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decreased, especially for those with greater than 15 years since first exposure. US EPA (1984) also
noted that smoking was a potential confounder, exposure analysis failed to show a dose-response trend,
and exposure to multiple chemicals was also a potential confounder. The SMR for respiratory cancer
was much higher in workers exposed in the isopropyl alcohol manufacturing unit to other chemicals in
addition to ECH than in the group exposed to ECH alone (SMRs = 214.8 and 63.3, respectively). US
EPA (1984) concluded that the studies by Enterline (1978, 1981) provide only limited evidence for the
human carcinogenicity of ECH.
Tassignon et al. (1983) studied the mortality of workers exposed to ECH in four European
manufacturing plants which produced ECH, epoxy resins, glycerin and other ECH-derived specialty
chemicals. Data was collected on 606 male workers with at least one year of exposure to ECH starting
at least 10 years before December 31, 1978. No excess cancer mortality due to ECH exposure was
observed; however, the authors noted that the small cohort size, short duration of the observation
period and the limited number of deaths due to low average age (42 years) limited the power of the
study.
Animal Studies
Female ICR/Ha Swiss mice were treated with ECH by dermal application, subcutaneous injection or
intraperitoneal injection (Van Duuren et al., 1974). Dermal applications were performed 3 times/week;
2 mg ECH in 0.1 ml acetone was applied to 50 animals for 83 weeks. Untreated and vehicle control
groups of 100 and 50 animals, respectively, were included. No increased incidence in skin tumors were
noted in the treated animals. Intraperitoneal injections were performed weekly for 64 weeks; 1 mg
ECH in 0.05 ml tricaprylin was injected into 30 animals. Untreated and vehicle control groups of 100
and 30 animals, respectively, were included. No treatment-related tumor induction was noted in the
exposed animals. Subcutaneous injections were performed weekly for 83 weeks; 1 mg ECH dissolved
in 0.05 ml tricaprylin was injected into 50 animals. Untreated and vehicle control groups of 100 and 50
animals, respectively, were included. An increased incidence of injection site tumors was noted (6/50
sarcomas, 1/50 adenocarcinomas) in the treated animals as compared to controls (no tumors in
untreated controls, 1/50 sarcomas in vehicle controls).
Laskin et al. (1980) exposed male non-inbred Sprague-Dawley rats to 10, 30 or 100 ppm ECH by
inhalation for the lifetime of the animals. Exposure durations were 6 hours/day, 5 days/week. Control
groups consisted of 50 untreated animals and 100 air-treated animals. All groups demonstrated a high
degree of early mortality, primarily due to respiratory disease (50% mortality by 64 weeks). Of a group
of animals exposed to 100 ppm ECH for 6 weeks, 18/140 developed nasal cavity tumors, which were
primarily squamous cell carcinomas. A group of 100 animals exposed for life (approximately 144
weeks) to 30 ppm developed 2 respiratory tract tumors; 1 larynx squamous papilloma and 1 nasal
squamous cell carcinoma. The laryngeal tumor was misidentified in the original manuscript as a nasal
tumor (US EPA, 1984). These tumor incidences were not significant when compared to those of the
control group; however, they were significant when compared to the 1920 historical control animals
from that laboratory, none of which had developed nasal squamous carcinoma. No nasal or respiratory
tract tumors were noted in a group of 100 animals exposed for life to 10 ppm. No equivalent nasal or
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