Corresponence EHP 101-1

Superfund and Public Health Policies: An ATSDR Response

We read with interest the article "Public Health Policies Regarding Hazardous Waste Sites and Cigarette Smoking: An Argument by Analogy" by Legator and Strawn (p. 8). The article raises a number of important points regarding the characterization of health risks presented by hazardous waste sites. In particular, the article argues that government policies and public health practice pertaining to hazardous waste sites should somehow be developed and pursued in ways analogous to how public health agencies have reacted to the health hazard of cigarette smoking. For reasons described in this letter, we differ with Legator and Strawn's arguments on two counts: 1) they are misinformed about how federal agencies are dealing with the health threats posed by hazardous waste sites, and 2) their proposed analogy between cigarette smoking and hazardous waste sites strikes us as being inadequate.

Turning first to the authors' attempt to develop an analogy between cigarette smoking and hazardous waste sites, it is not at all obvious to us that such a comparison can be made. We agree with Legator and Strawn that cigarette smoke contains a complex mixture of toxic substances, and acknowledge, based on our agency's experience, that some toxic waste sites release complex mixtures of substances into the environment. However, it is not true that exposure scenarios between cigarette smoking and hazardous waste sites are comparable. For example, unlike cigarette smoke, hazardous waste sites contaminate multiple environmental media in addition to air (1). Further, the degree of exposure can be vastly different, depending on such factors as proximity to hazardous waste sites, routes of exposure, and lifestyle, including smoking behaviors.

We also have difficulty in comparing the situation of cigarette smoking to hazardous waste sites because of the disparity in scientific knowledge. Considerable investment has been made in studying the toxicology of cigarette smoke constituents and the epidemiology of health consequences of smoking. In contrast, as pointed out by the National Research Council (2), there are an inadequate number of epidemiologic (and we would add toxicologic, as well) investigations pertaining to the health effects of hazardous wastes. Given the disparity in scientific data, how can meaningful comparisons between cigarette smoking and hazardous waste sites be made--especially if such comparisons, as argued by Legator and Strawn, are to be forged into public health policies?

Legator and Strawn's central thesis seems to be "The role of the public health agencies should be to identify those persons exposed to the compounds of concern. Having done so, the role of the regulatory agencies should be to eliminate the source of exposure or to relocate those persons exposed. No further assessment of the health risks is needed (our emphasis)." As the principal federal public health agency tasked under the Comprehensive Environmental Response, Compensation, and Liability Act (commonly called Superfund) with determining and acting upon the effects on human health of hazardous wastes, the Agency for Toxic Substances and Disease Registry (ATSDR) is centrally involved in making the kinds of determinations advocated by Legator and Strawn. Legator and Strawn seem to suggest that current practices by EPA and ATSDR somehow differ from their central thesis. In fact, both federal agencies give special emphasis to assessing the potential of current community exposures to hazardous substances released from waste sites as well as places where emergency releases of hazardous substances have occurred. Where site conditions require, current exposures of concern are mitigated through such actions as restricting access to the site, providing alternative sources of drinking water, conducting emergency removal actions, and relocating people. Under Superfund, all of these actions have been employed by EPA, where necessary, to interdict current exposures of communities to hazardous substances released from waste sites.

We are in full agreement with the philosophical linchpin of public health practice regarding environmental hazards: prevent exposure to the hazard and thereby prevent any adverse health effects. Having said this, one is confronted with very difficult questions in terms of implementing this philosophy. How do you measure or assess exposure (especially in light of limited scientific knowledge regarding uncertainties in bioavailability and a paucity of biomarkers for most hazardous substances)? What analytic means to assess exposure are available to the public health official? When measured or assessed, how much exposure constitutes a potential health hazard? And what should be done in situations where there is information about past environmental exposures that have been interdicted? (Are there latent health effects that should be of concern to the health agency?) At the heart of these questions is how to assess or measure human exposure to toxicants in the environment.

It is ATSDR's position that exposure assessments should usually commence with an evaluation of environmental contamination levels (including an assessment of the adequacy of such data), coupled with an assessment of potential exposure pathways. From this analysis, ATSDR will conduct human exposure measurements or derive plausible estimates where that course of action is beneficial, if methods exist for measuring or estimating the levels of toxicants of concern (3). To advance the science of biological markers for use in exposure assessments, ATSDR has also supported a long-term program of work at the National Research Council. From this effort with the National Research Council have come a number of significant recommendations on biomarkers for the following toxic endpoints: reproductive, pulmonary, neurobehavioral, and immune function (4). The ATSDR is currently implementing these recommendations in its program of epidemiological investigations of communities around hazardous waste sites and other areas of pollution.

ATSDR's approach to determining who is, or has been, exposed to hazardous substances released from waste sites and other contaminated areas is contained in its public health assessment, which is an evaluation of environmental contamination data, health effects information, and community health concerns in order to determine the hazard posed by individual waste sites (5). Concerning Legator and Strawn's comment about the quality of ATSDR's health assessments, the Agency acknowledges that our public health assessments of individual waste sites were of uneven quality during a period of time when we were under severe resource constraints (6,7). However, independent peer reviews of a statistical sample of recent public health assessments, together with guidance from the ATSDR Board of Scientific Counselors, indicate ATSDR's health assessments have been improved and are of good quality. Moreover, the public health assessments of Superfund sites conducted by ATSDR and 24 state health departments have been developed into a practical instrument that points health agencies toward those public health actions (e.g., exposure assessments, epidemiologic investigations, exposure registries, surveillance) that should be pursued in communities. Even with the efforts to measure exposure, the important question about latent, adverse health effects remains unanswered. As public health professionals in environmental health committed to protect the health of communities living near hazardous waste sites, we therefore strongly disagree with the authors' statement that "No further assessment of the health risks is needed."

Legator and Strawn also make two other points to which we wish to respond. They state "If information on each site were available in sufficient detail, populations from exposed communities could be aggregated or combined. Unfortunately, the data that would help determine the multiple sites for which similar effects could be anticipated does not yet exist." The ATSDR agrees with the approach of combining populations from sites with reasonably common characteristics; this is the exact approach taken in our National Exposure Registry program (8). As an example, the ATSDR Subregistry of Persons Exposed to Trichloroethylene consists of a registry of about 5000 persons in 13 communities. Chemical-specific exposure subregistries provide ATSDR with health information on persons with common chemical exposures and also provide a means for communicating health information back to the registrants.

In addition, more recently, ATSDR has developed the database necessary to combine site-specific information. The database is called HazDat. It contains all the environmental contamination, toxicology, and human health effects data from about 1300 Superfund sites. Recently, in conjunction with four state health departments, we conducted a study of lead exposure and toxicity in four different populations that were identified through use of HazDat. We anticipate releasing HazDat to the public later this year.

Ascertaining the dangers to public health of hazardous waste sites, together with implementing public health actions to protect against the effects of hazardous substances, is a challenging responsibility. The ATSDR's public policies and public health practices must be based on sound scientific principles and data. This must involve the communities affected by releases from waste sites and other sources of hazardous substance releases. We believe the statutory mandates in the Comprehensive Environmental Response, Compensation, and Liability Act that bear on public health are consistent with sound public health practices. The translation of these mandates into actions, to some extent in ways inferred by Legator and Strawn, is ATSDR's challenge. We believe we have made progress, but much awaits.

Barry L. Johnson
Assistant Surgeon General
Assistant Administrator,
Agency for Toxic Substances and Disease Registry

Maureen Lichtveld
Assistant Director for Public Health Practice
Division of Health Assessment and Consultation
Agency for Toxic Substances and Disease Registry

References

1. Susten AS. Findings from ATSDR's health assessments. J Environ Health 55:17- 21(1992).

2. National Research Council. Environmental epidemiology: public health and hazardous wastes. Washington, DC: National Academy Press, 1991;7-8.

3. Johnson BL. A precis on exposure assessment. J Environ Health 55:6-9(1992).

4. Johnson BL, Jones DE. ATSDR's activities and views on exposure assessment. J Exp Anal Environ Epidemiol (suppl 1): 1-17(1992).

5. Agency for Toxic Substances and Disease Registry. Public health assessment guidance manual. Chelsea, Michigan: Lewis Publishers, 1992.

6. U.S. GAO. Public health assessments--incomplete and of questionable value. Washington, DC: U.S. Government Accounting Office, 1991.

7. ATSDR. ATSDR's response to the GAO report on health assessments. Atlanta, Georgia: Agency for Toxic Substances and Disease Registry, 1991.

8. ATSDR. Policies and procedures for the National Exposure Registry. Atlanta, Georgia: Agency for Toxic Substances and Disease Registry, 1987.

Industrial Sources of Benzene Exposure

[Citation in PubMed] [Related Articles]

In volume 82 of EHP, Wallace presented some of the results of the EPA's Total Exposure Assessment Methodology (TEAM) study in an attempt to identify the major sources of exposure to benzene (1). He contended that the results showed ". . . that personal activities or sources in the home far outweigh the contribution of outdoor air to human exposure to benzene" (1: 166). Two tables of statistical data were presented to demonstrate this point.

We have previously commented on the severe problems affecting the benzene data for New Jersey (2) and on the confounding effects of the apparent inversion that occurred concerning the data for Los Angeles, California (1: Tables 1 and 2; LA1). We believe that further comment is necessary regarding the North Carolina and Baltimore, Maryland, data, which are reported in the Wallace paper.

The North Carolina data presented in Wallace's Table 1 do not have an outdoor counterpart in Table 2. The reason for this is that only six fixed-site outdoor samples were obtained (3). The arithmetic mean benzene concentration of those six samples was about 19 µg/m³ for both day and night, or about twice the level found in the personal air samples (4). However, neither personal exposures nor outdoor levels of benzene in North Carolina should have appeared in the paper because of the extremely high and variable levels of benzene contamination on the Tenax sampling medium. The contamination was 193 ± 216 ng benzene/tube for both personal and outdoor air samples. Regarding this contamination, the EPA report (5) says "The benzene determinations should also be viewed with suspicion. . ." We agree and believe that none of the North Carolina data should be used to draw major conclusions.

The Maryland data shown in Table 1 of Wallace's paper represents only half of the available data from that portion of the study. Wallace reports here data from the segment of the study that was downwind of an industrial district. Another segment of the study, equal in size, from an area upwind of potential industrial sources has apparently not been reported except in the final report prepared for EPA (6). Table 1 compares data from the upwind segment of the study to data from the downwind segment of the study. Outdoor benzene levels are not reported because they were obtained by a different sampling technique.

There is no serious question about the values from the second group of data from Los Angeles (LA2) and from Antioch-Pittsburg, California (AP), but subsequent comments and conclusions regarding benzene exposure or breath differences should be reconsidered based only on results from the remaining total of 30 smokers and 89 nonsmokers. These remaining subjects can hardly be considered to be representative of the U.S. population.

The correlations between passive smoking and benzene are very weak. This weakness is further demonstrated in another EPA report (7) that shows when the New Jersey and the California data for matched indoor and outdoor samples are regressed, only the first group of data for Los Angeles (LA1) show a significant correlation with the presence of a smoker in the home, and then only with p = 0.1 (probability that a smoker in the home was a significant variable). A later study conducted in Los Angeles (8), continuing primarily with the same homes at two different times of the year, was unable to show a significant difference between benzene in the air in the homes of smokers and those of nonsmokers. This result held true regardless of the season, the time of day, and the area of the house that was studied. What this later study did show was that the location of the outside samplers was important because there was not a good correlation between fixed or area samples and individual samplers located outside homes. This implies that the location of individual samples outside of homes is critical. We know of no published work in which this variable has been studied. Hence, when examining earlier data, the emphasis should be on matched indoor-outdoor results, and even then one should not be overly confident in the results.

Wallace's Figure 2, which compares West German data to U.S. data, appears to contain an error. Krause et al. (9) give the concentrations of benzene in West German homes as 9.3 and 6.9 µg/m³ for smoking and nonsmoking, respectively, not 11 and 6.5 µg/m³ as quoted by Wallace. We are also suspicious of the practice of comparing two different statistics, i.e., U.S. geometric means and West German medians.

We are aware of the breath levels of benzene in self-reported work exposure as discussed by Wallace et al. (10). Those results, obtained by the TEAM study in New Jersey when exhaust fumes infiltrated the van containing the spirometer, indicated that nonsmokers exposed to passive smoke more than 50% of the time at work could probably reduce their exposure by becoming smokers! Neither the experimental conditions during the New Jersey study nor the finding about the equivalent workplace exposure to benzene inspires much faith in the passive smoking conclusions from the TEAM study.

Readers with a need to incorporate the results of the TEAM study into their own findings would be well advised to critically review all of the TEAM study reports to determine when problems detracted from the significance of the study's conclusions and to what extent this occurred. Some important unanswered questions remain regarding the true impact of proximity to industrial sources, the potential for indoor sinks to ballast the effects of outdoor concentrations of benzene, whether smokers and nonsmokers have different lifestyles, and how representative these data are of the subjects' average day. Until these questions can be answered more conclusively, one can put little faith in risk analyses that use TEAM data.

We contend that the problems enumerated above invalidate the benzene exposures and risks shown in Wallace's Table 3. In addition to the problems with the appropriateness of the bases for the numbers in the calculations, examination of the numbers used in the exposure budget and risk analysis reveals some contradictory and unsupportable assumptions. For example, the text appears to say that two-thirds of the population are passive smokers, which we take to be 160 x 10⁶ individuals. The footnotes to Table 3 imply that 80% of the population is exposed to environmental tobacco smoke, which we take to be 190 x l0⁶. Table 3 claims a population at risk of 200 x 10⁶. Footnote c of Table 3 and the text imply that the average increase in benzene due to environmental tobacco smoke is 3 µg/m³ for 17 hr spent at home and at work. But the data in the EPA report indicated that there was essentially no difference between the homes of smokers and nonsmokers in the second Los Angeles and Antioch-Pittsburg studies (10), and these are the only data not subject to serious questions. Finally, the variables presented in Wallace's Table 3 are not independent. The 53 x 10⁶ smokers must be contained within the 200 (?) x 10⁶ passive smoker population.

Donald D. Rosebrook
EndoEnvironment, Inc.
Prairieville, LA

George H. Worm
Pel, Inc.
Baton Rouge, LA

References

1. Wallace LA. Major sources of benzene exposure. Environ Health Perspect 82:165- 169(1989).

2. Rosebrook DV, Worm GH. Personnel exposures, indoor-outdoor relationships, and breath levels of toxic air pollutants measured for 355 persons in New Jersey (letter to the editor). Atmos Environ (in press).

3. Pellizzari ED, Perritt R, Hartwell TD, Michael LC, Sheldon LS, Sparacino CM, Whitmore R, Leninger C, Zelon H, Handy RW, Smith D, Wallace LA. Total exposure assessment methodology (TEAM) study: Elizabeth-Bayonne, New Jersey; Devils Lake, North Dakota; and Greensboro, North Carolina, vol 2, EPA 600/G87/002b. Washington, DC: U.S. Environmental Protection Agency, 1987;662.

4. Pellizzari ED, Perritt R, Hartwell TD, Michael LC, Sheldon LS, Sparacino CM, Whitmore R, Leninger C, Zelon H, Handy RW, Smith D, Wallace LA. Total exposure assessment methodology (TEAM) study: Elizabeth-Bayonne, New Jersey; Devils Lake, North Dakota; and Greensboro, North Carolina, vol 2, EPA 600/G87/002b. Washington, DC: U.S. Environmental Protection Agency, 1987;appendix BB.

5. Pellizzari ED, Perritt R, Hartwell TD, Michael LC, Sheldon LS, Sparacino CM, Whitmore R, Leninger C, Zelon H, Handy RW, Smith D, Wallace LA. Total exposure assessment methodology (TEAM) study: Elizabeth-Bayonne, New Jersey; Devils Lake, North Dakota; and Greensboro, North Carolina, vol 2, EPA 600/G87/002b. Washington, DC: U.S. Environmental Protection Agency, 1987;270-272.

6. PEI Associates, Inc. Baltimore total exposure assessment methodology (TEAM) study. Final report prepared for EPA under contract no. 68-02-4406. Research Triangle Park, North Carolina:U.S. Environmental Protection Agency, 1988.

7. Wallace L. The total exposure assessment methodology (TEAM) study: summary and analysis, vol 1, EPA 600J6-87/002a. Washington, DC: U.S. Environmental Protection Agency, 1987;appendix B.

8. Pellizzari ED, Michael LC, Perritt K, Smith DJ, Hartwell TD, Sebestik J. Comparison of indoor and outdoor toxic air pollutant levels in several southern California communities. Final report prepared for EPA under contract no. 68-02-4544. Research Triangle Park, North Carolina:U.S. Environmental Protection Agency, 1989.

9. Krause C, Mailahn W, Nagel R, Schulz, Seifert B, Ulrich D. Occurrence of volatile organic compounds in the air of 500 homes in the Federal Republic of Germany. In: Indoor air '87: proceedings of the fourth international conference on indoor air quality and climate, vol 1. Berlin:Institute for Water, Soil and Air Hygiene, 1987;102-106.

10. Wallace LA, Pellizzari E, Hartwell TD, Perritt R, Ziegenfus R. Exposures to benzene and other volatile compounds from active and passive smoking. Arch Environ Health 42: 272-279 (1987).

Cigarettes: Point Source for Benzene Exposure?

In their letter, Rosebrook and Worm erroneously state that Tables 1 and 2 of my article in volume 82 of EHP (1) include values from the second batch of samples from New Jersey (which were taken in the summer of 1982). However, footnote a of Tables 1 and 2 clearly indicates that these values are for the fall of 1981. No data from the summer of 1982 are included in either table.

Rosebrook and Worm refer to the "confounding" effect of the inversion affecting the first group of Los Angeles, California, data. Such inversions, however, are fairly common in Los Angeles in the winter months, and any estimate of exposure must include both high and low exposure seasons. We made a return visit to Los Angeles in 1987 (2,3) and observed similar differences between high winter and lower summer exposures (Table 1).

The Maryland data (4) were collected by two contractors using two different sampling techniques (Tenax and evacuated canisters). I chose to report only the data collected by the same sampling technique and the same contractor as in all other TEAM studies, in the belief that these data would be the most comparable to data from other cities. However, because Rosebrook and Worm dispute the central finding of increased personal and indoor exposures compared with outdoor exposures, it is appropriate to compare indoor values collected with the canister to outdoor values collected with the canister (Table 2). These data, like those from the Tenax samplers, showed increased indoor values compared to outdoor.

It is unclear why Worm brings up the additional Maryland information only to then suggest discarding both it and the original Maryland data.

The North Carolina data are indeed more uncertain than the remaining data due to high and variable background contamination of benzene. If the North Carolina data are removed, the conclusions of the paper would be based on a total of about 600 different persons instead of about 620 and would be unchanged. Because all of these persons were selected on a probability basis to represent much larger populations, the total population represented is about 600,000 persons, even without the 130,000 residents of Greensboro, North Carolina.

Rosewood and Worm state that ". . .important unanswered questions remain regarding the true impact of proximity to industrial sources. . ." The New Jersey study involved 350 persons, many of whom lived close (<1 km) to major petroleum refining and petrochemical facilities, and many others lived farther away. No difference in exposure of the two groups was evident. For both groups, personal exposures were approximately triple the outdoor concentrations, putting a stringent upper limit on the portion of exposure that could be provided by the nearby industrial sources. Both the Los Angeles and Antioch-Pittsburg, California, locations were selected for proximity to major petroleum refining operations, and again no impact of these facilities on personal exposure could be discerned.

Recently, one additional large-scale personal monitoring study in Valdez, Alaska (5) has come to a similar conclusion: the single major source in that community (a pipeline terminal facility) contributes about 90% of the benzene emissions in that area but contributes only about 10% of residents' exposure to benzene. That estimate was based on a tracer gas emitted from the facility, providing additional objective evidence for the conclusion. The Valdez study also found that indoor sources and personal activities accounted for the majority of personal exposure to benzene, concluding that its findings confirm those of the TEAM studies.

Rosewood and Worm state that the correlations between passive smoking and benzene are weak, quoting from a table based on a subset (about one-quarter) of the available data. However, when all the data are included in the regressions, much stronger correlations are noted. Tables A-1 and A-2 of Wallace (6) show that the 258 New Jersey residents with one or more smokers in their homes had about double the daytime benzene personal air concentrations (p <0.0006) and about a 68% increase in their overnight benzene personal air concentrations (p<0.006) compared to the 90 persons with no smokers in their homes. Table A-11 shows a similar increase (about 50%) in the February 1984 overnight benzene personal air concentrations for the Los Angeles residents with a smoker in the home (p<0.001). The increase was not observed in California homes in May and June of 1984; however, windows in these homes were generally left open for ventilation and therefore had high air exchange rates, reducing the concentration of benzene in indoor air. I have discussed the relationship of benzene to active and passive smoking in greater detail elsewhere (7).

The median values for smoking and nonsmoking homes quoted by Rosewood and Worm from Krause et al. (8) were based on only 230 of the 488 homes eventually monitored. The values used in my paper (1) were based on the full 488 homes. Geometric means in the TEAM studies have consistently been very close to median values, as would be expected for log-normally distributed data, and as can be seen in the accompanying tables.

The estimates of the number of passive smokers were indeed inconsistent, ranging from 160 to 200 million. This number includes active smokers because all active smokers are also passive smokers, breathing increased benzene from their own sidestream smoke. If the lower figure were accepted, the estimated nationwide benzene exposure budget would be lowered by about 1%. In view of the increasing restrictions on smoking in the workplace and in public facilities, a still lower estimate of the number of passive smokers might be appropriate today.

If we omit the breath measurements for New Jersey, which may have been elevated for both smokers and nonsmokers, the mean breath levels measured at other locations are remarkably consistent at about 12-14 µg/m³ for smokers and 1-2 µg/m³ for nonsmokers. It is impossible to observe these data without concluding that smoking is the most powerful single source of exposure to benzene for many millions of persons.

Lance Wallace
U.S. Environmental Protection Agency