National Academies Press: OpenBook

Human Exposure Assessment for Airborne Pollutants: Advances and Opportunities (1991)

Chapter: 7 Current and Anticipated Applications

« Previous: 6 Models
Suggested Citation:"7 Current and Anticipated Applications." National Research Council. 1991. Human Exposure Assessment for Airborne Pollutants: Advances and Opportunities. Washington, DC: The National Academies Press. doi: 10.17226/1544.
×
Page 207
Suggested Citation:"7 Current and Anticipated Applications." National Research Council. 1991. Human Exposure Assessment for Airborne Pollutants: Advances and Opportunities. Washington, DC: The National Academies Press. doi: 10.17226/1544.
×
Page 208
Suggested Citation:"7 Current and Anticipated Applications." National Research Council. 1991. Human Exposure Assessment for Airborne Pollutants: Advances and Opportunities. Washington, DC: The National Academies Press. doi: 10.17226/1544.
×
Page 209
Suggested Citation:"7 Current and Anticipated Applications." National Research Council. 1991. Human Exposure Assessment for Airborne Pollutants: Advances and Opportunities. Washington, DC: The National Academies Press. doi: 10.17226/1544.
×
Page 210
Suggested Citation:"7 Current and Anticipated Applications." National Research Council. 1991. Human Exposure Assessment for Airborne Pollutants: Advances and Opportunities. Washington, DC: The National Academies Press. doi: 10.17226/1544.
×
Page 211
Suggested Citation:"7 Current and Anticipated Applications." National Research Council. 1991. Human Exposure Assessment for Airborne Pollutants: Advances and Opportunities. Washington, DC: The National Academies Press. doi: 10.17226/1544.
×
Page 212
Suggested Citation:"7 Current and Anticipated Applications." National Research Council. 1991. Human Exposure Assessment for Airborne Pollutants: Advances and Opportunities. Washington, DC: The National Academies Press. doi: 10.17226/1544.
×
Page 213
Suggested Citation:"7 Current and Anticipated Applications." National Research Council. 1991. Human Exposure Assessment for Airborne Pollutants: Advances and Opportunities. Washington, DC: The National Academies Press. doi: 10.17226/1544.
×
Page 214
Suggested Citation:"7 Current and Anticipated Applications." National Research Council. 1991. Human Exposure Assessment for Airborne Pollutants: Advances and Opportunities. Washington, DC: The National Academies Press. doi: 10.17226/1544.
×
Page 215
Suggested Citation:"7 Current and Anticipated Applications." National Research Council. 1991. Human Exposure Assessment for Airborne Pollutants: Advances and Opportunities. Washington, DC: The National Academies Press. doi: 10.17226/1544.
×
Page 216
Suggested Citation:"7 Current and Anticipated Applications." National Research Council. 1991. Human Exposure Assessment for Airborne Pollutants: Advances and Opportunities. Washington, DC: The National Academies Press. doi: 10.17226/1544.
×
Page 217
Suggested Citation:"7 Current and Anticipated Applications." National Research Council. 1991. Human Exposure Assessment for Airborne Pollutants: Advances and Opportunities. Washington, DC: The National Academies Press. doi: 10.17226/1544.
×
Page 218
Suggested Citation:"7 Current and Anticipated Applications." National Research Council. 1991. Human Exposure Assessment for Airborne Pollutants: Advances and Opportunities. Washington, DC: The National Academies Press. doi: 10.17226/1544.
×
Page 219
Suggested Citation:"7 Current and Anticipated Applications." National Research Council. 1991. Human Exposure Assessment for Airborne Pollutants: Advances and Opportunities. Washington, DC: The National Academies Press. doi: 10.17226/1544.
×
Page 220
Suggested Citation:"7 Current and Anticipated Applications." National Research Council. 1991. Human Exposure Assessment for Airborne Pollutants: Advances and Opportunities. Washington, DC: The National Academies Press. doi: 10.17226/1544.
×
Page 221
Suggested Citation:"7 Current and Anticipated Applications." National Research Council. 1991. Human Exposure Assessment for Airborne Pollutants: Advances and Opportunities. Washington, DC: The National Academies Press. doi: 10.17226/1544.
×
Page 222
Suggested Citation:"7 Current and Anticipated Applications." National Research Council. 1991. Human Exposure Assessment for Airborne Pollutants: Advances and Opportunities. Washington, DC: The National Academies Press. doi: 10.17226/1544.
×
Page 223
Suggested Citation:"7 Current and Anticipated Applications." National Research Council. 1991. Human Exposure Assessment for Airborne Pollutants: Advances and Opportunities. Washington, DC: The National Academies Press. doi: 10.17226/1544.
×
Page 224
Suggested Citation:"7 Current and Anticipated Applications." National Research Council. 1991. Human Exposure Assessment for Airborne Pollutants: Advances and Opportunities. Washington, DC: The National Academies Press. doi: 10.17226/1544.
×
Page 225
Suggested Citation:"7 Current and Anticipated Applications." National Research Council. 1991. Human Exposure Assessment for Airborne Pollutants: Advances and Opportunities. Washington, DC: The National Academies Press. doi: 10.17226/1544.
×
Page 226
Suggested Citation:"7 Current and Anticipated Applications." National Research Council. 1991. Human Exposure Assessment for Airborne Pollutants: Advances and Opportunities. Washington, DC: The National Academies Press. doi: 10.17226/1544.
×
Page 227
Suggested Citation:"7 Current and Anticipated Applications." National Research Council. 1991. Human Exposure Assessment for Airborne Pollutants: Advances and Opportunities. Washington, DC: The National Academies Press. doi: 10.17226/1544.
×
Page 228
Suggested Citation:"7 Current and Anticipated Applications." National Research Council. 1991. Human Exposure Assessment for Airborne Pollutants: Advances and Opportunities. Washington, DC: The National Academies Press. doi: 10.17226/1544.
×
Page 229
Suggested Citation:"7 Current and Anticipated Applications." National Research Council. 1991. Human Exposure Assessment for Airborne Pollutants: Advances and Opportunities. Washington, DC: The National Academies Press. doi: 10.17226/1544.
×
Page 230
Suggested Citation:"7 Current and Anticipated Applications." National Research Council. 1991. Human Exposure Assessment for Airborne Pollutants: Advances and Opportunities. Washington, DC: The National Academies Press. doi: 10.17226/1544.
×
Page 231
Suggested Citation:"7 Current and Anticipated Applications." National Research Council. 1991. Human Exposure Assessment for Airborne Pollutants: Advances and Opportunities. Washington, DC: The National Academies Press. doi: 10.17226/1544.
×
Page 232
Suggested Citation:"7 Current and Anticipated Applications." National Research Council. 1991. Human Exposure Assessment for Airborne Pollutants: Advances and Opportunities. Washington, DC: The National Academies Press. doi: 10.17226/1544.
×
Page 233
Suggested Citation:"7 Current and Anticipated Applications." National Research Council. 1991. Human Exposure Assessment for Airborne Pollutants: Advances and Opportunities. Washington, DC: The National Academies Press. doi: 10.17226/1544.
×
Page 234
Suggested Citation:"7 Current and Anticipated Applications." National Research Council. 1991. Human Exposure Assessment for Airborne Pollutants: Advances and Opportunities. Washington, DC: The National Academies Press. doi: 10.17226/1544.
×
Page 235
Suggested Citation:"7 Current and Anticipated Applications." National Research Council. 1991. Human Exposure Assessment for Airborne Pollutants: Advances and Opportunities. Washington, DC: The National Academies Press. doi: 10.17226/1544.
×
Page 236
Suggested Citation:"7 Current and Anticipated Applications." National Research Council. 1991. Human Exposure Assessment for Airborne Pollutants: Advances and Opportunities. Washington, DC: The National Academies Press. doi: 10.17226/1544.
×
Page 237
Suggested Citation:"7 Current and Anticipated Applications." National Research Council. 1991. Human Exposure Assessment for Airborne Pollutants: Advances and Opportunities. Washington, DC: The National Academies Press. doi: 10.17226/1544.
×
Page 238
Suggested Citation:"7 Current and Anticipated Applications." National Research Council. 1991. Human Exposure Assessment for Airborne Pollutants: Advances and Opportunities. Washington, DC: The National Academies Press. doi: 10.17226/1544.
×
Page 239
Suggested Citation:"7 Current and Anticipated Applications." National Research Council. 1991. Human Exposure Assessment for Airborne Pollutants: Advances and Opportunities. Washington, DC: The National Academies Press. doi: 10.17226/1544.
×
Page 240
Suggested Citation:"7 Current and Anticipated Applications." National Research Council. 1991. Human Exposure Assessment for Airborne Pollutants: Advances and Opportunities. Washington, DC: The National Academies Press. doi: 10.17226/1544.
×
Page 241
Suggested Citation:"7 Current and Anticipated Applications." National Research Council. 1991. Human Exposure Assessment for Airborne Pollutants: Advances and Opportunities. Washington, DC: The National Academies Press. doi: 10.17226/1544.
×
Page 242
Suggested Citation:"7 Current and Anticipated Applications." National Research Council. 1991. Human Exposure Assessment for Airborne Pollutants: Advances and Opportunities. Washington, DC: The National Academies Press. doi: 10.17226/1544.
×
Page 243
Suggested Citation:"7 Current and Anticipated Applications." National Research Council. 1991. Human Exposure Assessment for Airborne Pollutants: Advances and Opportunities. Washington, DC: The National Academies Press. doi: 10.17226/1544.
×
Page 244
Suggested Citation:"7 Current and Anticipated Applications." National Research Council. 1991. Human Exposure Assessment for Airborne Pollutants: Advances and Opportunities. Washington, DC: The National Academies Press. doi: 10.17226/1544.
×
Page 245
Suggested Citation:"7 Current and Anticipated Applications." National Research Council. 1991. Human Exposure Assessment for Airborne Pollutants: Advances and Opportunities. Washington, DC: The National Academies Press. doi: 10.17226/1544.
×
Page 246
Suggested Citation:"7 Current and Anticipated Applications." National Research Council. 1991. Human Exposure Assessment for Airborne Pollutants: Advances and Opportunities. Washington, DC: The National Academies Press. doi: 10.17226/1544.
×
Page 247
Suggested Citation:"7 Current and Anticipated Applications." National Research Council. 1991. Human Exposure Assessment for Airborne Pollutants: Advances and Opportunities. Washington, DC: The National Academies Press. doi: 10.17226/1544.
×
Page 248
Suggested Citation:"7 Current and Anticipated Applications." National Research Council. 1991. Human Exposure Assessment for Airborne Pollutants: Advances and Opportunities. Washington, DC: The National Academies Press. doi: 10.17226/1544.
×
Page 249
Suggested Citation:"7 Current and Anticipated Applications." National Research Council. 1991. Human Exposure Assessment for Airborne Pollutants: Advances and Opportunities. Washington, DC: The National Academies Press. doi: 10.17226/1544.
×
Page 250
Suggested Citation:"7 Current and Anticipated Applications." National Research Council. 1991. Human Exposure Assessment for Airborne Pollutants: Advances and Opportunities. Washington, DC: The National Academies Press. doi: 10.17226/1544.
×
Page 251
Suggested Citation:"7 Current and Anticipated Applications." National Research Council. 1991. Human Exposure Assessment for Airborne Pollutants: Advances and Opportunities. Washington, DC: The National Academies Press. doi: 10.17226/1544.
×
Page 252
Suggested Citation:"7 Current and Anticipated Applications." National Research Council. 1991. Human Exposure Assessment for Airborne Pollutants: Advances and Opportunities. Washington, DC: The National Academies Press. doi: 10.17226/1544.
×
Page 253
Suggested Citation:"7 Current and Anticipated Applications." National Research Council. 1991. Human Exposure Assessment for Airborne Pollutants: Advances and Opportunities. Washington, DC: The National Academies Press. doi: 10.17226/1544.
×
Page 254
Suggested Citation:"7 Current and Anticipated Applications." National Research Council. 1991. Human Exposure Assessment for Airborne Pollutants: Advances and Opportunities. Washington, DC: The National Academies Press. doi: 10.17226/1544.
×
Page 255
Suggested Citation:"7 Current and Anticipated Applications." National Research Council. 1991. Human Exposure Assessment for Airborne Pollutants: Advances and Opportunities. Washington, DC: The National Academies Press. doi: 10.17226/1544.
×
Page 256

Below is the uncorrected machine-read text of this chapter, intended to provide our own search engines and external engines with highly rich, chapter-representative searchable text of each book. Because it is UNCORRECTED material, please consider the following text as a useful but insufficient proxy for the authoritative book pages.

7 Current and Anticipalred Applications INTRODUCTION The previous chapters in this report dealt with the basic principles and methodological elements of exposure assessment. To illustrate the state of the science and its application to the mitigation of deleterious effects on health or nuisance effects, this chapter analyzes some current and emerging problems of exposure to environmental contaminants in the form of case studies: vola- tile organic compounds, environmental tobacco smoke, polycyclic aromatic hydrocarbons, lead, acidic particulate matter, substances in buildings that cause occupancy complaints (sick-building syndrome), chemicals released from manufacturing facilities, and radon. These do not represent all the important issues but illustrate the state of the science in particular areas, such as biologi- cal markers, multiroute exposure, and personal monitoring. Each section addresses the completeness and results of the approaches in question, the sophistication of the methods used, the requirement for improvement or redirection, the misapplication (if any) of results, and the use of scientific results in making regulatory decisions. Discussions of several of the case studies in the context of exposure through environmental media other than air, such as water, food, or soil, relate to the general framework for exposure assessment discussed in Chapter 1. Accordingly, approaches to assess exposure through inhalation should be considered within the framework of total exposure, which accounts for all exposures a person has to a specific compound regardless of environmental medium. Therefore, strategies to reduce air exposures to a given contaminant should consider exposures due to other media. If other media are found to contribute significantly to the total exposure even after air exposures are re- duced, agencies responsible for or groups experienced with the other medium should be apprised of the issue and play an active role in the development of integrated exposure reduction strategies. 207

208 ASSESSING HUMAN EXPOSURE Unless the hazard of a contaminant is unique or the source of the contami- nant exposure is well characterized, it is difficult to conduct an assessment on one contaminant out of a group present in specific microenvironments. When the contaminant does not have a unique health effect, it is necessary to identi- fy those situations where populations have important exposures. Once the exposure is assessed, that information should be used to perform studies to establish the magnitude of the health outcome from exposure in those situa- tions. These case studies focus on the development of a new paradigm for e~o- sure assessment in risk assessment, risk management, epidemiology, and the application of clinical intervention. The conclusions focus on broad implica- tions for the discipline of exposure assessment, notable advances, and remain- ing needs. The committee hopes that these case studies will stimulate con- tinued or accelerated development of basic principles of exposure assessment and suggest ways to improve the investigations required for specific air con- taminants and general problems. 1 VOLATILE ORGANIC COMPOUNDS Introduction Some volatile organic compounds (VOCs) such as benzene, formaldehyde, and vinyl chloride-are classified as hazardous because of their role in human carc~nogenicity. This discussion deals mainly with VOC exposure of the U.S. population in general; occupational exposure is not specifically considered. The discussion examines EPA's current approach to assessing exposure as part of regulatory investigations of selected VOCs as air contaminants and the advances made by EPA's Total Exposure Assessment Methodology (TEAM) study in evaluating human exposure to VOCs. Benzene is used to examine an eyposure-assessment dichotomy found between the TEAM study and EPA's regulatory investigations. Current Approaches to Exposure Assessment Under the Clean Air Act EPA is required, under Section 112 of the Clean Air Act, to establish National Emission Standards for Hazardous Air Pollutants (NESHAP) that provide an ample margin of safety to protect the public from harmful expo- sure to VOC contaminants. NESHAPs are set by considering major source

CURRENT AND ANTICIPATED APPLICATIONS 209 categories of emissions, determining exposures, calculating health risks associ- ated with each contaminant, and focusing regulation on categories with the greatest risk potential. EPA's selection of source categories is often based on the assumption that sources emitting the greatest amounts cause the greatest exposures. Outdoor stationary sources (e.g., chemical plants and petroleum refineries) are usually identified as the greatest contributors to exposure. The EPA approach to exposure assessment relies heavily on modeling and uses little, if any, actual monitoring data. The human-exposure model combines source emission rates with atmospheric-dispersion equations to predict concentrations of VOC contaminants at various receptor sites In the general population and test the effectiveness of various emission-control strategies. Modeling extremely long-term exposures, as is required for a NESHAP risk assessment for exposure to carcinogens, presents several major difficulties. The typical practice is to measure or model the concentration of a contami- nant at one time and determine lifetime exposure by multiplying that concen- tration by a fixed number of years, e.g., the average human lifetime. Model input data are source locations and estimated emission characteristics, popula- tion census data, and meteorological data. It is assumed that population density remains unchanged for 70 years and that ambient concentrations are constant for 24 hours/day throughout the assumed lifetime. , ~ However, the nature of sources of exposure can change substantially over a lifetime. Large facilities commonly have a design life of 30 years, so consid- erable change can be anticipated in the sources over the 70-year human life- t~me. In addition, individual time-activity patterns can vary substantially over very long periods. In the United States, people change their place of resi- dence often, and few live in the same place over a lifetime. Recent studies of exposures to some VOCs cast considerable doubt on the NESHAP modeling approach and showed clearly that most people's exposures depend far more on their activities than on whether they live near an industri- al source of benzene emissions. The TEAM study has shown that in many circumstances focusing on industrial sources is ineffective in determining human exposure to select VOCs (Wallace, 1987~. Total Exposure-Assessment Methodology Study Overview An assessment of human exposure to airborne VOCs has been carried out through the TEAM study. The program originally intended to develop tech

210 ASSESSII`JG HUMAN EXPOSURE niques to measure total human exposure to a broad range of toxic chemicals, including selected volatile and semivolatile organic compounds and metals, but analysis of those chemicals in air, water, and food presented serious method- ological problems except for a group of VOCs (Wallace, 1987~. An implicit hypothesis was that the observed personal exposures to selected VOCs could be related to point sources (e.g. from industry) and that the farther one moved from these sources the smaller the observed exposures would be. Stated another way, this implicit hypothesis was that there is no difference between VOC exposure estimates made from stationary monitoring networks and from direct personal-exposure measurements as made in the TEAM program. For the small group of VOCs measured, the hypothesis has been rejected. The TEAM study measured exposure to selected VOCs directly with per- sonal monitors that were worn by subjects. The monitors were designed to be small, and to permit unobtrusive but accurate and precise sampling. Monitoring of VOCs is complex, because VOCs are typically found at trace levels. Contamination and artifact problems can affect the reliability of the data, and the applied analytical methods generally require laboratory-based instruments (Moschandreas and Gordon, in press). An extensive quality- control and quality-assurance program was carried out to ensure the proper interpretation of data. Sufficient sample size and probability sampling were used to support inferences regarding the target population and to permit the extrapolation of results to the general population. (Probability sampling is an experimental design that provides unbiased estimates of statistics, including precision, by weighting probability of selection, stratification, and clustering.) The TEAM study measured 2=hour personal exposures to 20-35 target VOCs in air and drinking water, including halogenated alkalies, alkenes, and aromatic compounds. Subjects were monitored in urban (heavy and light industry) and rural environments. In addition to personal samples, concurrent outdoor samples were collected from the backyards of a subset of the subjects. A comparison of matched indoor and outdoor samples showed that the con- centrations of most of the chemicals were higher indoors. That conclusion has been confirmed by other studies that analyzed for a comparable set of VOCs (Molhave and Molter, 1979; Jarke et al., 1981; Seifert and Abraham, 1982; De Bortoli et al., 1984; Gammage et al., 1984; Lebret et al., 1984; Monteith et al., 1984~. In particular it should be noted that Molhave and Moller (1979) found higher concentrations of benzene indoors than outdoors.

CURRENT AND ANTICIPATED APPLICATIONS 211 Measurement Methods The sampling system used a single-tube containing Tenax sorbent through which a known volume of air was drawn with a personal sampling pump. The adsorbent and pump were combined in a vest that was worn by the test sub- ject. Two consecutive 12-hour samples were collected (6 a.m. to 6 p.m. and 6 p.m. to 6 a.m.~. While the subject slept and bathed, the vest was placed carefully in a convenient location. Because most subjects remained at home overnight, the overnight samples were considered indoor samples. Outdoor samples were taken simultaneously near the house. The indoor-outdoor relationships were then established. The disadvantages of Tenax are that it will not retain very volatile compounds (vinyl chloride and methylene chloride) well and it cannot be used to trap reactive compounds (such as formalde- hyde). Samples were thermally desorbed from the Tenax onto a gas chro- matograph, where the analyses were separated, and then detected using mass spectrometry, which is highly specific and sensitive. Recently, the TEAM study employed canisters for the indoor measurements. Biological Markers At the outset of the TEAM study, blood samples were taken at the end of the sapling period and analyzed for the selected VOCs. However, the inva- sive nature of the sampling and poor detection limits associated with the analysis of blood led to the discontinuation of the technique. Fortunately, breath samples were also taken at the end of the sampling period. Breath sampling involved the use of a special spirometer in which the person exhaled approximately 20 L of air into a Tedlar bag, the contents of which were passed through the same type of Tenax traps as used in the air sampling. The same analytical techniques were used for the breath samples as for the air samples. The breath studies showed significant correlations with the personal- monitoring analyses for all 11 prevalent chemicals and showed no correlation with outdoor-air analyses (Wallace, 1987~. To understand the relation of the breath analyses to the air measurements, it is necessary to know the rates of absorption, distribution, metabolism, and elimination of the analyses in the body (physical pharmacokinetics). In funda- mental studies, subjects remained in an exposure chamber for a specified period breathing selected VOCs at specified concentrations. The subjects then left the chamber and their respired breath was analyzed repeatedly after specific periods to establish the half-life of the VOCs in the blood. Half-lives ranging from a few hours (benzene) to 21 hours (tetrachloroethylene) were

212 ASSESSING lIUMAN EXPOSURE observed (Gordon et al., 1985~. Similar results have been seen by Jo et al. (in pressb) for chloroform. The half-lives can be used to determine the most appropriate sampling time for the use of breath measurement as an indicator of exposure. Questionnaires Two questionnaires were used. The first was a household questionnaire, which included age, sex, occupation, household characteristics and activity characteristics of the participant and other members of the household. The "formation was used to obtain a probability sample of subjects and to ensure the inclusion of highly exposed subjects in the studies. The second question- naire involved a 2lhour recall and was administered immediately after the end of the 2=hour monitoring period. The participants were asked whether they had been exposed to potential sources of target chemicals. Monitoring data were then compared with data from the second questionnaire. Variables related to smoking, occupation, home characteristics, personal activities, and automobile travel were found to be the most important determinants of expo- sure. Benzene concentrations were 30-50% higher in homes of smokers than in homes of nonsmokers. Subjects were heavily exposed to benzene (over 1 mg/m3) when filling automobile gas tanks; benzene exposure could often be related to automobile use, which also includes time spent inside of an automo- bile compartment (Wallace, 1989~. Models No models were used specifically to assess exposure in the TEAM study. However, the use of pharmacokinetic models was considered essential for the proper use and interpretation of breath measurements as indicators of eypo- sure. A simple two-compartment model accounted for the effect of the initial breath concentration and the residence time of VOC measured in the TEAM study within the body (Wallace et al., 1983~. The model successfully predicted the time needed for clearance of tetrachloroethylene from the body when compared with the chamber studies mentioned earlier (Gordon, 1985~. Benzene Results of the TEAM study indicate that personal benzene-exposure con

213 o I: ,, o o - C ~ ~ Y o .° E ~ ~ _ 3 o O i/- s~ 'A ~ . ~- I: C _ o E ° _c :, c ,, 3~ C) C) o .. ~ ~ 0 C)In as o o·- X CryC.) ~ to ~ C o C , ~ ~ _ ~- I,, CL ~C).>

214 ASSESSING HUMAN EXPOSURE centrations exceed ambient outdoor concentrations (Wallace, 1989~. Figure 7.1 shows industrial sources represent about 14% of total emissions of ben- zene, but their contribution to exposure is relatively small~nly about 3% of the total. Thus programs and regulations to reduce emissions from major stationary point sources could affect, at most, 3% of total exposure nation- wide. Nevertheless, a recent rule-making has established national emission standards for benzene from industrial source categories: maleic anhydride plants, ethy~benzene-styrene plants, benzene storage, equipment leaks, and coke by-product recovery plants. Other larger indoor and personal sources of exposure are not covered by this rule-making (EPA, 1988d). Exposures from active smoking, involuntary smoking, products in the home, and personal activities such as driving or painting have been estimated to account for more than 80% of nationwide exposure to benzene. The sources of exposure la- beled Motor vehicles (outdoor air)" do not include personal use, such as driving or riding in an automobile; such uses are included in Motor vehicles (travel).~ (Note that the TEAM subjects were drawn from areas with little use of wood stoves or kerosene heaters, which are potentially important sources of expo- sure to benzene (Wallace, 1989~. These important sources of exposure must be re-evaluated and considered for regulation and education. In addition, similar types of integrated analyses are necessary for other VOC contami- nants, which may have both indoor and outdoor sources. Recommendations To incorporate all significant exposure findings into future rule-makings for other hazardous VOCs, exposure analysts and risk managers need to Interact. Regulatory investigations should not be limited to some readily identifiable and measurable point sources that might have insignificant impacts on expo- sure. The findings of TEAM are at odds with conventional approaches used to control VOC exposure. Therefore a major rethinking of the approaches used to identify public health risk is warranted. Exposure analysts must con- tinue to refine techniques that can identify important sources of contaminant exposures, whether those sources are indoors or outdoors. The VOCs examined in the TEAM study were almost exclusively in a single exposure medium (air), were chemically stable, and had a volatility that permitted their effective collection and concentration with the sorbent Tenax New analytical techniques should be developed to broaden the range of ana- lytes that can be collected and measured, so that the "T" in TEAM will actually stand for "Total," and not for "Targeted compounds," as is now the case. In particular, greater attention should be given to analyzing for highly reactive

CURRENT AND ANTICIPATED ~4PPLIC:ATIONS 215 compounds. Passive dosimeters (Lewis et al., 1985) that match the time resolution of active monitors should continue to be developed, because they are less expensive and usually more convenient to wear. Better microenvironment monitoring data and time-activ~ty data, including quality assurance aDd quality control, are needed to improve the modeling of VOC exposures. ENVIRONMENTAL TOBACCO SMOKE Introduction The health herds associated with smoking have received extensive study and are well letdown. Thus, it is not surprising that there is now a growing concern that exposure to environmental tobacco smoke (ETS) might affect the health and comfort of nonsmokers. The health and nuisance effects of so- called involuntary smoking have been extensively reviewed in a National Re- search Council report (NRC, 1986) and in a report of the Office of Smoking and Health (1986~. Both reports concluded that exposure of nonsmokers to ETS results in acute irritation of the eyes, nose, and throat; unacceptable odor; upper-airway problems in children, including increased prevalence of respiratory symptoms (cough, sputum production, and wheezing), decreased lung function, increased lower-respiratory-tract illnesses, and increased rate of chronic ear infections; and increased risk of lung cancer. The reports also noted that other outcomes related to the growth and health of children had positive associations In studies, including low birthweight and reduced growth and development. However, the results of some of these studies continue to be debated, and other related studies are ongoing. Thus, it is unportant to examine ways to improve techniques to assess more accurately exposure to ETS. Until recently, epidemiological studies of the acute and chronic health effects of ETS have been handicapped by limitations in assessing exposures to ETS. Exposures occur at a u ide range of concentrations for highly variable periods and in numerous indoor environments. Unlike active smoking, expo- sure to ETS cannot now be easily assessed with standardized methods. Prev~- ous epidemiological studies of the chronic effects of ETS, particularly lung cancer, have determined exposure solely by questionnaires, which have not been standardized or validated. The questionnaires have usually obtained information on smoking habits of occupants of residences to permit assess- ment of ETS exposures and have not adequately addressed the Impact of occupational exposures. The use of such questionnaires might pose problems

216 ASSESSING-HUMAN EXPOSURE in misclassification of subjects by exposure status and obscure possible e~o- sure-effect relationships. In the past few years, new techniques have been developed that permit a more accurate assessment of individual exposures to ETS (Leaderer, 1990~. They are being applied to test hypotheses ~ epidemiological studies on the relationships between ETS and acute and chronic health and nuisance effects. The methods use advances in the applications of markers or profanes of ETS, air monitoring, modeling, questionnaire survey, and biological markers. Air<on~minant Measurement ETS is a complex mature of more than 3,800 chemicals in the particle and vapor phases. Given the broad range of chemicals that make up ETS, surro- gates or marker compounds have to be identified and measured if one is to assess exposures. Results of recent chamber studies indicate that two such markers are vapor-phase nicotine and the very general category of respirable suspended particles (RSP). In contrast u ith mainstream smoke, approximately 95% of the nicotine in ETS is in the vapor phase (Eudy et al., 1985; Eatough et al., 1986; Hammond et al., 1987~. It is not known how nicotine concentrations are related to con- centrations of other contaminants in ETS (particle or gas phase) or to those contaminants that might be associated with health (e.g., benzene) or nuisance effects. Results of recent chamber studies (Rickert et al., 1984) and one residential field study indicate that vapor-phase nicotine might be a good marker of ETS-generated RSP (Leaderer and Hammond, 1990~. Various active methods (Muramatsu et al., 1984; Hammond et al., 1987; Eatough et al., 1989) have been developed for sampling vapor phase or phase-distributed nicotine in air, and can be used to measure nicotine in different microenviron- ments or personal monitoring situations for periods ranging from a few hours to approximately 24 hours. A passive monitor has been developed from an active method of sampling for nicotine (Hammond et al., 1987) and from the knowledge that ETS nicotine exists primarily in the vapor phase. This passive monitor measures personal exposures to nicotine and nicotine concentrations in indoor environments in periods of 1 day to several weeks (Hammond and Leaderer 19871. It might permit the assessment of ETS ~,rnoc,~r~.~ in loran. segments of the population. The combustion of tobacco results in the emission of large quantities of RSP into the indoor environment-amounts that result in easy measurement of increases over background (Spengler et al., 1981~. A model that incorpo- rates an application of a mass-balance equation has been used for estimating rat :~_

CURRENT AND ANTICIPATED APPLICATIONS 217 ETS-generated RSP in various indoor microenvironments (Repace and Low- rey, 1980, 1982~. It is also being used to estimate ETS exposures retrospec- tively and to assess risk (Repace and Lowrey, 1990~. As input, the model uses known rates of RSP emission from tobacco combustion and data from several sources, including measured and estimated smoking densities, infiltration and ventilation rates, and deposition rates. The tapered element oscillating micro- balance could be used to continuously monitor indoor concentrations of RSP (Patashnick and Rupprecht, 1986~. Biological Marlters Physiological fluids can be analyzed for specific biological marker com- pounds indicative of exposure to ETS. Thiocyanate, carboxyhemoglobin, nicotine and cotinine, hydroxyproline, N-nitrosoproline, aromatic amines, and protein or DNA abducts have all been considered as Indicators of dose of tobacco smoke (NRC, 1986; Office of Smoking and Health, 1986~. Those biological markers indicate that exposure has taken place, but might not be directly related to the source or to the specific adverse effect under study. Furthermore, a biological marker of exposure might not be specific for the contaminant related to the effect, does not provide an exact measurement of ETS exposure in a single environment, and does not provide information on the environmental factors that affect the concentration in the environments in which people spend time. Biological markers of ETS exposure can also vary widely from person to person, because of differences in uptake, distribution, and metabolism. Some markers are not specific for ETS exposure (e.g., carboxyhemogIobin); while others (e.g., thiocyanate) might be useful for active smoke exposure, but not sensitive enough for ETS exposure. Cotinine and nicotine measurements in the blood, urine, and saliva are specific for tobacco- smoke exposure, and have been widely used as indicators of ETS exposure (NRC, 1986~; they are valuable in determining the total or integrated short- term (hours to days) dose of ETS across all locations in which a person spends time. Questionnaires Questionnaires have been used extensively in epidemiological studies for the classification of people into broad categories of ETS exposure on the basis of reported exposure. Questionnaires are also used to obtain information on the physical environments in which exposures take place, the factors affecting

218 ASSESSING HUMAN EXPOSURE the exposures in those environments (volume, number of cigarettes, etc.) and the amounts of time people spend in those environments. They afford an indirect measure of exposure and so cannot provide information on specific exposure magnitudes, although information obtained with them is essential for use In models aimed at predicting ETS concentrations in different environ- ments and total exposure. An effort is under way to develop a standardized questionnaire for estimating indoor concentrations of ETS-related contami- nants and personal exposures (Lebowitz et al., 1987~. Future Applications Advances in assessing ETS exposures are now being incorporated into epidemiolog~cal studies of the health and nuisance effects associated with ETS exposure. The use of any particular method in an epidemiological study is determined by the overall objective of the study and the resources available. Some studies use only one of the techniques available; others use several. Many studies use nested exposure-assessment designs, in which small samples of the study population are subjected to extensive direct and indirect measure- ment of exposure (questionnaires, personal monitoring, biological markers, etc.), and the whole study population is subjected to less intensive measure- ment methods (questionnaires). That approach can be cost-effective. One current study (Leaderer et al., 1989) tests the hypothesis that pregnant women passively exposed to ETS are at increased risk of delivering an infant with low birthweigbt, or before 37 weeks of gestation, with intrauterine growth retarda- tion. The study uses all the techniques of assessing ETS exposure discussed above in a nested design. That permits efficient use of scarce resources to obtain as complete an estimate of ETS exposure as possible and comparison of results of different exposure-assessment techniques. If successful, similar approaches should be considered for use by other exposure analysts in the design of studies of other pollutants or biological end points. POLYCYCLIC AROMATIC HYDROCARBONS Introduction The polycyclic aromatic hydrocarbons (PAHs) are a class of hydrocarbons found in polycyclic organic matter, a very broad class of compounds that have two or more fused rings and are produced by incomplete combustion. Many individual PAHs, as well as various PAH mixtures from different combustion

CURRENT AND ANTICIPATED APPLICATIONS 219 sources, are carcinogenic in animals and in humans (Santodonato et al., 1981; NRC, 1983b). Exposure to PAHs In workplace env~ron~nents has long been recognized as posing risks of skin and lung cancer (NRC, 1983b). Although that recognition led to concern about community exposures to PAHs and cancer risk, efforts to link outdoor concentrations of the compounds to lung- cancer rates over many years were largely unsuccessful, in part because it was difficult to detect a relatively small risk of cancer related to PAH-polluted air against a large background of lung cancer due to cigarette smoke using stand- ard epidemiological methods. In addition, there was also a failure to accu- rately assess personal exposures to PAHs, and epidemiological studies were based on the assumption that measurements of PAHs in outdoor air yielded a reasonable estimate of total exposures. In the last decade, indoor air has been recognized as much more important in exposure to PAHs because most of the population spends 80-90% of the day indoors. There has also been growing awareness that other pathways of exposure, such as diet, can be as important as airborne exposures (Santodonato et al., 1981; Lioy et al., 1988~. Outdoor sources of PAHs include combustion of wood, coal, oil, and gas; motor vehicles; and some industrial sources, such as coke ovens (Daisey et al., 1986~. Natural sources, such as forest fires, can also contribute to the atmo- spheric burden of PAHs. Many sources are present in indoor environments, including tobacco smoke (active and environmental), Invented space heaters, and food preparation (Howard and Fazio, 1980; Wilson et al., 1985; Traynor et al., 1987; Lioy et al., 1988~. PAHs produced from combustion of tobacco smoke are directly inhaled during smoking. A one-pack/day smoker inhales approximately 0.4 fig of benzoapyrene (BaP), which is only one of the many PAHs In the complex mixture of tobacco smoke. Nonsmokers can also be exposed to PAHs In environmental tobacco smoke. The ubiquitous nature of PAHs in the community environment requires the measurement or estimation of total inhaled PAHs in multiple microenviron- ments. In addition, PAH contamination of water, food, and soil can contrib- ute to personal exposures through other routes of entry into the body. Airborne concentrations of PAHs depends on the nature, location, mag- nitude, and duration of multiple combustion sources and vary widely. Lioy and Greenberg (1990), for example, compared urban and suburban locales and found wide variations in outdoor concentrations. Their analyses indicat- ed that the highest PAH concentrations occurred in communities that burned wood as a major source of space-heating. Personal exposures to PAHs from space-heating in communities depend on the kinds of space heaters used, time of year, time spent indoors and outdoors, direct emissions from heaters into indoor air, and penetration of PAHs in outdoor air into indoor environments. Daisey et al. (1989) showed that indoor concentrations of individual PAHs in

220 ASSESSING HUM,4N EXPOSURE homes with woodstoves were 2-47 times Heater during wood-burning than non-wood-burning periods. Both direct emissions into indoor air and penetra- tion from outdoor air were inferred to contribute to indoor concentrations; Many particulate PAHs penetrate to the indoors, because they are normally associated with respirable fine particles. The 2- and 3-nug PAHs are largely In the vapor phase and can also readily infiltrate into indoor environments. The penetration of particulate BaP has been demonstrated in nonsmoker homes as part of the Total Human Environmental Exposure Study (THEES) (Lioy et al., 1988~. Indoor BaP was significantly correlated (r > 0.80, p ~ 0.01) with simultaneous outdoor values for these homes. In fact, BaP penetration accounted for most of the inhalation exposure of the residents -of the non- smokers' homes studied. It is difficult to determine the contribution of various sources of airborne PAHs to human exposure. Determining human dietary intake of PAHs Is equally difficult. Exposure to PAHs In food depends not only on the source of food, but also on the style of cooking and personal eating habits (Howard and Fazio, 1980~. BaP can be deposited from outdoor air onto surfaces of agricultural crops, e.g., spinach, lettuce, and cabbage. The edible portions of those crops have relatively large surface areas exposed to the air and tend to collect large amounts of BaP. Beverages made from coffee beans and tea leaves contain BaP. General information can continue to be obtained from market-basket surveys, but population-based measurements of diets are necessary to define the magnitude of exposures in food, compared with other media. PAHs are typically found in the atmosphere and In other media as complex mixtures of several hundred compounds associated with organic compounds of many other classes. Low-molecular-weight PAHs, such as phenanthrene, are found In the vapor phase whereas high-molecular-weight PAH, such as BaP, are almost wholly in the particulate phase (Cautreels and Van Cauwen- berghe, 1978; Hunt and Pangaro, 1985; Pysalo et al., 1987~. Particulate PAHs in air are preferentially concentrated on particles smaller than 2-3 Em In diameter, because they generally result from direct emission from combustion sources, which produce predominantly smaller size particles (Pierce and Katz, 1975; Miguel and Friedlander, 1978; Van Vaeck and Van Canwenberghe, 1985~. The distribution of semivolatile PAHs (between the vapor and particu- late phases) depends on their sub-cooled liquid-phase vapor pressures (and thus on temperature) and on the surface area of the particles (Yamasaki et al., 1982; Bidleman et al., 1986; Bidleman, 1988; Ligocki and Pankow, 1989~. Sampling is difficult if all the PAHs are to be collected in a way that truly reflects their true physical state in the air. Inhalation exposures to PAHs ~n- cluded compounds present in both the vapor phase and the particulate phase

CURRENT AND ANTICIPATED APPLICATIONS 221 and the potential risk associated with them depends not only on the concen- trations and duration of contact with these compounds but on their distribu- tion between particulate and vapor phases (Boulos, 1985~. Differences in penetration of various PAHs to the indoors and in the Spoor distribution of PAHs between vapor and particulate phases are not well established. Data on those differences would assist in establishing inhalation-exposure relation- ships for total PAHs. For the quantitative analysis of total-PAH exposure, it is critical to develop sensitive techniques for sampling and analysis of particu- late-phase and vapor-phase material collected on low-flow personal samplers (e.g. less than 10 L/min). The relative amounts of the hundreds of different PAHs In a complex mixture from a combustion or industrial source can vary substantially (Daisey et al., 1986; Masclet et al., 1986~. The overall chemical composition of com- bustion emissions also varies. For example, cigarette smoke has higher pro- portions of mtrogen-containing organic compounds than do emissions from wood-burning or diesel and automobile exhaust (Schmeltz and Hoffmann, 1977; Albert et al., 1983; Daisey and Gundel, 1989~. Such differences result in differences in the biological potencies of complex matures. Mumford et al. (1987), for example, reported substantial differences in mutagenic activity in an Ames assay, in carcinogenic activity in mice, and in the chemical compo- sition of particulate matter from Chinese homes that used different fuels- smoky coal, wood, and smokeless coal. They also reported higher lung cancer rates In communities that used smoky coal than in communities that used the other two fuels. Albert et al. (1983) reported substantial differences in chemi- cal composition and biological potency of emissions from coke ovens, roofing tar, cigarette smoke, and various motor vehicles. It is difficult and expensive to measure all the PAH compounds in a com- plex mixture as part of an exposure assessment. Therefore, BaP, an animal carcinogen that is found in all PAH mixtures as a more easily measured indi- cator compound, has been widely used as a surrogate indicator compound to characterize exposure to many PAHs and other complex mixtures (Santodo- nato et al., 1981; Osborne and Crosby, 1987) . There is considerable evidence that BaP is at best a crude indicator of exposure to PAHs, to complex mix- tures containing PAHs, and to carcinogens of other classes (Albert et al., 1983; NRC, 1988~. The EPA report on toxic air pollution (EPA, 1985b), which used BaP as a surrogate for total PAHs, estimated that half the risk associated with exposure to BaP was probably due to other products of incom- plete combustion. That was probably an underestimate in that the report did not take into account differences in the potencies of various complex mixtures or, more important, indoor exposures to PAHs. It might be possible to meas- ure multiple index compounds to characterize exposures to complex PAH

222 ASSESSING HUMAN EXPOSURE mixtures with different biological potencies This, however, has not yet been done, and BaP continues to be used as the indicator compound for character- i~ng exposure to complex mixtures of PAHs. Hypothesis and Study Design Exposures to PAHs in community settings occur through multimedia path- ways, including air, water, soil, and food. There is a need to determine the contributions of various pathways and sources of the biologically active PAHs as a basis for reducing the risk of cancer. In the THEES (Total Human Environmental Exposure Study), exposure to BaP present in multiple media in an urban population is being investigated (Lioy et al., 1988~. The study includes simultaneous measurements of BaP in air (indoor, outdoor, and breathing-zone air), water, soil, and food. The results will be used in mass-balance studies on BaP metabolites in the partici- pants' urine and feces and on DNA adducts in their blood. This approach is being developed for generalization to assessments of exposure to other PAHs that require multimedia assessment. The multimedia microenvironmental results from the first phase of the study were averaged for smoker homes, nonsmoker homes, and a coal-burning home (Lioy and Greenberg, 1990~. Data compiled were for indoor and out- door air samples on 14 consecutive days, weekly composites of food consumed by the participants, spot samples of tap water, and the soil around each home. THEES showed that inhalation and food ingestion provided the greatest exposures (Lioy et al., 1988~. Inhaled BaP was derived primarily from indoor microenv~ronments (including BaP generated indoors and BaP that penetrated from outdoors). Tap water yielded minimal exposure. The homes where the highest calculated ingested doses occurred (more than 400 mg for one subject) also showed the highest inhalation doses, and that suggests a need for further research on the relationships of BaP inhalation and cooking. Inhalation re- sulted in the highest dose in 7 of the 12 exposure weeks in nonsmoker homes, but food ingestion yielded a higher mean dose during the high food-exposure week. These were doses 3-16 times greater than the inhaled dose. If one adds an estimate of direct BaP inhalation by smokers in the smoker homes as a separate category, their BaP doses will increase by a factor of more than 5. The second and third phases of THEES included personal and biological monitoring and provided information supporting the importance of food and inhalation routes of exposure and on the utility of current biological markers (Waldman et al., in press).

CURRENT AND ANTICIPA TED APPLICATIONS 223 Measurement Methods PAHs in air are usually collected using high-volume air samplers containing a filter to collect particles followed by an adsorbent trap to collect vapors. However, separating and collecting artifact-free supples of vapor- and part;- cle-phase PAHs are difficult using these samplers. These artifacts include adsorption of vapors by the filter matrix itself; PAH blow-off losses from or adsorption gains to particles coldected on the filter; and losses of PAHs from chemical reactivity with ozone and other reactive species drawn through the sampler (Van Vaeck et al., 1984; Finlayson-Pitts and Pitts, 1986; Coutant et al., 1988; Ligocki and Pankow, 1989~. Many scientists who sample air believe that an improved way to separate and collect both phases simultaneously would be to use a sampling train with a diffusion denuder followed by a filter and then by a sorbent. With this sample collection system, compounds in the vapor phase are removed by the diffusion denuder and, therefore, are not available to adsorb onto the particles coldected on the filter or onto the filter matrix itself during sampling. Particles pass through the denuder and are collected on the filter. The sorbent behind the filter collects vapor-phase compounds desorbed from the particles collect- ed on the filter. The sum of the analyte concentration on the filter and on the sorbent behind the filter provides the analyte's particle-phase concentration. Recent experiments by Coutant et al. (1988), using a denuder system simi- lar to that described above, have shown that at a high-volume filter face velo- city of about 33 cm/see, low-molecular-weight PAHs-phenanthrene, anthra- cene, fluoranthene, pyrene, chrysene, and ben7aanthracenc all displayed some tendency for volatilization losses from the filter. High-molecular-weight PAHs, such as BaP, did not appear to be affected. In principle, the sampler that they developed for experiments on sampling artifacts could be adapted and used to measure the vapor-phase and particulate PAHs in indoor air more accurately. But applications would require four rather than two analyses for each collected sample, because chemical interferences prohibit the analysis of vapor-phase PAH removed by the denuder. Thus, vapor-phase PAH must be determined by difference. Two samplers are used in this method, one with and one without a PAH denuder, to determine the concentrations of particu- late-phase PAH and total PAH, respectively The filters and backup sorbents for each sampler must be analyzed, requiring four analyses for each sample. Denuder systems that permit Resorption of collected vapors (Lane et al., 1988) would be very useful for collection of airborne PAH. Samples of particles or vapors on a sorbent are typically extracted with an organic solvent and concentrated, sometimes fractionated, and then commonly analyzed with gas chromatography-mass spectrometry (GC-MS) or high-pres

224 ASSESSING HUMAN EXPOSURE sure liquid chromatography (HPLC) with fluorescence detection. Wilson et al. (1985) have reported that extracts of PAHs from particulate matter and the sorbent can be analyzed directly (without cleanup) with positive-chemical- ionization GC-MS. They collected large air volumes (100 m3 in 8 hours) in indoor environments. Indoor air-sampling rates should be less than 5-10% of indoor air-exchange rates for the room with the sampler, to minimize the perturbation caused by sampling. This method could be modified by reducing the total solvent extract volume (and thus concentrating the sample) or using longer sampling times at a lower flow rate. In THEES (Lioy et al., 1988), samples of airborne particulate matter are being collected indoors and outdoors and analyzed for BaP. The samples are extracted, concentrated, and then separated and analyzed for BaP with thin- layer chromatography and in situ spectrofluorimetry. Analysis of PAHs in food samples typically involves extraction and digestion in alcoholic potassium hydroxide followed by various cleanup and separation steps (Howard and Fazio, 1980; Lawrence and Das, 1986; Grimmer and Jacob, 1987; Vaessen et al., 1988~. Considerable cleanup is generally required for food samples and losses of PAHs can be substantial. The PAH-enriched fraction is then analyzed with the same methods as for airborne PAHs. It is important to include both positive (known standards or surrogate compounds) and negative (field and lab blanks) controls in the sampling and analysis of PAH for exposure measurements and to determine and report the accuracy and precision of all measurements. Biological Markers There has been considerable development of methods for the analysis of biological markers of PAH exposure in the last decade. Methods have been developed for PAHs and their metabolites in urine (Becher and Bjorseth, 1983) and for PAM-DNA adducts in blood and tissue (Perera et al., 1982; Burlingame et al., 1983~. The method developed by Becher and Bjorseth for measurement of PAHs and their metabolites in urine involves reduction of the metabolites to the parent PAHs followed by HPLC with fluorescence detec- lion of total PAHs. That method has been used for biological monitoring of PAHs in workers in an aluminum plant. Other analytical methods are being explored for use with urine samples. Mass-spectrometric methods have also been developed for biological markers of PAH exposure (Burlingame et al., 1983~. Several investigators (Perera et al., 1987; Harris et al., 1985; Everson et al., 1986) have used an immunoassay for determination of PAM-DNA adducts in tissue samples and in blood samples from smokers, nonsmokers,

CURRENT AND ANTICIPATED APPLICATIONS 225 and workers in high-PAH-exposure industries. Application to the community exposure situation needs further research and development. Questionnaires Questionnaires should be used in any study of exposure to PAHs to provide information on the various sources that contribute to exposure. They should include questions on smoking; indoor sources, such as smokers in the home, kerosene heaters, woodstoves, fireplaces, and gas stoves; cooking practices, =d diet; and local outdoor sources. In the THEES (Lioy et al., 1988), a person in each participating household fills out a daily activity questionnaire that includes questions about time spent in the home, personal activities, indoor combustion sources, smoking, and ventilation. Information about hobbies, home repairs, and personal-product use is included and is necessary for defining the important pathways and sources of exposure. Details on the contents of each meal eaten at home and at other locations are also obtained. Models Several types of models have potential application in community exposure assessments for PAHs. The mass-balance model can be used in various ways to estimate indoor and outdoor inhalation of PAHs. Receptor models might be used to estimate the contributions of various sources to PAH exposures, if appropriate tracers can be identified for the major source types. The macromodel~eveloped by Traynor et al. (1988) for particulate matter, CO, and NOX in indoor air-could be developed to provide estimates of population exposures to PAHs and identify major sources and factors that contribute to large exposures. Future Needs PAHs emitted and accumulated in various environmental media require the development and application of sensitive personal-monitoring methods for determining the individual compounds present and routes of exposure to them. Research conducted on airborne BaP and other selected PAHs clearly demonstrates that they can accumulate indoors as well as outdoors. The data indicate that many 3-4 ring PAHs are present in both particulate and vapor phases. Therefore, new techniques for sampling PAHs simultaneously in both

226 ASSESSING HUMAN EXPOSURE phases are required for indoor-environment and personal-monitoring studies; they will increase the accuracy of exposure and risk assessments for total PAHs. The reactivity of PAHs requires further investigation, because it appears that a number of nitrogenated and oxygenated PAHs can be produced during sampling (Arey et al., 1988) or by atmospheric reactions (Pitts et al., 1985b; Greenberg and Darack, 1987). Some nitrogenated and oxygenated PAHs are directly emitted by combustion sources (F~nlayson-Pitts and Pitts, 1986~. Some of these components are highly mutagenic and will need to be factored into PAH exposure assessments. In addition, methods that Will minimize or eliminate artifacts during sampling or analysis will have to be developed. The THEES strategy has been developed for the measurement of BaP exposure through multiple pathways. Inhalation exposures could be derived from indoor combustion sources, penetration of outdoor air to the indoors, and personal activities, such as cooking and smoking. The strategy should be extended to other PAHs and important PAH derivatives to assist in studying related indoor and outdoor exposures and in identifying the primary routes of exposure for use in risk assessment and risk management. Those conducting the research and those involved with development and application must inter- act to ensure that the major pathways of exposure continue to be studied and effective strategies developed. LEAD Introduction Mined and processed since antiquity, lead is a ubiquitous toxic substance that poses special challenges for exposure assessment. Like a number of persistent environmental pollutants, lead appears in all media (NRC, 1987b). Over the past 3 decades, the decrease in the body burden of lead that is deemed to be toxic and the detection of widespread lead poisoning in young American children have spurred recognition of the importance of controlling an array of sources. The American Academy of Pediatrics and the American Public Health Association recommend routine testing of infants and children to reduce the neurological deficits inflicted by exposure to lead a previously silent epidemic that can permanently impair vital physiological functions and cognition in workers and children. Given the absence of adequate systematic environmental monitoring of lead and the lack of routine body-burden screening, lead-poisoned children all too often are the primary means of

CURRENT AND AIVTICIPA TED APPLICATIONS 227 identifying a lead-poisoned environment. Pinpointing precise sources remains difficult. Over the past 2 decades, measurement of airborne lead concentrations has provided a clear method for tracking and enforcing overall reductions in airborne exposure. Despite real success in reducing airborne lead exposure in the United States and concomitant reduction In blood lead, the Agency for Toxic Substances and Disease Registry (ATSDR, 19~) estimates that about 17% of ad children under five have enough lead in their blood to cause per- manent deficits In intelligence and development. Approximately 40% of all children in poverty in 1984 are believed to be so affected. Children absorb lead from multiple sources including air, drinking water, food, house dust, play area soil and dust, interior and exterior paints, improperly glazed ceramics, and toys (EPA, 1986c). Children are at special risk from lead exposure, because their higher rate of mineral turnover in bone allows them to absorb and retain more lead per unit of mass than adults and because the developing nervous system is espe- cially vulnerable to lead. Some children are exposed to high doses of lead through deliberate swallowing (e.g., pica), mouthing of lead-containing non- food objects, or hand-to-mouth activity after exposure to lead-contaminated dust or soil. The relative intensities and durations of exposure to lead also influence toxicity. The recommended mammal daily intake of lead for infants is 100 fig from all sources. In the late 1970s, one could slide a finger along a long table and accumulate more than 100 fig of lead in common, urban dust contributed by emissions from motor vehicles combusting gasoline containing lead. A single chip of 50% lead paint (500,000 parts per million) will produce acute poisoning if eaten by a young toddler. Daily ingestion of 1 or 2 liters of water with lead at or above 20 ~g/L occurs from 20% of public drinking water supplies in the United States. This level of lead can result in developmental problems, as can playing on the ground or floor in an area with modest lead contamination over the same period. We review here the recent history of the successful application of exposure assessment methods to the problem of airborne lead. This section discusses the development of evidence on the contribution of lead from gasoline, sta- tionary sources (including municipal incinerators), and dusts and soil to air- borne lead and notes the clear link between the recent decline in airborne lead and at least a portion of the decline in blood lead in the U.S. population.

228 ASSESSING HUMAN EXPOSURE Lead from Gasoline In the 1970s, as more and more cases of lead poisoning occurred in chil- dren who did not live in dwellings with lead-based pent, researchers explored the link between leaded gasoline and outdoor-air lead concentrations. It was found that most of the lead in the atmosphere resulted from combustion of leaded gasoline. Two regulations were promulgated by EPA. One (EPA, 1973) required the availability of unleaded fuel for automobiles designed to meet federal standards for emission of VOCs with lead-sensitive emission- contro] devices (e.g., catalytic converters); the second (EPA, 1986c) required a reduction of the lead content in leaded gasoline. As shown in Figure 7e2' the control of lead in gasoline over the last several years has resulted in a decrease in peak outdoor-air lead concentrations. Based on data from a larger number of monitoring stations, the downward trend shown in Figure 7.2 has continued. The most recent data from EPA show that in 19~ the ma~n- mum quarterly average concentration of lead in outdoor air was less than 0.1 Gym and approximately 3 x 103 tons of lead was emitted due to gasoline combustions (EPA, 1990~. Figure 7.3 shows findings of the National Health and Nutrition Evaluation Survey from 1976 to 1980, establishing a clear associ- ation between lead in children's blood and lead used in gasoline (NRC, 1980; Annest et al., 1983; Rabbinou~tz, 1990~. In a number of major U.S. cities, trends in childhood lead concentrations correlated closely with those of sales in leaded gasoline (NRC, 1980~. At one time, exposure to airborne lead accounted for 40-50% of blood lead in children (ATSDR, 1988~. Use of leaded gasoline has been declining since the 1970s and it is project- ed that the gasoline-lead phasedown now in progress ugly lower blood lead concentrations to less than 15 ~g/dL in millions of children between now and 1992; pediatric lead toxicity is considered to begin when blood lead exceeds 10 ~g/dL. But present and past airborne depositions (fallout) of lead onto soil and buildings All produce exposures for years to come, and continued monitoring of lead in air and other media remains important. Lead in the ambient air is routinely monitored in accordance with the Lead National Ambient Air Quality Standards (Fed. Reg. 1978, 1981~. In urban areas, airborne lead is presumed to be correlated directly with the remaining lead in gasoline, although municipal incineration and other point sources can also be important. Airborne Lead from Stationary Sources Stationary sources are fixed operations that emit lead. The United States

CURRENT AND ANTICIPATED ~PLI=TIONS 229 180 160 - - _ 120 140 UJ 2 J 1OO lo In C' c, 80 MU in o 60 J 40 20 l - ~_ x. 1~. AMBIENT AIR LEAD CONCENTRATION - : _ l _ ~ _ -LEAD CONSUMED IN GASOLINE 1975 1976 1977 1 978 1 979 1 980 CALENDAR YEAR 1.2 t.t a, : J UJ 1.0 ~ UJ C} MU J lo IS UJ > 0.7 ~ to 0.6 IS a 0.5 ~ X Or 0.4 ~ LO 03 ° o 0.2 0.1 O 1 981 1 982 ~ 983 1 984 FIGURE 7.2 Gasoline lead emissions and outdoor lead concentrations 1975-1984. Source: EPA (1986c).

230 Ip/B8'Sl3~3l aV31 aoO18 39~3~V __ >I a- I l l l ll I l ~ - - - lo z z go a, :~< cog Or \ J \ ~ ~- - Iq~L) \ \ ~ J ] - o -o o - o ~ o o' or ret - 8~l ~U:~ - 801 001~3d HlNOW~ H~d 03sn av31 1~101 .c Q) o A) 's OD a: - A) As 'e c, o ca 3 o es a: Ct C~ C) _. ._ ~5 ~> C> C~ o C~ r ~_ ~n ce . ;> Ct o o - ~: ._ C~ _` ~4,> C~ _ CO C) G) =5 ~ - C~ ~ .. ~, 8 o ~: o

CURREAtTAArDANTICIPATED^PLICATION5 231 today has 11 mines, five primary smelters and refineries, 60 secondary smelt- ers, 132 plants where lead-acid batteries are manufactured, and thousands of other local sources, including municipal incinerators, demolished structures, and uses of contaminated sewage sludge. The latter are especially difficult to pinpoint. The most severe pediatric lead poisonings In the United States have been noted ~ the vicinity of primary lead smelters (Baker et al., 1977; CDC, 1985~. Exposure from stationary sources might be concentrated, because of adverse climatic conditions, such as aridity, low winch speeds, and thermal inversions. Children are also being exposed to leaf] at some hazardous sites that are on the National Priorities List for Superfund remedial action (ATSDR, 1988~. Small numbers of children are affected, but their exposures are often large. Lead in Dusts and Soils Soil dusts, street dusts, and household dusts can all contain substantial amounts of lead deposited from air, although some is linked with degrading paint and municipal ash transportation or incineration. Direct exposure by inhalation is only one way that lead in the air can affect children. In time, lead settles out from the air and can be ingested through soil consumption and consumption of contaminated foods. Deposition of atmospheric lead over many years accounts for the high concentrations of lead found in soil and dust (Groth, 1981; CDC, 1985~. Studies in New Jersey (Caprio et al., 1974; CDC, 1985) and California (Johnson et al., 1975; CDC, 1985) have shown that chil- dren living within 100 feet of major roadways have higher blood lead concen- trations than those living farther away. Urban soil lead has numerous sources, such as the burning of trash rich in lead, the residue of demolished structures, the dumping and burning of lead batteries and their cases, the historical use of lead pesticides, emissions of refuse incinerators, and use of sewage sludge as fertilizer (Chancy and Mielke, 1986~. Lead from flaking paint, particularly in and around houses, can be an important lead source for soils (Chancy et al., 1984~. (Note: Yaffe et al. (1983) used stable isotopes of lead to trace paint lead to soil, from there to house dust, and from there to blood lead in children. Plant uptake of lead from soil and transport into edible plant tissues is another source of lead ex- posure (Chancy and Mielke, 1986~.)

232 ASSESSING HUMAN EXPOSURE Outdoor-Air Measurements At the beginning of 1988, EPA had 353 monitoring stations that directly measured lead in air in the United States. Roadside and neighborhood mon;- tors dominate the network now, but greater monitoring around point sources is planned. EPA's monitoring for lead in air uses hi~-volume samples with fiberglass filters. B;Q10g;Cal Markers The human body is an integrator of lead from different sources. Whether ingested or inhaled, lead accumulates in the blood, brain, and bone; the pro- portion retained is greatest after ingestion. In humans recent exposure to lead is commonly measured in terms of blood lead, which indicates exposure in the preceding 4 months. The heme biosynthetic pathway is exquisitely sensitive to lead. An increase in erythrocyte protoporphyrin or an increase in delta-aminolevulinic acid (ALA) in urine is often an early and reliable marker of functional impairment due to lead absorption (EPA, 1986c; ATSDR, 19~. Research is under way to measure cumulative lead exposures in the dentin of deciduous teeth or by x-ray fluorescence of major bones, such as the tibia. In any given population, a range of internally absorbed blood lead will reflect individual variation in metabolism of to~ncants and other host factors, such as nutritional status and age (ATSDR, 1988~. Lead in inhaled air is eventually absorbed in a two-part process: some absorbed from the pulmonary tract, and some swallowed and absorbed from the gastrointestinal tract (ATSDR, 1988~. Low concentrations in a number of media can add up to a large intake over time. Moreover, the developing fetus and the young remain at special risk, both because their metabolism is high and because their grouting brains more readily absorb lead. The biological basis of lead toxicity is closely linked to the ability of lead to bind to ligating groups in crucial biomolecular structures. Lead competes With calcium and other essential metals for binding sites and can inhibit en- yme activity. Anemia, a common manifestation of chronic lead intoxication, is associated with reduced hemoglobin production and shortened erythrocyte survival. An increase in erythroc~rte protoporphyrin is often construed as a marker of recent lead absorption in young children. Many believe that ALA in urine and inhibition of the activity of the entwine ALA-dehydrose (ALA-D) are the most sensitive markers; however, interpretive difficulties might arise, as mentioned in Chapter 4. Piomelli and others have shown, however, that blood lead can underesti

CURRENT AND ANTICIPA TED APPLICA TION5 233 mate cumulative exposure. They used EDTA chelation tests to stimulate the release of lead from bone and showed that substantial stores of lead can be found in children with modest blood lead concentrations (Piomelli et al., 1984~. Questionnaires The studies reported above did not use individual questionnaires. Rather, biological markers became the indicator or validator of sources of lead expo- sure. Thus, in investigations of a neighborhood near a smelter, blood lead concentrations in children were determined by hematofluor~meter evaluations of whole blood drawn by venipuncture, and these were correlated with dis- tance. Models In preparing its justification for the regulation of lead, EPA relied on a series of crude models that correlated gross figures on production of leaded gasoline with estimates of airborne lead and blood lead. More sophisticated models now use radiographic tracers to simulate lead deposition, absorption, and pharmacokinetics in the pulmonary tract and its environmental cross- media cycling (EPA, 1989a). Studies have confirmed the direct causal link between amounts of lead in gasoline, air, and blood. Conclusions The best integrator of recent exposure to lead in the young child is the blood, which reflects exposures that occurred over the preceding 4 months. However, inferential methods for determining the relative sources of blood lead In the child, such as the isotope-ratio method developed by Yaffe et al. (1983), are expensive. Table 7.1 summarizes various strategies for estimating exposure from a number of important sources described here. In few of the strategies have studies of individual activity patterns been undertaken. Most rely on extrapolations from a few samples or or surrogate indicators from production or consumption patterns. From the earliest Roman times, humans have been exposed to lead from numerous sources. Methods for estimating exposure to lead across media have changed, reflecting the field of exposure assessment itself and different

234 c) c) :s o D Ct C) o _. o ~: - $- o C~ U) S C, g ._ Ct ._ U: C~ o C~ C) .c o ~0 CD Ct m S: C) Ct o Q o ._ Ct5 m o ~_ C~ ._ CD o o ¢) - Ct CO 7 - o C~ i ~ ~~ ~ C D · ~ ~ ~· & ~_ O Ct O ·= ~ .Q ~O ~ O .5 ~ ·~ , ~ ~ ~Ct C.) Q) o - ~ C ~ ~o o ._ ~C) _ . ~ ~ ~_ ~Ct ~' ~ °~= ' ~ _ _ ~ _ ~._ _ .= .= ~.= o ~ ~ ~ `: C: - >` C: ~<~, 3 C: ~P~ ~P~ ~ ~ ~ C) C~ o C~ Ct ~: O ~._ ._ O _ C ~Ct e~ ~O .= ·= e ~Ct Ct

235 o Q. ~ o ~ ~ ~ ~ ~ i;= =$ g0;~-~7io ~.- A: Ct o ~ c: ~ _ X ~o D ~ a) Ct _ C) ID Ct ~O U) G) C) ~v ::i ~i~ ~ ~ ~_ ~_ ~ ~ _ O ~O~ ~ O ~ ~<-c ~ ~ Cal ._ O ~ Cal Ct ~3 c: ~ ,_ Cal ,~o ~5~ so:so: ._ ._._ ~5 Ct CtCt C) oo oo on - Can ·O o

236 ASSESSING HUMAN EXPOSURE hypotheses as to critical sources. Exposure to lead has often been estimated with crude surrogates of different source terms, such as production and con- sumption figures for specific applications. There is no systematic monitoring of environmental lead across media today, nor is there routine testing and screening of children for lead toxicity. More focused exposure studies are needed that include observation of activities of the young child, individual monitoring, and detailed cross-media uptake monitoring (which can be affected directly or indirectly by air emis- sion). Such studies would ensure that future control expenditures were appro- priately based on exposure-response relationships. ACIDIC PARTICULATE MATIER Introduction Airborne acidic particulate compound species, which include primarily sulfuric acid (H2SO4) and ammonium bisulfate (NH4HSO4), and surrogates have been measured by a number of researchers over the last 20-30 years, but their health effects have been appreciated only recently (Utell et al., 1983; Spektor et al., 1989; Koenig et al., 1989; Speizer, 1989; Spengler et al., 1990~. As discussed by Lippmann et al. (1987), there appear to be two different responses of humans to inhaled acidic aerosols: reflex bronchoconstriction and altered mucociliary clearance (which might lead to chronic bronchitis). Both are supported by numerous animal studies. Controlled human-exposure studies that have attempted to define a dose-response relationship have ~n- volved short-term exposures to acidic aerosol concentrations in excess of those typically found in outdoor air. However, the exposures were comparable with those estimated during specific pollution episodes (Lioy and Waldman, 1989~. For bronchoconstriction, the lowest observed-effects concentration of sulfuric acid in asthmatics was reported in four studies to be 68 ~g/m3 for 30 minutes at rest and 10 minutes of exercise (Koenig et al., 1989), 450 fig /m3 for 16 minutes (Utell et al., 1983), 1,000 ~g/m3 for 1 hour at rest (Spektor et al., 1989) and 75 ~g/m3 for 2 hours including rest and four 10-minute periods of exercise (Bauer et al., 1988) a wide range. The lowest observed-effects concentration for altered mucociliary clearance was reported iI1 two studies to be 100 ~g/m3 for 1 hour at rest (Leikauf et al., 1981, 1984; Spektor et al., 1989). Recent epidemiological evidence supports the hypothesis that chronic, low- level exposure to acidic particles can be associated with respiratory disease. That is very important, because the exposure pattern is typical of the ambient

CURRENT AND ANTICIPA TED APPLICA TION5 237 atmosphere (Lioy and Waldman, 1989). Speizer (1989) has reported that in four of the six cities in the Harvard study In which acidic particles were meas- ured, there was a better correlation of the prevalence of chronic bronchitis (as diagnosed by a physician) with hydrogen ion concentration in the particles than with total respirable-particle concentration. The Clean Air Science Advisory Committee (CASAC) of EPA recommend- ed to the administrator that an analysis of the available and emerging scientif- ic information on acidic particles be prepared and that exposure and health research be conducted to provide a scientific basis for a decision on the prom- ulgation of a National Ambient Air Quality Standard (NAAQS). This is based on the conclusions and recommendations in Acid Aerosol Issues Paper (EPA, 1989b). Hypothesis Health effects associated with exposures to acidic particles have been ob- served in controlled human studies, and epidemiological studies have yielded suggestive evidence of exposure-response relationships at exposures detected in the ambient environment. Therefore it is necessary to examine the occur- rence of exposures to and health effects of acidic particles in sensitive groups in the general population. Measurements The chemical variable relevant to health appears to be total particle acidity or sulfuric acid concentration, although the aqueous concentration of hydrogen ion in the airborne particles might be useful. There are several reasons for that. First, titratable acidity has been suggested as the appropriate indicator of irritant potency (Fine et al., 1987~. Second, animal-toxicity studies of acidic sulfate aerosols have shown that it is the acidity (i.e., the hydrogen ion concen- tration), rather than the acid anion concentration, that is related to respiratory effects (Lippmann et al., 1987)e Finally, although airborne acid aerosols are found as highly concentrated solution droplets whose acids might not be fully dissociated, the acids in the droplets become fully dissociated when the drop- lets are inhaled and later come to rest on the relatively alkaline surfaces of the respiratory tract. Therefore, particle acidity appears to be the relevant meas- ure from a public-health perspective. Based on a total of about 10 reported studies, typical outdoor concentra- tions of particle acidity range from 1 to 4D microequivalence of hydrogen ion

238 ASSESSING HUMAN EXPOSURE per cubic meter of air over 1-12 hours of sampling. The highest reported concentrations were associated with the longer sampling times (Tanner and Marlow, 1977; Pierson et al., 1989~. The associated exposure during a pollu- tion episode can be estimated from the reported concentration and the epi- sode duration and can be as high as approximately 1,000 pEq~H+) hr/m3 (I,ioy and Waldman, 1989~. An important exposure characteristic is particle size. Airborne acidic parti- cles can range in diameter from 0.01 to more than 10 ~m. The smallest particles are formed from condensation of acidic gases, such as sulfur trioxide. The largest are found in fogs. However, most airborne acidic particles have a mean diameter of 0.3-0.6 Em (on an aerodynamic mass basis). Depending on the size, the particles will be deposited in various regions of the respiratory tract. Particle size also determines the ratio of particle surface area to vol- ume, which in turn determines the rate of chemical neutralization by atmo- spheric and respiratory ammonia (Larson, 1989~. Very few measurements of acidic aerosol size distribution exist, so no estimate can be made of episode exposure as a function of particle size. Clearly, there is a great need for more complete exposure assessments than have resulted from epidemiolog~cal studies. Lioy and Waldman (1989) have identified at least three ambient situations (urban wintertime fogs, summer- time haze, direct source emissions) in which high acidic concentration can be anticipated, and Leaderer et al. (199Ob) have identified sources that could lead to indoor exposure. It is imperative to focus on situations that embody the most important exposure-response relationships in the outdoor and indoor environments. However, the metric of acidity of concern should be measur- able with methods developed for use in the field. Methods The most direct sampling method for strongly acidic particles involves drawing ambient air through a diffusion denuder tube and a collecting the particles on a Teflon filter. The denuder tube removes airborne bases, such as ammonia, that might otherwise neutralize some of the acidity collected on the filter. When the sample collection is complete, the filter is returned to the laboratory, and the acidity is extracted and titrated. That method has much appeal: it is relatively straightforward and involves an acid-base titration of aerosol acidity. Its drawbacks include relatively long collection times (it is not a continuous method), the need for laboratory analysis of the filters, and potential sampling artifacts. The potential sampling artifacts occur under two conditions: in sampling of acidic particles that coexist in the air with other,

CURRENT AND ANTICIPATED APPLIG4TION5 239 more alkaline particles, such as sea salt and surface dust; and in sampling of particles that are coated with an acidic surface layer, such as those studied by Amdur and coworkers (Amdur et al., 1986~. The first potential artifact results from the inability of the diffusion denuder to remove alkaline particles, which penetrate past the size selective inlet. Therefore these particles land on the same filter as (and potentially react withy the acidic particles of interest. The second potential artifact also results from the failure of the denuder to prevent chemical reactions between the particle and its acid coating. The second artifact is probably not too severe, because the acid-coated particles are not the major form of atmospheric acidity and are expected to be important only near some combustion sources. The other approach to measuring acidic particles focuses on the continuous measurement of specific acidic compounds, notably the ammonium salts of sulfuric acid, using a flame photometric detector modified to discriminate the species by using volatilization as a function of temperature (Tanner et al., 1980; Slan~na et al., 1985~. Continuous methods avoid many of the problems associated with filter sampling. However, these methods cannot distinguish ammonium bisulfate from ammonium sulfate, because these compounds have similar thermal-decomposition characteristics; airborne total acidity might therefore be underestimated. In addition, the methods do not measure total particulate acidity, but focus on a few sulfur compounds that contribute to the total. It is evident that ideal monitoring methods would measure titratable acidity in airborne particles or all acidic particle species. Ideal methods would not be subject to artifacts resulting from particle-particle reactions on filters and would be continuous and rapidly responding. No reported measurement method has all those attributes. Conclusions Once an acidic particulate contaminant of health concern is agreed upon, an intensive program should be developed to design or validate instrumental and analytical techniques for indoor and outdoor studies. Closely associated is the need to gather further information on acidic particle precursor sources and primary acidic particle sources, particle size distributions, the situations in which acid exposures can occur indoors and outdoors, and accurate predic- tive models of exposure. The techniques should then be used in epidemiologi- cal studies of chronic or acute effects. The results of exposure assessments related to atmospheric acidic species should provide a basis for comparisons of toxicity of acidic mixtures. Accurate measurement of exposure to acidic

240 ASSESSING HUMAN EXPOSURE particles in a variety of microenvironments is necessary if exposure analysts and other environmental health professionals are to define exposure-response relationships. Accurate exposure assessment is imperative for use by regula- tors and managers in establishing a basis for recommendations of mitigation steps necessary to minimize indoor and outdoor exposures and community health effects. SICK-BUILDING SYNDROME Introduction Environmental measurements made during the last decade have revealed that indoor concentrations of some air pollutants are often higher than out- door concentrations and sometimes even hider than outdoor health-based air quality standards (Spengler and Sexton, 1983; Spengler and Soczek, 1984; Wallace et al., 1986~. Furthermore, other research demonstrates that, on the average, people spend 80-90% of their time indoors (Szalai, 1972; NRC, 1981~. Thus, indoor exposures to some pollutants are greater than outdoor exposures because of higher indoor concentrations, longer exposure durations, or both. Because of the large amount of time spent indoors, some indoor exposures can be greater even when indoor concentrations are lower than those out- doors. Thus, it is important to identify and take into account all important microenvironments when determining total exposures to airborne contami- nants (Girman et al., 1987~. Many types of studies are being carried out to determine exposures in various indoor microenvironments and should consider using the state-of-the-art concepts as discussed throughout this report. One type of indoor study~he study of the sick-building syndrome (SBS)-especially could profit from the use of new methods. The incidence of SBS has increased with the development of energy-effi- cient buildings, the attendant reduction in ventilation, and the increased use of synthetic building materials and furnishings. Outbreaks of SBS are a cause for great concern, because of their impact on public health and the economic impact of direct expenses (for environmental exposure monitoring, medical care, and litigation) and indirect expenses (productivity losses and reduced marketability of office space). There are two types of building-related problems. One, called building- related illness (BRI), can be generally thought of as an outbreak in a set of occupants of subchronic disease or symptoms caused by one or a few environ- mental constituents near or above a health-effect threshold, such as legionel- losis caused by exposure to the bacteria of the genus Legion ella, hypersensitivi

CURRENT AND ANTICIPATED APPLICATIONS 241 ty pneumonitis caused by bioaerosol exposure, or eye Irritation caused by exposure to formaldehyde. The other, SBS, usually involves buildings in which no single environmental constituent examined exceeds the generally accepted threshold. Assuming that the health-effects threshold data are correct, the problem is thought to be multifactorial but could be caused by a single com- ponent not detected by current sampling and analysis methods. In SBS, occu- pants complain of subchronic discomfort (eye irritation, headaches, lethargy, etc.) at a prevalence greater than that associated with occupants of Healthy buildings (in which the prevalence is not well established, but might be around 20%~. The symptoms characteristically diminish when the occupants leave the building (Molhave, 1987; Woods, 1988~. The multifactorial cause of SBS is believed to involve a complex interplay of indoor pollutant-source emissions, both chemical and bioaerosol, from building materials and furnishings, building systems (e.g., ventilation and humidification systems), and building use; physical factors (temperature, light, noise, etc.~; human characteristics (race, sex, health status, sensitivity, etc.~; and the group dynamics in the building. Except in rare instances, baseline information on those parameters is lacking for noncomplaint (healthy) build- ings, so the basis for evaluating what is unique about a sick building is lacking (Berglund et al., 1987~. The current situation is analogous to attempting to treat a sick patient without knowledge of normal physiology. a- Cal Carrying out accurate risk assessments and developing appropriate mitiga- tion strategies to reduce adverse health outcomes in sick buildings are not possible without baseline information about the environmental characteristics of buildings without complaints, i.e., from healthy buildings, as well as similar data on sick buildings. Such information can come only from carefully execut- ed epidemiological studies that include both healthy buildings and sick build- ings. For example, Noma et al. (1988) have studied SBS through a statistical analysis of chemical concentrations in air samples collected from sick and healthy school buildings Many studies that could be classified as SBS studies have been reported, particularly in the proceedings of three international conferences on indoor air quality since 1981 (International Symposium on Indoor Air Pollution, Health and Energy Conservation, 1981; Third International Conference on Indoor Air Quality and Climate, 1984; and Fourth International Conference on Indoor Air Quality and Climate, 1987~. Although the studies varied in size and quali- ty, they shared a number of disturbing characteristics: they were not scien- tifically designed but rather were responses to complaints of building occupants; they were generally limited in their types of measurements, usually only monitoring for concentrations of contaminants near the occupational ex- posure limits; they seldom incorporated quality assurance plans; they generally

242 ASSESSING HUMAN EXPOSURE used no standardized protocols; and they were rarely designed to test clearly stated hypotheses. Data from such studies are often characterized as anecdotal by scientists. Although such anecdotal data can be of use in the early development of a scientific discipline to assist in generating hypotheses, they are of little scientif- ic value and, in fact, can do a disservice if they continue to be published in the scientific literature in the guise of results of studies. It is important to distinguish between public-health building investigations and SBS research studies. The primary objective of the former is to alleviate a problem or concern, and that of the latter is to test a hypothesis. The two objectives are not necessarily compatible. Therefore, regarding SBS, a sharp delineation should be made between anecdotal efforts and true research stud- ies; efforts of the anecdotal type should be referred to simply as building- complaint investigations. In recent years, a few studies have been conducted that can be considered SBS research studies, as opposed to building-complaint investigations. Finne- gan et al. (1984) attempted to show a relation between symptoms and building ventilation type; their study was seriously flawed in that no environmental characteristics were measured not even ventilation rates. Robertson et al. (1985) attempted a followup study in which some environmental measure- ments were made; it included only two buildings, and the measurements were limited to temperature, relative humidity, air velocity, and ion concentrations. Harrison et al. (1987) studied 2,587 workers in 27 buildings; but environmental measurements were limited to particulate matter, fungi, and bacteria. Hedge et al. (1987) correlated the symptoms of 4,373 office workers with types of building ventilation systems, but made no environmental measurements and reported no information on the age of the buildings, so their conclusions were tentative. The Danish town-hall studies measured 29 environmental characteristics- including chemical, biological, and physical and used detailed questionnaires regarding 4,369 employees (Skov and Valbjorn, 1987; Valbjorn and Skov, 1987~. The study represents a definite advance in SBS study methods, but only 14 buildings were studied, so it is difficult to analyze the data on the many symptoms and environmental characteristics. This presents a clear dilemma to the investigator with limited resources; i.e., to understand the multifactorial causal relations of SBS, one must obtain data of many kinds, but adequate analysis requires covering many buildings.

CURRENT AND ANTICIPATED APPLICATIONS 243 Hypothesis and Study Design This section discusses the various components that must be considered in the design of an SBS study. There is a very close relationship between the hypothesis and the study design. A hypothesis that states that USES is caused by multifactorial parameters is too general and vague to be tested with limited resources. A good SBS hypothesis is one that requires reasonable resources, yet resolves a public-health issue of concern. For example, a hypothesis that states that There is a statistically significant relation among some symptoms (such as sensory irritation) and some environmental factors (such as chemi- cals, biological aerosols, temperature, relative humidity, and ventilation) or psychosocial situations, for clerical staff working in open environments in office buildings with specific characteristics (such as size and ventilation char- acteristics)" can be tested with more limited resources. The resolution of such a hypothesis will be of use in developing mitigation strategies. With that type of hypothesis in mind, we discuss here the major considerations for the com- ponents of a study. We will not discuss considerations common to most epi- demiological studies, but will stress those peculiar to the SBS. Measurement Techniques (Analytical and Sampling) Because so little is known about SBS, any reasonable study will require a plethora of data of diverse categories, such as chemical, biological, physical (ventilation, relative humidity, temperature, noise, light, vibration), and psy- chosocial information and information on biological markers. Some data can be acquired through the use of questionnaires and time and activity reports, but a large amount must be obtained through costly microenvironmental measurements. It should be emphasized, however, that the techniques will have to be more sensitive than those typically used in industrial hygiene. Investigations to date usually have not indicated the presence of contaminants at concentrations approaching occupational exposure limits; that implies that the workplace is safe. However, it is obviously still a problem and the situa- tion is complicated by the fact that there are no standards or guidelines to assist the exposure analyst in evaluating the significance of substances found. Clearly, a new approach that focuses on immunological toxicology and expo- sure-response research on the symptoms associated with sick buildings is necessary. Developing a quality assurance program is more difficult for an SBS study than for most other environmental studies, because so many variables are involved and few standard methods or reference materials are available for

244 ASSESSING HUMAN EXPOSURE many chemical and biological species that appear to be of interest. Many of the standard methods used for outdoor or industrial environments require instruments too noisy and large to be used indoors. Thus, the Investigator must validate the method either before (which is preferable) or during the study using procedures such as parallel sampling with different methods In selected buildings or splitting of collected air samples among other laborato- ries. Biological Markers Markers sometimes can be useful in BRI (building-related illness) studies, particularly in ensuring that an exposure has occurred. Understanding of the SBS problem is insufficient to be able to predict whether markers might be useful in SBS studies. Of course, the marker used depends on the suspect contaminants. Although markers have been used extensively in the industrial setting (e.g., blood lead), not many problem buildings have been studied with markers. That is partly because investigators usually have little information on what substances are causing the problem and marker methods are often invasive. Two notable exceptions are measurements of breath and urine, and it is recommended that these be considered for development and use whenev- er possible. A spinoff of the use of biological markers is that building occupants tend to understand better and accept the meaning of measurements that describe their individual body burdens than measurements of the environment. The usefulness of markers was demonstrated In a California building that had a problem with pentachlorophenol eluted from interior wood treated with it. A combination of data on air and urine markers gave the investigators evi- dence that the building was the source of the problem and that mitigation efforts were fruitful, and also gave the building occupants some confidence that the problem was not out of control (Wesolowski et al., 1984~. Many building problems, however, are multifactorial and thus do not lend them- selves to such distinct monocontaminant resolution. Biological markers, even noninvasive ones, should not be used unless they are needed to test a useful hypothesis, because their use requires that the persons tested be given clear explanations of what their test results imply about their present and future health. In many cases, particularly at the rela- tively low body burdens often encountered, such information is not know n to the investigator. The same caution applies to indoor environmental measure- ments: occupants have a right to a clear interpretation of the health and dis- comfort implications of the data.

CURRENT AND ANTICIPATED APPLICATIONS 245 Questionnaires Questionnaires are used in SBS studies to survey the nature and magnitude of health and comfort complaints, to determine the spatial and temporal distributions of complaints, to assess confounders of reported effects (such as current health status of respondents and demographics), and to obtain ir~for- mation on environmental factors that might be related to complaints. Ques- tionnaires, when used to obtain information on environmental factors, can provide information on human exposures that could prove useful even if not accompanied by environmental measurements. They can also give information that helps to determine which environmental measurements should be used in a study. When used specifically as an exposure assessment tool in SBS studies, questionnaires use the respondent as a sensor of the workplace environment to assess such important variables as odor, sound, lighting, comfort, and envi- ronment acceptability; to characterize potential sick-building psychosocial factors (such as conflict at work, job satisfaction, and degree of control over work); and to provide surrogate measures of off-site (residence, outdoor, transportation, etc.) exposures to air contaminants in lieu of more expensive personal or microenvironmental monitoring. Questionnaires have been used in SBS studies (Finnegan et al., 1984; Rob- ertson et al., 1985; Gamble et al., 1986; Hedge et al., 1986; Leaderer et al., 1990a), but no standardized questionnaire is available. The lack of a stand- ardized questionnaire makes it difficult to compare data collected in various studies. The questionnaires used so far have typically obtained information on only a few of the factors that affect exposure, and only one reported study attempted to obtain information on a wide range of psychosocial factors (Hur- rell et al., 1990; Leaderer et al., 1990a). An effort is needed to develop and test a standardized questionnaire for use in SBS studies. Several characteristics of administration of a questionnaire must be careful- ly chosen before a study begins. They include the sample selection method (building census, stratified sample based on air-handling systems, etc.), the method of distribution and collection of questionnaires (telephone, post office, in-building mail system, etc.), and the method and number of followup at- tempts to ensure a high response rate. The choices should be determined on the basis of the hypothesis being tested and the characteristics of the building and population involved in the study.

246 ASSESSING HUMAN EXPOSURE Models The single compartment and multicompartment ma.cc-balance model dis- cussed in Chapter 6 can be used to good purpose in designing and conducting a study to elucidate the relationship between health effects and exposures to airborne contaminants. Those models can provide a conceptual framework for designing the sampling strategy to be used in various buildings, can help to predict exposure concentrations from various sources or infernug source strengths from concentration measurements, and can be useful In designing controlled human exposure experiments in which concentrations of indoor contaminants are varied. Empirical models constitute a second class of model that can often be used as hypothesis-generating and testing tools. Such models are typically multivar- iate. For an SBS study, some health end point would be related to env~ron- mental variables in a stepwise multiple regression. Conclusions The SBS problem has surfaced only in the last decade. Thus, the methods for understanding it have not had time or resources to be adequately devel- oped by exposure analysts. However, the database obtained from ~nvestiga- tions of BRI has suggested better approaches for the design of SBS studies and a need to develop measures to reduce exposure and the Incidence of SBS. Issues of technique include the development of more refined hypotheses; the use of a broader range of physical, chemical, and biological measurements; more complete and standardized health and activity questionnaires; and the use of more sophisticated models of total exposure. TOXICS RELEASE INVENTORY Introduction Title III of the Superfund Amendments and Reauthorization Act of 1986 (SARA), Public Law 99-499, is a free-standing statute titled "The Emergency Planning and Community Right-To-Know Act of 1986". In the development of SARA Section 313, it was acknowledged during discussions in Congress that the extent of human exposure to toxic chemicals released by industry was a major concern Congressional Record, H11205, December 5, 1985~. It was also expressed in Congress that much work is needed before human exposure

CURRENT AND ANTICIPATED APPLICATIONS 247 to toxic chemicals can be effectively managed and that acquisition of informa- tion is the next necessary step. Section 313 of SARA requires industrial facili- ties that manufacture, process, or use toxic chemicals to report annual envi- ronmental release information to the EPA. Initial requirements for submis- sion of the information are specified by EPA in the Toxic Chemical Release Reporting Final Rule (Fed. Reg., 1988a). The database resulting from the information reported to EPA is referred to as the Toxics Release Inventory (TRI). The TRI was seen as a means to gather information for three general objectives: (a) to identify the chemicals of the greatest concern; (b) to identify locations where the chemicals are manufactured, used, and released; and (c) to determine the quantities released into the environment (Congressional Record, S11772, September 19, 1985~. The initial list of toxic chemicals for TRI reporting contains 308 specific chemical compounds and 20 chemical categories and can be modified only by a rule-making, such as the deletion of titanium dioxide ¢Fed. Reg., 1988b). Information reported to the TRI includes routine releases (e.g., emissions from stacks) and accidental releases to air, land, and water. The first reports were filed on June 30, 1988. This case study examines the issues that should be addressed in the TRI to make it useful for assessing exposure to toxic chemicals. The purpose of the TRI is to inform the public and government officials about total releases of toxic chemicals. Section 313 of SARA requires EPA to develop the TRI information into a computerized database for public ac- cess. The information is intended, among other purposes, to assist research and aid in the development of various regulations, guidelines, and standards (EPA, 1988c). There are no requirements to perform risk assessments or to regulate any TRI-listed chemicals. To minimize the burden of data-gathering on industry, Section 313 of SARA allows release reports to be based on esti- mates; monitoring data and other available information are not required, but can be reported if available. Applications to Exposure Assessment Although the TRI provides useful information on estimated mass quantities of chemical releases, it does little to assist in understanding the potential for human exposure to those releases and resulting impacts on public health. The inclusion of accidental and routine emissions in the total releases reported to the TRI makes estimation of downwind concentrations and exposures techni- cally infeasible. The separate types of releases involve different exposure issues and require different analyses for determination of exposure and expo

248 ASSESSING HUMAN EXPOSURE sure impact. The TRI database is useful In identifying chemicals of concern, which may, with further analysis, provide data needed for exposure assess- ment. The TRI requires reporting of chemical quantities released directly into the environment or transferred to off-site locations, identity of releasing facility, geographical location (latitude and longitudes, identity of all sites to which the reporting facility transports chemical wastes, how the reported chemicals are used, and types and efficiency of on-site methods to treat chemical wastes. The data, by themselves, are inappropriate for assessing either acute or chron- ic exposures, because they are not linked specifically to the potential concen- trations and locations of exposure of the general population (Levin and Spence, 1989~. TRI data are only one type of input data for air-dispersion models (see Chapter 6) used to estimate potential downwind concentrations, which are then linked with human time-activ~ty data to assess potential e~o- sures (see Chapter 5~. Even the simplest dispersion models cannot be used to estimate downwind concentrations of released toxic chemicals on the basis only of TRI data. The TRI provides some data useful in determining downwind concentrations, such as facility location, latitude and longitude (to assist in describing meteorolog~- cal transport), and categorization of releases as either point sources (e.g., stack emissions) or fugitive releases. Additional data are needed for air-dis- persion analyses. Values of various model parameters on individual sources are needed: release temperature and discharge velocity, orifice diameter and height of release; frequency and duration of releases; and nearby structure characteristics likely to affect small-scale air movements. Because the TRI does not collect those additional data, industry is not likely to obtain and store them, so they cannot be obtained simply by calling the TRI coordinator at each facility and requesting them. Some facilities have taken the initiative of estimating potential exposure concentrations of released chemicals reported to the TRI. Such information more fully prepares facilities to respond to inquiries from the public about impacts of their toxic chemical releases on public health and the environment. Acute toxicity is the primary concern for assessment of exposure to acci- dental releases. To identify possible carcinogenic impacts, analysis of lifetime exposure to routine emissions is required. Even if all the necessary model data were provided for each release source, the results would be of little use for exposure assessment, because of the combination of data in the TRI on routine emissions and accidental releases. For example, at low concentrations, hydrogen cyanide (HCN) gas, an acute- ly toxic agent, can be detoxified by the body. However, at high concentrations, HCN causes breathing loss and death. Reporting all emissions of HCN on an

CURRENT AND ANTICIPATED APPLICATI0115 249 annual basis could give a false impression of potential exposures that had acute health outcomes. The estimation of exposure on an annual basis might be acceptable for long-term effects, but even a single breath of HCN at more than 2,300 ppm~v) would result in death. Only time will tell whether the TRI database will be applied incorrectly to Closure assessment activities. It is clear today, on the information submitted to the TRI database, that industry has committed resources to reduce emis- sions (Steyer, 1988) and EPA is expected to move more rapidly to develop regulations for several specific hazardous air pollutants. Implications The TRI reporting requirement will, in all probability, provide tangible environmental benefits. Data on releases to all media are important for understanding the impact of a chemical release on total human exposure and the global environment, but releases to air warrant special attention. Releases to air probably result in the most immediate, and perhaps the most important, exposures of the public living near an industrial facility that produces or uses toxic chemicals. Exposure to airborne toxic chemicals can occur directly through inhalation of contaminated air or through ingestion of food or water that contains contaminants deposited from the air. In the future, acutely and chronically toxic chemicals should be reported separately to allow proper focus of resources on the most important exposure issues. A source and receptor database needed for the proper exposure as- sessment for both acutely and chronically toxic chemicals should be carefully considered for inclusion in the data-collection effort In any revision of SARA Section 313. Industry burden of providing the additional information is an important aspect of the considerations. Because the technology used for exposure assessment is changing rapidly, it would be appropriate to define data needs in regulations, rather than in specific laws. Regulations could then be changed as necessary to respond to advances ~ exposure assessment without the need to amend laws. RADON Introduction Exposure of the general public to radon and its decay products appears to constitute an important naturally occurring environmental health risk. Radon

250 ASSESSING HUhlAN EXPOSURE decay products have clearly produced lung cancers in exposed underground miners (NRC, 1987a). However, there are considerable uncertainties in how the risks identified in the miner studies can be extrapolated to the general public. No clearly identified lung-cancer mortality in the general population ran yet be specifically linked to exposure to radon decay products (NCRP' 1984a,b). Four relatively small case-controlled studies have suggested a possible relationship between lung cancer and building construction or residential radon exposure (Axelson et al., 1979; Edling et al., 1984; Lees et al., 1987; Svensson et al., 1987), but there are no unequivocal measurements of the Inug-cancer risk associated with indoor radon. Because the estimated risks are higher than those associated with many other environmental agents suspected of having adverse health effects, there has been considerable inter- est In looking for clear evidence of radon-related lung cancer in the general population. The problem of protecting the public health has been exacerbated by the uncertainties in the exposures and the corresponding risk estimates. Risk- management decisions of EPA have suggested radon concentrations in indoor air that should trigger mitigation action, and those action concentrations if too low would result in unnecessary expenditures and concern. EPA reported in a September 1988 press conference that radon causes 2O,000 lung-cancer deaths a year in the United States. However, that estimate is at the high end of the range estimated by the National Council on Radiation Protection and Measurements (NCRP, 1984a,b), so the risk estimates are not in good agree- ment. Major factors affecting the uncertainty in risk estimates are related to the measurement of the proportion of exposure that is environmental. There are major difficulties in assessing exposure to natural airborne radio- activity, particularly to those radionuclides of greatest health-effect potential. It is universally agreed that the short-lived decay products of radon (hippo' 2~4Pb, alibi, and 2~4po) cause the presumed health effects, but radon Is gener- ally measured as a surrogate for these other radionuclides, because it is rea- sonably easy and inexpensive to measure the indoor radon concentration. One must be careful in extrapolating short-term screening measurements made under nontypical conditions (e.g., in a basement in a closed house during winter) to annual average exposures, although these nontypical-condition measurements may represent a maximum exposure condition. Methods for measuring long-term, average exposure to radon require further development, and better communication is necessary to explain the risk uncertainties to the public. The amount of airborne radon decay products in a room depends on sever- al factors, including the amount of radon to produce them, the concentration of airborne particles to which they can become attached, and the aerodynamic

CURRENT AND ANTICIPATED APPLICATIONS 251 processes that contribute to the deposition of radioactivity on surfaces in the room (walls, ceilings, furniture, etc). Thus, the actual concentration of a~r- boruc radioactivity is a complicated function of several environmental vari- ables. . ~ The health effects of radon decay products also depend heavily on their aerodynamic behavior in the indoor atmosphere. Particularly for Typo, parti- tioning between the unattached state and the attached forms (i.e., combined with pre-existing aerosol particles) has an important impact on the calculation of the dose to the lung from a given airborne decay-product concentration. In the dose models commonly used to relate tissue dose to airborne radioac- tiv;ity concentrations (Jacob; and Eisfeld, 1980; James et al., 1980), a substan- tially increasing effective dose to the target tissue is predicted with decreasing particle size down to about 3 nm. The increase in dose is due to the increase in effective deposition through molecular diffusion as particle size approaches that of free molecules. Small changes In particle size in this range result in large changes In the diffusion coefficient and in depositional behavior, particu- larly in regard to the location of deposition in the tracheobronchial tree. These models of delivered dose of alpha radiation to Jung tissue show radon to be a reasonable surrogate for exposure to the `decay products because several of the opposing factors in the exposure cancel each other. Hypothesis and Study Design The hypothesis of interest is that increased exposure to radon decay prod- ucts In the indoor environment increases the risk of induction of lung cancer. Exposure to tobacco smoke and differential residential mobility are substantial confounding factors in the estimation of health risk. Two epidemiological studies are attempting to relate lung cancer to envi- ronmental radon and decay-product exposure through retrospective measure- ment of indoor radon concentrations. One is being conducted by the state of New Jersey and the other by Argonne National Laboratory. Both are con- cerned with obtaining better risk estimates related to exposure of the general population to radon decay products and are using cases of lung cancer in white women as the subjects of case-controlled studies The New Jersey study (Schoenberg et al., 1987) is an earlier extension of a statewide population-based case-controlled interview study of New Jersey women. The cases include all of the female residents of New Jersey whose histologically confirmed primary cancers of the lung were newly diagnosed in the period from August 1982 to September 1983. For cancer patients who were interviewed, age- and race-matched controls were chosen from New

252 ASSESSING HUMAN EXPOSURE Jersey drivers-license files and from Health Care Financing Administration files for Medicare enrollees. For next-of-kin interviews, matched controls were selected from state death-certificate files. For the 1,306 cases identified, 994 patients or next-of-kin were interviewed; of the 1,449 controls chosen, 995 were interviewed. Some 53% of the interviews were with the patients, and the rest were with next-of-kin. The study began without consideration of indoor radon, and residential housing information had been collected only on the towns in which the sum jects lived. The subjects or next-of-kin were therefore recontacted to obtain street-address information. It was assumed that there is a minimal 10-year latency period between exposure and onset of cancer. Only one house was tested per subject because of resource limitations, so the study focused on subjects who lived for at least 10 years at an address in New Jersey during the period 1953-1972, about 10-30 years before the case diagnosis or control selection. It was found that 17% of the subjects had not lived in New Jersey for at least 10 years dunng 1953-1972 and that 10~o had not lived at any address for at least 10 years during the critical period. In another 2% of the cases, it was not possible to determine specific street addresses. It was possi- ble to obtain addresses for 1,216 subjects that met the criteria. Of those addresses, 82 no longer existed or were dwellings in upper floors of apart- ments, trailers, or other situations in which radon exposure would be expected to be negligible; that left 1,134 addresses. Short-term charcoal-canister meas- urements were made for a quick screening. For a better determination of the annual average concentrations, two alpha-track detectors were deployed in the 1,134 dwellings. In 10% of the dwellings, a third track-etch detector was collocated with one of the other detectors for quality assurance. The Argonne study provides a good example of a potentially useful study design. The study population comprises white females born in Pennsylvania who lived in eastern and central Pennsylvania, excluding Philadelphia and Pittsburgh, and died of lung cancer between 1970 and 1987. Controls will be chosen from white females born in Pennsylvania in the same years as cases, selected by random-digit dialing and random selection from vital statistics. A large number of lung cancer cases are available (more than 6,000 through 19843 in an area where there are likely to be high indoor radon concentra- tions. Separate case series will be defined by histopathological type of lung cancer and by smoking status. The first case series of about 500 cases in- cludes all lung cancers and categories of smokers. For each of the dwellings that the subjects have occupied and that can be identified, both short-term charcoal and long-term track-etch measurements will be made for all levels in the dwellings. When current occupants are willing, two sets of sequential 6-month track-etch samplers will be left and picked up by project personnel,

CURRENT AND ANTICIPATED APP~C4TIONrS 253 to ensure adequate response. Charcoal-canister measurements will be used to screen the dwellings to make preliminary assignments as to radon exposure. When current occupants are not willing to allow measurements, radon concen- tration will be based on the age and construction lope of the dwelling and its geological setting. Although data on a number of dwellings already permit building of a predictive model for indoor radon, the results from the coopera- tive dwellings with occupants win improve the database on which the models are built. The researchers also plan to measure radon-decay product concentrations to assess exposures to radon progeny more directly. There is no apparent plan to measure the radioactive particle size distributions. Thus, it will not be possible to assess the potential for deposition, and the analyses will have to include estimates of the effectiveness of the measured concentrations In pro- ducing specified doses. Measurement Methods Short-term charcoal and long-term track-etch detectors will be used. In both cases, it is assumed that current radon concentrations reflect past radon. If there have not been changes In the insulation, heating system, or general nature of a dwelling, the assumption should be reasonable. However, with the extensive energy-conservation efforts many homeowners made in the late 1970s and early 1980s, many homes might have been modified. Estimation of prior concentrations would then constitute a considerable problem. Another important problem is the concentration of decay products relative to the radon concentration. If, for example, one or more occupants smoked and then quit, indoor particle concentrations might be much lower now than in the past. Higher particle concentrations result In higher decay-product concentrations, but lower the concentrations of more diffusive unattached decay products and thus result in a lower average dose per unit of airborne radioactivity. Similarly, if a gas stove were traded for an electric unit, particle concentrations resulting from cooking would be lower; this could change the effective exposure to decay products. Air cleaners can substantially increase the unattached fraction, so EPA does not recommend the use of air cleaners to mitigate the effects of radon decay products. Models The choice of radon as the measured entity suggests the possibility of an

254 ASSESSING HURON E~OSU~ implicit use of dose models that make the following prediction: the inverse relationship between the concentration of airborne particles, the total decay products, and the unattached fraction cancels out the effects of particle con- centration on dose (James, 1988~. Therefore, exposure can be adequately measured by determining the integrated, average radon concentration. Such calculations have been presented by Vanrnarcke et al. (1985~. The capability to predict indoor radon concentrations Is central to the development of radon exposure models. Considerable effort is being devoted to the development of models of radon entry into houses as a function of soil characteristics (e.g., radium content and permeability), cInnatic conditions, and house characteristics (e.g., substructure type, type of heating system, and air- leakage area). Indoor radon concentrations are predicted by combining the models of radon entry into basements (Loureiro, 1987; Mowris and Fisk, 1988), generally with steady-state, two- or three-dimensional numerical codes that model the convective (pressure-driven) entry of soil gas (containing ra- don) through openings In the substructure. These models are being upgraded at Lawrence Berkeley Laboratory to account for diffusive entry of radon, spatial variability of soil properties, simultaneous transport of soil moisture, and transient effects. A smaller effort has been devoted to the entry of radon into houses with craw! spaces (Mowris and Fisk, 19~) and to the development of simplified closed-form or statistical models (Mowris and Fisk, 1988; Rev- zan, 1989~. None of these models has been adequately validated, although a current experimental effort by Lawrence Berkeley Laboratory should provide critical data on radon entry into basements during the next few years. Advances Both of the large studies discussed here are making direct measurements in at least one of the dwellings occupied by each of many lung-cancer subjects over a long period and thus should yield a reasonable estimate of radon con- centrations to which they have been exposed. In addition, information has been obtained on smoking behavior and mobility to try to account for these strongly confounding variables. The Argonne study will be partially supple- mented by direct measurement of concentrations of radon decay products although the particle size distributions and their potential influence on dose are not explicit parts of either study. New measurement methods have recently been developed that permit the determination of both concentrations and size distributions of radon decay products. The use of single screens in nonconventional diffusion batteries (graded screen arrays) and measurement of the radioactivity that passes

CURRENT AND ANTICIPATED APPLIC4TIOli/S 255 through each screen permit one to obtain size distribution over the range of 0.5-500 rim (Reineking and Porstend~orfer, 1986; Holub and Knutson, 1987; Ramamurthi and Hopke, 1988~. A new system can provide hourly measure- ments of concentrations and size distributions of each decay product, so it is now possible to measure directly the species that are responsible for hearth effects without resorting to assumptions and models (Ramamurthi, 1989~. This system can be used soon to test the variability of concentrations in ~ffer- ent size ranges directly so that a better understanding of the dynamics of inducer radon decay products will be possible.

Next: Glossary »
Human Exposure Assessment for Airborne Pollutants: Advances and Opportunities Get This Book
×
Buy Paperback | $90.00
MyNAP members save 10% online.
Login or Register to save!
Download Free PDF

Most people in the United States spend far more time indoors than outdoors. Yet, many air pollution regulations and risk assessments focus on outdoor air. These often overlook contact with harmful contaminants that may be at their most dangerous concentrations indoors.

A new book from the National Research Council explores the need for strategies to address indoor and outdoor exposures and examines the methods and tools available for finding out where and when significant exposures occur.

The volume includes:

  • A conceptual framework and common terminology that investigators from different disciplines can use to make more accurate assessments of human exposure to airborne contaminants.
  • An update of important developments in assessing exposure to airborne contaminants: ambient air sampling and physical chemical measurements, biological markers, questionnaires, time-activity diaries, and modeling.
  • A series of examples of how exposure assessments have been applied—properly and improperly—to public health issues and how the committee's suggested framework can be brought into practice.

This volume will provide important insights to improve risk assessment, risk management, pollution control, and regulatory programs.

  1. ×

    Welcome to OpenBook!

    You're looking at OpenBook, NAP.edu's online reading room since 1999. Based on feedback from you, our users, we've made some improvements that make it easier than ever to read thousands of publications on our website.

    Do you want to take a quick tour of the OpenBook's features?

    No Thanks Take a Tour »
  2. ×

    Show this book's table of contents, where you can jump to any chapter by name.

    « Back Next »
  3. ×

    ...or use these buttons to go back to the previous chapter or skip to the next one.

    « Back Next »
  4. ×

    Jump up to the previous page or down to the next one. Also, you can type in a page number and press Enter to go directly to that page in the book.

    « Back Next »
  5. ×

    To search the entire text of this book, type in your search term here and press Enter.

    « Back Next »
  6. ×

    Share a link to this book page on your preferred social network or via email.

    « Back Next »
  7. ×

    View our suggested citation for this chapter.

    « Back Next »
  8. ×

    Ready to take your reading offline? Click here to buy this book in print or download it as a free PDF, if available.

    « Back Next »
Stay Connected!