Hexavalent Chromium


Hexavalent chromium is also know as chromium-6, or Cr(VI).

It is currently regulated under a US drinking water standard for total chromium of 0.1 mg/L, set in 1991. The standard covers both Cr(VI) and Cr(III), although EPA assumes that a measurement of total chromium is 100 percent Cr(VI), the more toxic form.  EPA is currently revising its risk assessment for Cr(VI).

California completed development of a public health goal of 0.02 micrograms/L for Cr(VI) in 2011, based in part on a 2008 rodent study by the National Toxicology Program suggesting that oral exposure may lead to cancer in humans. The California Department of Health Services in 2014 adopted a drinking water standard for Cr(VI) of 10 micrograms/L.

Monitoring guidance

In May 2012, EPA finalized the third round of Unregulated Contaminant Monitoring. Assessment monitoring of Cr(VI) and total chromium is included.

Risk assessment

Revision of the Cr(VI) risk assessment began in 2001 with the NTP rodent study. An infusion of industry-funded research investigating the mode of action underlying toxicity from oral exposure to Cr(VI) began entering the peer-reviewed literature in 2011. An external panel advising EPA’s Integrated Risk Information System program advised EPA to take the time to include the results of this latest research. The USEPA IRIS program is currently developing a toxicological summary for public comment.

AWWA resources

AWWA’s DrinkTap website provides water utilities with information pertinent to communication about Cr(VI) to the public. Systems with specific questions should email AWWA Public Affairs.

Additional information

EPA activities

Third UCMR

In addition to EPA issuing Cr(VI) monitoring guidance in 2011, the agency in May 2012 finalized requirements for the third round of monitoring under the third Unregulated Contaminant Monitoring Rule, which includes monitoring for Cr(VI).

From January 2013 through December 2015, all community and nontransient noncommunity systems serving more than 10,000 persons, and a statistical sample of small systems, must monitor for Cr(VI) and 27 other unregulated contaminants. Systems in this group will also monitor total chromium at the same locations (points-of-entry to the distribution system and maximum residence time locations).

The minimum reporting level for Cr(VI) is 0.03 micrograms/L.

UCMR3 monitoring data was released in July 2016.

Risk assessment

In 2010 USEPA released an external peer-review draft assessment of health risks posed by Cr(VI). This draft assessment by the Integrated Risk Information System program frames oral exposure risks from Cr(VI) as carcinogenic and potentially toxic at very low concentrations in drinking water.

Research funded through the American Chemistry Council investigating the underlying toxicity from oral exposure to Cr(VI) began entering the peer-reviewed literature in 2011. An external panel convened by the IRIS program advised USEPA to take the time to include the results of this latest research and address a number of concerns with the agency's draft toxicology review. The IRIS process is an eight step process.  The first step is hazard identification; this step was completed in 2014. EPA has not posted a schedule for when the remaining steps in the process will be completed.

While individual states like California may determine that it is appropriate to adopt Cr(VI) drinking water standards, USEPA has identified revision of the IRIS risk assessment for Cr(VI) as a critical step in the agency’s process for deciding whether to regulate Cr(VI).

Completion of the IRIS assessment and compilation of national occurrence data from UCMR will provide information necessary to characterize the potential hazard posed by Cr(VI) in drinking water in the United States.

California regulation

The California Department of Public Health proposed a Cr(VI) drinking water standard of 0.010 mg/L in August 2013, and the California-Nevada Section of AWWA and national association filed joint comments (PDF) and supporting analyses (PDF).

CDPH finlized the standard in 2014.  Additional information about the CDPH standard and Cr(VI) occurrence in California is available on the CDPH website.

The California Office of Environmental Health Hazard Assessment had earlier set a final Public Health Goal for Cr(VI) of 0.02 micrograms/L in drinking water. The PHG is not an enforceable standard. 


Recent research


1. Welling R, Beaumont JJ, Petersen SJ, Alexeeff GV, Steinmaus C. 2014. Chromium VI and stomach cancer: a meta-analysis of the current epidemiological evidence.  Occup Environ Med. 2014 Sep 17. pii: oemed-2014-102178. doi: 10.1136/oemed-2014-102178.   

2. Schlosser PM, Sasso AF. 2014. A revised model of ex-vivo reduction of hexavalent chromium in human and rodent gastric juices. Toxicol Appl Pharmacol. 2014 Aug 20;280(2):352-361. doi: 10.1016/j.taap.2014.08.010.   


1. Jin LF, Wang YY, Zhang ZD, Yuan YM, Hu YR, Wei YF, Ni J. 2013. Cytotoxicity and genome-wide microarray analysis of intestinal smooth muscle cells in response to hexavalent chromium induction. Dongwuxue Yanjiu. June, 34(3):E93-E100 Abstract.

2. Kirman, C.R., LL Aylward, M. Suh, M.A. Harris, CM. Thompson, LC. Haws, D.M. Proctor, W. Parker, and S.M. Hays. 2013. Physiologically Based Pharmacokinetic Model for Humans Orally Exposed to Chromium. Chemico-Biological Interactions. 204(1):13-27. Manuscript.

3. O'Brien, T.J., H. Ding, M. Suh, CM. Thompson, B.L. Parsons, M.A. Harris, L.C. Haws, W.A. Winkelman, J.C Wolf, J.G. Hixon, A.M. Schwartz, M.B. Myers, L.C Haws, and D.M. Proctor. 2013. Assessment of K-Ras mutant frequency and micronucleus incidence in the mouse duodenum following 90-days of exposure to Cr(VI) in drinking water. Mutation Research. June, 754(1–2):15–21. Manuscript.

3. Seidel, C.J. and C.J. Corwin. 2013. Total chromium and hexavalent chromium occurrence analysis, Journal AWWA, June, 105(6):E-310-319. Manuscript.

4. Seidel, C.J., I.N. Najm, N.K. Blute, C.J. Corwin, and X. Wu. 2013. National and California treatment costs to comply with potential hexavalent chromium MCLs, Journal AWWA June, 105(6):E-320-336. Manuscript.

5. Thompson, C.M, D.M. Proctor, M. Suh, L.C. Haws, and M.A. Harris. 2013. Mode of Action Underlying Development of Rodent Small Intestinal Tumors Following Oral Exposure to Hexavalent Chromium and Relevance to Humans. Critical Reviews in Toxicology. 43(3):244-274. Manuscript.

6. Thompson, CM., C.R. Kirman, D.M. Proctor, LC Haws, M. Suh, S.M. Hays, and M.A. Harris. 2013. A Chronic Oral Reference Dose for Hexavalent Chromium—Induced Intestinal Cancer. Accepted Journal of Applied Toxicology. June 2, 2013. Manuscript.

7.  Witt KL, Stout MD, Herbert RA, Travlos GS, Kissling GE, Collins BJ, Hooth MJ. 2013. Mechanistic Insights from the NTP Studies of Chromium. Toxicol Pathol. 2013 Jan 18. [Epub ahead of print] Abstract.


1.  Kopec, A.K. , S. Kim, A.L. Forgacs, T.R. Zacharewski, D.M. Proctor, M.A., Harris, L.C. Haws, and C.M. Thompson. 2012. Genome-wide gene expression effects in B6C3F1 mouse intestinal epithelia following 7 and 90 days of exposure to hexavalent chromium in drinking water. Toxicology and Applied Pharmacology. 259(1):13-26. Manuscript.

 2.  Kopec, A.K., C.M. Thompson, S. Kim, A.L. Forgacs, and T.R. Zacharewski. 2012. Comparative toxicogenomic analysis of oral Cr(VI) exposure effects in rat and mouse small intestinal epithelia. Toxicology and Applied Pharmacology. Manuscript. 

 3.  Proctor, D., M. Suh, L.L. Aylward, C.R. Kirman, M.A. Harris, C.M. Thompson, H. Gurleyuk, R. Gerads, L.C. Haws, and S.M. Hays. 2012. Hexavalent Chromium Reduction Kinetics in Rodent Stomach Contents. Chemosphere. 2012 Oct;89(5):487-93. Epub 2012 June 8.

 4.  Thompson, C.M., D.M. Proctor, and M.A. Harris. 2012. Duodenal GSH/GSSG Ratios in Mice Following Oral Exposure to Cr(VI). Toxicological Sciences. 126(1): 287-288. doi:10.1093/toxsci/kfr337. Letter to Editor.

 5.  Thompson, C.M., J.G. Hixon, D.M. Proctor, L.C. Haws, M. Suh, J.D. Urban,and M.A. Harris. 2012. Assessment of Genotoxic Potential of Cr(VI) in the Mouse Duodenum: An In Silico Comparison with Mutagenic and Nonmutagenic Carcinogens Across Tissues. Regul Toxicol Pharmacol. 2012 Oct;64(1):68-76. Epub 2012 June 15.

 6.  Thompson, C.M., Federov, Y., Brown, D.D., Suh, M., Proctor, D.M., Kuriakose, L., Haws, L.C., Harris, M.A.. 2012. Assessment of Cr(VI)-Induced Genotoxicity Using High Content Analysis. PLoS ONE. 2012.7(8): e42720. Manuscript.

 7.  Wang X, Mandal AK, Saito H, Pulliam JF, Lee EY, Ke ZJ, Lu J, Ding S, Li L, Shelton BJ, Tucker T, Evers BM, Zhang Z, Shi X. 2012. Arsenic and chromium in drinking water promote tumorigenesis in a mouse colitis-associated colorectal cancer model and the potential mechanism is ROS-mediated Wnt/β-catenin signaling pathway. Toxicol Appl Pharmacol. 2012 Jul 1;262(1):11-21. doi: 10.1016/j.taap.2012.04.014. Epub 2012 Apr 19. Abstract.


1.  Thompson, C.M., L.C. Haws, M.A. Harris, N.M. Gatto, and D.M. Proctor. 2011. Application of the U.S. EPA Mode of Action Framework for Purposes of Guiding Future Research: A Case Study Involving the Oral Carcinogenicity of Hexavalent Chromium. Toxicological Sciences. 119(1): 20-40. Manuscript and Supplemental data

2.  Thompson, C.M., D.M. Proctor, L.C. Haws, C.D. Hébert, S.D. Grimes, H.G. Shertzer, A.K. Kopec, J.G. Hixon, T.R. Zacharewski, and M.A. Harris. 2011. Investigation of the Mode of Action Underlying the Tumorigenic Response Induced in B6C3F1 Mice Exposed Orally to Hexavalent Chromium. Toxicological Sciences. 123(1):58-70. Manuscript and Supplemental data.

3.  Thompson, C.M., D.M. Proctor, M. Suh, L.C. Haws, C.D. Hébert, J.F. Mann, H.G. Shertzer, J.G. Hixon, and M.A. Harris. 2011. Comparison of the effects on hexavalent chromium in the alimentary canal of F344 rats and B6C3F1 mice following exposure in drinking water: Implications for carcinogenic modes of action. Toxicological Sciences. 125(10: 79-90. Manuscript and Supplemental data.

4.  Zhitkovich A.. 2011. Chromium in drinking water: sources, metabolism, and cancer risks. Chem Res Toxicol. 2011 Oct 17;24(10):1617-29. doi: 10.1021/tx200251t. Epub 2011 Jul 28. Manuscript.