Below are the first 10 and last 10 pages of uncorrected machine-read text (when available) of this chapter, followed by the top 30 algorithmically extracted key phrases from the chapter as a whole.
Intended to provide our own search engines and external engines with highly rich, chapter-representative searchable text on the opening pages of each chapter. Because it is UNCORRECTED material, please consider the following text as a useful but insufficient proxy for the authoritative book pages.
Do not use for reproduction, copying, pasting, or reading; exclusively for search engines.
OCR for page 8
--> 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 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.
OCR for page 9
--> 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
OCR for page 10
--> 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 program 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 nonregulatory 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
OCR for page 11
--> 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
OCR for page 12
--> 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.,
OCR for page 13
--> 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 × 10-4 with a standard error of 0.1 × 10-4, and the model's average was either 0.9 × 10-4 or 1.2 × 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 × 10-4 and 1.2 × 10-4 and recommends that EPA continue to use 1.0 × 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
OCR for page 14
--> 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 × 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
OCR for page 15
--> cancer death risk from lifetime ingestion of radon dissolved in drinking water at a concentration of 1 Bq m-3 is 0.2 × 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 cells—that 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 × 10-4, 1.2 × 10-4, and 1.3 × 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 × 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 × 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 × 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
OCR for page 16
--> risks to susceptible populations—such 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 I Bq m-3 is 1.6 × 10-8. The adopted lifetime risk of stomach cancer for the same water concentration is 0.2 × 10-8; the committee could not make a distinction in ingestion risk for any specifically identified subpopulation other than the differences in gender. Figure I (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. 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 × 10-8 2.0 × 10-8 2.6 × 10-8 Inhalation (never-smokers)b 0.59 × 10-8 0.4 × 10-8 0.50 × 10-8 Inhalation (population)b 2.1 × 10-8 1.2 × 10-8 1.6 × 10-8 Ingestion 0.15 × 10-8 0.23 × 10-8 0.19 × 10-8 Total Risk (inhalation and ingestion) 2.2 × 10-8 1.4 × 10-8 1.8 × 10-8 a These rounded values combine the various subpopulations, with appropriate weighting factors taken from the 1990 U.S. Census. b Based on the radon decay product risks of BEIR VI Report (National Research Council 1999) and includes the incremental dose to showering with thc uncertainties in these estimates.
OCR for page 17
--> 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%. 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. 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 expo- 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 × 10-8 1.3 × 10-8 0.81 × 10-8 (B) Radon inhalation 0.05 × 10-8 0.054 × 10-8 (C) Ingestion 0.2 × 10-8 0.4 × l0-8 0.95 × 10-8 Stomach 1.6 × 10-9 2.0 × 10-9 4.9 × 10-9 Colon 0.059 × 10-9 0.46 × 10-9 1.4 × 10-9 Liver 0.058 × 10-9 0.33 × 10-9 0.25 × 10-9 Lung 0.034 × 10-9 0.55 × 10-9 1.2 × 10-9 General tissue 0.079 × 10-9 0.61 × 10-9 1.5 × 10-9 Total risk (A+B+C) 1.8 × 10-8 1.8 × 10-8 1.8 × 10-8 a Total for the U.S. population (averaging across sex and smoking stares). b EPA 1991b. c EPA 1994b.
OCR for page 18
--> sure 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. 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 (3,000–33,000) 13,600 Inhalation of radon progeny in outdoor air (120–1300) 720 520 Inhalation of radon progeny derived from the release of radon from drinking water 160 (25–290)d 86 Ingestion of radon in drinking water (5–50) 23 100 a Based on the 1998 estimated U.S. population of 270 million. b Based on data from BEIR VI (National Research Council 1999). c Based on a U.S. population of 250 million (EPA 1994b). d Values 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).
OCR for page 19
--> 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
OCR for page 20
--> 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 multimedia 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-
OCR for page 21
--> 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
OCR for page 22
--> 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. Non-economic 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.
Representative terms from entire chapter: