Document dn6kZ9yNBNLyYpOYJZEN71o5R

BFGoodric -i The BFGoodrich Company Geon Vinyl Division 61000ak Tree Boulevard Cleveland, Ohio 44131 216-447-6000 March 9, 1992 Mr. Robert H. Burneltt Executive Director The Vinyl Institute 155 Route 35 West Wayne Interchange p|laza Wayne, NJ 07470 II Dear Mr. Burnett: I am enclosing ano th er example of how the VI research program on HC1 and PVC in p rimates and rodents is helping to claify misconceptions abou t HC1 and ultimately PVC. Because of the VI r esearch and my publications on the toxicity of HC1, I was asked to participate in a workshop on the effects of HC1 in a nbient air. This provided us with an important opportuni ty to insure the accuracy of statements regarding the toxic ity of HC1. As you can see, the author notes on page 77 th at, " ------ the use of rodents in many of these studies has b aen questioned because of anatomical and physiological diffe rences between rodents and humans (Buckley et al. 1984)" and t aat, " ------ rodents differ markedly from primates in their 1 Dwer airway response to HC1. Exposures to high levels of HC1 :ause pulmonary edema in rodents, but not in primates (Kaplan et al., 1988). This difference appears to be due to differenc s in respiratory anatomy and the scrubbing ability of the uppe r airways." He also concludes on p. 80 that " ------ if toxic effects in humans result from ambient exposure they will ae limited to the upper airways. HC1 will probably be effect! /ely scrubbed from the inspired air at these levels of the respiratory system and will not penetrate into the deep lung Ln significant amounts." The first VI publication Kaplan et al. 1988 is listed on p.81. Sincerely, THE BFGOODRICH COMPANY Robert K. Hinderer, Ph. D. Director, Health, Tfc xicology and Product Safety 0309-2/jp cc: Dr. Harold Kaplan Don Knechtges Lou Maresca Mike Marshall Carl Mattia Bill Patient SPI-01372 INSTITUTE FOR ENVIRONMENTAL TOXICOLOGY fttKfl, 4 iffi, MICHIGAN STATE UNIVERSITY February 28, 1992 Robert K. Hinderer, Ph.D. B.F. Goodrich Company Health and Environmentall Sciences 3925 Embassy Parkway Akron, OH 44313-1799 Dear Bob: Thank you again lor participating in the Workshop on the Health Effects of HC1 .n Ambient Air and for your review of the proceedings of this me qting. These contributions were essential for the success of thifc endeavor. For your information, I have enclosed a reprint of t ie final Workshop report. Sincerely yours, Michael A. Kamrin, Ph.D Professor MAK/cm Enc. C-231 Ho) lcn Hall Lasl Lansing. Michigan 48824-1206 Plujnc 517/353-6469 LAX: 5 17/355-4603 MSI' n jn \llirmaiiv< imn/l.quul Of>t*rturtHv ImltiuUfn SPI-01373 REGULATORY TOXICOLOGY AND PHARMACOLOGY 15, 73-82 (1992) Workshop on the Health Effects of HCI in Ambient Air Michael a. Kamrin Institute for Environmental T( xicology, C-231 Holden Hall, Michigan State University, E tst Lansing. Michigan 48824 Received April 3, 1991 This article presents a summary of the proceedings of the Workshop on the Health Effects of HCI in Ambient Air, held in Det^ioit, Michigan, on October 15, 1990. Participants addressed three topic areas: sources, levels id chemistry of HCI in ambient air; toxicity of atmospheric HCI to humans and animals; and th : need for future research on toxicity and exposure. Consensus conclusions related to each of these topic areas, arising form the deliberations of the workshop participants, are presented. These i iclude: (I) atmospheric HCI will most commonly exist in the gaseous form; (2) long-range transpi)rt of HCI is probably of limited importance; (3) ambient HCI levels are in the low parts per billic n range; (4) irritation of the upper airways appears to be the most sensitive indicator of exposure; (5) such effects are likely to occur only at exposure levels much greater than those measured n ambient air, and (6) future health research should focus on occupationally exposed population and potentially sensitive subgroups, e.g., asthmatics. 1992 Academic Press, Inc. INTRODUCTION The objectives of the Workshc p on the Health Effects of HCI in Ambient Air were to evaluate (1) available information about sources, levels, and chemistry of hydrogen chloride in ambient air; (2) cum nt knowledge about the toxicity of atmospheric hy drogen chloride to humans and animals; and (3) the need for future research on the toxicity of and exposure to hydrygen chloride in ambient air. To accomplish this, a group of 32 scientists representin g a variety of disciplines and sectors met for a full day of intensive work on Octobei 15, 1990, in Detroit, Michigan. The Workshop was coordinated by the Institute for Environmental Toxicology, Michigan State University. In preparation for the meeting participants were provided with a number of materials. Included were six articles describing experiments on the health effects of HCI (Malek and Alarie, 1989; Burleig i-Flayer el al., 1985; Hartzell el al., 1988; Kaplan el al.. 1988; Albert el al., 1982; Se lakumar el al., 1985); a summary of the National Research Council (1987) evaluai ion of HCI; and two review articles on the health effects of acid aerosols (Spengler i ai, 1990; Soskolne el al., 1989a). One additional article describing a risk assessment of sulfuric acid (H2SO4) was distributed at the time of the meeting (Rao and Brown, 989). 73 SPI-01374 0273-2.300/02 $5.00 ('opvnghi 'O I'W.? In Academic I'resy Inc. All rights of rcponliK tion in am lorm reserved. 74 MICHAEL A. ICAMRIN The Workshop began w th three presentations to delineate the important health and environmental issues, 'articipants then were divided into smaller groups to facilitate discussion of the nu jor questions. These breakout sessions were structured to identify areas of consensus and those requiring further study. All participants then met as a group to hear sumip:aries of the breakout sessions and discuss the conclusions that were reached. The im dications of the group conclusions for assessing human risk were also addressed duing this final segment of the meeting, This report contains sun maries of each of the formal presentations followed by discussions of the issues rai;s;d in the respective presentations. The discussion sections summarize the views of the participants as expressed in both the breakout and the plenary sessions. In additio 1, the report reflects comments provided by participants subsequent to the Workshop in response to a draft version of this manuscript. While it was not possible to incorp<ofate all comments ofall individuals, this meeting summary reflects the consensus of the participants. HC1 IN AMBIENT AIR Sources and Levels SPI-01375 The first speaker, Gerald Keeler (University of Michigan) discussed sources of HC1, the nature of HC1 emissions md their atmospheric distribution and fate, and concen trations of HC1 in ambient air. The two major sources of atmospheric HC1 are fossil fuel burning and incineratior of domestic and industrial waste (Sturges and Harrison, 1989; Lightowlers and Cape, 988). The fossil fuel of most concern is coal. The amount of HC1 generated from bum ng of coal depends on its chloride content which varies from 0.0029 to 0.095% (Glac ney et al., 1984; Olmez, 1990). The chloride content of fuel oils is generally low, as i: the concentration in gasoline, where chloride is used as a scavenger for lead (Lightowlers and Cape, 1988; Pierson and Brachazek, 1983). The major contributors to the cl lorine content in municipal solid wastes are polyvinyl chloride and paper (Lightow ers and Cape, 1988; Michigan DNR, 1986). The relative contributions of incineration and coal burning can be estimated using information from existing faci ities. A high-capacity resource recovery facility, operating 24 hr a day, 5 days a week, alnd burning 650,000 tons of solid waste (containing 6.5 lb HCl/ton) per year is estim ited to emit uncontrolled emissions of about 2000 tons of HCI/year (Michigan DNR 1986; Brunner, 1985). A high-capacity coal-fired power plant, burning 2,000,000 to is/year of bituminous coal (with an HC1 content of 0.0925%), emits an estimated 1700 tons of HCI/year. Thus, these two types of sources appear to emit roughly equiv dent amounts of HC1 into the air. However, the source type that is the largest contrib utor to HCI in a particular geographical region depends on the amount and type of fu<^l consumed and the control equipment utilized on each facility. In addition to the combust on of coal and solid waste, there are a number of other sources that contribute to H :i in ambient air. These include glass manufacturing, iron-steel manufacturing, the ceramic industry, cement production, the chemical industry. rocket tiring, and natur il sources, e.g., volcanoes and sea salt (National Research Council, 1976; Fenton et al 1980; Clegg and Brimblecombc, 1985). In most areas, these secondary sources contri bute 10% or less to the total HCI emissions (Lightowlers HEALTH EFFECTS OF HC1 IN AMBIENT AIR 75 and Cape, 1988; National Re:search Council, 1976). Some exceptions are found in the states of New Jersey and Wes Virginia, where such sources are more significant (National Research Council, 197^) Environmental Distribution The salient physicochemicc 1 characteristics of HC1 are its high solubility in water, hygroscopic nature, strong reactivity, and complete ionization in solution (Lightowlers and Cape, 1988; National Research Council, 1976, 1987). Thus, the exact form of HC1 in the atmosphere at a particular time and place will depend on atmospheric factors such as humidity and he presence of other constituents. However, from the above physicochemical consid orations, it can be predicted that atmospheric HC1 will most commonly be in the gaseous form. Because of its solubility, H' 71 will rapidly dissolve in cloud water or rain and be i ^sphere. HC1 is a reactive gas and is quickly removed from the atmosphere by almo st any surface. Its dry deposition velocity is probably very similar to that of nitric aaid (HN03) gas and is dependent upon meteorological conditions such as wind speed and vertical temperature profile. Although HC1 may adsorb to inert particles when it is present at high levels and the humidity is high, it desorbs rapidly and is unlikely to be associated with particulates when it reaches the ground. Because of its reactivi y, it may interact with gases such as ammonia (NH3) and be neutralized. As a result of these removal processes, long-range transport of HC1 from the source area is probably of limited importance and significant levels are more likely to be found closer :o the emission source (Lightowlers and Cape, 1988). Environmental Data Few measurements of ambient HC1 concentrations have been reported. Most of the measurements were perforrp ed in Europe during the past decade (Table 1) (Clegg and Brimblecombe, 1985; Pio and Harrison, 1987; Matusca et al., 1984; Ruprecht and Sigg, 1990; Harrison et al., 989; Cadle et al., 1985; Dasch et al., 1989). As shown in Table 1, ambient concentra|tions are generally in the range of 1-100 nmol/m3, equivalent to about 0.025 to 2. ppb or 0.4-4 /xg/m3. Based on these data and physicochemical considerations, it I!. estimated that the maximum HC1 concentrations in locally impacted areas will be fiom 20 to 30 ppb (30-45 /ig/m3). Some higher values have been reported but they are 3pen to question due to the methodological difficulties (Pio and Harrison, 1987; Dascl ctal.. 1989). `There are insufficient data to determine how concentrations vary with time of day, season, source, or area character sties, e.g., urban vs rural settings. There are no measurements relating ambient co tjeentrations to a particular source, and no direct assessments of excursions from t c measured values. These data gaps suggest areas for further study. Analytical Questions SPI-01376 An issue related to the determination of ambient levels ol'HCI is the comparability oflhe different types of measure ttenl techniques. Sampling methods for atmospheric 76 Location/type Maritime/background Europe UK./rural UK/rural UK/urban Switzerland Dubendorf/urban Dubendorf/rural Po River/rural Ljubljana/urban Linz/urban/industrial Wien/urban Dortmund/urban United States N. Michigan/rural South Haven, MI Ann Arbor, MI MICHAEL A. KAMRIN TABLE I Atmospheric Levels of HCI Season Sample duration All Summer All All April 1982 Winter 1985 March 1986 Winter 1986/1987 November 1984 February 1985 Summer 1985 Winter 1983/1984 September-October 1980 Winter 1983/1984 July 1990 \ugust 1990 Weekly 2--4 hr Daily Weekly 1 hr Daily -- -- Daily Daily Daily Daily Daily Weekly 6 hr Daily Concentration range nmol Af3 (ppb) 2-8 (0.05-0.2) 27-82 (0.7-2) 7-50 (0.2-1.2) 15-31 (0.4-0.8) 5-84 (0.1-2) 0.8-82 (0.02-2) 7-37 (0.2-0.9) 4-87 (0.1-2.1) 3-13 (0.07-0.3) 3-11 (0.07-0.3) 6-46 (0.15-1.1) 3-43 (0.07-1) 10-310(0.2-7.6) 2-11 (0.05-0.3) 12-50 (0.3-1.2) 3-54 (0.07-1.3) HC1 must have a quantity tive means for separation of gaseous HCI from aerosols which contain chloride ioi. Furthermore, the sampling efficiency must be constant and independent of sampli ng conditions or there must be provisions for determining sampling efficiencies for ea:h sample. Methods that are commonly used are impingers/bubblers, absorbent tubes (silica gel), filter packs, and diffusii m denuders. Filter packs, diffusion samplers, and denuders are considered the method: of choice and many of the measurements listed in Table 1 were generated using filter packs. Although there are questions about how well this method measures the species of interest, it is preferred since it provides an estimate of the upper bound on ambient concentrations. One study has been performed comparing the filter pack and denuder methods for HCI determinations. This was done in Michigan under winter conditions and showed that the two techniques ga\ e similar values (Dasch et al., 1989). While this result is encouraging, additional comparisons are needed to determine whether this compa rability holds for other site : and other times of the year. In addition, studies of the comparability of these methods with the other two measurement devices, impingers and absorbent tubes, are net ded to assist in the interpretation of data already collected and to decide on the best and most cost-effective technique. Discussion SPI-01377 The question of the appl icability of such ambient measures of HCI to human exposures was raised. The poss blc approaches to exposure assessment include dispersion HEALTH EFFECTS OF HQ IN AMBIENT AIR 77 modeling and personal monit<pri ng. The dispersion modeling approach has one critical drawback in that it assumes tnat HC1 can be treated as a nonreactive gas and this is known to be inaccurate. Thus while such a model may be useful for assessing human exposure over short distances, its predictive power may decrease as distance and dispersion increase. The accuracy of personal monitoring techniques is subject to the same questions raised about the specificity, efficiency, and comparability of the various methods of measuring HC1 levels in ambient air. Available techniques need to be carefully evaluated and calibrated before personal monitoring will be useful for exposure assessments. HC1 AND HUMA HEALTH; EXPERIMENTAL STUDIES Two speakers addressed the effects of acid exposure on human health. The first, Yves Alarie (University of Pittsburgh), reviewed the data collected from experimental studies. These studies show thai the most common toxic reactions are sensory irritation of eye, nose, and throat; coughing; bronchoconstriction; and edema of conducting airways or alveoli. There are very few reported tudies on humans exposed to gaseous HC1 (Lehmann, 1886; Matt, 1889; Lehmann et al., 1908). Matt (1889) concluded that levels above 10 ppm (15,000 /zg/m3) lead to w<o|rk impairment; above 50 ppm (75,000 Mg/m3) to work hindrance; and above 100 ppm (150,000 Mg/m3) to an environment in which work is impossible. It should be emph isized that these results were derived from studies of healthy adult males; no studie: of possibly more sensitive human populations, such as children or individuals wit preexisting pulmonary impairment, have been per formed. A study of human exposure to large HC1 droplets was conducted, but the experiment lacked clear definition of exposure. In addition, the results are relevant to acid fogs only, so that the usefi lness of the work is limited (Fine et al., 1987). Acute studies on animals have been conducted at very high exposure concentrations, generally in the thousands of p< rts per million, so that the results are of questionable relevance to potential human health effects at much lower ambient concentrations (Danner el al., 1974; MacEwei and Vernot, 1974; Hartzell et al., 1985; Kaplan et al., 1985, 1988; Burleigh-Flaye - et al, 1985; Malek and Alarie, 1989). In addition, the use of rodents in many of these studies has been questioned because of anatomical and physiological differences between rodents and humans (Buckley et al., 1984). However, rodents, like primates, exhibit bronchoconstriction when exposed to irritants such as HC1 and the guinea pig has been used as a possible model for this response in humans (Kaplan et al., 1985). It should be noted, however, that rodents differ markedly from primates in their lower airway response to HC1. Exposures to high levels of HC1 cause pulmonary edema in rodents, but not in primates (Kaplan et al., 1988). This difference appears tc be due to differences in respiratory anatomy and the scrubbing ability of the upper airways. There is very little informatio a about long-term effects of HC1 in either humans or animals. One study showed thai a day, 5 days a week, for a lifeti ne, leads to laryngeal hyperplasia (Scllakumar et at.. 1985). This can be considered a owest observed adverse effect level, although it is not known whether this value is din ctly applicable to sensitive human subpopulations. Considering the limited amount of MCI data and similarities in the chemistry of I1C1 and FLSOj. it is useful to qxamine the extensive H.S04 data base to see if it is SPI-01378 78 MICHAEL A. KAMRIN consistent with the result:; of the HC1 experiments. Based on short-term studies of H2S04 exposure in humans, it appears that reversible airways construction occurs at 100-300 ng/rn3 in sensitij/ie individuals (Spengler et al., 1990). Since higher levels of HC1 are needed to pro iuce similar effects, it appears to be a less potent irritant than H2S04. With respect to long-term effects, studies in cynomolgus monkeys indicate that 30 Mg/m3 H2S04 appears to be a clear no effect level and that 300 Mg/m3 is the lowest effect level based on mild issue irritation (Alarie et al., 1975). Converting these concentrations to equivalent tines for HC1 on a molar basis and taking into account the lower potency of HC1 as an irritant, the level of HC1 at which no effects would be expected is between 0.2 arid 2 ppm (300-3000 Mg/m3). These values are not very different from the 10 ppm no effect level reported in human workers and the 10 ppm lowest effect level seen in rodents. Thus, the H2S04 data are consistent with and provide support for the n|o effect level values suggested by the results of the HC1 studies. Discussion Utilizing the above anal} sis in conjunction with available literature, the participants concluded that, even though the data base is meager for both acute and chronic effects, it is possible to provide a good estimate of the no effect level for HC1. Based on the one long-term rodent HC study showing laryngeal hyperplasia and the long-term H2S04 study in monkeys, t|he no effect level in humans is predicted to be between 0.2 and 10 ppm. It was noted that the changes observed in experimental animals at the lowest effect levels were ni inimal and were not accompanied by losses in function (Alarie et al., 1975). No com parable functional studies have been performed in humans, In addition, the participar t:s examined published data from rodent carcinogenicity studies and concluded that there is no evidence that HC1 is a rodent carcinogen (Sel- lakumar et al., 1985; Albeit et al., 1982). It was also evident frorr the discussion that the form of HC1 is critical to the as- sessment of toxicity. If, as suggested by the physicochemical information, HC1 mol- ecules exist in a gaseous 0 r nearly gaseous state in the atmosphere, they will likely become hydrated to a deg|ee when inhaled into the upper airways. The majority of the resultant HC1 micropa 1 tides will be scrubbed or neutralized in the upper airways in humans and thus will n }t be likely to result in significant pulmonary effects. This conclusion is consistent wi h results from studies in baboons which indicate that HC1 does not move past the na< opharyngeal area even when exposure is at high levels, up to 10.000 ppm (Kaplan et ai. 1988). One issue that was not resolved is the possible impact of HC1 on sensitive human subpopulations. Although the most sensitive group is not known, one higher risk subpopulation that has be en identified from H2S04 studies consists of adolescents susceptible to asthma (Ko^ nig et al.. 1989). Studies of effects of HC1 inhalation on adolescent asthmatics mig it provide additional useful information. Such a study is presently underway at the U niversity of Washington (Koenig. 1991). When the results of this research are availalb le, they should help to better assess the potential health effects from HC! exposure. SPI-01379 HEALTH EFFECTS OF HQ IN AMBIENT AIR 79 HC1 AND HUMAN HEALTH: EPIDEMIOLOGICAL STUDIES The second speaker address ng human health concerns, Colin Soskolne (University of Alberta, Canada), summar:zed epidemiological studies of workers exposed occupationally to sulfuric acid. Thpse data were included in the workshop because of the absence of epidemiological ies on the association between HC1 and upper airway effects and because of the simlilarities between HC1 and H2S04 in the experimental studies discussed in the previo|u:s section. In addition to published s(1 t|udies (Soskolne, 1982; Soskolne et ai, 1984, 1989a; Beaumont et al., 1987; Steenhnd et al., 1988), recently completed research has addressed the possible relationship between laryngeal cancer and long-term inhalation of sulfuric acid (Soskolne et al 1989b, 1990). These studies on workers from several industries suggest that long-tern (>25 years), high-level H2S04 exposure is associated with laryngeal cancer. After takjing confounding variables (such as tobacco and alcohol consumption) into account, tl e studies indicate odds ratios in the 4 to 13 range for this type of exposure. Supporting the association, risk was found to decrease as exposure decreased. In addition, by examining tHe pattern of odds ratios as a function of variable length exposure windows dating from first exposure through cancer diagnosis, it was possible to distinguish between total yd;ars of exposure and critical periods of exposure. This analysis suggests that the initial 25 years of high exposures contribute to the cancer incidence and that the 10 yea s prior to the cancer diagnosis contribute less to the effect. Discussion There are no epidemiological studies focusing solely on HC1, but some data were presented from a broad multifi ctorial occupational study suggesting that exposure of workers to 1 ppm (1500 Mg/n: ) of HC1 for 15 years was not associated with lung cancer (Bond et al., 1986). Unfjrtunately, details were not available, particularly with respect to possible effects on th upper airways, so it was not possible to compare this study to the sulfuric acid rese ireh. (Subsequent to the workshop, a more detailed analysis of the study was submitted for publication by Bond.) Even with such information, it appears that additior al epidemiological data are desirable to assess whether there is any association betweer occupational hydrogen chloride exposure and chronic health effects, particularly thosf occurring in the upper airways. The participants also conclud ;d that the relevance ofthe sulfuric acid epidemiological data to HC1 depends on wheth :r the effects noted can be ascribed strictly to acidity, an issue that remains to be reso ved. Even if acidity is the critical factor, there is reason to believe that the effects may be different because sulfuric acid, due to its greater hygroscopicity, will grow to a much larger particle size than hydrogen chloride in humid environments such as t(i e upper airways and thus have the potential to cause greater effects at these sites. CONCLUSIONS SPI-01380 The participants in the Wor<shop were in general agreement about the scientific conclusions described above. They also reached consensus on the implications of these 80 MICHAEL A. KAMRIN conclusions for assessinf the risk of HC1 in ambient air. First, measured levels of HC1 in ambient air are about 1 ppb (0.025-2.5 ppb). These values are at least a few orders of magnitude less than tie approximately 1 ppm (0.2-10 ppm) likely to cause either acute or chronic effects in humans. One area of uncertainty is possible effects on sensitive subpopulations, However, results from studies of H2S04 exposure in sensitive groups suggest that they are only fivefold more sensitive than the general population (Spengler et al., 1990). If these results are applicable to HC1, they suggest that ambient levels are unlikely to cai se effects in such subpopulations. Second, the form of E Cl in ambient air (gaseous or with a very limited amount of hydration) and its physio chemical properties, especially hygroscopicity and reactivity, suggest that even if toxic effects in humans result from ambient exposure they will be limited to the upper airways. HC1 will probably be effectively scrubbed from the inspired air at these levels of the i espiratory system and will not penetrate into the deep lung in significant amounts, t mother conclusion from physicochemical considerations is that human exposures wi 1 be limited in both time and space due to the transport and fate properties of HC1 in ambient air. Third, based on the li nited geographical distances HC1 is transported, it is clear that it is not a significani contributor to acid rain. However, in local areas, it could have environmental and economic impacts, such as corrosion. More careful exami nation of local movemen t of HC1 is needed to assess the extent of such impacts. In terms of future wo k, the consensus of the group was that additional health research should focus on jpidemiological studies of exposed workers and of sensitive subpopulations. More environmental research is needed to quantify atmospheric HC1 levels and determine their daily and seasonal variability. This work should include attempts to assess impacls of individual sources on ambient air concentrations. As part of this research, stud es of the reliability and comparability of the four different measurement techniques--impingers/bubblers, absorbent tubes, filter packs, and dif fusion denuders--should oe undertaken. In summary, the partici pants were able to reach general agreement about the levels of HC1 expected in ambie it air and the doses and types of adverse effects expected in to such levels. The participants also identified additional areas of research that might provide additional useful information about HC1 toxicity in humans. ACKNOWLEDGMENTS The Workshop was made poss i ble by the generous support provided by ABB Resource Recovery Systems; Air and Waste Management Asi>ciation, Michigan Chapter, East Central Section; Air Quality Division, Michigan Department of Naturtl Resources; American Lung Association of Michigan: American Lung Association of Southeastern Micqigan; Council on Environmental Quality. Michigan Department of Public Health: Michigan Manufacturers \ssociation; and Roy F. Weston, Inc. The author would also like to express his appreciation for the valuable contributions of the other members of the organizing committee: Dean Branson, Dow Chemical Compan r Lawrence J. Fischer, Michigan State University; RolfHartung, University ofMichigan; Bruce Peirano, US. I nvironmenlal Protection Agency; Alex Sagady, American Lung Association of Michigan; Catherine Simon, Michigan Department of Natural Resources; and Peter Warner. Wayne County (Michigan) Department ( f Public 1 Icalth. REFERENCES SPl-01381 At aril, Y. C., KlttiMM, A. A.. Lust v, W. M.. Ut rich. C. and Kaniy, R. J.. 11 (N75). Long-term ex|xisure to sulfur dioxide, sulfuric acid mist, fly ash, anil their mixtures. Arch h.'iictrun Health .10, 254- HEALTH EFFECTS OF HQ IN AMBIENT AIR 81 Albert, R. E., Sellakumar, A. R., I .askin, S,, Kuschner, M,, Nelson, N,, and Snyder, C. A. (1982). Gaseous formaldehyde and hydroge n chloride induction of nasal cancer in the rat. JNCI 68(4), 597-603. Beaumont, J. J., Leveton, J., Kno<, K., Bloom, T,, McQuiston. T., Young, M., Goldsmith, R., Steenland, N. K., Brown, D. P. and Halperin, W. E. (1987). Lung cancer mortality in workers exposed to sulfuric arid mist and ot ter acid mists. JNCI 79, 911 -921. Bond, G. G., Flores, G. H., ShellL INBERGER, R. J., CaRTMILL, J. B., FlSHBECK, W. A., AND COOK, R. R. (1986). Nested case-control st idy of lung cancer among chemical workers. Am. J. Epidemiol. 124, 53-66. r Emissions from Incineration. Chapman & Hall, New York. Buckley, L. A., Jiang, X. Z,, James R. A., Morgan, K. T., and Barrow, C. S. (1984). Respiratory tract lesions induced by sensory irrit mts at the RD50 concentration. Toxicol. Appl. Pharmacol. 74, 417- 429. Burleigh-Flayer, H., Wong, K. L,, vnd Alarie, Y. (1985). Evaluation of the pulmonary effects of HC1 using C02 challenges in guinea pigs. Fundam. Appl. Toxicol. 5, 978-985. Cadle, S. H., Dasch, J. M., and Mul wa, P. A. (1985). Atmospheric concentrations and the velocity to snow of nitric acid, sulfur dioxide, ard various particulate species. Atmos. Environ. 19, 1819-1827. Clegg, S. L., and Brimblecombe, F. (1985). Potential degassing of hydrogen chloride from acidified sodium chloride droplets. Atmos. Em iron. 19, 465-470. Darmer, K. I., Jr., KjnkeaD, E. R., an ) DiPasquale, L. C. (1974) Acute toxicity in rats and mice exposed to hydrogen chloride gas and aerosols Am. Ind. Hyg. Assoc. J. 35, 623-631. Dasch, J. M., Cadle, S. H., Kenneey, K. G., and Mulawa, P. A. (1989). Comparison of annular denuders and filter packs for atmosph:ric sampling. Atmos. Environ. 23, 2775-2782. Fenton, D. L., Purcell, R. Y., Hrdin a, D.. and Knutson, E. O. (1980). The washout of combustion-- hydrogen chloride. Atmos. Environ. 1<;, 1055-1062. Fine, J. M., Gordon, T., Thompson, (. E., and Sheppard, D. (1987). The role of titratable acidity in arid aerosol-induced bronchoconstrict on. Am. Rev. Respir. Dis. 135, 826-830. Gladney, E. S,, Burns, C. E., Perrin, D R,, Roselandts, I., and Gill, T. E. (1984). The 1982 Compilation ofElemental Concentration Data for N BS Biological. Geological, and Environmental Standard Reference Materials. NBS Special Publication 26 )-88. Harrison, R. M., Rapsomankjs, S., an d Turnbull, A. (1989). Land-surface exchange in a chemically- reactive system. Surface fluxes of HNC 3, HC1, and NH3. Atmos. Environ. 23, 1795-1800. Hartzell, G. E., Packham, S. C., Gra: id, A. F,, and Switzer, W. G. (1985). Modeling of toxicological effects of fire gases. III. Quantification o: post-exposure lethality ofrats from exposure to HC1 atmospheres. J. FireSci. 3, 195-207. Hartzell, G. E., Grand, A. F,, and Switzer, W. G. (1988). Modeling of toxicological effects of fire gases. VII. Studies on evaluation ofani nal models in combustion toxicology. J. Fire Sci. 6, 411-431. Kaplan, H. L., Grand, A. F., Switzer, IV. G., Mitchell, D. S., Rogers, W. R., and Hartzell, G. E. (1985). Effects of combustion gases onscape performance of the baboon and the rat. J. Fire Sci. 3, 228- 244. Kaplan, H. L., Anzueto, A., Switzer, \ f. G,, and Hinderer, R. K. (1988). Effects of hydrogen chloride on respiratory response and pulmonary unction of the baboon. J. Toxicol. Environ. Health 23, 473-493. Koenig, J. Q. (1991). Private communica Jon. Koenig, J. Q., Covert, D. S., and Pierson, W. E. (1989). Effects of inhalation of acidic compounds on pulmonary function in allergic adolescent subjects. Environ. Health Perspect. 79, 173-178. Lehmann, K. B. (1886). Experimental st idies on the influence of technical and hygienically important gases and vapours on the organism. Pats I and II. Ammonia and hydrogen chloride gas. Archiv. fur Hygiene 5, 1 -- 125. Lehmann. K. B.. Wilke, J.. Yamada, J., and Wiener, J. (1908). New investigations on the quantitative absorption of some poisonous gases by ani nals and humans via the respiratory tract and its parts. Ammonia, hydrochloric acid, sulphurous acid, accti : acid, and carbon disulphide. Archiv fur Hygiene 67, 57- lOu. Lightowlers. P. J., and Cape, J. N. (1981) Sources and fate of atmospheric HC1 in the U.K. and Western Europe. Atmos Environ 22, 7-15. MacUwen, J. D., and Vernot, E. H. (I< 74). The determination of the 60-minutc LC50 for hydrogen chloride in rodents. In Toxic Hazards Res. arch Unit Annual Technical Report, 1974, pp. 124-128. AMRL- TR-74-78. U S. Aerospace Medical Reser rch Laboratory, Wrighl-Pattcrson Air Force Base, Ohio. Mali k. D. E.. and Alarm;. Y. (19X9). Er;;ometer within a whole-body picthysmograph to evaluate per- lormanee of guinea pigs under toxic alim spheres. Toxicol Appl Pharmacol 101, .140-155. SPI-01382 82 MICHAEL A. KAMRIN Matt, L. (1889) Experimental' Beitrage zur Lehre von der Entwicklung Giftiger Gase aufden Menschen. Doctoral dissertation, Univer litat Wurzburg. Matusca, P., Schwartz, B., a jd Backman, K. (1984). Measurements ofdiumal concentration variations of gaseous HC1 in air in the s ibnanogram range. Atmos. Environ. 18, 1667-1675. Michigan Department of Natunl Resources Air Quality Division (Michigan DNR) (1986). Staff Activity Report (April). National Research Council (197 5). Chlorine and Hydrogen Chloride. National Academy of Science, Wash ington, DC. National Research Council (198 t). Emergency and Continuous Exposure Guidance Levels for Selected Air borne Contaminants. Vol. 7, At nmonia, hydrogen chloride, lithium bromide, and toluene. National Academy Press, Washington, DC. Olmez, I. (1990). Personal Communication toG. J. Keeler. Pierson, W. R., and Brachaz :k, W. W. (1983). Particulate matter associated with vehicles on the road. Aerosol Sci. Technol. 2, 1-40. Pio, C. A., and Harrison, R. vL (1987). The equilibrium of ammonium chloride aerosol with gaseous hydrochloric acid and ammonia under tropospheric conditions. Atmos. Environ. 21, 1243-1246. RaO, H. V., and Brown, D. R. (1989). "Sulfuric Acid Particle Levels and Potential Inhalation Effects-- A Quantitative Approach." Pre: ented before the Division of Environmental Chemistry, American Chemical Society, Miami, Florida, Septe Tiber 10-15, 1989. Ruprecht, H., and SlGG, L. (I( 90). Interactions of aerosols (ammonium sulfate, ammonium nitrate and ammonium chloride) and gase i (HC1, HN03) with fogwater. Atmos. Environ. A 24, 573-584. Sellakumar, A. R,, Snyder, C A., Solomon, J. J., and Albert, R. E. (1985). Carcinogenicity of form aldehyde and hydrogen chloric e in rats. Toxicol. Appl. Pharmacol. 81, 401-406. Soskolne, C. (1982). Upper Re: piratory Cancer among Refinery and Chemical Plant Workers: A CaseControl Study in Baton Rougt, Louisiana. Ph.D. dissertation, University of Pennsylvania, University Microfilms International. Soskolne, C., Zeighami, E,, Ha nis, N,, Kupper, L., Herrman, N., Amsel, J., Mausner, J., and Stellman, J. (1984). Laryngeal canc er and occupational exposure to sulfuric acid. Am. J. Epidemiol. 120(3), 358-369. Soskolne, C. L., Pagano, G., Cipollaro, M., Beaumont, J. J., and Giordano, G. G. (1989a). Epi demiologic and toxicologic evi< lence for chronic health effects and the underlying biologic mechanisms involved in sub-lethal exposure! to acidic pollutants. Arch. Environ. Health 44(3), 180-191. Soskolne, C, Jhangri, G., Burch, D., Howe, G., Siemiatyckj, J., Lakhani, R., and Miller, A. (1989b). "Laryngeal Cancer an 1 Occupational Exposure to Sulfuric Acid: A Case-Control, Augmented Secondary Analysis." Presentee before the Society for Epidemiologic Research, Birmingham, Alabama, June 1989. Soskolne, C., Jhangri, G., Ch eckoway, H., Risch, H., Siemiatyckj, J,, Lakhani, R,, Burch, D., Howe, G., and Miller, A. (19 0). "Sulfuric Acid Exposure in Laryngeal Cancer Induction and Latency Estimates from a Lagged Expose re Window Analysis." Presented before the International Epidemiological Association XII Scientific Meet ng, Los Angeles, CA, August 5-9, 1990. Spengler, J. D., BraUER, M., a'JD Koutrakis, P. (1990). Acid air and health. Environ. Sci. Technol. 24(7), 946-956. Steenland, K., Schnorr, T,, Beaumont, J,, Halperin, W. E., and Bloom, T. (1988). Incidence of laryngeal cancer and exposure to acid mists. Br J Ind. Med. 45, 766-776. Sturges, W. T,, and Harrison, R. M. (1989). The use of nylon filters to collect HCl: Efficiencies, inter ferences and ambient concentra ions. Atmos. Environ. 23, 1987-1996. Woolley, W. D. (1971). Decomr ositiort products of PVC for studies of fires. Br. Polym. J. 3, 186-193. SPI-01383