Update: May 2011
Current Massachusetts Regulatory Limit
ORSGL = 0.0003 mg/L
Federal Regulatory Limit
The U.S. EPA has not published an MCL for 1,4-dioxane.
Basis for Criteria
1,4-dioxane is likely to be carcinogenic to humans. Under the old U.S. EPA classification system, it was designated a B2 carcinogen. The ORSGL is calculated based on the IRIS chronic oral cancer potency factor and corresponds to the Drinking Water Program's target excess lifetime cancer risk of one in a million.
- Oral Drinking Water Cancer Unit Risk: 2.9 x 10-6 per ug/L (U.S. EPA, 2010)
- One in a million risk level calculated: 1 x 10-6 x 1 (ug/L)/2.9 x 10-6 = 0.34 ug/L (0.0003 mg/L)
Oral RfD: 0.03 mg/kg/day (US EPA, 2010)
liver and kidney toxicity; carcinogenicity
Likely To Be Carcinogenic to Humans/B2
The human data are inadequate for cancer risk assessment. Supporting data for the cancer classification comes from sufficient evidence for carcinogenicity in animal studies, including hepatic tumors in multiple species (three strains of rats, two strains of mice, and in guinea pigs); mesotheliomas of the peritoneum, mammary, and nasal tumors have also been observed in rats following 2 years of oral exposure to 1,4-dioxane.
The Kano et al., (2009) drinking water study was used as the principal study for derivation of an oral drinking water unit risk value. This study contained three dose groups and a control at lower doses than those used in previous studies. The most sensitive target organ for tumor formation was the liver. In addition, this study also noted increased incidence of peritoneal and mammary gland tumors. At a much lower incidence, nasal cavity tumors were also observed in high-dose male and female rats.
Several studies conducted in mouse skin and rat liver suggested that 1,4-dioxane does not initiate the carcinogenic process but is a promoter (Bull et al., 1986; King et al., 1973; Lundberg et al., 1987).
*LCMRL: 0.00004 mg/L
U.S. EPA Method 522
Modified SW-846 8260 SIM
Modified SW-846 8270 SIM
*In the late 1980's, the U.S. EPA replaced their designation of the PQL as a quantitation limit with the LCMRL. The LCMRL is defined as "the lowest true concentration for which the future recovery is predicted to fall, with high confidence (99% between 50% and 150% recovery)". The Agency has also developed a procedure for use in the drinking water program which allows laboratories to confirm that they can achieve a required Minimum Reporting Level (MRL) during their initial demonstration of capability. The U.S. EPA anticipates using standardized LCMRL/MRL procedures to support monitoring required under the Safe Drinking Water Act for unregulated contaminants (U.S. EPA, 2004).
EPA method 522 may be found at http://www.epa.gov/microbes/ordmeth.htm; however, there are a variety of alternative analytical protocols available that are based on existing modified methods that may be used to achieve a similar level of detection.
Other Regulatory Data
Any Health Advisories, Reference Doses (RfDs), cancer assessments or Cancer Potency Factors (CPFs) referenced in this document pertain to the derivation of the current guidance value. Updated information may be obtained from the following sources:
Health Advisories - The U.S. EPA provides guidance for shorter-term exposures for chemicals based on their non-cancer effects. Current health advisories may be more current than those used to derive MCLs and may be found at http://www.epa.gov/waterscience/drinking/standards/dwstandards.pdf
RfDs, cancer assessments and CPFs - For specific information pertaining to derivation of drinking water criteria, consult the Federal Register notice that announces the availability of the most current guidance for that chemical. In addition, information on other current RfDs and CPFs as well as cancer assessments for specific chemicals may be found in the U.S. EPA Integrated Risk Information System (IRIS) at http://www.epa.gov/iris/. Please note that the information in IRIS may differ from that used in the derivation process as published in the Federal Register notice.
Bull RJ; Robinson M; Laurie RD. 1986. Association of carcinoma yield with early papilloma development in SENCAR mice. Environ Health Perspect, 68: 11-17.
Kano H, Umeda Y, Kasai T, Sasaki T, Matsumoto M, Yamazaki K, Nagano K, Arito H, Fukushima S. 2009. Carcinogenicity studies of 1,4-dioxane administered in drinking-water to rats and mice for 2 years. Food Chem Toxicol, 47: 2776-2784.
King, M.E., Shefner, A.M. and Bates, R.R. 1973. Carcinogenesis bioassay of chlorinated dibenzodioxins and related chemicals. Env. Health Persp. 5:163-170.
Kociba, R.J., McCollister, S.B., Park, C., Torkelson, C.R. and Gehring, P.J. 1974. 1,4-dioxane. I. Results of a 2-year ingestion study in rats. Toxicol. Appl. Pharmacol. 30:275-286.
Lundberg, I., Hogberg, J., Kronevi, T., Holmberg, B. 1987. Three industrial solvents investigated for tumor promoting activity in the rat liver. Cancer Lett, 36: 29-33.
National Cancer Institute. (NCI) 1978. Bioassay of 1,4-dioxane for possible carcinogenicity, CAS No. 123-91-1. NCI Carcinogenesis Tech. Rep. Ser. No. 80. DHEW Publications NO. (NIH) PB-285-711.
U.S. EPA (U.S. Environmental Protection Agency). 2004. Revised Assessment of Detection and Quantitation Approaches. EPA 821-B-04-005. Engineering and Analysis Division. Office of Science and Technology. Office of Water.
U.S. EPA (U.S. Environmental Protection Agency). 2010. Integrated Risk Information System (IRIS). Washington, D.C. http://cfpub.epa.gov/ncea/iris/index.cfm (date accessed: May 2011).