Risk Assessment of Radon in Drinking Water Committee on Risk Assessment of Exposure to Radon in Drinking Water Board on Radiation Effects Research Commission on Life Sciences National Research Council NATIONAL ACADEMY PRESS Washington, D.C. 1999 Notice Committee Preface Contents Public Summary Executive Summary NOTICE: The project that is the subject of this report was approved by the Governing Board of the National Research Council, whose members are drawn from the councils of the National Academy of Sciences, the National Academy of Engineering, and the Institute of Medicine. The members of the committee responsible for the report were chosen for their special competences and with regard to appropriate balance. This report was prepared under EPA Contract EPA X825492-01-0 between the National Academy of Sciences and the Environmental Protection Agency. Library of Congress Cataloging-in-Publication Data Risk assessment of radon in drinking water / Committee on Risk Assessment of Exposure to Radon in Drinking Water, Board on Radiation Effects Research, Commission on Life Sciences, National Research Council.           p. cm.      Includes bibliographical references and index.      ISBN 0-309-06292-6 (casebound).      1. Drinking water--Contamination--United States. 2. Radon--Health aspects. 3. Indoor air pollution--Health aspects--United States. 4. Radon mitigation. 5. Health risk assessment--United States. I. National Research Council (U.S.). Committee on Risk Assessment of Exposure to Radon in Drinking Water.      RA592.A1 R57 1999                                     99-6134      615.9'02dc21 Risk Assessment of Radon in Drinking Water is available for sale from the National Academy Press, 2101 Constitution Avenue, N.W., Box 285, Washington, DC 20055; 1-800-624-6242 or 202-334-3313 (in the Washington metropolitan area); Internet, http://www.nap.edu Copyright 1999 by the National Academy of Sciences. All rights reserved. Printed in the United States of America COMMITTEE ON RISK ASSESSMENT OF EXPOSURE TO RADON IN DRINKING WATER JOHN DOULL (Chair), University of Kansas Medical Center, Kansas City, KS THOMAS B. BORAK, Colorado State University, Fort Collins, CO JAMES E. CLEAVER, Department of Dermatology, University of California, San Francisco, CA KEITH F. ECKERMAN, Oak Ridge National Laboratory, Oak Ridge, TN LINDA C.S. GUNDERSEN, US Geological Survey, Reston, VA NAOMI H. HARLEY, New York University School of Medicine, New York, NY CHARLES T. HESS, University of Maine, Orono, ME PHILIP K. HOPKE, Clarkson University, Potsdam, NY NANCY E. KINNER, University of New Hampshire, Durham, NH KENNETH J. KOPECKY, Fred Hutchinson Cancer Research Center, Seattle, WA THOMAS E. McKONE, University of California, Berkeley, CA RICHARD G. SEXTRO, Lawrence Berkeley National Laboratory, Berkeley, CA CLS ADVISER JONATHAN M. SAMET, Johns Hopkins University, Baltimore, MD NATIONAL RESEARCH COUNCIL STAFF STEVEN L. SIMON, Study Director, Board on Radiation Effects Research KAREN M. BRYANT, Project Assistant DORIS E. TAYLOR, Staff Assistant NORMAN GROSSBLATT, Editor SPONSOR'S PROJECT OFFICER NANCY CHIU, US Environmental Protection Agency BOARD ON RADIATION EFFECTS RESEARCH JOHN B. LITTLE (Chair), Harvard School of Public Health, Boston, MA R.J. MICHAEL FRY, Oak Ridge, TN* S. JAMES ADELSTEIN, Harvard Medical School, Boston, MA†‡ VALERIE BERAL, University of Oxford, United Kingdom EDWARD R. EPP, Harvard University, Boston, MA† HELEN B. EVANS, Case Western Reserve University, Cleveland, OH† MERRIL EISENBUD, Chapel Hill, NC (deceased August 1997) MAURICE S. FOX, Massachusetts Institute of Technology, Cambridge, MA§ PHILIP C. HANAWALT, Stanford University, Palo Alto, CA (member until 6/30/98)|| LYNN W. JELINSKI, Cornell University, Ithaca, NY WILLIAM F. MORGAN, University of California, San Francisco† WILLIAM J. SCHULL, The University of Texas Health Science Center, Houston, TX DANIEL O. STRAM, University of Southern California, Los Angeles, CA SUSAN W. WALLACE, University of Vermont, Burlington, VT H. RODNEY WITHERS, UCLA Medical Center, Los Angeles, CA NATIONAL RESEARCH COUNCIL STAFF EVAN B. DOUPLE, Director, Board on Radiation Effects Research RICK JOSTES, Senior Program Officer STEVEN L. SIMON, Senior Program Officer CATHERINE S. BERKLEY, Administrative Associate KAREN BRYANT, Project Assistant PEGGY JOHNSON, Project Assistant DORIS E. TAYLOR, Staff Assistant *New BRER Chair effective 7/1/98 †New members effective 7/1/98 ‡IOM §NAS.NAE ||NAS COMMISSION ON LIFE SCIENCES THOMAS D. POLLARD (Chair), The Salk Institute for Biological Studies, La Jolla, CA FREDERICK R. ANDERSON, Cadwalader, Wickersham & Taft, Washington, DC JOHN C. BAILAR, III, University of Chicago, IL PAUL BERG, Stanford University School of Medicine, Palo Alto, CA JOANNA BURGER, Rutgers University, Piscataway, NJ SHARON L. DUNWOODY, University of Wisconsin, Madison, WI JOHN L. EMMERSON, Indianapolis, IN NEAL L. FIRST, University of Wisconsin, Madison, WI URSULA W. GOODENOUGH, Washington University, St. Louis, MO HENRY W. HEIKKINEN, University of Northern Colorado, Greeley, CO HANS J. KENDE, Michigan State University, East Lansing, MI CYNTHIA J. KENYON, University of California, San Francisco, CA DAVID M. LIVINGSTON, Dana-Farber Cancer Institute, Boston, MA THOMAS E. LOVEJOY, Smithsonian Institution, Washington, DC DONALD R. MATTISON, University of Pittsburgh, Pittsburgh, PA JOSEPH E. MURRAY, Wellesley Hills, MA EDWARD E. PENHOET, Chiron Corporation, Emeryville, CA MALCOLM C. PIKE, Norris/USC Comprehensive Cancer Center, Los Angeles, CA JONATHAN M. SAMET, The Johns Hopkins University, Baltimore, MD CHARLES F. STEVENS, The Salk Institute for Biological Studies, La Jolla, CA JOHN L. VANDEBERG, Southwest Foundation for Biomedical Research, San Antonio, TX NATIONAL RESEARCH COUNCIL STAFF PAUL GILMAN, Executive Director ALVIN G. LAZEN, Associate Executive Director The National Academy of Sciences is a private, nonprofit, self-perpetuating society of distinguished scholars engaged in scientific and engineering research, dedicated to the furtherance of science and technology and to their use for the general welfare. Upon the authority of the charter granted to it by the Congress in 1863, the Academy has a mandate that requires it to advise the federal government on scientific and technical matters. Dr. Bruce M. Alberts is president of the National Academy of Sciences. The National Academy of Engineering was established in 1964, under the charter of the National Academy of Sciences, as a parallel organization of outstanding engineers. It is autonomous in its administration and in the selection of its members, sharing with the National Academy of Sciences the responsibility for advising the federal government. The National Academy of Engineering also sponsors engineering programs aimed at meeting national needs, encourages education and research, and recognizes the superior achievements of engineers. Dr. William A. Wulf is the president of the National Academy of Engineering. The Institute of Medicine was established in 1970 by the National Academy of Sciences to secure the services of eminent members of appropriate professions in the examination of policy matters pertaining to the health of the public. The Institute acts under the responsibility given to the National Academy of Sciences by its congressional charter to be an adviser to the federal government and, upon its own initiative, to identify issues of medical care, research, and education. Dr. Kenneth I. Shine is president of the Institute of Medicine. The National Research Council was organized by the National Academy of Sciences in 1916 to associate the broad community of science and technology with the Academy's purposes of furthering knowledge and advising the federal government. Functioning in accordance with general policies determined by the Academy, the Council has become the principal operating agency of both the National Academy of Sciences and the National Academy of Engineering in providing services to the government, the public, and the scientific and engineering communities. The Council is administered jointly by both Academies and the Institute of Medicine. Dr. Bruce M. Alberts and Dr. William A. Wulf are chairman and vice chairman, respectively, of the National Research Council. Preface At the request of the Environmental Protection Agency (EPA) pursuant to a congressional mandate (amendment to bill S. 1316 to amend title XIV of the Public Health Service Act commonly known as the Safe Drinking Water Act), the National Research Council has appointed a multidisciplinary committee to conduct a study and report on the health risks associated with exposure to radon in drinking water. The committee was also asked to prepare an assessment of the health-risk reduction associated with various mitigation measures to reduce radon in indoor air; to accomplish this task, the committee used the results of the latest scientific studies of risk assessment and relevant peer-reviewed research carried out by organizations and individual investigators. Finally, the committee was asked to summarize the agreements and differences between the various advisory organizations on the issues relevant to the health risks posed by radon in drinking water and radon-mitigation measures and to evaluate the technical and scientific bases of any differences that exist. The Committee on Risk Assessment of Radon in Drinking Water was appointed in May 1997, held its first meeting on July 14-15, 1997, and held six additional meetings during the next 9 months. The ability of the committee to comply with this extremely tight schedule is a reflection of the dedication and expertise of the committee members and the efforts of the committee staff. The committee acknowledges the help of those individuals or organizations who gave presentations during our meetings and/or provided information in response to requests by committee members or staff and to others who helped the committee in the completion of our task. Gustav Akerbloom, Swedish Radiation Protection Institute Hannu Arvela, Finnish Radiation/Nuclear Safety Authority Timothy Barry, Environmental Protection Agency David S. Chase, New Hampshire Radiologic Health Bureau Gail Charnley, Presidential/Congressional Commission on Risk Assessment and Risk Management Nancy Chiu, Environmental Protection Agency Jack Correia, Massachusetts General Hospital Bill Diamond, Environmental Protection Agency Joe Drago, Kennedy Jenks, San Francisco, CA Susumo Ito, Professor Emeritus, Harvard University Dan Krewski, Environmental Health Centre, Ottawa, Canada Jay Lubin, National Cancer Institute J.P. Malley, Jr., University of New Hampshire Sylvia Malm, Environmental Protection Agency Frank Marcinowski, Environmental Protection Agency Lars Mjones, Swedish Radiation Protection Institute Roger McClellan, Chemical Industry Institute of Toxicology Neal S. Nelson, Environmental Protection Agency David Paris, Waterworks, Manchester, NH Dan Pederson, American Water Works Association Frederick Pontius, American Water Works Association Jerome Puskin, Environmental Protection Agency Edith Robbins, New York University David Rowson, Environmental Protection Agency Richard Toohey, Oak Ridge Institute of Science and Education George Sachs, VA Medical Center, Los Angeles Anita Schmidt, Environmental Protection Agency Daniel J. Steck, St. John's University Grant Stemmerman, University of Cincinnati Neil Weinstein, Rutgers University Jeanette Wiltse, Environmental Protection Agency This report has been reviewed by individuals chosen for their diverse perspectives and technical expertise, in accordance with procedures approved by the National Research Council's Report Review Committee. The purpose of this independent review is to provide candid and critical comments that will assist the authors and the National Research Council in making their published report as sound as possible and to ensure that the report meets institutional standards for objectivity, evidence, and responsiveness to the study charge. The content of the review comments and draft manuscript remain confidential to protect the integrity of the deliberative process. We wish to thank the following individuals for their participation in the review of this report: Antone Brooks, Washington State University, Tri-Cities Bernard Cohen, University of Pittsburgh Douglas Crawford-Brown, University of North Carolina-Chapel Hill Robert E. Forster, The University of Pennsylvania School of Medicine Sharon Friedman, Lehigh University Patricia L. Gardner, New Jersey Department of Environmental Protection Roger O. McClellan, Chemical Industry Institute of Toxicology Gilbert Omenn, University of Washington Frank H. Stillinger, Bell Laboratories Rhodes Trussell, Montgomery Watson, Inc. The committee members would like to express their gratitude to the staff of the National Research Council's Board on Radiation Effects Research. The committee members are especially appreciative for study director Steven Simon's technical guidance and encouragement. They are also grateful to Karen Bryant and Doris Taylor for assistance with administrative details related to the committee's work. Contents Public Summary 1 Executive Summary 8 1   Introduction 23   The Origin of Radon 23   Absorbed Dose from Indoor Radon 27   Composition of the Report 31 2   Baseline Information on Indoor Radon and Radon in Water In the United States 32   Indoor Radon 32   Radon in Groundwater and Public Water Supplies 36   Ambient Radon 37 3   Transfer of Radon from Water to Indoor Air 50   Measurements of Transfer Coefficients 51   Modeling of Transfer Coefficient 52   Conclusions 57 4   Dosimetry of Ingested Radon and its Associated Risk 59   Intakes and Consumption of Water 59   Physicochemical Properties of Radon 60   Fate of Radon Decay Products in the Body 73   Cancer Risk Per Unit 222Rn Concentration in Drinking Water 76   Special Populations at Risk 81 5   Dosimetry of Inhaled Radon and its Associated Risk 82   Inhalation of Radon and Its Short-lived Decay Products 82   Risk Posed by Inhalation of 222Rn Decay Products 82   Lung Dose from 222Rn Gas 83   Dose to Organs Other Than the Lung from Inhaled 222Rn 84   222Rn Decay-Product Dose During Showering 84   Lung-Cancer Risk Posed by Inhalation of 222Rn Decay Products 93   Epidemiology of Childhood Exposure and Lung-Cancer Risk 100   Environmental and Domestic Epidemiology 100   Epidemiology of Cancer of Organs Other Than Lung 102   Evaluation of Risk Per Unit Exposure from Inhaled 222Rn in Air 103 6   Molecular and Cellular Mechanisms of Radon-Induced Carcinogenesis 105   Cells at Risk 105   Cellular Damage Induced by Radon Alpha Particles 107   Transformation of Cells by Alpha Particles in Vitro 110   DNA Damage and Its Repairthe Caretaker Genes 110   Deletion Mutagenesis and Chromosomal Changes Caused by Densely Ionizing Radiation 114   Control of Cellular Responses to Damagethe Arbitrator Gene 115   Apoptosisthe Undertaker Genes 116   Initial Genetic Changes in Carcinogenesisthe Gatekeeper Genes 118   Tumor Growth and Nutritionthe Caterers 119   Genetic Instability in Irradiated Cell Populationsthe Diversifiers 120   Mutations in a-Particle-Induced Tumorsthe Fingerprints 121   Epidemiologic, Biophysical, and Cell-Based Models of Radon-Induced Carcinogenesis 122 7   Defining Key Variabilities and Uncertainties 124   Reliability of a Health-Risk Assessment 126   Environmental Protection Agency Process for Assessing and Evaluating Uncertainties in Radon Risk 127   Issues in Uncertainty Analysis for Radon 129   The Committee's Evaluation of Uncertainties in Risk Assessment of Radon in Drinking Water 130   Communication of Uncertain Risk Information 137   Discussion and Recommendations 139 8   Mitigation 141   Mitigation of Radon in Indoor Air 141   Mitigation of Radon in Water 160   Conclusions 179 9   Multimedia Approach To Risk Reduction 180   Derivation of the Alternative Maximum Contaminant Level (AMCL) 181   Equivalent Risk-Reduction Scenarios 182     Scenario 1: High Radon Concentrations in Water 183     Scenarios 2-4: Effects of Distribution of Radon in Indoor Air 184     Scenario 5: Use of New Radon-Resistant Construction 187     Scenario 6: Multicommunity Mitigation 188     Scenario 7: Use of Outreach, Education, and Incentives 189     Scenario 8: Outreach for Other Health Risks 193   Equity and Implementation Issues and Risk Reduction 193   Summary 196 10   Research Recommendations 198 REFERENCES 200 GLOSSARY 223 APPENDIXES   A   Behavior of Radon and Its Decay Products in the Body 233   B   A Model for Diffusion of Radon Through the Stomach Wall 241   C   Water-Mitigation Techiques 249   D   Risks Associated with Disinfection By-products Formed by Water Chlorination Related to Trihalomethanes (THMs) 254   E   Gamma Radiation Dose from Granular-Activated Carbon (GAC) Water Treatment Units 257   F   EPA Approach to Analyzing Uncertainty and Variability 260 Index 269 Public Summary Radiation is a natural part of the environment in which we live. All people receive exposure from naturally occurring radioactivity in soil, water, air and food. The largest fraction of the natural radiation exposure we receive comes from a radioactive gas, radon. Radon is emitted from uranium, a naturally occurring mineral in rocks and soil; thus, radon is present virtually everywhere on the earth, but particularly over land. Thus, low levels of radon are present in all the air we breathe. There are three forms of radon, but the use of the term radon in this report refers specifically to radon-222. Although it cannot be detected by a person's senses, radon and its radioactive by-products are a health concern because they can cause lung cancer when inhaled over many years. A recent report by the National Research Council suggested that between 3,000 and 32,000 lung-cancer deaths each year (the most likely value is given as 19,000 deaths) in the United States are associated with breathing radon and its radioactive by-products in indoor air, but these deaths are mainly among people who also smoke. Most of the radon that enters a building comes directly from soil that is in contact with or beneath the basement or foundation. Radon is also found in well water and will enter a home whenever this water is used. In many situations such as showering, washing clothes, and flushing toilets, radon is released from the water and mixes with the indoor air. Thus, radon from water contributes to the total inhalation risk associated with radon in indoor air. In addition to this, drinking water contains dissolved radon and the radiation emitted by radon and its radioactive decay products exposes sensitive cells in the stomach as well as other organs once it is absorbed into the bloodstream. This report examines to what degree this ingested radon is a health risk and to what extent radon released from water into air increases the health risk due to radon already in the air in homes. Approximately half of the drinking water in the United States comes from ground water that is tapped by wells. Underground, this water often moves through rock containing natural uranium that releases radon to the water. Water from wells normally has much higher concentrations of radon than does surface water such as lakes and streams. Radon concentrations can be measured either in terms of a volume of air (becquerel of radon per cubic meter) or a volume of water (becquerel of radon per liter). The average concentration of radon in public water supplies derived from ground water sources is about 20 becquerel per liter (540 pCi). Some wells have been identified with high concentrations, up to 400 times the average. Surface water, such as in lakes and streams, has the lowest concentrations, about one-tenth that of most wells. Drinking-water quality in the United States is regulated by the Environmental Protection Agency (EPA) under the Safe Drinking Water Act (SDWA). Since radon is acknowledged as a cancer-causing substance, the law directs EPA to set a maximum contaminant level (MCL) for radon to restrict the exposure of the public to the extent that is possible, that is, as close to zero as is feasible. In 1991, EPA proposed an MCL for radon of 11 becquerel per liter (about 300 pCi per liter) for radon in drinking water. In 2000, the agency is required to set a new MCL based in part on this report. The law also directed EPA to set an alternative MCL (AMCL); an AMCL is the concentration of radon in water that would cause an increase of radon in indoor air that is no greater than the level of radon naturally present in outdoor air. Limiting public risk from radon by treating the water alone is not feasible because radon is also naturally present in the air. Thus, the AMCL is the tool that allows EPA to limit exposure to radon in water to a practical level, that is, allowing no more risk from the radon in water than is posed by the level of radon naturally present in outdoor air. The 1996 amendments to the Safe Drinking Water Act required EPA to fund the National Academy of Sciences (NAS) to determine the risk from radon in drinking water and also to determine the public-health benefits of various methods of removing radon from indoor air. In response to that agreement, the NAS established through its principal operating agency, the National Research Council, a committee which has evaluated various issues related to the risk from radon in drinking water and provides here the information needed by EPA to set the AMCL. The primary conclusion from the committee's investigation into the risk of inhaling radon as compared to drinking water containing dissolved radon is as follows: Most of the cancer risk resulting from radon in the household water supply is due to inhalation of the radioactive by-products that are produced from radon that has been released from the water into the air, rather than from drinking the water. (The risk from radon is higher among smokers because the combination of radon and smoke has a greater damaging effect than the sum of the individual risks.) Furthermore, the increased level of indoor radon that is caused by using water in the home is generally small compared with the level of indoor radon that originated in the soil beneath the home. Based on an analysis of the available data on radon concentrations outdoors and on the transfer from water to air, the Research Council committee arrived at these additional conclusions: The average outdoor air concentration over the entire United States is about 15 becquerel per cubic meter (405 pCi per cubic meter or 0.4 pCi per liter). The contribution to radon concentration in indoor air from household usage of water is very lowonly about one ten-thousandth the water concentration. The reason the resulting airborne concentration is so low is because only about half of the radon in the household water supply escapes into the air and then it is diluted into the large volume of air inside the home. Combining this information, the committee has determined that the level of radon in drinking water that would cause an increase of radon in indoor air that is no greater than the level of radon naturally present in outdoor air is about 150 becquerel per liter (4,050 pCi per liter). This conclusion will affect the public and water utilities in the following ways: 1. People who own their own wells are not legally obliged to do anything because the Safe Drinking Water Act does not regulate private wells. However, people who are served by private wells and who wish to minimize their risk should test their water and consider taking action to reduce the radon if the concentration in the water is above the AMCL. In addition, those people should also measure the indoor air concentration in their home and consider taking actions to reduce it if it is above EPA's recommended action levels. Lastly, as the earlier NRC report concluded, stopping smoking is the most effective way to reduce the risk of lung cancer and reduce the risks associated with radon. 2. Water supplies serving 25 or more people or with 15 or more connections are considered to be public water supplies. Those supplies, along with some special cases such as schools, will be subject to radon regulation if they rely on groundwater. In this case, there are three possibilities: (a) The radon in the water is already below the MCL. This will apply to the majority of people in the United Statesonly about 1 of every 14 individuals routinely consumes water with concentrations greater than the 1991 proposed MCL (11 becquerel per liter or 300 pCi/L). For water below the MCL, nothing needs be done. (b) The radon in the water is greater than the AMCL. In this case, radon reduction (mitigation) would be required by law after the regulation is final. Data available to the committee indicate that there are several types of water mitigation technology that could effectively reduce the radon concentration to the MCL. (c) The radon in the water is between the MCL and the AMCL. In this case, the concentration must be reduced to the MCL or, if there is an approved state plan, the risk to the population served by the water supply can be reduced by activities that reduce radon in air and/or water. The committee discussed a variety of methods to reduce radon entry into homes and the concentrations in the indoor air and in water. Ventilation systems can be used to reduce radon concentrations in indoor air to acceptable levels. Periodic testing would be needed to ensure the continued successful operation of individual air treatment systems. New homes can be constructed using methods to reduce airborne radon (radon resistant construction). However, there is not enough evidence at the present time to be certain these techniques are effective. Several water-treatment technologies to remove radon from water are very effective, however, they do not address the largest risk to the occupants of the house, namely radon in air. The EPA mandate is to reduce public risk caused by exposure to radon. For those communities where the public water supply contains radon at concentrations between the MCL and the AMCL, the law will allow individual states to reduce the risk to their population through multimedia measures to mitigate radon levels in indoor air. A state may develop and submit a multimedia program to mitigate radon levels in indoor air for approval by the EPA Administrator. The Administrator shall approve a state program if the health risk reduction benefits expected to be achieved by the program are equal to or greater than the health risk reduction benefits that would be achieved if each public water system in the state complied with the MCL. If the program is approved, public water systems in the state may comply with the alternative maximum contaminant level in lieu of the MCL. State programs may rely on a variety of mitigation measures, including public education, home radon testing, training, technical assistance, remediation grant and loan or other financial incentive programs, or other regulatory or nonregulatory measures. As required by SDWA, EPA is developing guidelines for multimedia mitigation programs. If there is no approved state multimedia mitigation program, any public water system in the state may submit a program for approval by the EPA Administrator, according to the same criteria, conditions and approval process that would apply to a state program. In this scenario, water utilities can minimize the level of risk to their consumerseven if the water they provide is higher than the MCL (but lower than the AMCL)by reducing airborne radon in some of the community's homes. Because the risk caused by inhaled radon is so much greater than that caused by radon that is swallowed in water, reducing the airborne radon in only a few homes may reduce public risk enough for the water utility to be in compliance with the multimedia program requirements. With regard to multimedia programs, the committee's report provides discussion of risk-reduction methods at the community level and of ways to evaluate the effectiveness of reducing radon-related risk within a community or region served by a water utility. One risk reduction technique is public education programs to encourage radon mitigation from indoor air. The previously conducted education and outreach programs reviewed by the committee were largely unsuccessful; therefore, the committee concluded that public education and outreach programs alone would be insufficient to achieve a measurable reduction in health risk. A multimedia mitigation program will reduce radon risks in indoor air in lieu of reduction to the MCL in drinking water. The specific design of each community water utility's program will depend on many factors. At the same time, complicated risk-reduction programs like those discussed here have many potential difficulties. For example, for water utilities that provide water that contains radon at levels between the MCL and the AMCL, the feasibility of using a multimedia mitigation program will depend on whether there are homes with relatively high indoor radon concentrations. Only in those homes is it feasible to reduce the air concentration sufficiently such that an expensive, large-scale water mitigation program in the region is not needed to satisfy the multimedia program requirements. The key issue is determining how many buildings must have air mitigation systems to obtain a reduction in public risk equal to that which could be achieved by reducing radon in the water supplied to the community. Moreover, air monitoring programs will be needed to identify the homes whose indoor air must be mitigated and effective outreach programs will be needed to educate the public about the need to modify these homes to reduce indoor radon so that the water utility can demonstrate the risk reduction needed for compliance. Finally, consideration needs to be given to how the costs of mitigation of private homes will be apportioned among homeowners and the water utilities or state government. Another potential problem is the present-day scarcity of trained personnel (particularly in the water utilities) that could design or maintain home air mitigation systems and carry out the tests needed to ensure continued performance of these systems. Finally, the committee recognizes that the reduction in risk by multimedia programs will not be distributed equally among the public. The mitigation of indoor-air radon in a small number of homes means risk reduction among only a few people who had high initial risk, rather than a uniform risk reduction for a whole population served by the water utility. The various analyses conducted allowed the committee to estimate the risk and annual number of fatalities caused by radon in water and to compare it with the risk caused by radon in air. The figure presented here summarizes the cancer risk posed by inhaling radon in air (with and without the addition of radon from using water in the home) and the risk posed by drinking water that contains dissolved radon. Specifically, in 1998 in the United States, there will be about 160,000 deaths from lung cancer, mainly as a result of smoking tobacco. Of those, about 19,000 are estimated to result from inhaling radon gas in the home; though most of these deaths will be among people who smoke. Of the 19,000 deaths, only 160 are estimated to result from inhaling radon that was emitted from water used in the home though most of these deaths would also among smokers. As a benchmark for comparison, about 700 lung-cancer deaths each year can be attributed to exposure to natural levels of radon while people are outdoors. The committee determined that the risk of stomach cancer caused by drinking water that contains dissolved radon is extremely small and would probably result in about 20 deaths annually compared with the 13,000 deaths from stomach cancer that arises from other causes. Except in situations where concentrations of radon in water are very high, reducing the radon in water will generally not make a large difference in the total radon-related health risks to occupants of dwellings. Using techniques to reduce airborne radon and its related lung-cancer risk makes good sense from a public-health perspective. However, there are concerns about the equity of the multimedia approach. The committee concludes that evaluating whether a multimedia approach to radon reduction will achieve an acceptable risk reduction in a cost-effective and equitable manner will be a complex process. It will require significant cooperation among EPA, state agencies, water utilities and local governments, especially because many of the communities affected by the radon regulation will be very small and they will need assistance in making decisions concerning the advantages or disadvantages of a multimedia program. Thus, each public water supply will find it necessary to study its own circumstances carefully before deciding to undertake a multimedia mitigation program instead of treating the water to reduce the radon dissolved in it. Executive Summary BACKGROUND Of all the radioisotopes that contribute to natural background radiation, radon presents the largest risk to human health. There are three naturally occurring isotopes of radon, but the use of the term radon in this report refers specifically to 222Rn, which is a decay product of 238U. A recent report by the National Research Council suggested that between 3,000 and 32,000 lung-cancer deaths annually (the most likely value for the number of deaths is 19,000) in the United States are associated with exposure to 222Rn and its short-lived decay products in indoor air, largely because radon substantially increases the lung-cancer risk for smokers. Most radon enters homes via migration of soil gas. Throughout this report, radon activity concentrations are cited in the SI1 unit of becquerel per cubic meter (Bq m—3; 1 Bq m—3 = 0.027 pCi L—1). The mean annual radon concentration measured in the living areas of homes in the United States is 46 Bq m—3. Radon has also been identified as a public-health concern when present in drinking water. Surface waters contain a low concentration of dissolved radon. Typically radon concentrations in surface waters are less than 4,000 Bq m—3.2 Water from ground water systems can have relatively high levels of dissolved radon, however. Concentrations of 10,000,000 Bq m—3 or more are known to exist in public water supplies. Many of the water supplies containing substantial concentrations of radon serve very small communities (<1,000 people). Data on radon in water from public water supplies indicate that elevated concentrations of radon in water occur primarily in the New England states, the Appalachian states, the Rocky Mountain states, and small areas of the Southwest and the Great Plains. Because radon is easily released by agitation in water, many uses of water release radon into the indoor air, which contributes to the total indoor airborne radon concentration. Ingestion of radon in water is also thought to pose a direct health risk through irradiation of sensitive cells in the gastrointestinal tract and in other organs once it is absorbed into the bloodstream. Thus, radon in drinking water could potentially produce adverse health effects in addition to lung cancer. Drinking-water quality in the United States is regulated by the Environmental Protection Agency (EPA) under the Safe Drinking Water Act originally passed in 1974. In the 1986 amendments to the act, EPA was specifically directed to promulgate a standard for radon as one of several radionuclides to be regulated in drinking water. Because of delays in implementing the regulation of radionuclides in drinking water, EPA was sued. In a consent decree, EPA agreed to publish final rules for radionuclides in drinking water, including radon, by April 1993. EPA proposed national primary drinking water regulations for radionuclides in 1991. Because radon is a known carcinogen, its maximum contaminant level goal (MCLG) was automatically set at zero. A maximum contaminant level (MCL) of 11,000 Bq m—3 was subsequently proposed as the level protective of public health and feasible to implement taking costs into account. Public comments on the proposed regulations suggested that the MCL for radon be set somewhere from less than 1,000 Bq m—3 to 740,000 Bq m—3; a large majority favored setting the MCL at value higher than 11,000 Bq m—3. In 1992, Congress directed the Office of Technology Assessment to analyze the EPA health risk assessment and outline actions that could address regulation of radon, considering both air and water. Also in 1992, the Chaffee-Lautenberg amendment to the EPA appropriation bill for FY 1993 directed the agency to seek an extension of the deadline for publishing a final rule until October 1993 and to submit a report, reviewed by EPA's Science Advisory Board (SAB), to Congress by July 1993. That report was to address the risks posed by human exposure to radon and consider both air and water sources, the costs of controlling or mitigating exposure to waterborne radon, and the risks posed by treating water to remove radon. The SAB review of the report questioned EPA's estimates of the number of community water supplies affected, the extrapolation of the risk of lung cancer associated with the high radon exposures of uranium miners to the low levels of exposure experienced in domestic environments and the magnitude of risk associated with ingestion. The SAB report also emphasized that the risk of cancer from radon in domestic settings was a multimedia issue and that the risk for radon in water must be considered within the context of the total risk from radon, which is dominated by radon in indoor air. The Office of Management and Budget also expressed concern about EPA's analysis of the cost of mitigation. In the agency's FY 1994 appropriation bill, Congress ordered EPA to delay publishing a rule for radon in drinking water. The 1996 amendments to the Safe Drinking Water Act required EPA to contract with the National Academy of Sciences (NAS) to conduct a risk assessment of radon in drinking water and an assessment of the health-risk reduction benefits associated with various measures to reduce radon concentrations in indoor air. EPA is also required to publish an analysis of the health-risk reduction and the costs associated with compliance with any specific MCL before issuing a proposed regulation. The law also directed EPA to promulgate an alternative maximum contaminant level (AMCL) if the proposed MCL is less than the concentration of radon in water "necessary to reduce the contribution of radon in indoor air from drinking water to a concentration that is equivalent to the national average concentration of radon in outdoor air." Under the law, states may develop a multimedia mitigation progam which if approved by EPA would allow utilities whose water has radon concentrations higher than the MCL, but lower than the AMCL, to comply with the AMCL. The multimedia programs to mitigate radon in indoor air may include "public education; testing; training; technical assistance; remediation grants, loan or incentive programs; or other regulatory or non-regulatory measures." If a state does not have an EPA-approved multimedia mitigation program, a public water supply in that state may submit such a program to EPA directly. Public water supplies exceeding the AMCL and choosing to institute a multimedia mitigation program to achieve equivalent health risk reductions must, at a minimum, treat their water to reduce radon in water concentrations to less than or equal to the AMCL. The present report was written to address the issues just discussed. CRITICAL ISSUES It has been difficult to set a standard for radon, as opposed to other radionuclides in drinking water, because of the absence of authoritative dosimetric information for radon dissolved in water. Furthermore, radon presents a unique regulatory problem in that its efficient transfer from water into indoor air produces a risk from the inhalation of its decay products. Thus, it is regulated as a radionuclide in water, but a major portion of the associated risk occurs because of its contribution to the airborne radon concentration. Because of the relatively small volume of water used in homes, the large volume of air into which the radon is emitted, and the exchange of indoor air with the ambient atmosphere, radon in water typically adds only a small increment to the indoor air concentration. Specifically, radon at a given concentration in water adds only about 1/10,000 as much to the air concentration; that is, typical use of water containing radon at 10,000 Bq m—3 will on average increase the air radon concentration by only 1 Bq m—3. There is always radon in indoor air from the penetration of soil gas into homes, so only very high concentrations of radon in water will make an important contribution to the airborne concentration. Even though water generally makes only a small contribution to the indoor airborne radon concentration, the risk posed by radon released from water, even at typical groundwater concentrations, is estimated to be larger than the risks posed by the other drinking water contaminants that have been subjected to regulation, such as disinfection by-products. Thus, in most homes, the risk to the occupants posed by indoor radon is dominated by the radon from soil gas, which is not subject to regulation, and a change in the radon in drinking water would produce a minimal change in the risk posed by airborne radon. This problem led to the suggestion that mitigation of radon in indoor air be considered an alternative means of achieving risk reduction equal to or greater than that which would be achieved by reducing the concentration of radon in drinking water. The ingestion of radon in water also presents a possible risk. Questions were raised with respect to the ingestion risk assessment that EPA used in the 1991 proposed regulations and in the revised multimedia risk assessment of 1994. The questions were related to the applicability of some of the data used as the basis of the risk model and to the resulting assumptions that were used to estimate risk. The substantial uncertainties in the radon health risks other than those posed by inhalation add to the problems of setting an appropriate MCL to protect public health. Thus, a reevaluation of the ingestion risks was needed. COMMITTEE CHARGE EPA contracted with NAS to address the issues cited above, and the committee on the Risk Assessment of Radon Gas in Drinking Water was formed in the National Research Council's Board on Radiation Effects Research. The specific tasks assigned to the committee were: To examine the development of radon risk assessments for both inhalation and ingestion of water. To modify an existing risk model if that was deemed appropriate or to develop a new one if not. To review the scientific data and technical methods used to arrive at risk coefficients for radon in water. To assess potential health-risk reduction benefits associated with various mitigation measures to reduce radon in indoor air. The final report includes: Estimates of cancer risk per unit activity concentration of radon in water. Assessment of the state of knowledge with respect to health effects of radon in drinking water for populations at risk, such as infants, children, pregnant women, smokers, elderly persons, and seriously ill persons. Review of information regarding teratogenic and reproductive effects in men and women due to radon in water. Estimates of the transfer coefficient relating radon in water to average radon concentrations in indoor air. Estimates of average radon concentrations in ambient air. Estimates of increased health risks that could result from methods used to comply with regulations for radon in drinking water. Discussion of health-risk reduction benefits obtained by reducing radon using currently available methods developed for reducing radon concentrations in indoor air and comparison of these benefits with those achievable by the comparable reduction of risks associated with mitigation of radon in water. FINDINGS AND CONCLUSIONS The committee's report addresses each of those points, and its conclusions are summarized below. The order of presentation below follows that in the report. Occurrence of Radon in the United States National data on indoor radon, radon in water, and geologic radon potential indicate systematic differences in the distribution of radon across the United States. Geologic radon-potential maps and statistical modeling of indoor radon exposures make it clear that the northern United States, the Appalachian and Rocky Mountain states, and states in the glaciated portions of the Great Plains tend to have higher than average indoor radon concentrations. Some smaller areas of the southern states also have higher than average indoor radon concentrations. Data on radon in water from public water supplies indicate that elevated concentrations of radon in water occur in the New England states, the Appalachian states, the Rocky Mountain states, and small areas of the Southwest and the Great Plains. National Average Ambient Radon Concentration The ambient concentration of radon varies with distance from and height over its principal source in the ground (rocks and soil) and from other sources that can locally or regionally affect it, such as lakes, mine or mill tailings, vegetation, and fossil-fuel combustion. However, diurnal fluctuations due to changes in air stability and meteorologic events account for most of the variability. Average ambient radon concentrations were measured by EPA over nine seasons at 50 sites across the United States. Most, but not all, sites coincided with the capital city of the state but did not statistically represent the population across the U.S., nor were the measurement at these sites necessarily representative of average ambient radon concentrations in each state. But the EPA data set is the only one with a fully national extent. The committee does not believe that the data are sufficiently representative to provide a population-weighted annual average ambient radon concentration. An unweighted arithmetic mean radon concentration of 15 Bq m—3, with a standard error of 0.3 Bq m—3 was calculated based on the EPA data set, and the committee recommends use of this value as the best available national ambient average concentration. After reviewing all the other ambient radon concentration data that are available from other specific sites, the committee concluded that the national average ambient radon concentration would lie between 14 and 16 Bq m—3. Transfer Coefficient The transfer coefficient is the average fraction of the initial average radon concentration in water that is contributed to the indoor airborne radon concentration. The average transfer coefficient estimated by a model and the average estimated from measurement data are in reasonable agreement. The average of the measurements was 0.9 x 10—4 with a standard error of 0.1 x 10—4, and the model's average was either 0.9 x 10—4 or 1.2 x 10—4 depending on the choice of input parameter values. Having considered the problems with both the measurements of the transfer coefficient and the measurements that are the input values into the model, the committee concludes that the transfer coefficient is between 0.8 x 10—4 and 1.2 x 10—4 and recommends that EPA continue to use 1.0 x 10—4 as the best central estimate of the transfer coefficient that can now be obtained. Biologic Basis of Risk Estimation The biologic effects of radon exposure under the low exposure conditions found in domestic environments are postulated to be initiated by the passage of single alpha particles with very high linear energy transfer. The alpha-particle tracks produce multiple sites of DNA damage that result in deletions and rearrangements of chromosomal regions and lead to the genetic instabilities implicated in tumor progression. Because low exposure conditions involve cells exposed to single tracks, variations in exposure translate into variations in the number of exposed cells, rather than in the amount of damage per cell. This mechanistic interpretation is consistent with a linear, no-threshold relationship between high-linear energy transfer (high-LET) radiation exposure and cancer risk, as was adopted by the BEIR VI committee. However, quantitative estimation of cancer risk requires assumptions about the probability of an exposed cell becoming transformed and the latent period before malignant transformation is complete. When these values are known for singly hit cells, the results might lead to reconsideration of the linear no-threshold assumption used at present. Ingestion Risk The cancer risk arising from ingestion of radon dissolved in water must be derived from calculations of the dose absorbed by the tissues at risk because no studies have quantified the risk. Studies of the behavior of radon and other inert gases have established that they are absorbed from the gastrointestinal tract and readily eliminated from the body through the lungs. The stomach, the portal of entry of ingested radon into the body, is of particular concern. The range of alpha particles emitted by radon and its short-lived decay products is such that alpha particles emitted within the stomach are unable to reach the cells at risk in the stomach wall. Thus, the dose to the wall depends heavily on the extent to which radon diffuses from the contents into the wall. Once radon has entered the blood, through either the stomach or the small intestine, it is distributed among the organs according to the blood flow to them and the relative solubility of radon in the organs and in blood. Radon dissolved in blood that enters the lung will equilibrate with air in the gas-exchange region and be removed from the body. The committee found it necessary to formulate new mathematical models of the diffusion of radon in the stomach and the behavior of radon dissolved in blood and other tissues. The need for that effort arose from the lack of directly applicable experimental observations and from limitations in the extent to which one can interpret available studies. The diffusion of radon within the stomach was modeled to determine the expected time-integrated concentration of radon at the depth of the cells at risk. The result, based on a diffusion coefficient of 5 x 10—6 cm2 s—1, indicated that a conservative estimate of the integrated concentration in the wall was about 30% of that in the stomach content. The committee also found it useful to set forth a physiologically-based pharmacokinetic (PBPK) model of the behavior of radon in the body. Various investigators have assessed the retention of inhaled and ingested radon in the body, but their observations do not relate directly to the distribution of radon among the tissues. The PBPK is formulated using information on blood flow to the tissues and on the relative solubility of radon in blood and tissue to determine the major tissue of deposition (which was adipose tissue) and retention within this tissue. The PBPK model is consistent with the observations regarding radon behavior in the body. Unlike previous estimates of the radiation dose, the committee's analysis also considered that each radioactive decay product formed from radon decay in the body exhibited its own behavior with respect to tissues of deposition, retention, and routes of excretion. The committee's estimates of cancer risk are based on calculations with risk-projection models for specific cancer sites. The computational method was that described in EPA's Federal Guidance Report 13. An age- and gender-averaged cancer death risk from lifetime ingestion of radon dissolved in drinking water at a concentration of 1 Bq m—3 is 0.2 x 10—8. Stomach cancer is the major contributor to the risk. The actual risk from ingested radon could be as low as zero depending on the validity of the linear, no-threshold dose response hypothesis, however, the committee has estimated confidence limits on the ingestion risk (see chapter 4). Inhalation Risk Lung cancer arising from exposure to radon and its decay products is bronchogenic. The alpha-particle dose delivered to the target cells in the bronchial epithelium is necessarily modeled on the basis of physical and biologic factors. The dose depends particularly on the diameter of the inhaled ambient aerosol particles to which most of the decay products attach. These particles deposit on the airway surfaces and deliver the pertinent dose, and the dose can vary, because of changes in particle size, by about a factor of 2 in normal home conditions. The dose from radon gas itself is smaller than the dose from decay products on the airways, mainly because of the location of the gas in the airway relative to the target cellsthat is, the source-to-target geometry. The dose from radon gas that is soluble in body tissues is also smaller than the decay-product dose. Two of the underground-miner studies showed no statistically significant risk of cancer in organs other than the lung due to inhaled radon and radon decay products. The dosimetry supports that observation, although there is a need to continue the miner observations. The risk of lung cancer associated with lifetime inhalation of radon in air at a concentration of 1 Bq m—3 was estimated on the basis of studies of underground miners. The values were based on risk projections from three follow-up studies: BEIR IV (National Research Council 1988), NIH (1994) and BEIR VI (National Research Council 1999). These three reports used data from 4 to 11 cohorts of underground miners in seven countries and developed risk projections of 1.0 x 10—4, 1.2 x 10—4, and 1.3 x 10—4 per unit concentration in air (1 Bq m—3), respectively. The three values were for a mixed population of smokers and nonsmokers. The value adopted by the committee is the rounded average derived from the two BEIR-VI model results and equals 1.6 x 10—4 per Bq m—3. The lung-cancer risk to smokers is statistically significantly higher than the risk to nonsmokers. Given the adopted transfer coefficient of 1 x 10—4, the risk of lung cancer (discussed in two reports of the National Research Council and one of the National Institutes of Health) posed by lifetime exposure to radon (222Rn) in water at 1 Bq m—3 was calculated to be 1.6 x 10—8. Summary of Risk Estimates The risk estimates developed by the committee for radon in drinking water are summarized in table ES-1. Although the committee was asked to estimate the risks to susceptible population--ssuch as infants, children, pregnant women, smokers, and elderly and seriously ill persons--there is insufficient scientific information to permit such estimation except for the lung-cancer risk to smokers, which is presented separately in the table. The adopted lifetime risk of lung cancer for a mixed population of smokers and nonsmokers, men and women, resulting from the air exposure to radon from a waterborne radon concentration of 1 Bq m—3 is 1.6 x 10—8. The adopted lifetime risk of stomach cancer for the same water concentration is 0.2 x 10—8; the committee could not make a distinction in ingestion risk for any specifically identified subpopulation other than the differences in gender. TABLE ES-1 Committee Estimate of Lifetime Risk Posed by Exposure to Radon in Drinking Water at 1 Bq m—3   Exposure Pathway Lifetime risk   Male Female U.S. Populationa Inhalation (ever-smokers)b 3.1 x 10—8 2.0 x 10—8 2.6 x 10—8 Inhalation (never-smokers)b 0.59 x 10—8 0.4 x 10—8 0.50 x 10—8 Inhalation (population)b 2.1 x 10—8 1.2 x 10—8 1.6 x 10—8 Ingestion 0.15 x 10—8 0.23 x 10—8 0.19 x 10—8 Total Risk (inhalation and ingestion) 2.2 x 10—8 1.4 x 10—8 1.8 x 10—8   aThese rounded values combine the various subpopulations, with appropriate weighting factors taken from the 1990 U.S. Census. bBased on the radon decay product risks of BEIR VI Report (National Research Council 1999) and includes the incremental dose to showering with the uncertainties in these estimates. The committee was asked to review teratogenic and reproductive risks. Figure 1 (see Public Summary) puts the inhalation and ingestion risks into perspective by direct comparison of annual cancer deaths. The number of lung-cancer deaths in the United States is estimated to be 160,100 in 1998 (ACS 1998). Using the average of the two BEIR-VI risk models and adjusting for the 1998 increase in the number of lung-cancer deaths, the committee estimates there will be about 19,000 lung-cancer deaths in 1998 attributable to radon and the combination of radon and smoking. The committee estimated there might be about 20 stomach-cancer deaths in 1998 (with a subjectively determined uncertainty range from 1 to 50 deaths) attributable to the ingestion of radon in drinking water as compared to 13,700 stomach-cancer deaths that are estimated to develop in the United States in 1998 from all causes (ACS 1998). Based on an estimated national mean value of radon in drinking water, the committee estimates 160 lung cancer deaths in 1998 (with a subjectively determined range from 25 to 280 deaths) attributable to indoor radon (in air) resulting from the release of radon from household water. The committee's analysis indicates that most of the cancer risk posed by radon in drinking water arises from the transfer of radon into indoor air and the subsequent inhalation of the radon decay products, and not from the ingestion of the water. The committee was asked to review teratogenic and reproductive risks. There is no scientific evidence of teratogenic and reproductive risks associated with radon in tissues from either inhalation or ingestion. Comparison of the Present Analysis with the Previous EPA Analyses The committee's analysis results in a modest reduction of the overall risk associated with radon in drinking water compared with the two previous analyses conducted by the EPA. However, the magnitudes of the risks associated with the different exposure pathways are different, as shown in table ES-2. The committee's analysis estimates that the inhalation pathway accounts for about 89% of the estimated cancer risk and ingestion accounts for 11%. In contrast, EPA's 1994 analysis suggested that inhalation accounted for 47% of the overall risk and ingestion accounted for 53%. TABLE ES-2 Comparison of Individual Lifetime Risk Estimates Posed by Radon in Drinking Water at a Concentration of 1 Bq m—3   Exposure Pathway Committee Analysisa 1991 EPA Proposed Ruleb 1994 Revised EPA Analysisc (A) Radon progeny inhalationa 1.6 x 10—8 1.3 x 10—8 0.81 x 10—8 (B) Radon inhalation       0.05 x 10—8 0.054 x 10—8 (C) Ingestion 0.2 x 10—8 0.4 x 10—8 0.95 x 10—8   Stomach 1.6 x 10—9 2.0 x 10—9 4.9 x 10—9   Colon 0.059 x 10—9 0.46 x 10—9 1.4 x 10—9   Liver 0.058 x 10—9 0.33 x 10—9 0.25 x 10—9   Lung 0.034 x 10—9 0.55 x 10—9 1.2 x 10—9   General tissue 0.079 x 10—9 0.61 x 10—9 1.5 x 10—9 Total risk (A+B+C) 1.8 x 10—8 1.8 x 10—8 1.8 x 10—8   aTotal for the U.S. population (averaging across sex and smoking status). bEPA 1991b. cEPA 1994b. Based on the committee's analysis, the estimated inhalation risk has increased while the estimated ingestion risk has decreased. The committee did not do any new analysis for the inhalation risk. An average risk value based on three studies: BEIR IV, NIH, and BEIR VI (NRC 1988; Lubin et al. 1994; NRC 1999; respectively) was adopted. The committee did conduct a new analysis of the ingestion risk, based on a model developed for this study. This model reduces the overall ingestion risk factor by about a factor of 5, and suggests that, in contrast with the previous EPA analysis, almost all of the ingestion risk is attributed to the stomach. The estimated ingestion risk factors for various organs are compared in table ES-2. TABLE ES-3 Comparison of estimated cancer deaths per year due to exposure to radon and estimated possible ranges due to uncertainty   Exposure Pathway Committee Analysisa Revised EPA Analysisc Inhalation of radon progeny in indoor air 18,200b 13,600   (3,000-33,000)   Inhalation of radon progeny in outdoor air 720 520   (120-1300)   Inhalation of radon progeny derived from the release of radon from drinking water 160 86   (25-290)d   Ingestion of radon in drinking water 23 100   (5-50)     aBased on the 1998 estimated U.S. population of 270 million. bBased on data from BEIR VI (National Research Council 1999). cBased on a U.S. population of 250 million (EPA 1994b). dValues derived from rescaling the analysis of the EPA-SAB (1994b) report using 1998 population and mortality data and risk estimates from BEIR VI (National Research Council 1999). There are a number of factors underlying the analysis of the risk associated with radon in drinking water, in addition to the lifetime radiation risk factors described above. These include the amount of water ingested, the effective exposure duration and the overall water-to-air transfer factor. The EPA reanalysis (EPA 1994b) used a direct tapwater consumption rate of 1 L d—1, an exposure time of 70 y, and assumed that 20% of the radon in the tapwater is released from the water in the process of transferring the water from the tap to the stomach (tapwater is defined as water ingested directly, without agitation or heating). The committee used an age- and gender-specific tapwater usage rate that corresponds to an age- and gender-average rate of 0.6 L d—1 and assumed all of the radon remained dissolved in the water during the transfer process. Both the EPA and the committee analyses used a transfer factor of 1 x 10—4 for purposes of estimating the contribution radon dissolved in water makes to the overall indoor air radon concentration. The estimated number of cancer deaths per year from public exposure to radon are compared in table ES-3. Ranges estimated by this committee are approximate and are based on judgment using the best available information. Uncertainty Analysis Estimating potential human exposures to and health effects of radon in drinking water involves the use of large amounts of data and the use of models for projecting relationships outside the range of observed data. The data and models must be used to characterize population behaviors, engineered-system performance, contaminant transport, human contact, and dose-response relationships among populations in different areas, so large variabilities and uncertainties are associated with the resulting risk characterization. The report provides an evaluation of the importance of and methods for addressing the uncertainty and variability that arise in the process of assessing multiple-route exposures to and the health risks associated with radon. The data, scenarios, and models used to represent human exposures to radon in drinking water include at least four important relationships (i) The magnitude of the source-medium concentration, that is, the concentrations of radon in the water supply and in other relevant media, such as ambient air, (ii) the contaminant concentration ratio, which defines how much a source-medium concentration changes as a result of transfers, transformation, partitioning, dilution, and so on before human contact, (iii) the extent of human contact, which describes (often on a body-weight basis) the frequency (days per year) and magnitude (liters per day) of human contact with a potentially contaminated exposure medium (tap water, indoor air, or outdoor air), and (iv) the likelihood of a health effect, such as cancer, associated with a predicted extent of human contact. The latter area of uncertainty includes that of the dose-response model assumed. Uncertainties in modeling the movement of radon with the wall of the stomach (model structure), in the model parameters, and the lack of relevant experimental observations are the critical sources of uncertainty. The key points discussed included one overarching issue, that being how uncertainty and variability can affect the reliability of the estimates of health effects for any exposure scenario and related control strategies. Mitigation of Radon in Air There has been considerable research on and practical experience with the use of active (mechanical) systems for the control of radon entry into buildings. Use of such systems, when they are properly installed and operating, can typically yield indoor airborne radon concentrations below 150 Bq m—3 and can often result in concentrations of about 75 Bq m—3. Although there is considerable experience with the design and installation of active systems, monitoring programs are needed to ensure the continued successful operation of individual active systems. Another possible way to reduce risks associated with exposure to airborne radon is to design and build radon-resistant new buildings. Although the technical potential for building radon-resistant buildings has been demonstrated under some circumstances, the scientific basis for ensuring that it can be done reliably and as a consistent outcome of normal design and construction methods is inadequate. With the exception of the results in research conducted in Florida, there are no comparative data on which to base estimates of the overall effects of radon-resistant construction methods on reducing concentrations of radon in indoor air radon concentrations. Mitigation of Radon in Water Several water treatment technologies have been used to effectively remove radon from water. However various issues and secondary effects must be addressed in connection with each method, including intermedia pollution (transfer of radon from water to air) in the case of aeration and the retention of radionuclides (gamma-ray exposure and waste disposal) in the case granular activated carbon (GAC) adsorption. If water must be treated to meet either the AMCL or the MCL, disinfection might be required to meet the pending groundwater rule. In this case, the risk associated with the disinfection byproducts, as estimated by the committee, will be smaller than the risk reduction gained from radon removal. The committee has estimated the equivalent gamma dose from a GAC system designed to remove radon from a public water supply. The dose depends heavily on the details and geometry of the system and should be predicted with an extended-source model that can be modified to simulate the actual dimensions of the treatment units. Multimedia Approach to Risk Reduction The 1996 Safe Drinking Water Act Amendments permit EPA to establish an alternative maximum contamination level (AMCL) if the MCL is low enough so that the contribution of waterborne radon to the indoor radon concentration is less than the national average concentration in ambient air. The AMCL is defined such that the waterborne contribution of radon to the indoor air concentration is equal to the radon concentration in outdoor air, which is taken to be the national average ambient radon concentration. In the situations where radon concentrations in water are greater than the MCL but less than the AMCL, states or water utilities can develop a multi-media approach to health risk reduction. The EPA is required to publish guidelines including criteria for multimedia approaches to mitigate radon in indoor air that result in a reduction in risk to the population living in the area served by a public water supply that contains radon in concentrations greater than the MCL. The committee has examined some of the implementation issues involved in a multimedia mitigation approach through a sequence of scenarios that explore the possible options. The MCL will be determined by EPA based on a variety of considerations including their risk assessment, measurement technology, and best available treatment options and thus, a specific value has not yet been determined. The ratio of the average ambient radon air concentration to the transfer coefficient defines the AMCL. On the basis of the committee's recommended values for the average ambient radon concentration and the average transfer coefficient, the AMCL would be 150,000 Bq m—3 (about 4,000 pCi L—1). Water in excess of the AMCL must be mitigated at least to the AMCL, and alternative means can then be used to provide a health-risk reduction equivalent to what would be obtained by mitigation of the water to the MCL. However, because of the relatively small cost difference between mitigating the water to the AMCL and to the MCL, the committee believes that in most cases multimedia mitigation programs will probably not be considered for public water supplies with water concentrations in excess of the AMCL. For high radon concen tration water, it will generally be most cost-effective to mitigate radon in water to the MCL. For water supplies with radon concentrations between the MCL and the AMCL, the feasibility of implementing a multimedia mitigation program depends on the availability of homes in which the airborne radon concentration is high (greater than 150 Bq m—3). EPA has divided the country into three regions of different potentials for elevated indoor radon concentration. For water supplies in areas of low indoor air radon potential, it will be difficult to identify and mitigate enough homes to achieve an equivalent or better health-risk reduction by treating the air. For such water supplies, it is unlikely that a public water system's multimedia mitigation program will be practical unless the water concentration of radon is only slightly above the MCL. In areas of medium and high indoor air radon potential, it is more feasible to mitigate a small number of high-indoor-concentration homes to provide an equivalent health-risk reduction at a cost less than the cost of mitigating the water. In this scenario, the public water supply would have to actively recruit high-indoor-air radon concentration homes and mitigate them. Incentives could perhaps be used to get participation of homeowners in these multimedia programs. In addition, the utilities would have to monitor and maintain the air mitigation systems routinely. This scenario would require water utilities to become involved in air mitigation in individual homes, something with which they are likely to have little experience. Reduction of radon in indoor air can be an alternative means of reducing overall risks associated with radon. One way to achieve this is to install active (mechanical) systems to reduce radon entry into existing or new houses. Adequate testing (long-term measurements in the living space to reflect actual exposures) will be necessary to determine which existing houses should be mitigated. Routine follow-up measurements will be needed, both to determine the risk reduction achieved by the mitigation and to ensure continued successful operation of the mitigation systems. To ensure that health-risk reductions are at least as great as the reductions that would result from reducing the water radon concentration to the MCL, the number of homes with air mitigation systems should be 10-20% greater than the calculated minimum number of homes. Radon-resistant new construction methods could also be used although the technical and practical bases of their implementation are still poorly developed. Evaluation of the baseline radon exposure would require use of radon-monitoring data from existing houses in the community of interest or estimates of average indoor concentrations based on calculated radon potentials for the region. Careful attention to the follow-up monitoring results would be important, both for determining how much radon reduction has resulted (on the basis of aggregate comparisons) and for determining whether radon persists at unacceptable concentrations. Various educational and outreach programs reviewed by this committee indicate that, in general, public apathy about the potential risks of exposure to radon has generally remained, despite numerous and sometimes costly public education efforts. Though the evaluation of many of these programs has not been rigorous, on the basis of the reported results, the committee concludes that an education and outreach program would be insufficient to provide a scientifically sound basis for claiming equivalent health-risk reductions and that an active program of mitigation of homes would be needed to demonstrate health-risk reduction. Furthermore, the mitigation of indoor-air radon concentrations in a small number of homes means risk reduction among only a few people who had high initial risk, rather than uniform risk reduction for a whole population served by the water utility. This approach raises questions of equity among the various groups that are being exposed to various levels of risk associated with radon. Equity issues would also result if the airborne-radon risks in one community were traded for the risks in another without a resulting identical or improved public health effect and a commensurate economic benefit to both communities. Noneconomic considerations could play a large role in the evaluation of multimedia mitigation programs and might be the deciding factors in whether to undertake such a program. In any planning process, a careful program of public education, utilizing experts in risk communication, will be essential to give the public an adequate perspective of the tradeoffs in risks being proposed and of the health and economic costs and benefits that will be produced by the various alternatives. EPA and the state agencies responsible for water quality will continue to be faced with the problem of the health risks associated with the presence of radon in drinking water. The increment in indoor radon that emanates from the water will generally be small compared with the average concentration of radon already present in the dwellings from other sources. Thus, except in situations where concentrations of radon in water are very high, the reduction of radon in water will generally not make a substantial reduction in the total radon-related health risks to occupants of dwellings served by the water supply. However, the risks associated with the waterborne radon are large in comparison with other regulated contaminants in drinking water. Using mitigation of airborne radon to achieve equivalent or greater health-risk reductions therefore makes good sense from a public-health perspective. However, there are concerns that the equity issues associated with the multimedia approach and other related issues will become important in obtaining agreement by all of the stakeholders. This issue will require each public water supply and the regulatory agency overseeing it to study the circumstances carefully before deciding to implement a multimedia mitigation program in lieu of water treatment. Notes 1 International System of Units (SI) adopted in 1960 by the 11th General Conference on Weights and Measurements (see for example NIST 1995; NIST 1991). 2 Note that 1 cubic meter (m3) is equivalent in volume to 1,000 L. Thus, 4,000 Bq m—3 is equivalent to 4 Bq L—1.