Arsenic in Drinking Water: 2001 Update
Robert A. Goyer, M.D.
Professor Emeritus, University of Western Ontario
Chair, Subcommittee to Update the 1999 Arsenic in Drinking Water Report
Committee on Toxicology
Board on Environmental Studies and Toxicology
Division on Earth and Life Studies
National Research Council
Environment, Technology and Standards Subcommittee
U.S. House of Representatives
October 4, 2001
Good morning Mr. Chairman and members of the Committee. I am Robert Goyer, M.D., Professor Emeritus of Pathology at the University of Western Ontario, and I am pleased to appear before you today on behalf of the National Research Council’s (NRC) Subcommittee to Update the 1999 Arsenic in Drinking Water Report, which prepared the report Arsenic in Drinking Water: 2001 Update, released in September 2001. In addition to serving as chair of that subcommittee, I served as chair of the Subcommittee on Arsenic in Drinking Water, which prepared the NRC report Arsenic in Drinking Water released in 1999.
Following the release of the 1999 report, EPA reviewed its regulations for arsenic in drinking water, and on January 22, 2001, EPA issued a pending standard for arsenic in drinking water of 10 ìg/L. That pending standard was primarily based on dose-response models and extrapolation from a cancer study of a Taiwanese population exposed to high concentrations of arsenic in its drinking water. On March 23, 2001, EPA published a notice that delayed the effective date of the arsenic rule pending further study of options for revising the MCL for arsenic. To incorporate the most recent scientific research into its decision, EPA’s Office of Water subsequently requested that the NRC independently review studies on the health effects of arsenic published since the 1999 NRC report.
In response to EPA’s request, the NRC assigned the project to the Committee on Toxicology (COT) and convened the Subcommittee to Update the 1999 Arsenic in Drinking Water Report. The members of that subcommittee were selected by the NRC from the academic community and other organizations for expertise in relevant scientific disciplines. The 2001 subcommittee was charged with the task of preparing a report updating the scientific analyses, uncertainties, and findings of the 1999 report on the basis of relevant toxicological and health-effects studies published since the 1999 NRC report, and to evaluate the analyses subsequently conducted by EPA in support of its regulatory decision-making for arsenic in drinking water. The subcommittee addressed only scientific topics relevant to toxicological risk and health effects of arsenic. It did not address questions of economics, cost-benefit assessment, control technology, exposure assessment in U.S. populations, or regulatory decision-making. It did not comment or make recommendations on risk management or policy decisions.
The subcommittee considered several hundred new scientific articles on arsenic published since the 1999 NRC report. It also heard presentations from the EPA administrator; other EPA representatives; the EPA Science Advisory Board; other scientists with expertise in arsenic toxicity; federal, state, and local government agencies; trade organizations; public-interest groups; and concerned individuals.
The subcommittee concluded that there is a sound database on the carcinogenic effects of arsenic in humans that is adequate for the purposes of a risk assessment, and that the data indicate arsenic causes cancer in humans at doses that are close to drinking water concentrations that occur in the United States. Arsenic-induced lung and bladder cancers should continue to be the principal focus of arsenic risk assessment for regulatory decision making. Unlike many other chemicals, arsenic data are sufficient so that there is no need to extrapolate from animals to humans or from very high doses to low doses. Since the 1999 NRC report, additional studies have been published that strengthen the association between arsenic and cancer. There are 4 major new epidemiological studies: three studies that show a positive relationship between cancer (bladder and lung) and arsenic, and one study from Utah that does not show such a relationship. However, the study from Utah has several limitations that make it insufficient for use in a quantitative risk assessment. The human data from southwestern Taiwan used by EPA in its risk assessment remain the most appropriate for determining quantitative lifetime cancer risk estimates.
The major findings of the Arsenic in Drinking Water: 2001 Update confirmed the conclusion of the 1999 report that chronic exposure to arsenic is associated with an increased incidence of bladder and lung cancer at arsenic concentrations below the current MCL. This conclusion was strengthened by new epidemiological studies. The subcommittee confirmed that the southwestern Taiwanese study, which was the basis of the 1999 report, is the optimal study for determining the cancer risks from chronic exposure to arsenic. However, the present report suggests that risks for bladder and lung cancer are greater than the risk estimates on which EPA based its January 2001 pending rule. Reasons for the increased risk estimate include: (a) use of a different biostatistical model that provided a better fit to the available data, (b) use of an external rather than internal comparison population, (c) improved assumptions for determining arsenic exposures and, finally, (d) relating the risks to the Taiwanese population to US cancer rates. Estimates of risks from low-level exposures were based on a Poisson linear extrapolation from observed data. Available data on the mode of action do not provide evidence for a threshold or non-linear dose-response. Several biochemical effects have been observed in cells in vitro at concentrations that might exist in urine following the ingestion of drinking water containing arsenic concentrations of 3-50 micrograms per liter, a range that is currently the focus of low-dose risk assessment.
There are also numerous studies showing an association between noncancer health outcomes for arsenic, such as cardiovascular (hypertension) effects and diabetes mellitus, and more limited evidence for reproductive effects.
The subcommittee identified a number of uncertainty factors and population variability that might influence the risk estimates, including genetic factors, age sex, and simultaneous exposure to other cancer causing compounds. There is also uncertainty regarding the possible interaction between arsenic ingestion and smoking in the causation of cancer. Research should be conducted on a priority basis to reduce those uncertainties which are relevant to arsenic risk assessment. More research is needed on the possible association between arsenic exposure cancers other than skin, bladder, and lung, as well as noncancer effects, particularly impacts on the circulatory system (high blood pressure, heart disease, and stroke), diabetes, and reproductive outcomes. Future studies of the relationships between arsenic ingestion and both noncancer and cancer outcomes should be designed to have sufficient power to determine risks in potentially susceptible subpopulations, including children; they should consider factors (e.g., smoking, diet, genetics) that could influence susceptibility to arsenic; and they should collect detailed exposure information, all in an effort to reduce uncertainty in the risk assessment. In addition, more information is needed on the variability in metabolism of arsenic among individuals and the effect of that variability on an arsenic risk assessment. Laboratory and clinical research is also needed to define the mechanisms by which arsenic induces cancer to clarify the risks at lower doses.
The theoretical lifetime excess risk for bladder and lung cancer combined is estimated to be approximately 1 in 1000 at 3 micrograms per liter.
Thank you for inviting me to testify before the House Science Committee. I would be happy to answer any questions you have.