This CICAD on 1,2-diaminoethane (ethylenediamine) was based on a review of human health concerns (primarily occupational, but also including an environmental assessment) prepared by the United Kingdom's Health and Safety Executive (Brooke et al., 1997). Data identified up to the end of 1994 were covered in the original review. An additional literature search up to July 1997 was conducted to identify any new information that had been published since the review was completed. Information on environmental fate and effects was based on the report of the German Chemical Society's Advisory Committee on Existing Chemicals of Environmental Relevance (BUA, 1997). The preparation and peer review of the source documents are described in Appendix 1. Information on the peer review of this CICAD is presented in Appendix 2. This CICAD was approved as an international assessment at a meeting of the Final Review Board, held in Tokyo, Japan, on 30 June - 2 July 1998. Participants at the Final Review Board meeting are listed in Appendix 3. The International Chemical Safety Card (ICSC 0269) produced by the International Programme on Chemical Safety (IPCS, 1993) has also been reproduced in this document. 1,2- Diaminoethane (CAS No. 107-15-3), commonly known as ethylenediamine (EDA), is a synthetic colourless to yellowish liquid at normal temperature and pressure. It is strongly alkaline and is miscible with water and alcohol. The main use for EDA is as an intermediate in the manufacture of tetraacetyl ethylenediamine, ethylenediaminetetraacetic acid (EDTA), organic flocculants, urea resins, and fatty bisamides. It is also used, to a much smaller extent, in the production of formulations for use in the printed circuit board and metal finishing industries, as an accelerator/curing agent in epoxy coatings/resins, and in the manufacture of pharmaceutical products. EDA is present as a contaminant (<0.5%) in commercially supplied fatty amines, which are used as wetting agents in bituminous emulsions. It is also used in the synthesis of carbamate fungicides, in surfactant and dye manufacture, and in photography development chemicals and cutting oils. EDA is a degradation product of ethylenebis(dithiocarbamate) fungicides. No atmospheric effects are expected, as reaction of EDA with hydroxyl radicals is likely to be rapid (half-life 8.9 h), and washout of volatilized EDA is expected. Volatilization to the atmosphere is likely from soil but not from water. Adsorption to soil particulates is strong through electrostatic binding; leaching through soil profiles to groundwater is not expected. Complex formation with metals and humic acids is expected. Biodegradation is the most likely source of breakdown in the environment and should be quite rapid; adaptation of microorganisms may improve degradation. Breakdown is less rapid in seawater than in fresh water. Bioaccumulation is unlikely. EDA has moderate acute toxicity in animals. It is a primary irritant, being corrosive when undiluted, and is also a skin sensitizer. EDA has not been tested for mutagenicity to current regulatory standards, and there are no assays for clastogenic activity or for the potential to express activity in somatic cells in vivo. Thus, there is insufficient information to draw firm conclusions regarding the mutagenic potential of EDA. EDA was not carcinogenic in animals. Non-neoplastic effects on the liver (pleomorphic changes to hepatocytes) have been observed in rats following oral dosing for 2 years at 45 mg EDA/kg body weight per day and above, with no effects seen at 9 mg EDA/kg body weight per day. Although the significance of these hepatic cell changes for human health is unclear, as well as whether or not they are a consequence of oral exposure (i.e., they might not occur via other routes, as they may be related to first-pass effects), they cannot be discounted, and the risk of their development should be characterized. In oral gavage dosing studies, effects on the rat eye (retinal atrophy and, at higher doses, cataract formation) were observed at doses of 100 mg EDA/kg body weight per day and above. Doses of 200 and 100 mg EDA/kg body weight per day and above were associated with renal damage in rats and mice, respectively. There was also some indication of effects in the spleen in mice and rats at doses of 400 mg EDA/kg body weight per day and above and in the thymus in rats at 800 mg/kg body weight per day. In inhalation studies, no effects were seen in rats at about 150 mg/m3 (60 ppm), and slight depilation was the only treatment-related effect observed at about 330 mg/m3 (132 ppm). Because diluted EDA is a skin irritant and a skin sensitizer, there may be a risk of developing irritant and/or allergic dermatitis if suitable personal protective equipment is not used in the occupational environment where skin contact can occur. EDA is also capable of inducing a state of respiratory tract hypersensitivity and provoking asthma in the occupational environment, and this is considered to be the major health effect of concern. The mechanism for the induction of the hypersensitive state is not proven, although the skin sensitizing potential of EDA and the limited evidence of immunological involvement in workers with EDA-provoked asthma are suggestive of an immunological mechanism. However, irrespective of the mechanism involved, the available data do not allow either elucidation of dose-response relationships or identification of the thresholds for induction of the hypersensitive state or provocation of an asthmatic response. The sample risk characterization in this document has, in order to assess the risks of other systemic effects, evaluated the risk of hepatic effects in occupationally exposed individuals. It concludes that when EDA is used in closed systems, the exposure, both measured and predicted from models, is substantially (by 100-fold or greater) less than the no-observed-effect level (NOEL) in rats; thus, adverse effects on the liver are unlikely. Exposure of the general public to EDA could not be evaluated owing to the lack of available data. Toxic thresholds for microorganisms may be as low as 0.1 mg EDA/litre. However, toxicity tests in culture media should be treated with caution, as the EDA may complex with metal ions. Effects may therefore be indirect, resulting from the loss of bioavailability of essential elements. LC50s for invertebrates and fish range from 14 to >1000 mg/litre. A no-observed-effect concentration (NOEC) for Daphnia reproduction has been reported at 0.16 mg/litre. Given the wide range of acute and chronic test results, a predicted no-effect concentration (PNEC) for aquatic organisms was taken as 16 μg/litre, based on application of an uncertainty factor of 10 to the lowest reported NOEC for Daphnia reproduction. Conservative assumptions for predicted environmental concentration (PEC) produce PEC/PNEC ratios indicating some concern from initial concentrations (i.e., at first release into the river or estuary). However, more refined exposure estimates indicate low risk to aquatic organisms.