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Chapter 3 Exposure Assessment

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EXPOSURE ASSESSMENT INTRODUCTION This chapter discusses the relationship of exposure assessment to the design and conduct of epidemiologic studies of air pollution. After presenting a working definition of exposure assessment, it discusses the pertinent history of air pollution monitoring and a framework for contemporary exposure assessment. The chapter then identifies the types of pollutants that the Committee feels require attention, indicating some physical, chemical, and spatiotemporal properties that are relevant to exposure assessment. Sections on special approaches to indoor pollutants and monitoring considera- tions follow, including opportunities for providing optimal exposure data in future epidemiologic studies. Finally, several important characterization studies are reviewed. Exposure assessment refers to a set of multidisciplin- ary activities that describe who is exposed to how much of what substances, for how long, and under what conditions. Exposure assessment, whether based on direct measurement or modeling, is a vital part of all environmental epidemiology. Exposure assessment of air pollutants is particularly complex, because pollutants do not occur independently, but as mixes of natural, indus- trial, transportation, and residential emissions. The focus of interest in this chapter is human exposure. Hazards to the environment, such as from acid deposition, are important, but are not the subject of this report. In an epidemiologic study, exposure assessment can be addressed before, during, and after the collection of 89

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health effects data. Conducted beforehand, it can lead to improvement in study design by treating the issues of subject selection, sample size, scale and frequency of monitoring, and usefulness of such tools as fixed-site monitors and descriptive questionnaires. Exposures can then be remeasured, in conjunction with health effects measurement, to provide a basis for a quantitative estimate of the association between exposure and effect. Exposure assessment has many purposes in air pollution research aside from providing exposure variable measure- ments for epidemiologic studies. Independent and parallel efforts to describe exposure may aim, for example, to determine the effectiveness of efforts to lower exposures, compare possible risks between various populations with different exposure conditions, develop siting and timing strategies for routine ambient air monitoring, and weigh the importance of various components of multisource and multimedium exposures. Obviously, some of these functions require assumptions about quantitative risk relationships based on previous health effects studies. Also, rather than incorporate new exposure assessment and costs into each epidemiologic study, we can often rely on information and assumptions derived from well-designed, independently conducted exposure assessment research. The central theme of this chapter is that the integra- tion of exposure assessment into an epidemiologic study and the decisions as to which aspects of exposure assess- ment to emphasize will depend on the nature of the specific research question. To be effective under current conditions, exposure assessment in air pollution epidemi- ology must be flexibly based on reasonable biologic modeling of exposure and effect and must comprise the degree of detail required by the research question. Thus, environmental monitoring should not be restricted arbitrarily from the outset to indoor or outdoor sources or to fixed or personal monitors. The advance in measurement technology increases the variety of potential epidemiologic studies, but does not in itself provide a valid rationale for a given study. m e mere ability to measure exposure to a pollutant precisely is not a sufficient reason to launch a study; indeed, many studies that are possible might be unimpor ten t or of unlikely productivity. 90 -

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The ultimate goal of exposure assessment in epidemi- ologic studies of air pollution is to minimize the mis- classification of study subjects by exposure magnitude or type. Common variations in outdoor and indoor concentra- tions and the proportions of time people spend in differ- ent locations can yield substantial overlap in the true total exposure between subjects assigned to high- and low-exposure groups. This applies whether exposure mag- nitude is assigned on the basis of categorical descriptor variables or ambient monitoring from central stations. Misclassification is a major reason for loss of sensitiv- ity in such studies; it increases the likelihood that a study will fail to detect a real association between an air pollution exposure and a health effect. The problem of exposure misclassification is described in more detail in Appendix C and several recent papers. 6 ~ O EXPOSURE, DOSE, AND BIOLOGIC MARKERS Most epidemiologic studies of air pollution have assumed that exposure, however measured, constitutes an adequate surrogate of the dose of a given pollutant. Recent advances in toxicology and molecular epidemiology have clarified the meaning of these terms and emphasized some important distinctions.S 6 nExposure" (see Figure 1) commonly refers to concentrations of pollutants measured in the environment. As to dose itself, two distinctions can be made: n internal doses is the amount of a substance or its metabolites in body tissues, and "biologically effective dose" is the amount that interacts with a par- ticular target tissue or its surrogate. In this report, however, "exposure, n unless otherwise specified, refers to all kinds of exposure, from ambient air to critical target organ. Research is required to relate a specific ambient exposure to the dose received by a given target tissue in the respiratory tract and to relate that dose, in turn, to a specific health effect. This research will ultimately benefit future epidemiologic studies of air pollution. One of the major constraints in determining the rela- tionship between exposure to air pollutants and the development of nonneoplastic diseases of the respiratory tract is the lack of biologic markers of exposure. Biologic markers that would indicate the cumulative dose of specific pollutants or types of pollutants to the 91

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Outdoor Emission Sources Outdoor Concentrations . Dispersion, conversion, and removal factors (including weather) ~ Building penetration, . . Indoor Emission Sources - Dispersion, conversion, and removal factors ~ ~ (including ventilation) or door l ~ Co ncentrations air exchange, conversion, and removal factors - Time-activity patterns Time-activity patterns Total Personal Exposure Host factors 1 ~ Internal Dose Host factors Biologically Effective Dose (to Critical Target Tissues) Host factors Health Effect FIGURE 1 Framework for exposure assessment. 92

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respiratory tract would be invaluable in determining precise relationships between exposures and disease. HISTORICAL BACKGROUND As analytic techniques became available around the turn of the century, air pollution investigations moved beyond crude and subjective forms of exposure assessment (e.g., number of foggy days, amount of coal use, or dis- tance from emission sources) to measurement of pollution surrogates, such as dust fall or total acidity. Air monitoring in major European cities for sulfur dioxide, SC2, and smoke began in the 1930s. In the United States, federally sponsored surveys of urban air pollution began in the middle 1950s, and routine monitoring was common by the late 1960s. Today, air pollution monitoring is a highly developed field of applied science. Sophisticated analytic devices are available for measuring many con- taminant gases continuously; and particles can be separated by size and analyzed for chemical composition (see box on instrumentation). However, many of the established air pollution monitor ing networks were not designed to test explicit biologic models of the health effects of air pollution. Pollutant monitoring typically provided averaged concentration data, usually over 24 hours or a full year, except for hourly data on ozone, O3, and carbon monoxide, CO. Cumulative exposure, frequency of concentration peaks, lag effects, and combined pollutant exposure indexes could not be explored in the air pollution epidemiology of the 1940s, 1950s, and 1960s. Current standards for SO2 and total suspended particles (TSP), based on past data, can thus be surrogates for other exposure times or pollutant species that are really responsible for the effects of concern. Likely candidates include size-fractionated particles and acid aerosols and gases. Until very recently, most air pollution epidemiology investigated relationships between adverse health outcomes in a population and average ambient air pollution concentrations. Most often, data from relatively few central outdoor monitoring stations were used to represent the exposure of all subjects in an entire residential community. Indoor sources that could contribute to total personal exposures to many of the 93 -

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* * * * * * * * * * * * * * * * * * * * * * * * * * * * * * * been developed for use In a variety or situations, both indoors and outdoors, and they are easily adaptable for providing data on cumulative exposure, time-lagged responses, and frequency of periodic exposure peaks. Quantitative chemical analysis now offers precision and sensitivity far greater than those required for most epidemiologic studies. A NOTE ON AVAILABLE INSTRUMENTATION * Since the early 1970s, instruments and techniques for * monitoring exposure to air pollutants have grown sub- * stantially in sophistication. Many types of continu- * ous and integrating (discrete period) samplers have * * * * * * * * * * * * * * * * * * * * * * * * Personal monitors are available in two basic types: * * active monitors, which use a pump to draw a measured * * volume of air into a collecting medium; and passive * monitors, which are small lightweight badges that * * sample by passive diffusion of chemicals. The recent * * _:~;A A~l~r~n~d ~~ A: 1~;~ t__A~ ; ~ ~_. ;~l~1 =_l~r * * * * * * * * * * rapid development of diffusion badges is particularly notable, because they have become inexpensive and * inconspicuous enough to be used for large popula- * Lions. However, personal monitors are still all of the integrating type; the choices of sampling and * averaging times are limited by available instruments- * tion. Detailed information on specific equipment can * be found elsewhere.~5 3 ~ * * * * * * * * * * * * * * * * * * * * * * * * * * * * * * * pollutants encountered outdoors were rarely considered. Studies implicitly assumed that the differences in outdoor concentrations of some pollutants between cities or be- tween regions within a community were more important determinants of individual or population exposures than housing or other personal factors. In past decades, when outdoor concentrations in many urban areas were higher than today, they might in fact have been the most impor- tant determinants of population exposure to SO2, TSP, benzo[a]pyrene (BaP), and other major industrial and utility-derived pollutants. If differences in exposure within groups are small, compared with differences between groups, the use of fixed monitors at representative sites in the community might suffice. But pollutants with 94

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important indoor sources or sharp variations in outdoor concentrations from place to place within people's daily mobility range could yield large differences in exposures within groups and require some incorporation of personal measuring techniques. Therefore, although outdoor ambient measurements might still be appropriate for some current questions in air pollution epidemiology, future studies will have to look at exposure in a more sophisticated context. FRAMEWORK FOR EXPOSURE ASSESSMENT In the last decade, recognition of the complexity of the determinants of individual exposure to air pollutants and the impact of misclassification has led to the need for a new conceptual framework for exposure assessment. Figure 1 depicts the relationship of indoor and outdoor pollutant sources and concentrations to each other and to total personal exposure. "Total personal exposure" refers here not only to the total, time-integrated cumulative exposure, but to the number and character of significant peak exposures, because in air pollution studies exposure assessment can develop from a biologic model of the exposure-effect relationship that involves cumulative exposures, peak exposures, or both. We are beginning to understand the interaction of key factors in determining total exposure to some pollutants. Outdoor emission sources contribute to outdoor concentrations, which in turn penetrate to a degree into indoor environments; and indoor sources also contribute to indoor concentrations. The relative importance of indoor and outdoor concentra- tions in determining personal exposure (average or peak) to a given pollutant depends on several factors, including the location of the predominant source of the pollutant, the daily time-activity patterns of exposed people, other host factors, and the pollutant's entry into, mixing in, and removal from a structure. More detail on the impact of indoor pollutants on air pollution epidemiology will be provided in a later section. With our present knowledge, we can divide air pollutants into three categories by source: . Outdoor, e.g.' SO2' sulfates, O3' and lead. Outdoor and indoor, e.g./ fine particles! nitrogen dioxide, and CO. 95

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Indoor, e.g., volatile organic chemicals, formaldehyde, woodsmoke, and radon. Of course, these categories might not apply in exceptional situations, such as in communities near industrial point sources. Total personal exposure to an air pollutant is a conceptually important measure for epidemiology. Among the exposure measures that are practically attainable, total personal exposure is the most valid predictor of the risk of any air-pollution-related health effect in a given person. Ideally, perfect individual exposure data (with no misclassification) could come only from measure- ment of biologically effective personal dose (see Figure 1). All methods of measuring individual exposure are essentially surrogates and can be ranked according to their crudeness or likelihood of misclassification error: Total personal exposure: direct personal monitoring in breathing zone. . data. Total personal exposure: indirect area monitoring. Predictive models using questionnaire and other Questionnaire data (categorical descriptors) without modeling. To assess total personal exposure to air pollutants, one can sample near the breathing zone of the subject with portable instruments or one can find the time- weighted sum of concentrations measured in a series of locations in which the subject spends the day. The latter, indirect approach requires time-activity logs and portable area monitors (rather than smaller monitors that are worn) for measuring microenvironmental concentrations. It is important to distinguish between direct measure- ment and indirect estimations of total personal exposure. Indirect estimations necessarily assume that contaminant concentrations within the microenvironment are uniform-- for example, that within an office or a particular room in a home the concentration measured at one point accu- rately represents the entire small area. However, mul- tiple measurements often reveal widely varied concentra- 96

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tions within a microenvironment. m e design of a monitoring program can mitigate this oversimplication to some extent. Research is also underway to improve the statistical handling of data from indirect personal exposure assess- ment and to resolve unexplained discrepancies with direct measurements. It might ultimately be more practical and cost-effective to pursue the indirect estimation approach for some epidemiologic studies, inasmuch as accurate, inconspicuous, and affordable personal monitors are not available for all pollutants and quality control of personal monitoring is more difficult than that of area monitoring. Furthermore, on the basis of the pollutants involved, a substantial fraction of the variance in human exposures might be explained by monitoring in relatively few locations. As the complex interaction of the variables becomes clarified in exposure assessment research, accurate predictive models for estimating average or peak exposures can be developed for some types of pollutants .2 B These models, which can use various kinds df data to minimize the need for actual measurements, are potentially appli- cable to epidemiologic studies. Future studies might use combinations of measurement and modeling approaches. Several factors can modify personal exposure or dose and should be addressed in planning exposure assessment for epidemiologic studies: Activitv: The amount of an air pollutant inhaled depends in part on ventilatory rate. Exercise or manual work can influence total dose. . Respiratory tract anatomy and physiology: The relationships among lung volume, ventilatory rate, and body size vary with age and race. Infants have a high ratio of ventilation to body size and can therefore have greater pollutant dose per unit of tissue than older people. The accessibility of various sensitive regions of the lung to pollutants also varies between persons. A smoker with a damaged mucociliary mechanism might receive a greater dose from a given Ambient exposure than a nonsmoker. Weather: Meteorologic conditions can affect the concentrations of pollutants, including those formed 97

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air that contains them. Characterization of such com- ponents is essential in selecting study populations with critical contrasts in exposure. A much improved kind of exposure assessment research, which will assist in the design of epidemiologic studies is the resolution of sources that contribute to measured air concentrations. Most of the work to date has been done on the outdoor sources of particulate matter. Infor- mation on the approach called source-receptor modeling can be found in EPA reports and original research papers. 2 ~ 3 48 A variety of mathematical techniques are available, including chemical-element balances 7 and multiple-regression factor analysis.25 The main product of each technique is an estimate of the percentage of particle mass in a given sample of air that can be attri bused to an individual source or type of source. This information will be very useful in the development of measures to regulate the contributions of sources that are found to produce a health effect in an exposed population. It will also be helpful in explaining the variation in personal exposure within a sampled area that could be attributable to variation in individual proximity to sources. - EPA has recently published its rationale for converting the TSP standard to one based on PMlo, in recognition that not only the concentration of suspended particles but also particle size and site of deposition in the respiratory tract are important determinants of the risk of health effects.55 In the future, it should be recognized that the potential health effects of inhaled particles also depend on the inherent toxicity or bio- logic activity of the particles, whether fine or coarse. For example, not all particles can be expected to be as toxic as alpha-quartz, a substance known to be highly toxic to the pulmonary alveolar macrophage (PAM) and to be highly fibrogenic. Several groups have compared the ability of mineral dusts to kill cultured cells with their fibrogenicity in whole animals, to validate the ability of the in vitro cytotoxicity test to predict in viva activity.22 23 5t Recently, Hill and Hobbs compared the toxicity of several types of coal-combustion fly ash with that of a positive reference standard, DQ12 quartz. They found that the fly ash had little or no toxicity to PAM cells at concentra- 114

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tions up to 500 ug/ml of culture medium, although the quartz caused a large leak of enzymes from the cells at a concentration of 250 ~g/ml.2 2 Rats were then exposed by inhalation to the same two dusts, and the relative pulmonary toxicities of the dusts were evaluated by analysis of bronchoalveolar ravage (BAL) fluids. Al though both dusts caused inflammation, as measured by neutrophil cell counts in BAL fluid, only the quartz increased the protein in BAL fluid, and the increase in enzymes in the fluid was much higher in the quartz-exposed than in the ash-exposed rats. 2 3 Thus, in this study the in viva test validated the use of the PAM toxicity assay as a predictor of in viva toxicity. With the use of such end points as cell viability and release of enzymes, it can be suggested that the PAM cytotoxicity test can be used to rank the oulmonarv toxicity of environmental dusts. . . . . . . . . . Bioassays could play a very important role in prescreening a community in the design stages of an epidemiologic study. If incorporated into a study, bioassays might provide important clues for interpreting differences in responses (rates of illness or effects on pulmonary function) in the community. _ _ is, Short-term biologic tests to determine exposure to harmful chemicals have been used most successfully to determine exposure to mutagenic-carcinogenic agents in high-risk populations. An example from air pollution research is the recent study of urinary mutagenic activity in children residing near a Montana smelter. In contrast, with the notable exceptions of blood lead and carboxyhemoglobin measurements, there are no biologic methods for monitoring the extent of exposure of the general population to EPA criteria air pollutants. Such methods might be particularly difficult to develop for short-lived reactive pollutants that exert their effects in the lung. Biologic measures of oxidant exposure should therefore be sought in surrogate targets, such as red cells or serum proteins.3 4 - e ~ When biochemical techniques have been developed much further, they might permit the precise measurement of biologically effective dose. However, measures of external exposure will still be important in determining relationships between environmentally monitored and internally absorbed concentrations of pollutants and will remain vital to epidemiology as long as such measures are the basis for regulation . 115

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To assist in the characterization of a pollutant sample with respect to predicting the dose received by tissues, information on the effect of its physical and chemical matrix can be obtained. The nature of this matrix affects the bioavailability of inhaled chemical pollutants. The potential health effects of inhaled benzo[a]pyrene, for example, might depend on whether it is inhaled as a pure compound (a rare occurrence), inhaled after adsorption on particles, or inhaled as a component of a droplet of a complex organic mixture. The formulation affects the retention time of organic com- pounds in the lung .4 9 - 5 2 Thus, knowledge of the amount of a specific type of chemical in the atmosphere is often no longer sufficient for predicting its health effects. As the ability to characterize pollutants improves, exposure assessment becomes an increasingly sophisticated tool for epidemiologic studies of air pollution. REFERENCES 1. Allen, P.W. Regional Air Pollution Study: An overview. Preprint No.#73-21. Proceedings of the 66th Annual Meeting of the Air Pollution Control Association. Pittsburgh, Pa.: Air Pollution Control Association, 1973. 2. Anderson, M.K., E.T. Brookman, R.J. Londergan, J.G. Watson, and P.J. Lioy. Receptor Model Technical Series: Source Apportionment Techniques and Considerations in Combining Their Use. Vol. 5. Publication No. EPA/450/4-84/020. Research Triangle Park, N.C.: U.S. Environmental Protection Agency, 1985. 191 pp. [Also available from the National Technical Information Service, Springfield, Va., as NTIS/PB85-111524.] Annest, J.L., J.L. Pirkle, D. Makoc, J.W. Neese, D.D. Bayse, and M.G. Kovar. Chronological trend in blood lead between 1976 and 1980. N. Engl. J. Med. 308:1373-1377, 1983. 4. Beck, W.B., and G.K. Tannahill. An overview of the Houston area oxidant study. #78-30.1. Proceedings of the 71st Annual Meeting of the Air Pollution Control Association. Pittsburgh, Pa.: Air Pollution Control Association, 1978. 116

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5. Binder, R.E., C.A. Mitchell, H.R. Hosein, and A. Bouhuys. Importance of the indoor environment in air pollution exposure. Arch. Environ. Health 31:277-279, 1976. 6. Bross, I. Misclassification in 2 x 2 tables. Biometrics 10:478-486, l9S4. 7. Cannon, J.A. Air quality effects of residential wood combustion. J. Air Pollut. Control Assoc. 34:895-897, 1984. 8. Cleveland, W.S., B. Rleiner, J.E. McRae, and J.L. Warner. Photochemical air pollution: Transport from the New York City area into Connecticut and Massachusetts. Science 191:179-181, 1976. 9. Cobourn, W.G., and R.B. Husar. Diurnal and seasonal patterns of particulate sulfur and sulfuric acid in St. Louis, Missouri, July 1977-June 1978. Atmos. Environ. 16:1441-1450, 1982. 10. Copeland, K.T., H. Checkoway, A.J. McMichael, and R.H. Holbrook. Bias due to misclassification in the estimation of relative risk. Am. J. Epidemiol. 105:488-495, 1977. 11. Countess, R.J., G.T. Wolff, and Sea. Cadle. The Denver winter aerosol: A comprehensive chemical characterization. J. Air Pollut. Control Assoc. 31:1194-1200, 1981. 12. Daisey, J.~. Organic compounds in urban aerosols. Ann. N.Y. Acad. Sci. 338:50-69, 1980. 13. Dattner, S., and P. Hopke, Eds. Receptor Models Applied to Contemporary Pollution Problems. Pittsburgh, Pa.: Air Pollution Control Association, 1983. 368 pp. 14. Davis, D.L., and S. Gusman. Exposure assessment: Introduction. Toxic Subst. J. 4:4-11, 1982. 15. Electric Power Research Institute. Electric Power Research Institute/Gas Research Institute Workshop on Personal and Portable Monitoring Equipment, December 5-8, 1984. Palo Alto, Cal.: Electric Power Research Institute. (in press) 117

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16. Frezieres, R.G., A.H. Coulson, R.M. Katz, R. Detels, S.C. Siegel, and G.S. Rachelefsky. Response of individuals with reactive airway disease to sulfates and other atmospheric pollutants. Ann. Allergy 48:156-165, 1982. 17. Friedlander, S.K. Chemical element balances and identification of air pollution sources. Sci. Technol. 7:235-240, 1973. 18. Gladen, B. and W.J. Rogan. Misclassification and the design of environmental studies. Am. J. Epidemiol. 109:607-616, 1979. . 19. Hamilton, H.L., Jr., and S.N. Jones. Seminars/ Workshop Proceedings: Persistent Elevated Pollution Episodes (PEPE), March 1979. Publication No. EPA-600/9-81-016. Research Triangle Park, N.C.: U.S. Environmental Protection Agency, 1979. 599 pp. 20. Harkov, R., B. Kebbekus, J.W. Bozzelli, P.J. Lioy, and J.~. Daisey. Comparisons of selected volatile organic compounds during the summer and winter at urban sites in New Jersey. Sci. Total Environ. 34:259-274, 1984. 21. Hidy, G.M., P.K. Mueller, D. Grogjean, B.R. Appel, and J. Wesolowski, Eds. The Character and Origins of Smog Aerosols: A Digest of Results from the California Aerosols Characterization Experiments. Vol. 10. Wiley-Interscience, 1980. 776 pp. Hill, J.O., and C.H. Hobbs. Comparative cytotoxicity of DQ12-quartz and fly ash particles from coal combustion. Toxicol. Lett. 10:399-403, 1982. 23. Hobbs, C.H., R.L. Carpenter, D.E. Bice, J.L. Mauderly, J.A. Pickrell, S.A. Silbaugh, F.F. Hahn, R.F. Henderson, and R.K. Wolff. Comparative inhalation toxicity of fly ash from pulverized and fluidized bed combustion of coal, pp. 401-407. In M.B. Snipes, T.C. Marshall, and B.S. Martinez, Eds. Inhalation Toxicology Research Institute Annual Report, 1981-1982. Publication No. LME-102, 1982. Albuquerque, N.M.: Inhalation Toxicology Research Institute. 118

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Holland, D., and D. Mage. Carbon Monoxide Concentrations in Four U.S. Cities During the Winter of 1981. Publ. No. EPA 600/59-83-025. Research Triangle Park, N.C.: U.S. Environmental Protection Agency, 1983. 75 pP. 25. Kleinman, M.T., B.S. Pasternack, M. Eisenbud, and T.J. Kneip. Identifying and estimating the relative importance of sources of airborne particulates. Environ. Sci. Technol. 14:62-65, 1980. 26. Kleinman, M.T., C. Tomczyk, B.P. Leaderer, and R.L. Tanner. Inorganic nitrogen compounds in New York City air. Ann. N.Y. Acad. Sci. 322:115-123, 1979. 27. Leaderer, B.P., D.M. Bernstein, J.M. Daisey, M.T. Kleinman, T.J. Rneip, E.O. Knutson, M. Lippmann, P.J. Lioy, K.A. Rahn, D. Sinclair, R.T. Tanner, and G.T. Wolff. Summary of the New York Summer Aerosol Study (NYSAS). J. Air Pollut. Control Assoc. 28:321-327, 1978. 28. Leaderer, B.P., R.T. Zagraniski, M. Berwick, and J.A.J. Stolwijk. Assessment of exposure to indoor air contaminants from combustion sources: Methodology and application. Am. J. Epidemiol., 1985. (in press) 29. Lioy, P.J. Ambient Measurements of Sulfate Species in the United States. Preprint #83-8.3. Proceedings of the 76th Annual Meeting of the Air Pollution Control Association. Pittsburgh, Pa.: Air Pollution Control Association, 1983. 30. Lioy, P.J., and J.M. Daisey, with T. Atherholt, J Bozzelli, F. Darack, R. Fisher, A. Greenberg, R. Harkov, B. Kebbekus, T.J. Kneip, J. Louis, G. McGarrity, L. McGeorge,and N.M. Reiss. The New Jersey Project on Airborne Toxic Elements and Organic Substances (ATEOS): A summary of the 1981 summer and 1982 winter studies. J. Air Pollut. Control Assoc. 33: 649-657, 1983. 31. Lioy, P.J., and M.J. Lioy, Eds. Air Sampling Instruments for Evaluation of Atmospheric Contaminants. 6th ed. Cincinnati, Oh.: American Conference of Governmental and Industrial Hygienists, 1983. 600 pp. 119 .

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Lippmann, M., P.J. Lioy, G. Liekauf, K.B. Green, D. Baxter, M. Morandi, B. Pasternak, D. Fife, and F.E. Speizer. Effects of ozone on the pulmonary function of children, pp. 423-446. In M.A. Melman, S.D. Lee, and M.G. Mustafa, Eds. Advances in Modern Environmental Toxicology. Vol. V. Princeton, N.J.: Princeton Scientific Publishers, 1983. McMillin, C.~., L.B. Mote, and D.G. DeAngelis. Potential Atmospheric Carcinogens: Phase I. Identification and Classification. Publication No. EPA 600/2-80-015. Research Triangle Park, N.C.: U.S. Environmental Protection Agency, 1980. 255 pp. 34. Morgan, D.L., A.F. Dorsey, and D.B. Menzel. Erythrocytes from ozone-exposed mice exhibit decreased deformability. Fund. Appl. Toxicol 5:137-143, 1985. . Mueller, P.K., and G.M. Hidy. The Sulfate Regional Experiment: Report of Findings. Vols. 1-3. EPRI Publ. No. EA-1901. Palo Alto, Cal.: Electric Power Research Institute, 1983. 36. National Council on Radiation Protection and Measurements. Exposures from the Uranium Series with Emphasis on Radon and Its Daughters. NCRP Report No. 77. Bethesda, Md.: National Council on Radiation Protection and Measurements, 1984. 37. National Research Council, Committee on Indoor Pollutants. Indoor Pollutants, pp. 307-322. Washington, D.C.: National Academy Press, 1981. 38. National Research Council, Committee on Indoor Pollutants. Indoor Pollutants. Washington, D.C. National Academy Press, 1981. 537 pp. 39. National Research Council, Committee on Medical and Biologic Effects of Environmental Pollutants. Ozone and Other Photochemical Oxidants. Washington, D.C.: National Academy of Sciences, 1977. 719 pp. 120

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