and a specific metabolic profile within that cell type would be consistent with that susceptibility.

Elimination can be assumed to occur from the above evidence of recovery when exposure to the compound ends. Due to its hydrophilicity, the expected route of elimination for dibromoethane would be the urine.