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the Nature of Risk Assessment Recent criticisms of the conduct and use of risk assess- ment by regulatory agencies have led to a wide range of proposed remedies, including changes in regulatory stat- utes and the development of new methods for assessing risk. The mandate to this Committee was more limited. Our obj ective was to examine whether alterations in institutional arrangements of Procedures, particularly the organizational separation of Disk assessment from regulatory decisionrmaking and the use of uniform guide lines for inferring risk from available scientific ~nfor- mation, can improve federal risk assessment activities. Before undertaking to determine whether organizational and procedural reforms could improve the performance and use of risk assessment in the federal government, the Committee examined the state of risk assessment and the regulatory environment in which it is performed. In this chapter, we define risk assessment and differentiate it From other elements in the regulatory process, analyze the types of judgments made in risk assessment, and examine its current government context. Because one chronic health hazard, cancer, was highlighted in the Committee's congressional mandate and has dominated public concern about public health risks in recent years, most of our report focuses on it. Furthermore, because activities i n four agencies-the Environmental Protection Agency (EPA), the Food and Drug Administration (FDA), the Occupational Safety and Bealth Administration (OSEA), and the Consumer Product Safety Commission (CPSC) have given rise to many of the proposals f or changes in r isk assessment practices, our review focuses on these four agencies. The conclu- sions of this report, although directed primarily at risk assessment of potential carcinogens as performed by these 17

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18 four agencies, may be applicable to other federal programs to reduce health risks. TERMINOLOGY Despite the fact that risk assessment }gas become a subject that has been extensively discussed in recent years, no standard definitions have evolved, and the same concepts are encountered under different names. The Committee adopted the following terminology for use in this report. BISR ASSESS AND FISI; M~GEME:NT We use risk assessment to mean the characterization of the potential adverse health effects of human exposures to environmental hazards. Risk assessments include several elements: description of the potential adverse health effects based on an evaluation of results of epidemiologic, clinical, toxicologic, and env~ro~ental research; extrapolation from those results to predict the type and estimate the extent of health effects in humans under given conditions of exposure; judgments as to the number and characteristics of persons exposed at various intensities and durations and summary judgments on the existence and overall magnitude of the p~li~health problem. Risk assessment also includes characterization of the uncertainties inherent in the process of inferring risk . The term risk assessment is often given narrower and broader meanings than we have adopted here. For same observers, the term is synonymous with quantitative risk assessment and emphasizes reliance on numerical results. Our broader definition includes quantification, but also includes qualitative expressions of risk. Quantitative estimates of risk are not always feasible, and they may be eschewed by agencies for policy reasons. Broader uses of the term than ours also embrace analysis of perceived risks, comparisons of risks associated with different regulatory strategies, and occasionally analysis of the economic and social implications of regulatory decisions-- functions that we assign to risk management. The Committee uses the term risk management to describe the process of evaluating alternative regulatory actions and selecting among them. Risk management, which is car- ried out by regulatory agencies under various legislative

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19 mandates, is an agency decision-making process that entails consideration of political, social, economic, and engineering information with risk-related information to develop, analyze, and compare regulatory options and to select the appropriate regulatory response to a potential chronic health hazard. The selection process necessarily requires the use of value judgments on such issues as the acceptability of risk and the reasonableness of the costs of control. S'~:~S IN RISK AS SESSME:NT - Risk assessment can be divided into four major steps: hazard zOentif ication, dose-response assessment, exposure assessment, and risk characterization. A risk assessment might stop with the first step, hazard identification, if no adverse effect is found or if an agency elects to take regulatory action without further analysis, for reasons of policy or statutory mandate. Of the four steps, hazard identification is the most easily recognized in the actions of regulatory agencies. It is defined here as the process of determining whether exposure to an agent can cause an increase in the inci- dence of a health condition (cancer, birth defect, etc.). It involves characterizing the nature and strength of the evidence of causation. Although the question of whether a substance causes cancer or other adverse health effects is theoretically a yes-no question, there are few chemi- cals on which the human data are definitive. Therefore, the question is often restated in terms of effects in laboratory animals or other test systems, e.g., Does the agent induce cancer in test animals?. Positive answers to such questions are typically taken as evidence that an agent may pose a cancer risk for any exposed hens. Information from short-term in vitro tests and on struc- tural similarity to known chemical hazards may also be considered. Dose-response assessment is the process of character- ~zing the relation between the dose of an agent adminis- tered or received and the incidence of an adverse health effect in exposed populations and estimating the incidence of the effect as a function of human exposure to the agent. At takes account of inters' ty of exposure, age pattern of exposure, and possibly other variables that might affect response, such as sex, lifestyle, and other modifying factors. A dose-response assessment usually

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20 requires extrapolation from high to low dose and extrapo- lation from animals to humans. A dose-response assess- ment should describe and justify the methods of extrapola- tion used to predict incidence and should characterize the statistical and biologic uncertainties in these methods. Exposure assessment is the process of measuring or estimating the intensity, frequency, and duration of Herman exposures to an agent currently present in the environment or of estimating hypothetical exposures that might arise from the release of new chemicals into the environment. In its most complete form, it describes the magnitude, duration, schedule, and route of exposure; the size, nature, and classes of the hen populations exposed; and the uncertainties in all estimates. Exposure assessment is often used to identify Feasible prospective control options and to predict the effects of available control technologies on exposure. ~~L china -~515~ is the process of estimating the incidence of a health effect under the various colons of human exposure described in exposure assessment. It is performed by combining the exposure and dose-response assessments. The summary effects of the uncertainties in the preceding steps are described in this step. The relations among the four steps of risk assessment and between risk assessment and risk management are depicted in Figure I-1. The type of research information needed for each step is also illustrated. SCIENTIFIC BASIS FOR RISK ASSESSMENT Step l. Bazard Identification Although risk assessment as it is currently practiced by federal agencies for the estimation of carcinogenic risk contains several relatively new features, the scientific basis for much of the analysis done in risk assessment is well established. This is especially true of the first step in the assessment process, hazard identification. - Four general classes of information may be used in this step: epidemiologic data, animal-bioassay data, data on in vitro effects, and comparisons of molecular structure. Euidemiol ogic Data Well-conducted epidemiologic studies that show a posz- tive association between an agent and a disease are

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21 LU cD z y u) cD cn u' y u, - - o o ~ - ~ o c, Q o o — C' — C) ~ .O E c, CO ~ o ._ V o _ C~ _ _ _ C3 C o ~ _ ~, ._ _ ~ _ C — ~ a~ ~ ~ ~ C) Z C' — — C' _, ~, a~ cc I ~ ~ _ _ , ~ _ ° C2. C) 4-C ~ {l, =5 ~- C~ — C:S — C C) ~ ~ s .3 _ C: -— ~ — . ~ a, c, C) ~ ~ ~ - 1 o _ ._ C~ ~ ,%; ·_ ._ _ C) C) C~ C' CZ ,~ ~ _ c ~ ._ C; _ — 2 , - _ ~s c, cc s _ ._ o C ~ C, — C C~ =; C, ._ ~ C) ~ ~ C) ._ , o ._ ._ C) cn ~ o ._ V CO o .3 ~ _ 6 c~ _ ~ _ V~ C) '— ~ — X cC ° ~ C~ — C-) — o ~ C) C C, X ' — ~ ~ o~ S: 0 ~S £ S~ S: ~n ~R m x ~2 S~ w o m ~: c: c LD cn LL G C) V7 C, C, ~ ,_ -3 — tl; _ _ o V' o o ._ _ _ o _ V J o X (5 ,= CO _ ~ o _ _ C} ~n ~ C) ~n _ C~ C' o — ~ CC , o _ ~ o | ~ _ ~ o ~ o - E mE ~ ~— ~1 ,= ,,l, ~ o~

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22 accepted as the most convincing evidence about human risk. This evidence is, however, difficult to accumulate; often the risk is low, the number of persons exposed is ~mall, the latent period between exposure and disease is long, and exposures are mined and multiple. Thus, epidemiologic data require careful interpretation. Even if these prob- lems are solved satisfactorily, the preponderance of chemicals in the environment has not been studied with epidemiologic methods, and we would not wish to release newly produced substances only to discover years later that they were powerful carcinogenic agents. These limitations require reliance on less direct evidence that a health hazard ex: sts. Animal—Bioassav Data The most commonly available data in hazard zdentifica~ talon are those obtained from animal bioassays. The infer- ence that results from animal experiments are applicable to humans is fundamental to toxicologic research; this premise underlies much of experimental biology and medi- cine and is logically extended to the experimental obser- vation of carcinogenic effects. Despite the apparent validity of such inferences and their acceptability by most cancer researchers, Mere are no doubt occasions in which observations in animals may be of highly uncertain relevance to humans. Consistently positive results in the two sexes and In several strains and species and higher inciden<:es at higher doses constitute the best evidence of carcinogen nici1:y. More often than not, however, such data are not available. Instead, because of the nature of the effect and the limits of detection of animal tests as they are usually conducted, experimental data leading to a posz- tive finding sometimes barely exceed a statistical thresh- old and may involve tumor types of uncertain relation to human carcinogenesis. Interpretation of same animal data may therefore be d'ff icult. Notwithstanding uncertainties associated with interpretation of she animal tests, they have, In general, proved to be reliable indicators of car- cinogenic properties and will continue to play a pivotal role in efforts to identify carcinogens. Short-Term Studies , Considerable experimental evidence supports the propose sition that most chemical carcinogens are mutagens and that many mutagens are carcinogens. As a result, a positive response in a mutagenicity assay is supportive

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23 evidence that the agent tested is likely to be carcino genie. Such data, in the absence of a positive annoy bioassay, are rarely, z! ever, sufficient to support a conclusion that an agent is carcinogenic. Because short- term tests are rapid and inexpensive, they are valuable for screening chemicals for potential carcinogenicity and lending additional support to observations from animal and epidemiologic investigations. Comparisons of Molecular Structure Comparison of an agent's chemical or physical proper- ties with those of known carcinogens provides some evi- dence of potential carcinogenicity. Experimental data support such associations for a few structural classes; however, such studies are best used to identify potential carcinogens for further investigation and may be useful in priority-setting for carcinogenicity testing. Step 2. Dose-Response Assessment In a small nether of instances, epidemiologic data permit a dose-response relation to be developed directly from observations of exposure and health effects in humans. I f epidemiologic data are available, extrapolations from the exposures observed in the study to lower exposures experienced by the general population are often necessary. Such extrapolations introduce uncertainty into the esti- mates of risk for the general population. Uncertainties also arise because the general population includes some people, such as children, who may be more susceptible than people in the sample from which the epidemiologic data were developed. The absence of useful human data is common for most chemicals being assessed for carcinogenic effect, and dose-response assessment usually entails evaluating tests that were performed on rats or mice. The tests, however, typically have been designed for hazard identification, rather than for determining dose-response relations. Onder current testing practice, one group of animals is given the highest dose that can be tolerated, a second group is exposed at half that dose, and a control group is not exposed. (The use of high doses is necessary to maximize the sensitivity of the study for determining whether the agent being tested has carcinogenic pose:: teal.) A finding in such studies that increased exposure leads to an increased incidence has been used primarily

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24 to corroborate hazard identif ication, that is, to show that the agent does indeed induce the adverse health effect. The testing of chemicals at high doses has been challenged by soree scientists who argue that metabolism of chemicals differs at high and low doses; i.e., high doses may overwhelm normal detoxification mechanists and provide results that would not occur at the lower doses to which humans are exposed. An additional factor that is often raised to challenge the validity of animal data to indicate effects in man is tha. metabolic differences among animal species should be considered when animal test results are analyzed. Metabolic differences can have important effects on the validity of extrapolating from animals to man if, for exile, the actual carcinoma gen is a metabol~te of the administered chemical and the animals tested differ markedly from horns in their prom auction of that metabolite. A related point is that the actual dose of carcinogen reaching the affected tissue or organ is usually not known; thus, dose~response informal tion, of necessity, is based on administered dose and not tissue dose. Although data of these types would certainly improve the basis for extrapolating from high to low doses and from one species to another, they are difficult to acquire and often unavailable. Regulators are interested in doses to which humans might be exposed, and such doses usually are much lower than those administered in animal studies. Therefore, dose-response assessment often requires extrapolating an expected response curve over a wide range of doses from one or two actual data points. In addition, differences in size and metabolic rates between man and laboratory animals require that doses used experimentally be con versed to reflect these differences. Low-Dose Extrapolation One may extrapolate to low doses by fitting a mathemat- ical model to animal dose-response data and using the model to predict risks at lower doses corresponding to those experienced by humans. At present, the true shape of the dose-response curve at doses several orders of magnitude below the observation range cannot be deter- mined experimentally. Even the largest study on record-- the EDGE study involving 24,000 animals--was designed only to measure the dose corresponding to a 1% increase in tumor incidence. However, regul atory agencies are often concerned about much lower risks (1 in 100,000 to 1

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25 in 1,000). Several methods have been developed to extrap- olate from high doses to low doses that would correspond to risk of such magnitudes. A difficulty with low-dose extrapolation is that a number of the extrapolation methods f it the data f rom animal experiments reasonably well, and it is impossible to distinguish their validity on the basis of goodness of fit. (From a mathematical point of view, distinguishing among these models on the basis of their fit with experimental data would require an extremely large experiment; from a practical point of view, it is probably impossible). As Figure 7-2 shows, the dose-response curves derived with different models to d iverge below the experimental doses and may diverge sub- stantially In the dose range of interest to regulators. Thus, low-dose extrapolation must be more than a curve- f itting exercise, and considerations of biological plau- sibility must be taken into account. Although the five models shown in Figure I-2 may fit experimental data equally well, they are not equally plausible biologically. Most persons in the field would agree that the supralinear model can be disregarded, because it is very difficult to conceive of a biologic mechanism that would give rise to this type of low dose response. The threshold model is based on the assumption that, below a particular dose (the .threshold. dose of.a given carcinogen) there is no adverse effect. This con- cept is plausible, but not now confirmable. The EDb1 study showed an apparent threshold for bladder cancers caused by 2-acetylaminofluorene; when the data were repotted on a scale giving greater resolution IOTA, 1981), the number of bladder tumors consistently ins creased with dose, even at the lowest doses, and no threshold was detected. Another aspect of the debate over thresholds for inducing carcinogenic effects Is the argument that agents that act through genotoxic mecha- nisms are not likely to have a threshold, whereas agents whose effects are mediated by epigenetic mechanisms are possibly more likely to have a threshold. The latter argument is also currently open to scientific challenge. Finally, apparent thresholds observable in animal b~o- assays cannot be equated with thresholds for entire populations. Even if a threshold exists for individuals, a single threshold would probably not be applicable to the whole population. Animal-to-Buman Dose Extrapolation In extrapolating from animals to humans, the doses used in bioassays must be adjusted to allow for differ-

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26 lo-2 10-4 - ~s - C~ A ~ 10 6 6 cr: X Lo 10-8 / /Subl Sneer ~ I 10 lo | 1 0.01 i' Supralinear '~7 I ~ / 0.1 Sublinear I | Threshold I 1 1.0 10.0 DOSE (,uglweek) FIGURE I-2 Results of alternative extrapolation models for the same experimental data. UNCLE: Dose-response functions were developed (Crump, in press) for data from a benzopyrene carcinogenesis experiment with mice conducted by Lee and O'Neill (1971).

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27 ences in size and metabolic rates. Several methods cur- rently are used for this adjustment and assume that animal and human risks are equivalent when doses are measured as milligrams per kilogram per day, as milligrams per square meter of body surface area, as parts per million in air, diet, or water, or as milligrams per kilogram per life- time. Although some methods for conversion are used more frequently than others, a scientific basis for choosing one over the other is not established. S ten 3. Exposure Assessment The f ~ rst task of an exposure assessment is the determiner tion of the concentration of the chemical to which humans are exposed. This may be known from direct measurement, but more typically exposure data are incomplete and must be estimated. Models f or estimating exposure can be com- plex, even in the case of structured activity, as occurs in the workplace. Exposure measurements made on a small group (e.g., workers in a particular industrial firm) are often applied to other segments of the worker population. Exposure assessment in an occupational setting consists primarily of estimation of long-term airborne exposures in the workplace. However, because an agent may be present at various concentrations in diverse occupational set- tings, a census of exposures is difficult and costly to conduct. In the community environment, the ambient con- centrations of chemicals to which people may be exposed can be estimated from emission rates only if the transport and conversion processes are known. Alternative eng~neer- ~ng control options require different estimates of the reduction in exposure that may be achieved. For new chew icals with no measurement data at all, rough estimations of exposure are necessary. Some chemical agents are of concern because they are present in foods or may be am sorbed when a consumer product is used. Asses rents of exposure to such agents are complicated by variations in diet and personal habits among different groups in the population. Even when the amount of an agent in a food can be measured, differences in food storage practices, food preparation, and dietary frequency often lead to a wide variation in the amount of the agent that individual s ingest. Patterns of use affect exposure to many consumer products; for example, a solvent whose vapor is poten- tially toxic may be used outdoors or it may be used in a small, poorly ventilated room, where the concentration of vapor in the air is much higher.

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40 determine whether regulatory action is warranted, risk assessment serves at least two major functions in regular tory decisions: first, it provides an initial assessment of risks, and, if the risk is judged to be important enough to warrant regulatory action, it is used to evalu- ate the effects of different regulatory options on expo- sure. In addition, it may be used to set priorities for regulatory consideration and for further toxicity testing. These varied functions place different requirements on risk assessors, and a single risk assessment method may not be sufficient. A risk assessment to establish testing priorities may appropriately incorporate many worst-case assumptions if there are data gaps, because research should be directed at substances with the most crucial gaps; but such assumptions may be inappropriate for analyzing regulatory controls, particularly If the regal later must ensure that controls do not place undue strains on the economy. In establishing regulatory priorities, Me same inference options should be chosen for all chem~- cals, because the main point of the analysis is to make useful Disk comparisons so that agency resources will be used rationally. Bowever, this approach, which may be reasonable for priority-setting, may have to yield to more sophisticated and detailed scientific arguments when a substance's cnmmercia1 life is at stake and the agency's decision may be challenged in court. Furthermore, the available resources and the resulting analytic care devoted to a risk assessment for deciding regulatory policy are likely to be much greater for analyzing control actions for a single substance than for setting priorities. THE AGENCIES TEAT BEGUL~TE The approach to risk assessment varies considerably among the four federal agencies. Differences stem pr~r~ly from variations in agency structure and differences in statutory mandates and their interpretation. Organizational Arrangements The Food and Drug Administration (FDA) is a component of the Department of Bealth and Buman Services, whose Secretary is the formal statutory delegate of the powers exercised by FDA. FDA is headed by a single official,

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41 the Commissioner of Food and Drugs, who is appointed by and serves at the pleasure of the Secretary of the Depart- ment of Health and Baton Services. It is organized in product-related bureaus, each of which employs its own scientists, technicians, compliance off icers, and adminis- trators. FDA has a long (75-year) and strong scientific tradition. According to a recent Office of Technology Assessment summary, FDA had taken or proposed action on 24 potential carcinogens by 1981. Like FDA, the Environmental Protection Agency (EPA) is headed by a single official, but EPA's Administrator is appointed by the President subject to Senate confirmation. Also like FDA, EPA resembles a confederation of relatively discrete programs that are coordinated and overseen by a central management. The agency was established in 1970, but many of its programs (e.g., air and water pollution control and pesticide regulation) predate its formation and previously were housed in and administered by other departments. Other programs, such as those for toxic substances and hazardous waste, are rather new. EPA's research, policy evaluation, and, until recently, enforce- ment efforts were separated organizationally from the program offices that write regulations. EPA has had the widest experience with regulating carcinogens; as of 1981, it had acted on 56 chemicals in its clean~water program, 29 in its clean~air program, 18 in its pesticide program, and two in its drinking-water program. The Occupational Safety and Bealth Administration (OS=) is part of the Department of Labor. The agency' s head Is an Assistant Secretary of Labor, who requires Senate confirmation. Although Fl)A and EPA derive their scientific support largely from their own full-time employees, until the late 1970s OSEA relied on other agencies, primarily the National Institute of Occupant tional Safety and Bealth, an agency of the Department of Health and Human Services. This division reflects a conscious congressional choice in 1970 to place ache health experts on whom OSEA was expected to rely in an outside environment believed more congenial to scientific inquiry and less vulnerable to political influence. As of 1981, 18 potential carcinogens had been acted on by OSEA. The Consumer Product Safety Commission (CPSC) enforces five statutes, including the Consumer Product Safety Act and the Federal Hazardous Substances Act. Both empower CPSC to regulate unreasonable risks of injury from prod- ucts used by consumers in the home, in schools, or in

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42 recreation. The much smaller CPSC differs sharply from the other three agencies in two important respects: it does not have a single administrative head, but instead is governed by five Commissioners, who can make major regulatory decisions only by majority vote; and the Comm' ssioners are appointed for f ixed terms by the President with Senate confirmation. Before 1981, CPSC had acted on five potential carcinogens. The four agencies have attempted to coordinate risk assessment activities in the past, most notably through the Interagency Regulatory Liaison Group (DOG), which formed a work group on risk assessment to develop a guides line for assessing carcinogenic risks. Assisted by scien- tists from the National Cancer Institute and the National Institute for Environmental Health Sciences, it examined the various approaches used by the four agencies to evalu- ate evidence of carcinogenicity and to assess risk. The IRLG (1979a,b) then integrated and incorporated these evaluative procedures into a document, "Scientific Bases for Identification of Potential Carcinogens and Esteem tion of Risks, which described the basis for evaluation or carcinogenic hazards identified through epidemiologic and experimental studies and the methods used for quanti- tat~ve estimation of carcinogenic risk. Requlatorv Statutes* Examination of the statutes that the four agencies admit ister reveals important differences in the standards that govern their decisions. The Office of Technology Assess- ment has summarized {Table I-2) statutes that pertain to the regulation of carcinogenic chemicals. In particular, the statutes accord different weights to such criteria as risk, costs of control, and technical feasibility. In addition, different modes of regulation vary in their capacity to generate the scientific data necessary to perform comprehensive risk assessments. Several laws require agencies to balance regulatory costs and benefits. Examples of balancing provisions are found in the Safe Drinking Water Act; the Federal Insecti- cide, Fungicide, and Rodenticide Act; the Toxic Substances *This discussion draws heavily on the Office of Techr nology Assessment report, Technologies for Determining Cancer Risks from the Environment, }981.

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43 Control Act; and the section on fuel additives in the Clean Air Ace. Under such provisions, a risk assessment can be used to express the nature and extent of public- health benef its to be attained through regulation. Some regulatory programs involve the establishment of technology-based exposure controls. This approach is Followed, for example, in portions of the clean-water program and the part of the hazardous-wastes program that deals with waste incineration standards. In such pro- grams, ~ risk assessment may be used to show the human exposure that corresponds to a specific degree of risk or to calculate the risk remaining after control technologies are put in place. Some statutes mandate control techniques to reduce risks to zero whenever hazard is affirmed. Such tech- niques include outright bans of products, as envisioned in the Delaney clause in the Federal Food, Doug, and Cosmetic Act. In addition, if the concept of a threshold below which carcinogens pose no risk is not accepted, strict interpretations of ample margin of safety language in federal clean-air and clean-water legislation would require that exposures to carcinogenic pollutants be reduced to zero. The role of risk assessment in cases where mandatory control techniques must reduce risks to zero may be simply to affirm that a hazard exists. m e difference between programs that involve premarket- inn approval of substances and programs that operate through post hoc mechanisms, such as environmental em~s- sion limits, may have an important influence over the quality of risk assessments. The most important effect of this difference may lie in the fact that premarketing approval programs (such as those for pesticides, for new human drugs, and for new food additives empower an agency to require the submission of sufficient data for a compre- hens~ve risk assessment, whereas other programs tend to leave agencies to fend for themselves in the acquisition of necessary data. There can be little question that differing statutory standards for decision affect the weight that agencies accord risk assessments. Like differences in the mode of regulation, they probably have affected the rigor and scope of many assessments. If risk is but one of several criteria that a regulator must consider or if data are expensive to obtain, it would not be surprising if an agency devoted less effort to risk assessment. However, the Committee has not discovered differences in existing statutes that should impede the adoption of uniform,

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47 ~ ~ v ' ~ ° co ~ 5 E E C| .. | ~ tr c,'° !3 =- `, E ,C 2' - . ~ al ~ a 0 C' O ~ C,—~ 0 OD^i~- ~ ~ 2 c ~ D as ! ~ ~ ~ O ID as ~ O O lC— ID · — C _ ~ O - cat of as ~ 0 ~ ~ o ~ 2 ~ ~ '_ ' ° ~ ', C !.-2~.l§.~.--~ I..- il~ls~r=~ ail - ~ '-a E hi, e< 0 c

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48 government-wide risk assessment guidelines. Indeed, it is not satisfied that there are legal bases for inter- agency differences in the performaw e--as distinct from the use--of risk assessment for chronic health hazards. CONCLUSIONS On the basis of a review of the nature and the policy context of risk assessment, the Committee has drawn the following general conclusions: 1. Risk assessment is only one aspect of the process of regulatory control of hazardous substances,, 24~3ctc~` - ~marov~ments in risk assessment to eliminate controversy over federal risk management decisions. Restrictive regulation nas seemed onerc~u:~ rev Can "-— turers, distributors, and users of products judged useful and valuable; conversely, inaction and delay with respect to regulatory proceedings have appeared callous and irresponsible to others. . These dissatisfactions have been manifested in many ways, including criticizer of risk assessment processes. The Committee believes that much of this criticism is inappropriately directed and gives rise to an unrealistic expectation that modifying risk assessment procedures will result in regulatory decisions more acceptable to the critics. Certainly risk assessment can and should be Improved, with salutary effects on the appropriateness of regulatory decisions. However, risk management, although it uses risk assessment, is driven by political, social, and economic forces, and regulatory decisions will continue to arouse controversy and conflict. 2. }lis}c assessment is an analytic process that is firmly based on scientific considerations, but it also requires iudsments to be made when the available informal tion is incomplete. both scientist`: no! P~ilE[~YLi4~Ya~CL Jon ris}c assessment is that the information on which decisions must be based is usually inadequate. Because the decisions cannot wait, the gaps in information must be bridged by inference and belief, and these cannot be evaluated in the some way as facts. Improving the quality and comprehensiveness of knowledge is by far the most effective way to Improve risk assess-

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49 meet, but some limitations are inherent and unresolvab, e, and inferences will always be required. Although we conclude that the mixing of science and policy in risk assessment cannot be eliminated, we believe that most of the intrusions of policy can be identified and that a major contribution to the integrity of the risk assess- ment process would be the development of a procedure to ensure that the judgments made in risk assessments, and the underlying rationale for such judgments, are made explicit. 3. Two kinds of policy can potentially affect risk assessment: that which is inherent in the assessment Process itself and that which Governs the selection of regulatory options. The lay i should not be allowed to control the former, risk assessment Policv. Risk management policy, by its very nature, must entail value judgments related to public perceptions of risk and to information on risks, benefits, and costs of control strategies for each substance considered for regulation. Such information varies from substance to substance, so the judgments made in risk management must be case- specific. If such case-specific considerations as a substance's economic importance, which are appropriate to risk management, influence the judgments made in ye risk assessment process, the integrity of the risk assessment process will be seriously undermined. Even the perception that risk management considerations are influencing the conduct of risk assessment in an important way will cause the assessment and regulatory decisions based on them to lack credibility. 4 . Risk assessment suf ~ of a mechanism for addressing generic issues in isolation , from specific risk management decisions. spent has progressed in recent years, there is currently no mechanism for st ulating and monitoring advances on generic questions in relevant scientific fields or for the timely disseminar tion of such information to risk assessors. REFERENCES Cramp, R. S. In press. Issues related to carcinogenic risk assessment from animal bioassay data. Paper

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50 presented May 1981 at the International School of Technological Risk Assessment, a NATO Advanced Study Institute, Erice, Italy. IRLG (interagency Regulatory Liaison Group), Work Group on Risk Assessment. 1979a. Scientific }cases for identification of potential carcinogens and estimation of risks. Fed. Reg. 44 :39858. IREG (Interagency Regulatory Liaison Group), Work Group on Risk Assessment. 1919b. Scientific bases for identification of potential carcinogens and estimation of risks. 3. Natl. Cancer Inst. 63 :242. Lee, P. N., and J. A. O'~eill. 1971. The effect both of time and dose applied on tumor incidence rate In benzopyrene skin painting experiments. Brit. J. Cancer 25: 759-770 . National Academy of Sciences. 1981. The Health Effects of Nitrate, Nitrite, and N=Nitroso Compounds. Washington, I).C.: National Academy Press. 544 pp. OTA tOffice of Technology Assessment). 1981. Assessment of the Technologies for Determining Cancer Risks from the Environment. 240 pp.