Bis(2-chloroethyl) ether

Toxicological Summary

Workers - Hazard via inhalation route

Systemic effects

Acute/short term exposure

DNEL related information

Local effects

Acute/short term exposure

DNEL related information

Workers - Hazard via dermal route

Systemic effects

Acute/short term exposure

DNEL related information

General Population - Hazard via inhalation route

Systemic effects

Acute/short term exposure

DNEL related information

Local effects

Acute/short term exposure

DNEL related information

General Population - Hazard via dermal route

Systemic effects

Acute/short term exposure

DNEL related information

General Population - Hazard via oral route

Systemic effects

Acute/short term exposure

DNEL related information

Additional information - General Population

BCEE is metabolized within the body and has only a low risk for bioaccumulation.

The acute oral LD50 for rat is 75 mg/kg bw, the dermal LD50 is 9 mg/kg bw (assuming that the information was based on test material and not ai) and the inhalation LC50 is 0.33 mg/L. A 13 hr inhalation period with rat resulted in an NOAEL of 205 mg/m³.

Within a period of 130 days, an air concentration of 420 mg/m³, inhaled by rats and guinea pigs 7 hours daily, 5 days per week, led to delayed weight gain of the male animals as opposed to the untreated control animals. The quality of this information is unclear since no further information was provided.

Volunteers inhalatively exposed to concentrations of about 550 ppm were reported to have suffered after a short time period from unbearable severe irritation to the eyes and nose combined with cough, gag reflex and nausea. The irritation was still noticeable at 260 and 100 ppm but no longer at 35 ppm. The odor, characterized as repugnant, was still distinguished even at 35 ppm.

This strong irritation reaction is considered a good warning system against poisoning.

The ATSDR report concludes:

"The principal reason for concern with BCEE is its apparent carcinogenic potential. The most direct evidence indicating that BCEE is carcinogenic is the increased incidence of hepatomas in two strains of mice dosed orally for 80 weeks (Innes et al. 1969). This is supported by limited data indicating that BCEE is mutagenic in some bacterial test systems, although several studies have yielded negative results. On the other hand, increased incidence of mouse liver hepatomas has been questioned as a reliable indication of true carcinogenic potential (Maronpot et al. 1987), and BCEE was not observed to cause a significant increase in tumors in a chronic feeding study in rats (Weisburger et al. 1981) or in parenteral exposure studies in mice (Theiss et al. 1977; Van Duuren et al. 1972) and rats (Norpoth et al. 1986). Also, no binding of BCEE to DNA and no foci of ATPase-deficient cells (a sign of pre-neoplastic effects) were detected in liver of rats exposed to BCEE (Gwinner et al. 1983), and no evidence of heritable chromosome damage was detected in a preliminary study in mice (Jorgenson et al. 1978). Consequently, while the positive carcinogenicity findings in mice are adequate to conclude that BCEE may be a human carcinogen, the evidence on this point is limited."