Document 5b1oM421MkvOo90QwQw6J3VjJ

Special Communications The Environment and the Lung Changing Perspectives Jonathan M. Samet, MD, Mark J. Utell, MD The focus of public health concern and research in regard to environmental lung diseases has changed across the century. .Illustrative agents include radon, indoor asbestos, environmental tobacco smoke, acidic aerosols, and oxidant gases. Tremendous progress has been made in understanding and preventing environmental lung diseases. However, we remain concerned about adverse consequences of breathing polluted outdoor and indoor air. In the persistent concerns about adverse effects of polluted air on the lung, a new emphasis is pervasive; the focus has shifted from avoiding clinical disease among highly exposed individuals to protecting the population from an unacceptable burden of risk. The technique of qua! ititative risk assessment has become increasingly Important for characterizing the safety of environmental agents. The resulting emphasis on the final risk projection and attendant uncertainties may overly emphasize gaps in our knowledge. ' (JAMA. 1991;266:670-675) AS THE 20th century ends, we are con cerned and fearful about the adverse consequences of breathing polluted air, whether outdoors or indoors, and are asking for reduction of known and po tential hazards. Yet, during this centu ry the environmental causes of many lung diseases have been identified, the pathogenetic mechanisms underlying the development of some of these dis eases have been described, and control measures have been implemented with at least partial success for a number of the injurious agents. In the United States and many other developed coun tries, elaborate regulations and en forcement mechanisms are in place to From the Pulmonary and Critical Care Division, De partment of Medicine, and the Mew Mexico Tumor Reg istry, Cancer Center, University of New Mexico, Albu querque (Dr Samet); and the Departments of Medicine and Environmental Health Sciences, University of Rochester(NY) School of Medicine, and the Pulmonary and Critical Care Unit and Occupational Medicine Pro gram, University of Rochester Medical Center (Dr Utell). Reprint requests to New Mexico Tumor Registry, Medical Center, 900 Camino de Salud NE, Albuquer que, NM 87131 (DrSamet). ensure that air outdoors and in work places does not pose unacceptable health risks; indoor air pollution has been recently recognized as a potential threat to health as well and programs have been implemented to address some of its hazards, for example, radon and asbestos. Despite the increasing scientific evi dence and the far-reaching array of con trol measures, the public is still con cerned about breathing the often visibly polluted air that remains in many cities and even rural locations and is learning that indoor air may be contaminated with the same chemicals that are re leased by industry and vehicles, and even by such invisible pollutants as ra don. While regulations have controlled many of the hazards of workplaces heavily contaminated by dust and fumes, new types of manufacturing have introduced novel and uninvesti gated exposures, and changing work environments have led to the emer gence of new clinical problems, such as "sick-building syndrome," and concern that some cases of recognized diseases, like asthma, may be caused or exacer bated by changes in the indoor and out door environments. In the persistent concerns about ad verse effects of poEuted air on the lung, a new emphasis is pervasive; the focus has shifted from the'avoidance ofclinical disease among highly exposed individ uals toward the protection of the gener al population from an unacceptable bur den of disease at much lower exposures, and an attempt to ensure that even the most susceptible persons are not ad versely affected. This same emphasis extends equally to other environmental exposures and to diseases other than those affecting the lung. Quantitative risk assessment, a four-step process, has become a widely used tool for judg ing the safety of environmental agents, providing a framework for summarizing the evidence on health risks from toxico logic studies, controUed exposures of volunteers, and epidemiologic research with information on exposure to injuri ous agents (Table l).1 The results ofrisk assessment can be used to identify areas for research, to assign priorities among environmental hazards, and to select approaches for managing risks. It must be recognized, however, that quantita tive risk assessment is a new method ology and that its role in regulation is stiU evolving.1 This shift in emphasis from higher exposures producing clinical disease to lower levels projected to increase popu lation risks has raised new questions and challenges for research on environ mental lung disease. Providing assur ance of safety, a level of risk judged to be acceptable,2 requires precise and confident characterization of risks, and the scope of research needs to extend 670 JAMA, August 7,1991 -Vol 266, No. 5 The Environment and the Lung--Samet & Utell 202G090468 Table 1.--The Four Steps of Risk Assessment* Hazard identification: The determination of whether an agent is causally linked to the health effect ofconcern Dose-response assessment: The determination of the relation between level of exposure and risk of the health effect Exposure assessment: Description of the extent of human exposure Risk characterization: Description of the human risk, including uncertainties `Based on reference 1. beyond testing for an exposure-disease association to quantification of risk at various levels of exposure and assess ment of factors that modify the expo sure-disease relationship. Data from extensive animal studies and largescale epidemiologic investigations are often required. This study addresses the changing fo cus across the century of public health concern and research in regard to envi ronmental lung diseases. We review se lected agents to illustrate the shift from disease prevention in individuals to risk reduction for the whole population and the difficulty ofanswering the questions now raised with regard to safety for many agents. We begin by considering the broad groups of environmental agents that produce lung disease and the mechanisms of disease patho genesis. MECHANISMS OF LUNG INJURY BY ENVIRONMENTAL AGENTS The environmental agents in indoor and outdoor air of greatest contempo rary concern are diverse, causing both malignant and nonmalignant diseases (Table 2). Continued concern about the risks of these and other causes of envi ronmental lung disease is justified by the myriad pollutants inhaled in the var ious indoor and outdoor environments where time is spent each day, the di verse mechanisms by which these pol lutants cause disease, and the wide range of susceptibility to pollutants in the population. Because we inhale 10 000 to 20 000 L of air daily, doses of pollutants present even at low concen trations may become biologically signif icant with sustained exposure. Fortu nately, the lung has physical, chemical, and immunologic defense mechanisms for clearing and detoxifying inhaled agents, although the defense systems may be overwhelmed by large pollutant doses or may not be fully effective against some pollutants. Atmospheric pollutants are present in the form of gases, fibers, or particles. Penetration of pollutants into the lung and retention at potential sites of injury depend on the physical and chemical properties of the agents.8 Highly water- Table 2.--Selected Agents Causing Environmental Lung Disease of Current Concern and Associated Adverse Effects Agent Acidic aerosols Asbestos Environmental tobacco smoke Nitrogen dioxide Photochemical pollution (ozone) Radon Silica Vblatile organic compounds Effect(s) Exacerbate asthma and COPD,* respiratory symptoms, reduced lung function Lung cancer, mesothelioma, pleural disease Lung cancer, respiratory infection, respiratory symptoms, reduced lung function Exacerbate asthma, respiratory infection and symptoms, reducdd lung function Exacerbate asthma and COPD, respiratoty symptoms, reduced lung function Lung cancer Silicosis, lung cancer Cancer; neuropsychological effects, respiratory irritation Chronic obstructive pulmonary disease. soluble gases, such as sulfur dioxide and formaldehyde, are almost completely extracted by the upper airway of a rest ing subject during a brief exposure, whereas less soluble gases, such as ni trogen dioxide and ozone, penetrate to the small airways and alveoli. Pollut ants in particulate form are usually found in nature as aerosols. The pene tration ofparticles into the lung and the sites of deposition within the lung de pend on the aerodynamic size ofthe par ticle. Those greater than 10 p.m are ef fectively removed in the upper airway, whereas smaller particles penetrate and are deposited in the airways and alveoli. Fibers are defined arbitrarily as particles having a length at least three times the width. The handling of fibers by the respiratory tract depends on fi ber width and length and susceptibility to dissolution. Exercise increases the amount ofairinhaled and the proportion of oral breathing, and thereby increases the dose of inhaled pollutants. The diverse mechanisms by which in haled gases and particles injure the lung, although not yet fully understood, can be broadly grouped as acute irrita tion and inflammation, chronic inflam mation accompanied by a fibrotic re sponse for some agents, immediate and cell-mediated immune responses, and carcinogenesis (Table 3). The likelihood of an adverse response to an inhaled pollutant depends on the degree of ex posure to the pollutant, the site ofdepo sition and the rate of clearance, and the individual characteristics of the ex posed person that determine suscepti bility. The relationship between expo sure and response may have different forms, depending on the mechanisms by which the pollutant causes disease (Fig ure). The shape and slope of the expo sure-response relationship have sub stantial implications for assessing the risks of environmental agents.1 Curves having a threshold that must be ex ceeded to produce disease indicate that levels below the threshold are without risk; by contrast, a curve without a threshold implies that any level ofexpo sure conveys some risk. For example, the linear no-threshold relationship, widely used to assess risks of carcino gens for regulatory purposes, is consid ered to be protective of public health because no level of exposure is without effect. The assumption of a linear no threshold model for carcinogenesis re mains highly controversial." Distin guishing among the theoretical curves in the Figure cannot be readily accom plished using either animal experiments or human data, and exposure-response relationships should be assumed on the basis ofbiologic plausibility.1 ILLUSTRATIVE POLLUTANTS OF CURRENTCONCERN This section briefly considers the cur rently available evidence and concerns about risk for several air pollutants, se lected to be illustrative of the changing emphasis of concern across the century. The pollutants discussed include asbes tos, radon, environmental tobacco smoke, acidic aerosols and sulfur diox ide, and oxidant pollutants, including ozone and nitrogen dioxide. Radon Radon, a naturally occurring radioac tive gas in the decay series of uranium238 that is known to cause lung cancer in underground miners, is ubiquitous in indoor environments.7,8 The decay prod ucts of radon are themselves radioac tive and release cancer-causing alpha particles, which are directly responsible for radon's carcinogenicity. The prob lem of cancer in underground miners was first reported over 100 years ago,9 and radon was considered as a possible cause of the excess lung cancer in these miners by early in the century.* Epide miologic studies of underground min ers, initiated in the 1950s and later, soon provided convincing evidence that ra- 2026090469 JAMA, August 7,1991 --Vol 266, No. 5 The Environment and the Lung--Samet & Utell 671 Exposure Examples of theoretic exposure-response relation ships. Line A shows a linear exposure-response relationship with a threshold, while line B .shows a linear nonthreshold relationship. Lines C and D are examples of nonlinear relationships (reprinted with permisson from reference 2). don caused lung cancer in miners and some information on the quantitative risk of lung cancer in relation to expo sure. Regulations were implemented during the 1960s and 1970s to protect miners against excess lung cancer.*10 * * * * By the mid-1980s, it was widely rec ognized that radon was present in homes, sometimes reaching concentra tions comparable with levels in uranium mines, lb guide the development of public policy by state and federal agen cies, estimates of lung cancer risk were needed across the range of concentra tions measured in homes. Because epi demiologic studies directly addressing these risks could not be quickly per formed, the risks found in the studies of miners were extrapolated to the gener al population, yielding estimates that indoor radon may cause approximately 10 000 to 20 000 lung cancer deaths an nually in the United States.8,11,12 Several sources of uncertainty have reduced confidence in the extrapolation of risks from miners to the general popula tion.13,1* Should the risks observed at the higher exposures in miners be extrapo lated to lower exposures using a linear nonthreshold relationship? Are the quantitative risks higher or lower for the general population compared with the risks forminers? In comparison with evidence from male adult miners, pre dominantly eigarette smokers, what are risks of exposure for children, for wom en, and for never-smokers? Some have even questioned the carcinogenicity of indoor radon.15 Reducing the uncertain ties in assessing the risk ofindoor radon poses a complex challenge for biomedi cal research. Improved understanding of carcinogenesis may lead to better Table 3.--Principal Mechanisms Associated With Environmental Lung Disease Mechanism Bronchoconstriction Inflammation Fibrosis Cancer Agents Sulfur dioxide, addle aerosols Ozone, environmental tobacco smoke Asbestos, silica Radon, asbestos, formaldehyde, active smoking, and environmental tobacco smoke support for a particular model of the relationship between exposure and lung cancer risk. Many ease-control studies of indoor radon and lung cancer are now in progress with the objective of direct ly estimating risk due to indoor expo sure, and several studies have already been reported.8'16 However, the results of these studies are likely to be affected by difficult methodologic problems, and extremely large and unfeasible studies would be needed to fully address uncer tainties and provide confident state ments about risk.17 * * ' As we begin the 1990s, the risks of indoor radon remain extremely contro versial, even though radon is an estab lished occupational carcinogen and ex tensive epidemiologic data from miners provide convergent risk estimates.8,18 The continued controversy and wide spread perception of uncertainty ap pear to reflect the complexity of the questions that must be answered in sup port-of policy development rather than weaknesses in the existing data. Risk assessment may highlight the gaps in scientific knowledge and, as illustrated by indoor radon and lung cancer, reduce confidence in good data by calling for answers to questions that cannot be readily answered. Indoor Asbestos Asbestos, a group of naturally occur ring fibrous minerals, has been widely used in insulation and other materials in schools, public and commercial build ings, and residences. Man-made fibers are now widely used as a replacement for many of these applications. At the start of the century, clinical cases pro vided clear evidence that occupational exposure to asbestos caused asbestosis, a fibrotic disorder of the lung.1' During the 1960s and 1960s, the results of epi demiologic studies of workers showed that occupational asbestos exposure also caused lung cancer and mesothelio ma.20 Although the information on expo sures of workers in these studies was limited, quantitative relationships be tween estimated exposures and cancer risk were addressed in some of the studies. Asbestos fibers can be released into the air of buildings from human activi ties that disturb asbestos-containing material or by maintenance activities involving asbestos-containing materi als. Thus, persons potentially at risk from asbestos exposure indoors include persons handling or contacting the ma terial during job activities or cleaning asbestos-contaminated areas, and gen eral building occupants if they inhale contaminated air. Because of the well- documented and widely known disease risks in historical cohorts of asbestos- exposed workers, the presence of as bestos-containing material in buildings has prompted great public concenvand legislative programs to reduce risks of indoor asbestos. The Asbestos Hazard Emergency Response Act requires in spection of schools for asbestos and sat isfactory in-place management or, in some cases, removal. New research ini tiatives have been implemented to ad dress asbestos in public and commercial buildings. Public and private efforts for manag ing asbestos-containing material have been undertaken to reduce the expo sures of custodial and maintenance workers and of general building occu pants, including general office workers and schoolchildren. Even though con centrations of asbestos fibers in build ings are extremely low, persons in the category of general building occupants have been considered to be at risk for lung cancer and mesothelioma21-3; re cent estimates of exposures23,2* are somewhat lower than earlier esti mates21,22 as more data have become available on indoor concentrations. The risks for the general population can only be estimated by extrapolating from the risks in asbestos workers to the general population. Exposure-disease relation ships are generalized across exposure scenarios typically differing by orders of magnitude to obtain risk projections for the general population, which are j, * subject to great uncertainty. While in rocreasing information is becoming avail- O able on concentrations ofasbestos fibers indoors, epidemiologic studies cannot (T) directly assess the risks ofindoor asbes tos for such populations as schoolchil- f dren and office workers because of the ^ large sample sizes needed. ^ Environmental Tobacco Smoke **5 By mid-century, a marked increase was evident in lung cancer deaths among men, and ease-control studies carried out to explain the epidemic quickly provided consistent evidence that cigarette smoking was a strong 672 JAMA, August 7,1991 --Vol 266, No. 5 The Environment and the Lung --Samet & Utell cause oflung cancer. By 1964, sufficient epidemiologic data on smoking and health were available to support a con clusion by the Advisory Committee to the Surgeon General that cigarette smoking caused lung cancer in men.25 Further research has shown that smok ing is a cause of many malignant and nonmalignant diseases.26 Nonsmokers inhale environmental tobacco smoke, a mixture of sidestream smoke and exhaled mainstream smoke. During the late 1960s and early 1970s, several reports suggested that expo sure of children to environmental tobac co smoke by the smoking of their par ents increased their risk for respiratory infections and respiratory symptoms27,28; in the late 1970s, adverse ef fects of parental smoking on lung func tion in children were first reported.29 In 1981, reports oftwo epidemiologic stud ies, one in Japan and the other in Greece, indicated that never-smokers married to smokers were at increased risk for lung cancer.36'81 Other studies with similar findings were reported during the 1980s, and by 1986 the Inter national Agency for Research on Can cer,32 the National Research Council,38 and the US Surgeon General81 had con cluded that passive smoking caused lung cancer in never-smokers. In reach ing their conclusions, both the Interna tional Agency for Research on Cancer and the Surgeon General's Report em phasized the biologic plausibility of the epidemiologic evidence, assuming that there is no threshold of exposure for respiratory carcinogenesis and thus any exposure conveys some risk. In contrast to the strong and causal associations of active smoking with lung cancer, the risks of exposure to environ mental tobacco smoke found in epidemi ologic studies have been lower, and methodologie problems have been dis cussed as an alternative explanation to causality for the association.3586 The ex tent of the lung cancer risk to neversmokers caused by exposure to environ mental tobacco smoke has been particularly contentious, largely be cause nonsmokers in public buildings and workplaces involuntarily inhale en vironmental tobacco smoke, and unac ceptable risks for this exposure would provide a basis for limiting smoking in these locations. The lung cancer risk of exposure to environmental tobacco smoke has been primarily assessed by generalizing the exposure-response re lationship from the studies of neversmokers exposed to the smoking oftheir spouses.37'38 Uncertainties are evident in this approach, including the lack of in formation on total exposure to environ mental tobacco smoke and the many as sumptions inherent in deriving a general exposure-response relationship from studies of never-smokers exposed at home. Because of the methodologie difficul ties of assessing lifetime exposure to environmental tobacco smoke and pre cisely describing risks that are not sub stantially elevated, these uncertainties in assessing the lung cancer risk ofenvi ronmental tobacco smoke may never be fully resolved, although they remain a 'subject of research. Yet, full resolution would seem unnecessary for the evolu tion of public policy on environmental tobacco smoke, a carcinogen with a readily controllable source. In the case of environmental tobacco smoke, it would be unfortunate ifpotentially irre solvable scientific uncertainties thwart ed control. Acidic Aerosols/Suifur Dioxide The sulfur dibxide/partieulate matter type of pollution, formed primarily as a result of combustion of sulfur-contain ing fossil fuels, represents a widespread form of pollution in industrialized soci eties.39 The large-scale mid-century pol lution disasters in Donora, Pa, in 1948 and in London, England, in 195241'42 probably involved extremely high lev els, by current standards, of acid aero sols and sulfur dioxide. During the Lon don fog of 1952, an estimated excess of 4000 deaths occurred, primarily among the elderly and those with a chronic res piratory disease. A recent reexamina tion of London mortality data for the years 1968 through 1972 showed a cor relation between daily mortality and sulfuric acid aerosol levels on the prior day. Statutory regulations promulgated in the early 1970s by the Environmental Protection Agency under the Clean Air Act resulted in significant reductions in levels of total particles and sulfur diox ide. However, local reductions in pollu tion were often achieved by the use of tall stacks, particularly for power plants, which resulted in the pollutants being emitted high into the atmosphere, where prolonged residence time per mitted their transformation into acid species. An emerging concern about the effects of these acidic aerosols has now extended beyond environmental effects on trees and lakes to human health. Although still limited in extent, new epidemiologic data suggest, adverse ef fects of acidic aerosols. A consistent as sociation was reported between hospi tal admissions for respiratory disease in Southern Ontario and daily levels of sul fates, ozone, and temperature.81 The Six Cities Study, conducted by Harvard University in six eastern and midwest- em US cities, demonstrated links be tween particle exposure and respira tory disease in children.16 Chronic cough and bronchitis symptoms were associat ed with hydrogen ion concentration, a measure ofacidity, rather than with sul fate levels or total levels of particles. Furthermore, controlled human studies have established remarkable sensitivity in exercising asthmatics to the bronchoconstrictor effects ofsulfur dioxide46 and acidic aerosols47,48 at concentrations sim ilar to those at higher outdoor levels. Data showing that acidic aerosols are a widespread form of pollution and the emerging health evidence have led to new research in the United States and elsewhere. While the air pollution epi sodes earlier in the century provided clear and dramatic evidence that acidic aerosols can increase mortality, the present levels of exposure have prompt ed questions concerning more subtle ef fects on mortality and morbidity. Pro viding certain answers to these questions is a difficult challenge for the scientific community. Epidemiologic studies are limited by the difficulty of measuring exposure and of singling out the effect of acidic aerosols from other factors, particularly for such nonspecif ic health effects as increased symptoms and reduction of lung fimetion. Con trolled exposures of volunteer subjects provide information concerning short term effects, but this approach cannot fully represent the exposures sustained in the community. Nonetheless, the regulatory appara tus turns to the results of epidemiologic and human toxicologic research as a ba sis for policy. On a 5-year cycle, the Environmental Protection Agency re evaluates the "science" to either modify or support the current sulfur dioxide and particulate matter standards. Thus, acidic aerosols may be eventually listed for regulation.49 Oxidant Gases Ozone and nitrogen dioxide (N02) are oxidant gases that contaminate outdoor air in many urban and industrial loca tions. Ozone is one component of the pollution mixture commonly referred to as "smog," and its concentration is used as an index of the degree of smog pollu tion. Indoor environments may be con taminated by oxidants from outdoor air and by NOz produced indoors by com bustion appliances, such as gas stoves and space heaters. At high concentra tions, oxidants cause extensive lung in jury, including pulmonary edema and bronchopneumonia in animals and in hu mans; however, effects at levels cur rently measured in outdoor and indoor air in the United States have been diffi 2026090471 JAMA, August 7, 1991 -Vol 266, No. 5 The Environment and the Lung -- Samet & Uteil 673 cult to characterize. A better under standing of the effects of oxidant pollut ants is extremely important; despite extensive control efforts, more than one half of the US population still lives in communities where the National Ambi ent Air Quality Standard for ozone is exceeded,51 and many homes with gas stoves have N02 levels that approach the standard for outdoor air.52 In fact, although outdoor air contamination by oxidants has been the subject of sub stantial research and of great regula tory concern, pollution of indoor envi ronments by N02 has been recognized as the predominant determinant of per sonal exposure in most locations.53 Investigating the health effects ofthe oxidant pollutants requires multidisci plinary research involving toxicologic and epidemiologic approaches.52 For ex ample, studies show that N02 exposure increases the frequency and severity of respiratory tract infections in animals'4; we are conducting research to test the hypothesis that N02 exposure also in creases the incidence and severity of respiratory tract infections in humans. In laboratory studies, volunteer sub jects are exposed to NOz in a chamber, cells are obtained from the respiratory tract by bronchoalveolar lavage, and the ability of the cells to kill virus is assessed. We recently reported that al veolar macrophages obtained from healthy volunteers after a 3-hour con tinuous exposure to 1120 qg/m3 of N02 inactivated influenza virus in vitro less effectively than cells collected after air exposure.55 In an epidemiologic study addressing this same hypothesis, over 1000 infants have been followed up from birth with prospective observation for respiratory tract illnesses and monitor ing oftheir homes for N02. * Persistent questions concerning the long-term effects of residence in smogpolluted locations, such as Southern California, will probably require large epidemiologic studies and further stud ies involving the exposure of volunteers to describe the range of susceptibility and to address the mechanisms of toxic ity. While the costs of this research may be high, exposure to oxidant pollutants is widespread, and the exposures of a substantial proportion of our population may be associated with adverse effects. CONCLUSIONS Although we have selected a few of the contaminants that cause environ mental lung disease, many other agents with a similar array of changing con cerns with regard to disease risk and safety could be listed; for example, sili ca, the cause of silicosis, is a suspect carcinogen at contemporary occupa tional levels of exposure, and concern has been raised about the human carci nogenicity of man-made fibers. We sug gest that the lessons to be learned from the example agents may be generalized to other pollutants. Active cigarette smoking, occupa tional asbestos exposure, radon in un derground mines, and high levels of acidic aerosols were remarkably strong causes of disease under the exposure conditions originally investigated. In fact, cases of disease caused by expo sure to these agents were initially iden tified through descriptive case series rather than more formal epidemiologic investigation. The subsequent re search, both epidemiologic and toxico logic, was successful in establishing causal exposure-disease associations and informative in characterizing expo sure-response relationships. However, current concerns over lower concentra tions of these same agents cannot be so readily answered, nor can they be an swered with sufficient certainty to sat isfy all interested parties, who poten tially include not only the general public but also involved manufacturers, par ties to litigation, environmental groups, and regulators. * The technique ofquantitative risk as sessment is increasingly applied to gauge the risks ofenvironmental pollut ants (Table 1). However, the frequent focus on the final risk projection--for example, stating that radon causes 10 000 to 20 000 eases oflung cancer an nually in the United States--may inap propriately heighten debate over the projected numbers, even though the numbers are produced by a simplistic and mathematical representation of complex biological processes. More over, controversy concerning uncer tainties in risk projections may detract from less ambiguous research findings. For example, radon is an established carcinogen, although any projection of the risks of indoor radon is subject to diverse uncertainties. Because malig nancy fits more readily into a risk as sessment framework than nonmalignant outcomes, emphasis by regulatory agencies appears to unduly weight ex posures causing cancer. In using quanti tative risk assessment to manage risks, the difficulties of communicating risks may further limit the capability of achieving public health goals." It should be recognized that steps can be taken to reduce risks of environmen tal lung disease despite the types ofcon troversies and points of uncertainty that we have considered. For some pol lutants, the individual can reduce risks. For example, prevention and cessation of smoking control the hazards of both active and passive smoking. Radon con centrations in homes can be measured inexpensively, and techniques are avail able for mitigating and avoiding unac ceptable radon concentrations. Guid ance is available for other indoor air pollutants, including asbestos. For oth er pollutants, only national policy and regulation can reduce risk. For exam ple, reduction oflevels of acidic aerosols or ofozone can be effected only by multi faceted regulatory strategies directed at sources. Tremendous progress has been made across the century in understandingand preventing environmental lung dis eases. The shift of our concern to mor bidity at lower levels of exposure and more subtle effects on mortality paral lels strong trends of declining levels for some pollutants. Certain diseases, eg, asbestosis and silicosis, are entirely preventable and the occurrence of new cases is now regarded as a sentinel event, signaling an unacceptable expo sure. Toxicologic studies have provided many new insights into effects of envi ronmental agents on the lung, although much remains to be learned about basic mechanisms of toxicity. The present emphasis on risk assessment and risk reduction, which raises many uncer tainties and new questions, should not detract from these past accomplish ments. The scientific community has been challenged by difficult questions, some of which may never be answered with complete certainty. Nevertheless, it is the results of research that have shifted our public health emphasis to concerns about lower and lower levels of exposure. We anticipate that research on the environment and the lung will continue to support the evolution of public policy, while raising even more difficult questions relevant to public health. This study was supported by grant ES02679 from the National Institute for Environmental Health Sciences; contracts 87-4 and 88-8 from the Heaith Effects Institute, an organizationjointly funded by the US Environmental Protection Agency (Assis tance Agreement X-812059) and automotive manu facturers; and grant DE-FG04-90ER6G950 from the US Department of Energy, Office of Energy Research. References 1. National Research Council, Committee on the Institutional Means for Assessment of Risks to Public Heaith. Risk Assessment in the Federal Government: Managing the Process. Washington, DC: National Academy Press; 1983. 2. Lowrance WW. Of Acceptable Risk: Science and the Determination ofSafety. Los Altos, Calif: William Kaufmann Inc; 1976. 3. Utell MJ, Samet JM. 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