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Polycyclic Aromatic Hydrocarbons: Evaluation of Sources and Effects (1983)

Chapter:3 ATMOSPHERIC TRANSFORMATIONS OF POLYCYCLIC AROMATIC HYDROCARBONS

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Suggested Citation:"3 ATMOSPHERIC TRANSFORMATIONS OF POLYCYCLIC AROMATIC HYDROCARBONS." National Research Council. 1983. Polycyclic Aromatic Hydrocarbons: Evaluation of Sources and Effects. Washington, DC: The National Academies Press. doi: 10.17226/738.
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Suggested Citation:"3 ATMOSPHERIC TRANSFORMATIONS OF POLYCYCLIC AROMATIC HYDROCARBONS." National Research Council. 1983. Polycyclic Aromatic Hydrocarbons: Evaluation of Sources and Effects. Washington, DC: The National Academies Press. doi: 10.17226/738.
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Suggested Citation:"3 ATMOSPHERIC TRANSFORMATIONS OF POLYCYCLIC AROMATIC HYDROCARBONS." National Research Council. 1983. Polycyclic Aromatic Hydrocarbons: Evaluation of Sources and Effects. Washington, DC: The National Academies Press. doi: 10.17226/738.
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Suggested Citation:"3 ATMOSPHERIC TRANSFORMATIONS OF POLYCYCLIC AROMATIC HYDROCARBONS." National Research Council. 1983. Polycyclic Aromatic Hydrocarbons: Evaluation of Sources and Effects. Washington, DC: The National Academies Press. doi: 10.17226/738.
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Suggested Citation:"3 ATMOSPHERIC TRANSFORMATIONS OF POLYCYCLIC AROMATIC HYDROCARBONS." National Research Council. 1983. Polycyclic Aromatic Hydrocarbons: Evaluation of Sources and Effects. Washington, DC: The National Academies Press. doi: 10.17226/738.
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Suggested Citation:"3 ATMOSPHERIC TRANSFORMATIONS OF POLYCYCLIC AROMATIC HYDROCARBONS." National Research Council. 1983. Polycyclic Aromatic Hydrocarbons: Evaluation of Sources and Effects. Washington, DC: The National Academies Press. doi: 10.17226/738.
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Suggested Citation:"3 ATMOSPHERIC TRANSFORMATIONS OF POLYCYCLIC AROMATIC HYDROCARBONS." National Research Council. 1983. Polycyclic Aromatic Hydrocarbons: Evaluation of Sources and Effects. Washington, DC: The National Academies Press. doi: 10.17226/738.
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Suggested Citation:"3 ATMOSPHERIC TRANSFORMATIONS OF POLYCYCLIC AROMATIC HYDROCARBONS." National Research Council. 1983. Polycyclic Aromatic Hydrocarbons: Evaluation of Sources and Effects. Washington, DC: The National Academies Press. doi: 10.17226/738.
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Suggested Citation:"3 ATMOSPHERIC TRANSFORMATIONS OF POLYCYCLIC AROMATIC HYDROCARBONS." National Research Council. 1983. Polycyclic Aromatic Hydrocarbons: Evaluation of Sources and Effects. Washington, DC: The National Academies Press. doi: 10.17226/738.
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Suggested Citation:"3 ATMOSPHERIC TRANSFORMATIONS OF POLYCYCLIC AROMATIC HYDROCARBONS." National Research Council. 1983. Polycyclic Aromatic Hydrocarbons: Evaluation of Sources and Effects. Washington, DC: The National Academies Press. doi: 10.17226/738.
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Suggested Citation:"3 ATMOSPHERIC TRANSFORMATIONS OF POLYCYCLIC AROMATIC HYDROCARBONS." National Research Council. 1983. Polycyclic Aromatic Hydrocarbons: Evaluation of Sources and Effects. Washington, DC: The National Academies Press. doi: 10.17226/738.
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Suggested Citation:"3 ATMOSPHERIC TRANSFORMATIONS OF POLYCYCLIC AROMATIC HYDROCARBONS." National Research Council. 1983. Polycyclic Aromatic Hydrocarbons: Evaluation of Sources and Effects. Washington, DC: The National Academies Press. doi: 10.17226/738.
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Suggested Citation:"3 ATMOSPHERIC TRANSFORMATIONS OF POLYCYCLIC AROMATIC HYDROCARBONS." National Research Council. 1983. Polycyclic Aromatic Hydrocarbons: Evaluation of Sources and Effects. Washington, DC: The National Academies Press. doi: 10.17226/738.
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Suggested Citation:"3 ATMOSPHERIC TRANSFORMATIONS OF POLYCYCLIC AROMATIC HYDROCARBONS." National Research Council. 1983. Polycyclic Aromatic Hydrocarbons: Evaluation of Sources and Effects. Washington, DC: The National Academies Press. doi: 10.17226/738.
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Suggested Citation:"3 ATMOSPHERIC TRANSFORMATIONS OF POLYCYCLIC AROMATIC HYDROCARBONS." National Research Council. 1983. Polycyclic Aromatic Hydrocarbons: Evaluation of Sources and Effects. Washington, DC: The National Academies Press. doi: 10.17226/738.
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Suggested Citation:"3 ATMOSPHERIC TRANSFORMATIONS OF POLYCYCLIC AROMATIC HYDROCARBONS." National Research Council. 1983. Polycyclic Aromatic Hydrocarbons: Evaluation of Sources and Effects. Washington, DC: The National Academies Press. doi: 10.17226/738.
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Suggested Citation:"3 ATMOSPHERIC TRANSFORMATIONS OF POLYCYCLIC AROMATIC HYDROCARBONS." National Research Council. 1983. Polycyclic Aromatic Hydrocarbons: Evaluation of Sources and Effects. Washington, DC: The National Academies Press. doi: 10.17226/738.
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Suggested Citation:"3 ATMOSPHERIC TRANSFORMATIONS OF POLYCYCLIC AROMATIC HYDROCARBONS." National Research Council. 1983. Polycyclic Aromatic Hydrocarbons: Evaluation of Sources and Effects. Washington, DC: The National Academies Press. doi: 10.17226/738.
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Suggested Citation:"3 ATMOSPHERIC TRANSFORMATIONS OF POLYCYCLIC AROMATIC HYDROCARBONS." National Research Council. 1983. Polycyclic Aromatic Hydrocarbons: Evaluation of Sources and Effects. Washington, DC: The National Academies Press. doi: 10.17226/738.
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Suggested Citation:"3 ATMOSPHERIC TRANSFORMATIONS OF POLYCYCLIC AROMATIC HYDROCARBONS." National Research Council. 1983. Polycyclic Aromatic Hydrocarbons: Evaluation of Sources and Effects. Washington, DC: The National Academies Press. doi: 10.17226/738.
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Suggested Citation:"3 ATMOSPHERIC TRANSFORMATIONS OF POLYCYCLIC AROMATIC HYDROCARBONS." National Research Council. 1983. Polycyclic Aromatic Hydrocarbons: Evaluation of Sources and Effects. Washington, DC: The National Academies Press. doi: 10.17226/738.
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Suggested Citation:"3 ATMOSPHERIC TRANSFORMATIONS OF POLYCYCLIC AROMATIC HYDROCARBONS." National Research Council. 1983. Polycyclic Aromatic Hydrocarbons: Evaluation of Sources and Effects. Washington, DC: The National Academies Press. doi: 10.17226/738.
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Suggested Citation:"3 ATMOSPHERIC TRANSFORMATIONS OF POLYCYCLIC AROMATIC HYDROCARBONS." National Research Council. 1983. Polycyclic Aromatic Hydrocarbons: Evaluation of Sources and Effects. Washington, DC: The National Academies Press. doi: 10.17226/738.
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Suggested Citation:"3 ATMOSPHERIC TRANSFORMATIONS OF POLYCYCLIC AROMATIC HYDROCARBONS." National Research Council. 1983. Polycyclic Aromatic Hydrocarbons: Evaluation of Sources and Effects. Washington, DC: The National Academies Press. doi: 10.17226/738.
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Suggested Citation:"3 ATMOSPHERIC TRANSFORMATIONS OF POLYCYCLIC AROMATIC HYDROCARBONS." National Research Council. 1983. Polycyclic Aromatic Hydrocarbons: Evaluation of Sources and Effects. Washington, DC: The National Academies Press. doi: 10.17226/738.
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Suggested Citation:"3 ATMOSPHERIC TRANSFORMATIONS OF POLYCYCLIC AROMATIC HYDROCARBONS." National Research Council. 1983. Polycyclic Aromatic Hydrocarbons: Evaluation of Sources and Effects. Washington, DC: The National Academies Press. doi: 10.17226/738.
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Suggested Citation:"3 ATMOSPHERIC TRANSFORMATIONS OF POLYCYCLIC AROMATIC HYDROCARBONS." National Research Council. 1983. Polycyclic Aromatic Hydrocarbons: Evaluation of Sources and Effects. Washington, DC: The National Academies Press. doi: 10.17226/738.
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Suggested Citation:"3 ATMOSPHERIC TRANSFORMATIONS OF POLYCYCLIC AROMATIC HYDROCARBONS." National Research Council. 1983. Polycyclic Aromatic Hydrocarbons: Evaluation of Sources and Effects. Washington, DC: The National Academies Press. doi: 10.17226/738.
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Suggested Citation:"3 ATMOSPHERIC TRANSFORMATIONS OF POLYCYCLIC AROMATIC HYDROCARBONS." National Research Council. 1983. Polycyclic Aromatic Hydrocarbons: Evaluation of Sources and Effects. Washington, DC: The National Academies Press. doi: 10.17226/738.
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Suggested Citation:"3 ATMOSPHERIC TRANSFORMATIONS OF POLYCYCLIC AROMATIC HYDROCARBONS." National Research Council. 1983. Polycyclic Aromatic Hydrocarbons: Evaluation of Sources and Effects. Washington, DC: The National Academies Press. doi: 10.17226/738.
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Suggested Citation:"3 ATMOSPHERIC TRANSFORMATIONS OF POLYCYCLIC AROMATIC HYDROCARBONS." National Research Council. 1983. Polycyclic Aromatic Hydrocarbons: Evaluation of Sources and Effects. Washington, DC: The National Academies Press. doi: 10.17226/738.
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Suggested Citation:"3 ATMOSPHERIC TRANSFORMATIONS OF POLYCYCLIC AROMATIC HYDROCARBONS." National Research Council. 1983. Polycyclic Aromatic Hydrocarbons: Evaluation of Sources and Effects. Washington, DC: The National Academies Press. doi: 10.17226/738.
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Suggested Citation:"3 ATMOSPHERIC TRANSFORMATIONS OF POLYCYCLIC AROMATIC HYDROCARBONS." National Research Council. 1983. Polycyclic Aromatic Hydrocarbons: Evaluation of Sources and Effects. Washington, DC: The National Academies Press. doi: 10.17226/738.
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Suggested Citation:"3 ATMOSPHERIC TRANSFORMATIONS OF POLYCYCLIC AROMATIC HYDROCARBONS." National Research Council. 1983. Polycyclic Aromatic Hydrocarbons: Evaluation of Sources and Effects. Washington, DC: The National Academies Press. doi: 10.17226/738.
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Suggested Citation:"3 ATMOSPHERIC TRANSFORMATIONS OF POLYCYCLIC AROMATIC HYDROCARBONS." National Research Council. 1983. Polycyclic Aromatic Hydrocarbons: Evaluation of Sources and Effects. Washington, DC: The National Academies Press. doi: 10.17226/738.
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Suggested Citation:"3 ATMOSPHERIC TRANSFORMATIONS OF POLYCYCLIC AROMATIC HYDROCARBONS." National Research Council. 1983. Polycyclic Aromatic Hydrocarbons: Evaluation of Sources and Effects. Washington, DC: The National Academies Press. doi: 10.17226/738.
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Suggested Citation:"3 ATMOSPHERIC TRANSFORMATIONS OF POLYCYCLIC AROMATIC HYDROCARBONS." National Research Council. 1983. Polycyclic Aromatic Hydrocarbons: Evaluation of Sources and Effects. Washington, DC: The National Academies Press. doi: 10.17226/738.
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Suggested Citation:"3 ATMOSPHERIC TRANSFORMATIONS OF POLYCYCLIC AROMATIC HYDROCARBONS." National Research Council. 1983. Polycyclic Aromatic Hydrocarbons: Evaluation of Sources and Effects. Washington, DC: The National Academies Press. doi: 10.17226/738.
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Suggested Citation:"3 ATMOSPHERIC TRANSFORMATIONS OF POLYCYCLIC AROMATIC HYDROCARBONS." National Research Council. 1983. Polycyclic Aromatic Hydrocarbons: Evaluation of Sources and Effects. Washington, DC: The National Academies Press. doi: 10.17226/738.
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Suggested Citation:"3 ATMOSPHERIC TRANSFORMATIONS OF POLYCYCLIC AROMATIC HYDROCARBONS." National Research Council. 1983. Polycyclic Aromatic Hydrocarbons: Evaluation of Sources and Effects. Washington, DC: The National Academies Press. doi: 10.17226/738.
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Suggested Citation:"3 ATMOSPHERIC TRANSFORMATIONS OF POLYCYCLIC AROMATIC HYDROCARBONS." National Research Council. 1983. Polycyclic Aromatic Hydrocarbons: Evaluation of Sources and Effects. Washington, DC: The National Academies Press. doi: 10.17226/738.
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Suggested Citation:"3 ATMOSPHERIC TRANSFORMATIONS OF POLYCYCLIC AROMATIC HYDROCARBONS." National Research Council. 1983. Polycyclic Aromatic Hydrocarbons: Evaluation of Sources and Effects. Washington, DC: The National Academies Press. doi: 10.17226/738.
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Suggested Citation:"3 ATMOSPHERIC TRANSFORMATIONS OF POLYCYCLIC AROMATIC HYDROCARBONS." National Research Council. 1983. Polycyclic Aromatic Hydrocarbons: Evaluation of Sources and Effects. Washington, DC: The National Academies Press. doi: 10.17226/738.
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Suggested Citation:"3 ATMOSPHERIC TRANSFORMATIONS OF POLYCYCLIC AROMATIC HYDROCARBONS." National Research Council. 1983. Polycyclic Aromatic Hydrocarbons: Evaluation of Sources and Effects. Washington, DC: The National Academies Press. doi: 10.17226/738.
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Suggested Citation:"3 ATMOSPHERIC TRANSFORMATIONS OF POLYCYCLIC AROMATIC HYDROCARBONS." National Research Council. 1983. Polycyclic Aromatic Hydrocarbons: Evaluation of Sources and Effects. Washington, DC: The National Academies Press. doi: 10.17226/738.
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Suggested Citation:"3 ATMOSPHERIC TRANSFORMATIONS OF POLYCYCLIC AROMATIC HYDROCARBONS." National Research Council. 1983. Polycyclic Aromatic Hydrocarbons: Evaluation of Sources and Effects. Washington, DC: The National Academies Press. doi: 10.17226/738.
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Suggested Citation:"3 ATMOSPHERIC TRANSFORMATIONS OF POLYCYCLIC AROMATIC HYDROCARBONS." National Research Council. 1983. Polycyclic Aromatic Hydrocarbons: Evaluation of Sources and Effects. Washington, DC: The National Academies Press. doi: 10.17226/738.
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Suggested Citation:"3 ATMOSPHERIC TRANSFORMATIONS OF POLYCYCLIC AROMATIC HYDROCARBONS." National Research Council. 1983. Polycyclic Aromatic Hydrocarbons: Evaluation of Sources and Effects. Washington, DC: The National Academies Press. doi: 10.17226/738.
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Given the high mutagenic potency of nitro-PAHs, it appears appropriate to speculate on the fate of these compounds in ambient air. Four nit r~-PAHs have been reported in urban particulate matter--6-nitro- BaP, 1 3-nitrofluoranthene, 1, 5 1-nitropyrene, and 5-nitroacenaph- thene85--and indirect evidence of the presence of nitro-PAHs in Wayne County3 Michigan, air has been presented on the basis of mutagenicity assays conducted with nitroreductase-deficient strains.483 89 Photolysis of nitro-PAHs, such as 9-nitroanthracene, yields the corresponding diones (e.g., 9,10-anthraquinone), both in solutig29 and on silica gel.7 On exposure of pyrene to N02' Jager and Hanus noted the appearance of new products after 4 h, and the nitropyrene yield decreased substan- tially. However, the retention times of these as yet unidentified com- pounds were different from those of the pyrene diones. The atmospheric relevance of these and other pathways should be investigated further. REACTIONS OF PAHs WITH SULFUR DIOXIDE Jager and Rakovic43 have reported the fonnation of sulfonic acids and other sulfur-containing compounds on exposure of BaP and pyrene (adsorbed on fly ash and on alumina) to SO2 at a high concentration (10% in air). These sulfonic acids are also easily prepared in the liquid phase by reaction of PAHs with sulfuric acid at room temperature.88 Tebbens et al.82 observed significant consumption of BaP adsorbed on soot from a propane burner and exposed to SO2 at 50-80 ppm for 4 h, both in the dark and under irradiation. At lower SO2 concentrations more relevant to ambient pollution, PAHs do not appear to react readily with SO2. Hughes et al.37 observed no reaction between SO2 at parts-per-million concentrations and BaP or pyrene adsorbed on silica gel, alumina, and coal fly ash. Butler and Crossley7 exposed 20 PAHs adsorbed on carbon (soot) to SO2 at 5 ppm in air for up to 100 d. The matrix air contained water vapor, and thus some sulfuric acid was presumably present. Within the stated analytic preci- sion, no significant reaction was observed for phenanthrene, coronene, fluoranthene, chrysene, BaP, pyrene, benz~ajanthracene, benzotghi]- perylene, and anthanthrene. Because the 20 PAHs studied include both highly reactive and essentially inert compounds with respect to reaction with, for example, O3 and N02, the conclusions of Butler and Crossley7 as to the absence of significant reaction with SO2 can probably be extended to many of the PAHs present in polluted air. However, SO2 and sulfuric acid may play a role as catalysts for other PAH reactions, including nitration, and this possible catalytic role should be inves ligated. REACTIONS OF PAHs WITH OTHER OXIDIZING SPECIES Reactions of adsorbed PAHs with atmospheric pollutants other than 03, S02, and NO2 have received very little attention. Pitts et _ .75 exposed BaP deposited on a glass filter to peroxyacetylnitrate 3-11

[CH3CO(OO)NO2, or PAN] at about 1 ppm for 16 h and observed the formation of BaP diones and other oxidation products. Ambient concen- trations of PAN in the Los Angeles atmosphere often reach 30 ppb during episodes of photochemical smog,29 so PAN may contribute, with Of, to the oxidative degradation of PAHs in photochemically polluted air. Reactions of PAHs with free radicals, including the hydroxyl (OH) and hydroperoxyl (HO2) radicals (well documented in the bulk liquid phase), have not been studied in the context of atmospheric pollution. On the basis of studies conducted with aromatic compounds, such as toluene, the OH photooxidation products in the presence of NOx include particulate- phase hydroxynitrotoluene and dihydroxynitrotoluene as major pro- ducts.31 It is possible that atmospheric oxidation of PAHs initiated by reaction with the OH radical results in the formation of nitro, hydroxy, and hydroxynitro derivatives. PHOTOCHEMICAL REACT IONS OF PAHs The mechanisms involved in photochemical reactions of PAHs with singlet oxygen in the bulk-liquid phase have received considerable atten- tion and have been the object of several comprehensive reviews.24~66 As is illustrated in Figure 3-6 for anthracene, products of these reactions include the PAR diones, formed either directly or by further reaction of primary endoperoxide products, as well as other oxygenated compounds. Photomodifications of BaP and other PAHs in the adsorbed state have received significant attention with respect to both product distribu- tion and influence of substrate. Product studies are in good agree- ment, and the chemical distribution of PAR phototransformations in the adsorbed state closely resembles that obtained in the bulk-liquid phase. However, reactivity reportedly varies widely as a function of substrate, and that makes it difficult to extrapolate laboratory studies to the ambient atmosphere. Falk, Markul, and Kotinl7 first reported on the photodecomposi- tion of 10 PAHs, including BaP, deposited on Whatman #1 paper filters and exposed to air in the dark, to air under irradiation, and to synthetic smog prepared by the reaction of O3 with gasoline. Their experiments were conducted with pure PAHs, as well as with PAHs adsorbed on gasoline-engine exhaust soot. On exposure of light in air, all PAHs adsorbed on soot were more resistant to photodecomposition than the same compounds in the pure form. Tebbens et al.81~82 investigated photo- transformations of BaP, perylene' pyrene, and fluoranthene adsorbed on soot or deposited on paper, acetylated, and glass-fiber filters. Losses of BaP of up to 40: were observed on irradiation for some 45 min in air; the major reaction products were the three BaP diones and a carboxylic acid derivative. Thomas _ al.83 reported similar results for BaP. Phototransformations of BaP and other PAHs have also been observed on a variety of substrates, including alumina,39~51 silica gel,39~40~5 cellulose,39~45 acetylated cellulose,39 soil,l9 carbon micro 3-12

needles,3 atmospheric particulate matter,21 and coal fly ash.50 A summary of the products of heterogeneous photooxidation of BaP on various substrates is given in Figure 3-7. For comparison, Table 3-8 lists half-lives and percent losses cellulose TLC plates45 and determined for a number of PAHs deposited on on Whatman #1 paperl7 and adsorbed on sootl7 and on fly ash.50 Although the four sets of data are directly comparable for only two compounds, perylene and BaP, the effect of substrate on PAH phototrans- formations is evident. PAHs deposited in the pure form on cellulose TLC plates exhibit short half-lives, from 23 min for anthracene to about 20 h for BaP.45 On Whatman paper, pure PAHs appear more resistant to photooxidation; egg., the half-life for perylene is about 2 d, compared with only 4 h on cellulose TLC plates. In the adsorbed state, PAHs appear to be much more resistant to photooxidation, with losses of only 10Z on soot after 48 h of irradiation.17 On fly ash, only modest photodecom- position rates (up to 20%) are observed, in striking contrast with rapid photooxidation in the liquid phase and on silica gel.50 If one neglects in a first approximation the important differences in experimental conditions, it appears from the data listed in Table 3-8 that PAHs adsorbed on atmospheric particles may be somewhat resistant to photo- oxidation, with half-lives ranging from several days to several weeks, depending on the reactivity of each compound. Korfmacher _ al.50 have discussed the possible physical and chemical factors involved in the resistance of PAHs to-photooxidation when adsorbed on fly ash. Resistance to photooxidation on soot, although even more relevant to urban pollution, where submicrometer particles contain a substantial fraction of carbonaceous material,30 has not been fully investigated. In addition, specific PAH-substrate interactions have to be considered. For example, Korfmacher et al.49 and Kotin et al.53 observed rapid decomposition in the dark of some PAHs adsorbed on fly ash and on soot. Until more data become available, caution must be exercised in extrapolating laboratory results to PAH photooxidation in the atmosphere. INTERACTIONS OF DEPOSITED PAHs WITH AMBIENT POLLUTANTS It i8 somewhat surprising 3 in view of the critical need to obtain overall PAH chemical deposition rates over a range of ambient condi- tions, that only a few studies have investigated interactions of PAHs with ambient polluted air. Pitts _ al.75 exposed pure BaP deposited on a glass filter to particle-free ambient Riverside, California, air for 3 d. BaP was partially oxidized under these conditions, yielding BaP diones and a variety of oxygenated (but not nitro) derivatives. In contrast, Fox and Olive21 found only trace amounts of anthraquinone from anthracene (a reactive PAH in the studies discussed above) adsorbed on ambient parti- culate matter (suburban location near Austin, Texas) and exposed to atmos- pheric gases for 4 d in the dark. Comparison of the results of these two studies suggests that, as noted for photooxidation, PAHs appear more 3-13

resistant to degradation in the adsorbed state than in the pure form. Peters and Seifert70 exposed glass-f iber filters impregnated with 4C-labeled BaP to ambient air in Berlin, Germany, and noted substantial losses of BaP, typically 75% over 24 h. Simultaneous determination of 14C activity 'only 10% loss in 24 h) established that BaP losses were due to chemical reaction, rather than to BaP evaporation from the filter. In addition, a relationship was noted between BaP reaction rates and ambient O3 concentrations. A recent investigation of PAH concentrations in the plume of a coal-fired power plant as a function of distance from the stack has been reported by Kalkwarf and Garcia. 44 Fluoranthene ~ BaP ~ pyrene ~ and BeP in the plume were found to be 50% reacted 3, 6, 8, and 12 kn from the stack, respectively (with correction for plume dilution and dispersion). The loss of the PAHs was attributed to their reaction with committed NO2 and SO2. PAHs IN AMBIENT AIR Source identification i s a key problem in the development of a pollution abatement or control program. In 1973, Friedlander22 des- cribed a technique to identify the sources of air pollutants in emission inventories for particulate matter. Many chemical elements--such as sodium, chlorine, silicon, and aluminum--are found in natural back- ground aerosols of the atmospheres of urban and industrial basins, such as Los Angeles. These are differentiated from other chemical tracers--such as lead, vanadium, zinc, and barium--which are attributable to human activities ~ see Figure 3-8) . Thus, if some of the ma jor sources are known in a given area, the source contributors to the atmosphere can be iden- tif fed and calculated by measuring the elemental concentrations at a given point and f itting the data into a mathematical model. One of the ma jar problems in using this technique has been the need for instrumentation for real-time measurement of the tracer elements. The use of trace metals for identification of sources of particles was examined by Moyers et al. in 1977.65 With these tracers, several sources of particulate species in desert, rural, and urban atmospheres could be determined. In 1979, Daisey et al.l4 described three methods for source identi- fication for the PAHs in the complex mix of the atmosphere. Although the evaluations of these methods are in the early stages, it was found that statistical modeling does not depend on source emission data, if the ambient-air measurement data base is large. In 1981, Daisey and Kneipl3 reported that it was possible to use multivariate regression models of ambient-air data for apportioning the contributions of emission sources to airborne particulate organic matter. The contributing sources of respir- able particles were determined by analysis of the ambient-air measurement data taken in New York City: 19: were from automobiles and related sources, 40Z were from oil-burning, and 15% were soil-like particles. Although this study using tracer chemicals had good results, the methods should be validated for predictive use by testing in other locations. 3-14

A comprehensive discussion and critique of environmental sampling and analytic methods used for polycyclic organic matter are in the EPA report.79 Lee et al. ,58 in a book on the analytic chemistry of PAHs, discussed sampling of mobile and stationary sources, ambient air, water, food, soils, and the aquatic environment. The cleanup and separation pro- cesses for the various collection media include solvent partitioning for analysis by column, paper, thin-layer, gas, and high-pressure liquid chromatography. The percentages of recovery with the analytic methods for the various PAHs were described by Lee et al., but are not discussed here. In 1967, Hangebrauck et al.,34 in a review of known sources of PAHs, gave the results of a survey made by the National Center for Air Pollution Control to screen the processes likely to produce emission in urban air. Although the survey was not intended to establish statistically the average emission from the sources, the data from it do characterize and classify the rate of emission of several PAHs from four major source categories: heat generation, refuse-burning, industrial processes, and motor vehicles. The 1972 NRC report Particulate Polycyclic Organic Mattered estimated that heat and power generation produced BaP at SOO metric tons/yr; refuse-burning, at 600 tons/yr; coke production, at 200 tons/yr; and motor vehicles, at 20 tons/yr. BaP has often been used as a surrogate in estimating source contributions of complex mixtures of PAHs. Surrogate chemicals have been used commonly in monitoring environ- mental quality, for various reasons--e."., analytic methods are often available only for the surrogate, and it costs less to monitor only one chemical. However, a PAH surrogate may not be useful unless studies have been conducted to characterize the PAH profile and percentage relation- shi~s for each type of environment. For example, in 1979, Bjorseth et al. showed that the relative distribution of PAHs is not the same in all environments. Figure 3-9 shows comparisons of the percentages of PAHs found in the particulate matter from an aluminum plant and a Soderberg paste plant. He recommended that a parent PAH profile (PPP) be estab- lished before a surrogate compound was chosen. In 1981, Gammage and Bjorseth23 stated that there are no established techniques for real-time monitoring of selected PAHs and that BaP is not a universally accepted proxy or surrogate for PAHs. It is known that the numerous PAHs found in the outdoor air can be radically different, qualitatively and quanti- tatively, from those in the workplace environment and that monitoring one compound as a surrogate for others is unreliable. The recommendation was made again that a PEP be determined before a proxy or surrogate compound was chosen. Cons iderable information is available to show the profile of the -various PAHs from various sources. Comparison of the rate of PAH emission between different categories is complicated, owing to the different units used to measure them: Ug/BTU, ~g/barrel of oil, Agog of particles, ~g/lb of material processed, ~g/m3, ~g/mi. Qualitative comparisons of PAH amiss ion sources do appear feasible and can identify the various contri- butors to the overall pollution burden. Lists of the PAHs found in the 3-15

following five broad categories have characterized the variety of sources and identified some of the major contributors: heat and power generation, refuse-burning, industrial processes, motor vehicles, and natural sources. In the 1978 review of the sources of PAHs, Baum,4 using data assembled by EPA in 1974, estimated that 97% of the BaP emitted in the United States could be attributed to stationary fuel combustion. The major contributors were the inefficient combustion of coal in residential furnaces, coke ovens, and refuse fires. This is in close agreement with the NRC report Particulate Polycyclic Organic Matter, which stated that 90% of the annual nationwide BaP emission was attributable to coal- and wood-fired residential furnaces, coal-refuse fires, and coke production. A wide range in concentrations of BaP (0.1-388 ng/m3) has been reported by Colucci and Begemanl0 for U.S. and foreign cities (see Table 3-9). These results are for measurements taken between 1952 and 1966. The objective of the authors was to study BaP concentrations in the atmosphere in relation to automobile traffic. They used tracers to identify auto- motive and nonautomotive sources and calculated correlation coefficients of BaP with CO (a motor-vehicle tracer) as 0.65, with lead (a gasoline- vehicle tracer) as 0.74, and with vanadium (an oil tracer) as 0.54.* The seasonal variations show that the concentrations were highest in fall and winter and lowest in spring and summer. The winter vanadium concen- trations were twice the summer concentrations; that indicates that the higher amount of BaP was attributable to combustion of residual fuels used for heating or to the lower inversion heights prevalent during cold weather. The concentrations of BaP in England, Italy, Norway, Sweden, and GermanOy, as shown in Table 3-10 for 1953-1964, were given in the report by Louw,6 for the purpose of comparing the findings Sin South Africa. The concentrations of BaP ranged between 5 and 49 ng/m . One sample, taken near a road-tarring operation, was extremely high' 1~113 ng/m ~ In Ontario, Canada, five locations were sampled for BaP by Katz et al.46 from April 1975 through March 1976. The highest concentration was obse3rved in Hamilton (3,498 ng/m3), and the lowest in Sudbury (111 ng~m ); the latter was attributed to the electrostatic precipitators in use at the nickel-copper smelter 5 mi away. The concentrations are given in Table 3-11. A study was conducted in Karlsruhe, Germany, to determine the relative amounts of BaP from residential heating systems and automobile traffic (see Figure 3-10). The concentrations ranged from 0.1 ng/m3 (at the low-traffic Municipal Garden) to 28 ng/m3 (at a railroad underpass). With lead as the tracer, it was determined that the highest concentration caused by automobiles was in the underpass. The low concentration in the lithe correlations indicate that 42-55% of the variation in BaP concen- trations is related to motor-vehicle tracers and 29% to stationary oil-burning. 3-16

Municipal Garden during summer was attributed to deposition of airborne particles on leaves, trees, and shrubs. During the winter, the increase in the concentration of BaP was attributed to increased residential heat- ing. The air samples taken at Karlsruhe Nuclear Research Center, 11 km (by air) north of the city, had the lowest concentrations, except for those in the Garden during May and June. BaP was determined in four locations around the industrial city of Essen, Germany, by Grimmer et al.,28 from October 1978 to March 1979. There were four sampling sites at each of five locations. The authors concluded that the concentrations of BaP in ambient air varied by a factor of more than 10 from one station to another during the cold-weather heat- ing period. Thus, they did not give any average values; the approximate ranges of concentration at each location were as follows: 1-75 ng/m3 in an area that used hand-stoked coal-heating in residences,-1.5-21 ng/m3 in an area with oil-heating only, 10-100 ng/m3 in a tunnel with car traffic, 15-210 ng/m3 in an area with coke ovens, and 1-75 ng/m3 in an area described as rural, outside the city. Two very thorough studies of the PAR content of Los Angeles air have been made by Gordon and Bryan26 and Gordon.25 The earlier study was of four locations in the Los Angeles basin (see Figure 3-11), and the latter included 13 sampling locations ~ see Figure 3-12 ~ . Analyses were performed for 14 PAHs, including BaP, sampled over the course of a year. From the relationship between meteorology, traffic density, and PAR concentrations, the authors concluded that most (at least 607) of the PAHs was contributed by automobile traffic, but that the concentrations were lower than in many other cities. This result was expected, because of the extensive use of natural gas and hydrothermal energy in the West and the nonuse of coal in Los Angeles. The warm climate also limits wood-burning in fireplaces. The Colucci and Begemanll results demonstrated much higher ambient BaP concentrations in urban areas that depend extensively on coal, oil, and wood combustion. They determined that the automotive contribution to Detroit ambient BaP was only 5-42%, with typical BaP concentrations 3 times as high as in Los Angeles. 3-17

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TABLE 3-5 Heterogeneou~ Photo-oxidation and Ozonolys is Hal f-Live~ of PAHs on TLC Platesa Half-Life, h Ozonolys is in Dark PAH Anthracene Benz ~ a ~ anthracene ~2~ -J 1.23 2.88 Dibenz ~ ah ~ anthracene 2 . 71 Dibenz ~ ac ~ anthracene 3 .82 . Photo-oxidat ion ~ quartz-lamp irrad ia t ion in air) 0.2 4.2 9.6 9.2 Pt~o~co-oxidat ion and Ozonolys i8 0.15 1.35 4.8 4.6 Pyrene 15.72 4.2 2.75 Benz o ~ a ~ pyrene 0.62 5.3 0.58 o .4b o .3c o .2b 0 e08C Benzote~pyrene7.6 21.1 5.38 Benzotbifluoranthene52.7 8.7 4.2 10.8b __ 3.6b 2 .gc Benzo~k~fluoranthene 34.9 13.eb 3 ,3c aData from Lane and Katz57 and Katz et al.45 bO3 = 0.7 ppm. CO3 = 2 .3 ppm. 3-23 1 .gc 14.1 3.9 3 .1b 0.9c

TABLE 3-6 Reaction of Adsorbed PAHs with Nitrogen Dioxide PAH-NO2 Nitro Reaction Nitro Derivative Effect of Half-life,a Derivatives Yield Substrate PAH d Identified Measured Investigated _ Phenanthrene 30 Mononitro, b isomer not specifiedb Anthracene __ 9-Nitroc ?d Fluoranthene 27 3-Nitroband b _ 8-nitrob Chrysene 26 6-Nitrob~c b c __ __ Pyrene 14 l-Nitrob,C,e 6,c,e c,e and dinitroe Benzo[a]pyrene Benzo[e]pyrene 24 Perylene 6-Nitro,C,f c,f 1-nitro, 3-nitro,f and dinitroC __ 3-Nitrod~f f Benz ~ a ] anthra ce ne 1 1 Benzo ~ gh i ] perylene 8 __ Anthantl~rene 3. 7 -- ~~ Fluorene -- 2-Nitrob b Coronene 29 -- - Carbazole -- Two b unspecif fed isomersb aData from Butler and Crossley.7 bData from Tokiwa et al.84 CData from Jager and Hanus.42 c dData from Gundel et al.33 eData from Hughes _ al.37 fData from Pitts 3-24 al.75

TABLE 3- 7 Yields of Nitro PAHs as Function of Substratea Nitro-PAH yield, ~g/100 ~ g of PAR I-Ni troDYrene Dark UV Light Daylight Subs bate Carbon 0.45 O. 38 Alumina, deactivated 2.4 2.3 Alumina, activated 1.9 2.0 Fly ash Silica gel aData from Jiger and Hanus . 42 36.8 41.8 3-25 0.40 2.6 6-Ni tro-BaP, Daylight Trace 7.9 2.8 - 8.2 57.3 ~ 112.5 15~8 25.5

T.ABLE 3-8 Influence of Substrate on Photo-Oxidation of PAH Half-life, h, ~ Destruction in 48 hb Pure PAH on Pure PAH Loss, %, Cellulose on Whatman Adsorbed Adsorbed on PAH TLC Platea Paper on Soot Fly AshC . Anthracene Benz E a ~ anthracene 0.2 4.2 Dibenz [ate] antl~racene 9 .6 Dibenz ~ ac ~ anthracene 9 .2 17-26 Pyrene 4.2 42 1 5-13 Benz 0 ~ a ~ pyrene 5 . 3 2 2 10 9-17 Benzoteipyrene 21.1 -- 7 - Benzo [b ~ fluoranthene 8 .7 Benzo ~ k ~ f luoran tl~ene 14 . 1 An thanthrene Ph enan th rene Fluoranthene Benz o ~ gh i ~ perylene Coronene Chrysene aData from Katz et al.45 bData from Falk et al,17 __ 44 60 - - 0 24 4 0 O O __ o __ CData from Korfmacher et al.50 Different light sources (xenon, quartz, etc . ~ . Times up to 100 h. 3-26 __

k TABLE 3-9 Benzo [a Jpyrene Content of Urban Aira Benzo~a]pyrene Content, ng/m3 Location Spring Summer Fall Winter New York: Commercial 0.5-8.1 0.7-3.9 1.5-6.0 0.5-9.4 Freeway 0.1-0.8 0.1-0.7 3.3-3.5 0.7-1.3 Residential 0.1-0.6 0.1-0.3 0.6-0.8 0.5-0.7 Detroit: Commercial 7.2 -- -- 5.0-17.0 Freeway -- 4.0-6.0 3.4-7.3 9,2-13.7 Residential -- 0.2 -- 0.9-1.8 Atlanta 2.1-3.6 le 6-4 ~ 0 12-15 2. 1-9. 9 Birmingham 6.3-18 6.1-10 20-74 23-34 Detroit 3.4-12 4.1-6.0 18-20 16-31 Los Angeles 0.4-0.8 0.4-1.2 1.2-13 1.1-6.6 Nashville 2.1-9.0 1.4-6.6 30-55 25 New Orleans 2.6-5.6 2.0-4.1 3.6-3.9 2.6-6.0 Philadelphia 2.5-3.4 3.5-19 7.1-12 6.4-8.8 Pittsburgh -- 0-23 2.~-37 8.2 San Francisco 0.8-0.9 0.2-1.1 3.0-7.5 1.3-2.4 Hamburg, Germany 14.72 10-26 66-296 94-388 London, England 25-48 12-21 44-122 95-147 Sheffield, England 20-44 21-33 56-63 64-78 Cannock, England 4-16 6-11 27--31 27-32 London: Traff ic 20 11 57 68 Background 11 1 3 8 4 2 Milan, Italy 12 3 25 150 Copenhagen, Denmark 6 5 14 15 Prague, Czechoslovakia -- 13-36 Budapes t, Hunga ry -- 17-32 South Af rice: Pretoria -- 10 Johannesburg Durban Osaka, Japan Commercial A. / ~ . / Residential 3.3 1. 4 53-145 72-141 22-28 22-49 5-28 r . ~ - 9.4 14 3.8 6.7 Sidney, Australia 0.6-2.4 0.6-1.8 2.5-7.4 3.8-8.2 aReprinted with permission from Colucci and Begeman; TO copyright 1971 American Chemical Society. 3-27

TABLE 3-10 At. Benzota~pyrene Concentrations in Pretoria, Johannesburg, Durban, and Other Large Citiesa Benzo[a]pyrene Concentration, ng/m3 Corrected for Country City Period of SamplingUncorrectedBenzo[k]fluoranthene S. Afr. Pretoria 26-27 Aug. 1963b 67 22 23-24 Sept. 1963b 83 28 20-21 Jan. 1964C 31 10 Johannes- 27-28 Apr. 1964b 6S 22 burg 4-5 May 1964b 141 47 18-19 May 1964b 146 49 12 May 1964 3,340 1,113 Durban 10-11 June 1964b 42 14 11-12 June 1964b 16 5 16-17 June 1964b 83 28 England Merseyside (i) Jan.-Dec. 1958 11 108 and other 1954-1957b 17 166 northern ~ ii) 1954-1957b 6 37 localities Salford Nov. 1952-Mar. 1953 197 290 Sheffield June 1949-Apr. 1950 20 28 Cannock July 1949-June 1950 4 32 Italy Milan Jan.-Oct. 1958 3 231 Norway Oslo Feb.-Dec. 1955 0.86 15.2 Sweden Stockholm Mar.-July 1960 1.1 10.0 Germany Hamburg Sept. 1961-Apr. 1963 10.1 388 aAdapted from Louw.60 "Winter. . CSummer; determined by direct chromatography of the cyclohexane-soluble fraction of sample on thin-layered al~mina. dRoad-tarring operation. 3-28

ED ~ ~ ~Go ~of e ~·· . ~ ~O ~O~ _ ~ 00 U] ~ C · - · - C~ O I, r-04 ~ k1 ~·eeee _I 04 _O-O _ ~US ~e O C) COCat · ~ ~TICCal ·~d C) be ~O ' - \8 1_ 0\ So -= ~ 00 ~CalO _~ C) ~·· 1~ ~_ 0 ~cadED ~- 1 ~ ~ By ~_ Cal ~ (V~ 1 ~ ~O ~I N r_ ~ 1 ~Go~-_ . E _uso _ ~_ ~_1 ~C_ - ~ - O ¢ o . - ~D I_ U~ ···· ~00oO Cd C O C' ~ ~r~ . e ~0 ~00 O ~ ~ CO c' u, 1 o C) o o · - · - OO ct U] ct U. 1 u' ·_' c~ - - ~u o o · ct c01 ~1 °1 ^ 0 1 ~: ~e ~ ~ .- ~ `: ~ ~ e ~_ ~ C ~_ ~_~- cn 0 0 ~ s~ c: . - o ~ ~o ~ ~ o ~E o ~o o ~ U, ~U, 3-29 N et ¢ O O ~0 c ~oa Ct ~0 Ct ~ 11

4' 141 ma: al i' lo it l. ~t ~'LJ am' Air Particulates 14 I 231 625 :~ 1~ .1 i. . . '' 1 ; ; ! ll 10 22 25 '23 , 1' ,j l 1, l J. ! 46~I~J~ 3L ~2 Kerosene Soof ,~ 38 3117 Lyle 47 ~ 11 1 1 1 33 3[ 1 Charles River Sediment I;C~ J$? FIGURE 3-1. Gas chromatograms of PAR mixtures obtained from (top) soot from kerosene flame, (middle) urban air particles, and (bottom) sediment of Charles River in Boston. 3-30 1 (~4

Peak Identifications 2 Biphenyl 4 Acenaphthylene 8 Fluorene 10 C14H8 14 Phenanthrene 15 Anthracene . 18 Methylphenanthrene 19 4H-Cyclopenta[def] phenanthrene 22 Fluoranthene 23 Benz~eJacenaphthylene 25 Pyrene 27 Methylfluoranthene 30 Benzotghi~fluoranthene 31 ClgHlo (unknown) . . 32 Cyclopenta~cd~pyrene 33 Benz~ajanthracene 34 Chrysene 35 Methylchrysene 37 Benzofluoranthene 38 Benzoteipyrene 39 Benzota~pyrene 40 Perylene 42 C21Hl2 (unknown) C21H12 (unknown) 44 Indenot1,2,3-cd~pyrene 46 Dibenz~acianthracene 47 Benzotghi~perylene 48 Anthanthrene 3-31

lot \ 2: ~ I. ~ ~. I*1 0 10 20 30 40 SO ~ 70 80 90 1= D157 F~0" ~ osro~ I ` - l FIGURE 3-2. Total PAN concentrations vet. distance from Boston for Massachusetts gOy samples. Reprinted with permission from Windsor and Rites; copyright 1979, Pergamon Press, Ltd. '4t _ 13 ~ 12 a. ~ ~ SO _ g g 7 ° 6 S ~ 3 - ~o 2 1 I ~I-- I ~I - I · ~I- L- 2.2 _ 2.0 I.B o 1.6 1.4 ~ I .2 G 1.0 ~ D.8 ,,, 0.6 .' 0.~= 0.2 ID 1820 1840 1860 1830 1~0 '920 1940 1960 19BO 1~0~01 D£DO\lI.O~ I Of ~ . 1. . . FIGURE 3-3 . Total PAH abundance in the various Pettaquamscut t River sediment core sections vs . date of deposition (solid line, left scale); BaP abundance in Gosser Planer Sea vs. date of deposition (dotted line, right scale). Reprinted with permission from Hites et al. ;35 copyright 1980, Pergamon Press, Ltd. 3-32

1 w~oN Al on l l D__ / o t3 I) sol. ~ 2" o - En (I,~) ~ -. 282 l COOH am_ (2 I) / 12~' ~. / ~d. ~ 2 - ~W o.l'-l.s~o, o.s - ~ 57~ ~ SPEW - -~`a~ Spurn dctc~ ~ be sad Oh Godson pant - a / ~ I 0 _ \ a / TYCOON \ ~ \ \ ~ ~ Ate o 1?1 0: o Ids Ir~tt} ||enz~n - ~K And _t2:~(1 FIGURE 3-4. Major reaction pathways and tentative structure of products of gas-phase ozonolysis of BaP. Most structures given as examples of possible isomers. Reprinted with permission from Van Vaeck et al.;36 copyright 1980, John Wiley & Sons Ltd. 3-33 ,'wW or ad ~ 332 of sad ad

4 H NO2 NP2 NO2 (B) O2 ~: O2 ~ loloJ Lo lo I NO2 Nitrocarbazole (2 unspecified isomers) 9 -Nitroanthracene Nitrophenanthrene ~ isomer not specif led) . 1-Nitropyrene (also dinitropyrene, isomer not specif led) 3-Nitrofluoranthene (A) and 8-nitrof luoranthene (B) 6 -Nib ochrys ene FIGURE 3-5. Nitro products identified in heterogeneous reactions of PAN with nitrogen dioxide. 3 -34

ANON NO2 (A) ANON (a) 2 (C) .. H2 ANON FIGURE 3 -5 . ~ cont inued) -Nitroperylene 1-Nitrobenzoia] pyrene (A) 3 -nit robenzo [ a] pyr en e (8) and 6 -nitrobenzo [ a] pyrene (C) --also dinitro-BaP is omer not specif fed 2 -Nitrof luorene 3 -35

I 0 1 0 1 - Q of [~3 o 9,10-Endoperoxide (yie l d, 2-7% ) 9,10-Anthraquinone (12-19X) 1-Hydroxy-9,10- anthraquinone (2-5X) Dione dimer (3-132) FIGURE 3-6. Products of heterogeneous photooxidation of anthracene on atmospheric particulate matter. Reprinted with permission from M. A. Fox and S. Olive, Science 205:582-583, 1979;2t copyright 1979 by the American Association for the Advancement of Science. 3-36

l hi, o tl At, fOT 1 1, 6-Dione ~0 3,6-Dione 11 o o 11 6, 12-Dione POOH [~C OOH ~20 A~ydride 7H-Benz He] - anthracene - 7 - one 3 ~ 4 -d icarboxyl ic acid - FIGURE~3-7. Products identified in heterogeneous photooxidatiou of BaP. Reprinted with permission from Tebbens et al. 3-37

1 NO2 - - - NO, HC ~ \ - ~HC~\ so2 ~H~ NH, ~.. _ HCI ~ Air | O" PHASE H2O CHEMICAL ELEMENT IN ~LLUT-ED ATMOSPHERES FIGURE 3-8. Inner ring encloses elements present in natural background (soil dust and marine aerosol) second ring, primary particulate matter introduced by man; outermost ring, secondary material formed in atmosphere. Elemental carbon added to seco22 ring. Reprinted with permission from Friedlander; copy riSht 1973 American Chemical Society. 3-38

·/0 of Tolol 100 at_ JO ~0 20 10 S 2 1 Q5 0.3 0.2 0.1 _ A HI l 1- /\ - / I f ~ I I I Ail' \ `~ , \ \ 1 1 ~ I I ~ 1 ICE ~ .=e ~= ~ Y ° C ° FIGURE 3-9 . Parent PAN profile of PAR in part iculate matter from aluminum plant (dashed line) and Soderberg paste plant (solid line). Soderberg paste plant is one in which electrodes used in production of aluminum are made of anthracite or of anthracite and petroleum coke. During baking of these electrodes, volatile components are produced from anthracite ore base. Reprinted with permission from Bjorseth; 6 copyright Ann Arbor Science Publishers, Inc. 3-39

- ~o JO 10 E ~ - 0 2 - - c 1 0,` 0,2 0,1 ! t L At, En' i1 it 1 1 -_T .. . i- 1 .. ,. . ., , ~ . ... 0,1 45 1 2 5 10 20 30 ~ 1. ~ ADA IX , ma, If 50 70 80 90 95 98 99 99,5 99,9 Probability ·1. I I f ! Il it 1 1 i 1 I ASH 1 Lit FIGURE 3-10. Frequency distribution of airborne BaP concentra- tion at different measuring sites in area of Rarleruhe. 1, nuclear research center, Rarl~ruhe, November 1974-March 1975; 2, municipal garden, May-June 1975; 3, railroad underpass, May-June 1975; 4, muni- cipal garden, October 1975-March 1976; 5, railroad underpass, October 1975-March 1976. 3-40

Component Location Total particulate mass, ug/m3 215 131 102 40 Benzene solubles. ug/m3 21.7 13.2 8.3 2.6 Lead,pg/m3 ~.35 2.50 1.97 0.50 Traffic density X 10-3,vehiCIe mi/mi2/day 200 130 95 8 PAN, ng/m3 Coronene 6.4 3.2 2.8 0.20 Pyrene 2.0 1.4 3.8 0.18 fluoranthene 1.9 0.8 3.4 0.12 "nz(~- anthracene 1.1 0.8 3. ~0.04 Chrysene 2.6 1.6 3.8 0.04 Benzo(e) pyreno 3.0 1.B 3.2 0.09 Bonzo(a) pyrene 1.1 O.S 3.5 0.03 Benzo(~) fluoranther. 1.6 0.9 1.8 0.09 Ebn20(1) flwranmen. 0.6 0~3 0.8 0.01 "nzo(k) tiuorant~ne 0.8 0.3 1.3 0.03 PeryIe" 0.5 0.3 1.2 0.01 Anthanthrene 0.d 0.2 1 .1 0.01 BeniO(Dh,] ~ peryIene B.2 4.2 7.1 0.21 Indeno( 1 .2.3-ed) - - pyrene 1.2 0.4 . 0.3 0.03 , , ~$_, L hw!>~5~),~- ~A `' ~ ~ ~,~ ~oS2 - L~ FIGURE 3-11. Component 8 in Los Angeles airborne particles . Composite June 1971-June 1972. Map shows approximate location of sampling sites. Reprinted with permission from Gordon and Bryan; copyright 1973 American Chemical Society. 3-41

PAR 1 2 3 4 5 6 7 8 9 10 11 12 13 PYR 0.41 0.36 FLT 0.28 0.23 BAA 0.18 0.13 CHY 0.62 0.44 BEP 0.8 1 0.75 BAP 0.4 7 0.32 BJF 0.17 0.13 BKF 0.16 0.14 ANT 0.25 0.18 G EE 2.86 2.73 INP 1.10 1.09 COR 1.83 0.46 0.37 O.50 0.40 0.32 0.20 0.32 0.26 Q 18 0.15 O.18 0.15 0 68 0.36 O.60 0.49 1.01 0.73 |.04 0.85 0.63 0.41 O.45 0.36 0.25 0.17 0.19 0.15 0.26 0.16 0.19 0.15 0.35 0.28 0.25 0.21 3.78 3.02 3.79 3.08 1.22 1.11 1.51 1.22 2.54 2.06 0.49 0.4 7 0.60 0.48 0.33 0.30 0.39 0.3 1 0.26 0.21 0.22 0.18 0.65 0.76 0.72 0.59 1.06 1.00 1.26 1.02 0.56 0.54 0.54 0.44 0.18 0.23 0.22 0.18 0.21 0.23 0.23 0.18 0.29 0.26 0.3 1 0.25 4.33 3.84 4.57 3.69 1.89 1.55 1.82 1.47 3.06 2.47 0.76 0.84 0.61 0.46 0.50 0.61 0.40 0.30 0.44 0.23 0.23 0.1 7 0.92 1.02 0.75 0.57 1.34 1.22 1.30 0.98 0.77 0.76 0.56 0.42 0.28 0.26 0.23 0.17 0.27 0.29 0.23 0.18 0.42 0.38 0.32 0.24 5.01 4.02 4.72 3.56 2.05 1.96 1.88 1.41 3.16 2.38 0.67 0.33 0.55 0.21 0.24 0.12 0.68 0.40 0.88 O.69 0.53 0.30 0.14 0.12 0.25 0.13 0.25 0.17 2.67 2.52 1.18 1.00 1.69 Upper value in each pair = observed; lower value calculated using the average PAH/COR Italicized observed values exceed calculated values by at least three times the coefficien 0.34 0.39 0.25 0.25 0.10 0.15 0.53 0.48 0.92 0.83 0.41 0.36 0.14 0.15 0.14 0.15 0.18 0.20 2.99 3.02 1.33 1.20 2.02 0.34 0.33 0.38 0.30 0.21 0.2 1 0.25 0.19 0.12 0.11 0.14 0.11 0.42 0.38 0.46 0.36 0.77 0.65 0.80 0.63 0.35 0.24 0.35 0.27 0.14 0.10 0.14 0.11 0.16 0.11 0.14 0.11 0.15 0.13 0.20 0.1 5 3.05 2.3 1 2.9 1 2.29 1.18 0.90 1.16 0.91 1.95 1.53 ~ ratio for areas 3, 11, and 13. t of variance among 3, 1 1, and 13. 0.42 0.2S 0.44 0.3C 0.30 0.22 0.28 0.19 0.17 0.11 0.16 0.11 0.66 0.45 0.53 0.37 0.89 0.70 0.92 0.63 0.38 0.27 0.40 0.27 0.15 0.11 0.16 0.11 0.19 0.11 0.17 0.11 0.17 0.12 0.22 0.1 5 3.4 1 2.32 3.35 2.30 1.48 1.0 1 1.33 0.9 1 2.24 1.54 Ares 1 2 3 4 5 6 7 8 9 10 11 12 13 Automobile Traffic Density (ATD), 10-5 Mi/Da/Mi2 (5) 0.75 1.2 1.5 1.5 2.0 1.2 0.65 0.4 0.8 1.05 0.95- 0.95 0.9 Sample Yields, Gym' Suspended Particulate Matter Geom. mean year 84.2 87.2 74.5 85.5 85.8 109.5 128.0 118.8 106.8 82.4 66.1 83.9 79.0 Benzene-soluble Particulate Matter Geom. mea n, year 7.7 9.6 6.5 9.0 8.4 11.3 1 0.8 9.2 7.9 7.3 5.3 6.8 5.9 10m' FIGURE 3-12. Observed PAR annual geometric mean concentrations' ng/m3, and calculated on basis of patterns in coastal areas. Map shows approximate ligation of sampling sites. Reprinted with permission from Gordon; copyright 1976 American Chemical Society. 3-42

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78. Santodonato, J., P. Howard, D. Basu, S. Lande, J. K. Selkirk, and P. Sheehe. Health Assessment Document for Polycyclic Organic Matter. Report EPA-600/9-79-008. Research Triangle Park, N.C.: U.S. Environ- mental Protection Agency, Office of Health and Environmental Assess- ment, 1979. [475] pp. (preprint) 79. Santodonato, J., P. Howard, D. Basu, S. D. Lee, and L. Grant, Eds. Health and Ecological Assessment of Polynuclear Aromatic Hydrocarbons. Environ. Path. Toxicol. (Special Issue) 5~1~:1-372, 1981. 80. Sehmel, G. A., and S. L. Butter. Particle deposition rates on a water surface as a function of particle diameter and air velocity. J. Rech. Atmospheriques 8:911-920, 1974. 81. Tebbens, B. D., M. Mukai, and J. F. Thomas. Fate of arenes incorporated with airborne soot: Effect of irradiation. Amer. Ind. Hyg. Assoc. J. 32:365-372, 1971. Tebbens, B. D., J. P. Thomas, and M. Mukai. Fate of arenes incorporated with airborne soot. Amer. Ind. Hyg. Assoc. J. 27:415-422, 1966. 83. Thomas, J. F., M. Mukai, and B. D. Tebbens. Fate of airborne benzo[a]- pyrene. Environ. Sci. Technol. 2:33-39, 1968. 84. Tokiwa, H., K. Nakagawa, K. Morita, and Y. Ohnisha. Mutagenicity of nitro derivatives induced by exposure of aromatic compounds to nitrogen dioxide. Mutat. Res. 91: 195-205, 1981. 85. Tokiwa, H., R. Nakagawa, and Y. Ohnishi. Mutagenic assay of aromatic nitro compounds with Salmonella typhimurium. Mutat. Res. 91:321-325, 1981. 86. Van Vaeck, L., G. Broddin, and K. Van Cauwenberghe. On the relevance of air pollution measurements of aliphatic and polyaromatic hydrocarbons in ambient particulate matter. Biomed. Mass Spectrom. 7:473-483, 1980. 81. Van Vaeck, L.' and K. Van Cauwenberghe. Cascade impactor measurements of the size distribution of the major classes of organic pollutants in atmospheric particulate matter. Atmos. Environ. 12:2229-2239, 1978. 88. Vollmann, H., H. Becker, M. Corell, and H. Streeck. Beitrage zur Kenntnis des Pyrens und seiner Derivate. Justus Liebigs Ann. Chem. 531: 1-159, 1937. 89. Wang, C. Y., M-S. Lee, C. M. King, and P. 0. Warner. Evidence for nitro- aromatics as direct-acting mutagens of airborne particles. Chemosphere 9:83-87, 1980. 90. Windsor, J. G., Jr., and R. A. Hites. PolycycLic aromatic hydrocarbons in Gulf of Maine sediments and Nova Scotia soils. Geochim. Cosmochim. Acta 43: 27-33, 1979. 3-48

4 BIOLOGIC EFFECTS OF SMOKE, EMISSION, AND SOME OF THEIR PAH COMPONENTS The environment is a major contributor to the development of a variety of pathologic conditions in humans. Indeed, Doll and Peto43 have estimated that as much as 13% of all human deaths from cancer may be attributed to exposure to harmful polluting substances in our environment. The purposes of this chapter are to describe the biologic activity of various kinds of polluting emission and some of their PAH components and to attempt to relate the toxic impact of such emission to its content of specific PAHs. (See Chapter 3 for discussion of particle size and respiratory uptake, Chapter 6 for discussion of PAH transfer in tissues, and Chapter 9 for recommendations.) It considers biologic activity in bacteria, animal-cell systems, and intact animals, as well as the nature and advantages of some biologic models used in emission toxicology. Hilado and colleagues65~68 have reported considerable morbidity in experimental animals that were exposed to the products of combustion of hard woods, such as birch and oak, or soft woods, such as fir and pine; they noted no difference in toxicity between the products of these hard and soft woods. The problem of interpreting results related to wood is compounded by the presence of preservatives and other additives in the wood. It is often difficult to establish whether any observed toxicity is caused by the combustion products of the wood itself or of a contaminating additive. And it has not been established whether the PAHs generated during combustion contribute more to the observed toxicity than the gaseous products. Considerable additional work with subacute and chronic exposure is required to characterize toxicity, particularly in view of the current increase in such emission. Toxicity has been measured in rats and mice intermittently expose' to diesel exhaust for periods up to 308 h. 110 The total cumulative particulate exposure varied from 7.75 to 1,310 mg/m3-h. However, only minimal changes from normal were observed. Glutathione reductase and lactic acid dehydrogenase activities, which might serve as indicators of lung-cell damage, were increased in ravage fluid after wk of exposure at the high dosage; although exposure was continued, they returned to normal by 6 wk. Neutral protease activity was increased in ravage fluid after 1 wk of exposure at the medium dosage (30.6 mg/m3-h) and the high dosage, but returned to normal by the twelfth week of continued exposure. It is of interest that no alteration in cytochrome P450 activity was observed in either mouse or rat liver at any time in any group. After 12 wk of exposure at the highest dosage, an increase in the number of macrophages was seen in the ravage fluid. 4-1

tar TOXICITY TO SPECIFIC ORGANS AND ORGAN SYSTEMS IN ANIMALS . .. Manifestations of toxicity to specific organs and organ systems were detected in animals that were exposed to various kinds of emission. PULMONARY FUNCT ION . Many studies have been conducted in which animals were exposed to dielel-exhaust particles (generally 0.1-0.2 Am in size). Abraham et al. reported little change in pulmonary resistance or in airway reactivity to a carbachol aerosol in conscious sheep exposed for 30 min to diesel-exhaust particles. Battigelli7 exposed human volunteers for up to 1 h to diesel exhaust at total hydrocarbon concentrations of 2-6 ppm (comparable with the environment in railroad shops) and then measured pulmonary resistance as an index of function. With this rather insensitive assay of only relatively short duration, no changes in function were observed. Mauderly et al.ll° measured tracheal mucociliary clearance of a 99mTc-macroaggregated albumin suspension that had been instilled intratracheally in rats 1 wk before exposure to diesel exhaust for 1, 6, or 12 wk. They also examined the morphology o f the lung and trachea with scanning electron microscopy. In the group of animals that had been exposed at high dosages (cumulative particle exposure of 151, 822, or 1,310 mg/m3-h, respectively, after 1, 6, or 12 wk of exposure), clearance of the suspension was increased after 1 wk; by 12 wk. it was below normal. In this group, a tendency toward reduced numbers of ciliated cells was noted. Furthermore, a dose-related increase in pulmonary macrophages was apparent. Many of these cells contained diesel particles as inclusions. No changes were seen in the morphology of the alveoli or airways. In the groups of animals that were exposed during the same times at lower dosages (30.6, 203, or 317 mg/m3-h), a reduction in clearance was the more prevalent response. However, in the pulmonary function part of this study, in no group of exposed mice or rats was any significant alteration in pulmonary function observed. A similar lack of effect on pulmonary function after diesel-exhaust exposure of rats was reported by Pepelko 5 and by Gross.58 In the study of Pepelko et al., rats were exposed for 20 in/d, 7 d/wk, for 28 d to a 1:4 raw or irradiated exhaust from a six-cylinder Nissan diesel engine. Gross exposed rats to diesel-exhaust particles at 1,500 ~g/m3 for 20 in/d, 5 d/wk, for up to 267 d, but suggested that a longer chronic exposure of the rats to the particles might result in lung disease. Because guinea pigs are generally more susceptible to pulmonary lesions, they were similarly exposed to diesel-exhaust particles for periods varying from 2 wk to 3 mo at 250-6,000 ~g/m3. As reported for other species, the number of pulmonary a lveolar macrophages

increased, and they tended to accumulate at the bronchoalveolar junctions. Occasional localization of the particles in alveolar Type epithelial cells and sporadic increases in Type II cells were observed. However, all these morphologic changes would be classified as minimal with regard to pulmonary toxicity. A different tack was taken by Mauderly et al.ll° and by Campbell _ al.l7 to demonstrate an alteration in pulmonary function after exposure of rats or mice to diesel-exhaust particles. In the former study, exposed rats were inoculated with 32P-labeled Pseudomonas aeruginosa at the oropharynx, and the killing and clearance of these organisms were ascertained 48 h later; no significant difference in either measure was observed. In the latter study, mice that had been exposed to light-duty diesel exhaust (up to 8 in/d, 7 d/wk, for 46 wk) were treated with aerosols of Streptococcus pyogenes or Salmonella typhimurium; mice that had been exposed to exhaust showed slightly increased toxic responses to streptococci. These results were confirmed in later studies by Campbell et al.17a showing greater mortality of infected mice exposed to diesel than to gasoline (catalyst-treated) engine exhausts. In brief, minimal changes are observed in pulmonary function and morphology after exposure to diesel-exhaust particles. Although many morphologic studies have been conducted in animals that have received some individual PAHs intratracheally or otherwise, there is little information on resulting alterations in pulmonary function. The morphologic changes that are generally classified as metaplastic are discussed later in this chapter. NERVOUS SYSTEM Evaluating the effects of any potential toxin on the development and function of the nervous system experimentally is very difficult. Laurie and colleagues97~98 set about to determine the effects of chronic diesel-exhaust exposure of neonatal rats on spontaneous locomotor activity and on performance in a bar-pres~ing task. The neonatal rats were exposed to the exhaust at 6 mg/m for 8-20 hid for 17-42 d, starting on day 1 or 2 of life. Performance was assessed during weeks 5-16. The activity was depressed both during exposure and in the group tested after exposure, compared with a control group; i.e., they required more extensive training. Because published reports had indicated that the gaseous components lacked any such effect, the authors concluded that the particles or their PAH components were the responsible factors. Laurie and Boyes97 measured the somatosensory and visual evoked potentials in control rats and rats that had been exposed to diesel exhaust during neonatal life. Although only small abnormalities were noted in the visual evoked potential, significantly longer latencies for all the peaks of somatosensory evoked potential were seen in the exposed rats. Because the latter potentials are in the central nervous system, the authors suggested that diesel-exhaust exposure may lead to failure to develop a normally functioning nervous system. These types of studies have not been conducted with animals exposed to individual PAHs, or to mixtures thereof, so it is not known 4-3

whether these organic components are responsible for the nervous system lesions. IMMUNE SYSTEM . The effects of chronic diesel-exhaust exposure of rats on the immune system were assessed by Mauderly et al.ll° They placed rats in chambers and exposed them to diesel-exhaust particles for various periods under dynamic conditions and gave them sheep red blood cells intratracheally. The numbers of lymphoid cells that produced IgM antibody to sheep red cells were determined in lymph nodes and spleen 7 d after inoculation with the sheep red cells. Only minimal or no effects on the induction of immunity were observed. Those studies are of particular interest, in view of the long- known damaging effect of some PAHs on lymphoid tissue. In 1937, Haddow and co-workers59 reported the systemic toxic effects of PAHs, calling attention particularly to damage to lymphoid tissue. Acute exposure of mice to 3-methylcholanthrene reportedly resulted in damage to the thymus that was followed by thymoma formation, a marked reduction in the weights of the spleen and the mesenteric lymph nodes, and degeneration of bone marrow cells.l84 Newborns appeared particularly sensitive, suffering a wasting disease that culminated in death. This toxic effect has also been noted after administration of 7,12-dimethylbenzanthracene (7,12-DMBA) to rats.23~128 Repeated administrations of dibenz[ah]anthracene, benz[a]anthracene, or anthra- cene to mice resulted in an increase in stem cells in lymph glands, a decrease in mature lymphoid cells and a decrease in spleen weight (only for dibenz[ah]anthracene).76 In rats, findings were similar after treatment with dibenz[ah~anthracene; the effects with anthracene were much less dramatic. The total immune response of an organism is an expression of the sum of humoral and cell-mediated effects. Humoral effects derive from the activity of B lymphocytes, which on maturation to plasma cells elaborate immunoglobulins; cell-mediated immunity is expressed by T cells. The effects of chronic administration of benzo[a]pyrene (daily subcutaneous injection for 14 d, for a total of 50-400 mg/kg of body weight) on the humoral immune response were summarized by Dean et al. 8 There was a marked decrease in this response. (The noncarcinogen benzo[e]pyrene (BeP) was without effect.) A variety of T-cell responses have been tested for sensitivity to benzotaipyrene (BaP) administration.l2~38~39,l04 The effects of chronic BaP administration, to a total of 400 mg/kg of body weight' on T-cell function were much less marked than those on B-cell activity. Little effect on the incidence of the B6 tumor in inoculated mice or on the growth of the B16 melanoma after intravenous challenge was observed. Furthermore, the resistance of mice to Listeria monocytogenes was unaltered by administration of BaP, although the expulsion of the parasite Trichinella spiralis was reduced. BaP administration resulted 4-4

in myelotoxicity, as determined by in vitro clonal bone-marrow assays. But delayed hypersensitivity reactions in the host were unaffected. summary, the effects of BaP administration on a variety of T-cell functions were not very s igni ficant. It has long been known that care inogenic PAHs are i~mnunosuppres- sive; indeed, this aspect of their action was believed responsible, at least in part, for their ability to cause neoplasia. After treatment of mice with 3-methylcholanthrene (3-MC), dibenz~ah~anthracene, or BaP, a prolonged depression of the immune response to sheep red cells was noted; the noncarcinogens BeP and anthracene were ineffective in this regard.l07'l63 The effects of the PAHs have been reviewed by Baldwin,4 who reported a good correlation between degree of immuno- suppression and carcinogenicity. In Although the previously cited work implied a link between the two activities, Dale and Hedges37 and Stutmanl64 definitively dissociated immunosuppression from carcinogenicity. Using guinea pigs, Dale and Hedges concluded that the effects of the PAHs were due to generalized toxicity and were not likely to persist long enough to lead to neoplasia. Stutman produced tumors in mice with very low doses of 3-MC--doses that did not influence the immune status of the animals. To conclude, some PAHs at high doses can alter the immune status of animals when administered to the point of general toxicity, whereas exhaust and emission have not been shown to do so. SKIN The major changes occurring in skin after application of emission or PAHs are associated with neoplasia and are discussed later in this chapter. KIDNEY The toxicity of diesel fuel to kidney and other tissues has been described in only one report: a sailor cleaned his hair with diesel fuel and was later hospitalized for renal failure.6 This acute intoxication also resulted in damage to the liver, the gastrointestinal tract, and the lungs. The information presented does not allow further definition of the toxic components responsible for the pathologic condition. GLANDS, REPRODUCTION, AND TERATOLOGY Although individual PAHs have pathologic effects on some glandular tissue, little toxicity has been reported after administration of various kinds of emission. The oral administration of 7,12-DMBA to 4-5

female mice caused the destruction of small oocytes and reduction in the number of growing and large oocytes.93 This compound also caused specific destruction of the adrenal cortex in the rat.13 3-MC administration resulted in destruction of the primordial oocytes in the mouse.l09 3-MC or BaP given intraperitoneally produced abnormally shaped sperm indicative of damage to the primary spe``Ilatocytes and spermatogonia.l83 With regard to reproduction and teratology, only few PAHs have been tested. The feeding of BaP to female rats resulted in no abnormalities in their ovarian cycle, ovulation, fertilization, or implantation, and few resorptions were observed in treated pregnant rats. 83 Similar findings have been reported for the mouse.139 SHORT-TERM MODEL SYSTEMS FOR DETECTING EFFECTS Whole-animal experiments for assessing toxicity are often expensive and time-consuming. Therefore, alternative approaches have been developed. A variety of short-term biologic model systems are avail- able for assessing the effects of exhaust, its particulate components, and pyrene analogues. These systems are characterized by the use of multiple end points to measure genotoxicity, the use of both bacterial and mammalian cell lines, the use of end points that can be evaluated in relatively short periods (i.e., 1 d to 6 wk)2 and the incorporation of an exogenous source of metabolic activation for generating the active PAN metabolites. Each end point in concert with a particular cell system has its own unique strengths and weaknesses. Recognizing this fact, the regulatory agencies have required a battery of short-term tests, to provide a more complete picture of the potential biologic activity of a test chemical. The categories of available short-term tests are presented in Table 4-1, with a partial list of some of the particular tests given in Table 4-2 (see Hollstein et _.74 for details) Examples of the use of these tests in a short-term battery are presented in Tables 4-3 and 4-4. Table 4-3 demonstrates the guidelines that the Federal Insecticide, Fungicide, and Rodenticide Act (FIFRA) recommended; tests recommended by the Organisation for Economic Cooperation and Development (OECD) are presented in Table 4-4. In general, these batteries include the evaluation of three or more end points from the following list: toxic effects, mutagenesis, DNA damage and repair, chromosomal alteration, and neoplastic transformation. TOXIC EFFECTS Toxicity is usually manifested by such end points as cell death, increase in generation time, decrease in respiration, decrease in rate of macromolecular synthesis, and release of particular cell-bound proteins. Many of these end points have been used in bacteria, 102 pro tozoa,75 algae,172 invertebrates,172 fish 148 and mammalian 4-6

cells.88 Cell death is also used concomitantly with virtually every assay system, to determine the numbers of cells at risk. MIJTAGENE S I S A mutation is any heritable change in the phenotype of an organism or cell resulting from a change in its DNA. A mutation need not be reflected in a change in function. The phenotypic expression of such a change can be detected in a variety of cellular proteins. Examples of genetic markers that use mutagenesis as the end point are given in Table 4-5. The bacterial systems are best exemplified by the Salmonella typhimurium test strains developed by Ames et al.3 This system measures the reversion rate to histidine prototrophy in five test strains that carry specific frameshift and base-pair substitutions at the his locus and a series of mutations at the other loci to make the bacteria more sensitive to chemically induced mutation. The deep rough mutation (rfa ), ultraviolet-light sensitivity (uvr B ), nitrate reducLase deficiency (chl-), biotin deficiency (bio~), and introduction of R factor plasmids are examples of alterations of these test strains to make them more sensitive to chemically induced mutagenesis. Because reversion to his prototrophy is being measured, a battery of strains (three to five) must be tested, to ensure detection of point mutation, frameshift mutation, and intragenic deletion. To circumvent this problem, there have been attempts to standardize a forward-mutation assay with S. t`~himurium. Forward mutations at both the arabinose-resistance (grail ~ and 8-azaguanine-resistance (8-Azr~l56 genes have been described. These assays have the advantages of detecting virtually all mutagenic events, detecting mutagenesis at more than one genetic locus (probably at least three), and requiring the use of only one test strain. Mutagenesis testing in mammalian cells has used cell types that range from the rapidly growing, easily handled cell lines, such as CHot55 and V-79, 20~27 to the more difficult testing of in vivo-derived human lymphocytes .3 Advantages of the CHO and V-79 cells include high plating and cloning efficiencies, pseudodiploidy, and the ability to monitor mutagenesis at a variety of genetic loci. disadvantage is that these cells have little or no capacity to metabolize xenobiotics, especially pyrenes. Recent results54 suggest that hamster-derived cell lines, such as CHO, have limited capacity to remove 06-alkylated guanine; thus, they may be def icient in DNA repair. The merits and limitations of the three most widely used loci for testing with mammlian cells are presented in Table 4-6. Such end points as resistance to purine analogues, to 5-bromodeoxyuridine (5-BUdR), and to ouabain collectively can detect most of the potential genotoxic effects of PAHs.77 These end points are now being used simultaneously to limit the possibility of false-negative conclusions. In assays for purine-analogue resistance, mutants lacking the enzyme of the purine salvage pathway, bypoxanthine-guanine phosphoribosyl

transferase (HGPRT), are identified by their resistance to toxic analogues, such as 8-azaguanine or 6-thioguanine. In assays for ouabain resistance, mutants are detected by their ability to grow in the presence of the glycoside ouabain. The basis of the latter muta- tion is an alteration in the receptor for the membranal sodium- potassium ATPase system. In the assay for 5-BUdR resistance, an alteration of the enzyme thymidine kinase is responsible for the mutant phenotype. The altered enzyme is unable to "activate" 5-BUdR by catalyzing its conversion to a deoxyribonucleotide; the latter is required for cell death. Such cells as C3HlOTl/2 and BALB/3T3 have also been used in mutagenesis studies; these cells have easily detectable hydrocarbon- metabolizing activity.36~92 However, they are hypotetraploid, may not detect some recessive mutations, and may not detect some mutations that are expressed codominantly.95 These cells express a high degree of contact inhibition and low saturation density and thus can be used in bioassays of neoplastic transformation. Recent studies have suggested that such cells can be used to detect simultaneously the mutagenic and transforming capacities of test chemicals.35 Primary cell strains and in vivo-derived cells have been used in mutagenesis assays; although they have high PAH-metabolizing capacities and are diploid, the difficulty in growing, handling, and evaluating data from these mixtures of cells is an important disadvantage.120 DNA DAMAGE AND REPAIR Assays for DNA damage and repair have also used both bacterial and mammalian cells. Primary DNA damage in mammalian cells has been measured by such end points as selective toxicity in strains of cells deficient in ONA repair,144 increase in rate of DNA elusion under alkaline conditions,165 formation of specific pyrene-DNA adducts, 133 increase in rate of unscheduled DNA synthesis, 162 increase in incorporation of specific d~es,ll and increase in incidence of sister chromatic exchange. 80 DNA repair is a specific response to DNA damage. The covalent interaction of chemicals with ONA provokes an enzymatic repair of the damaged regions of DNA.142 Repair synthesis can be measured in a variety of ways, but incorporation of radioactive precursors into DNA is the simplest.29~60 A DNA damage-repair system that shows promise in detecting chemically induced DNA alteration uses the rat hepatocyte.l79 This assay has the advantages of using nondividing cells (normal semiconservative DNA replication is suppressed) and using freshly cultured cells that have high endogenous capacity for carcinogen metabolism or activation. It has recently been shown to be effective in detecting the ability of a variety of chemical carcinogens (including many different PAHs) to damage ONA.136 An increase in sister chromatic exchange (SCE) may be one of the best measures of DNA damage in humans. This end point, which involves incorporation of 5-BUdR into DNA during two cycles of replication and making the two chromatics stain differently, so that exchanges of 4-8

material are scorable, seems to develop as the consequence of presumably long-lived DNA lesions in the S phase of the cell cycle.l26 The exact mechanism of SCE formation is not understood, although it is well known that the frequency of SCE is increased by exposure of cells to known mutagens in viva or in vitro.2, 127~161 In fact, a linear correlation between mutations induced at specific loci and SCE has been demons bated in CHO cel 1~ .20 This assay has been used to monitor the exposure of humans to potentially harmful chemiCa1~51, 94~ 118 and even to cigarette 9moke.76 The in viva techniques for detection of SCE can be applied in two basic ways. One method involves 5-BUdR incorporation into bone-marrow cell DNA by inoculation of solutions or implantations of 5-BUdR pellets directly into animals2 and exposure of the animals to the chemical under study; this method has been used to detect in viva DNA damage via such substances as cyclophos~hamide,9 styrene,31 benzene,ll7 urethane,24 and cigarette smoke. The second method involves the incorporation of 5-BUdR into lymphocyte cultures during mitogen-induced activation in vitro; this has been used in the human studies mentioned above. Good baseline data on the incidence and variation of SCE in humans now exist.l8 SCE has also been shown to persist for several days or even months after~chemical exposure and thus can serve as an index of acute or chronic exposure to chemicals.94~118~161 Comparison of rates of formation of SCE and specific ON.A adducts suggests that, for several types of mutagens, induction of SCE does not necessarily result from a single specific ONA lesion.166 CHROMOSOMAL ABERRATION Assays for chromosomal aberration are also used to monitor for the mutagenic activity of test chemicals. These assays detect major rearrangements in the chromosomal or chromatic structure and include such end points as chromosomal or chromatic breaks, chromatic trans- location, dicentric chromosomes, ring chromosomes, balanced transloca- tion, and inversion.46~108 Another test for acutely altered chromo- somes is the micronucleus test, in which chromosomal damage leads to fragmentation of chromosomes or malfunction of the spindle apparatus, so that whole chromosomes lag behind the rest and, accordingly, form micronuclei.8l These techniques can be used with tissues derived either in vitro or in viva much like those used for analysis of SCE. Generally, agents that induce point mutation also induce chromosomal aberration. In humans, mitogen-activated lymphocytes can be used to monitor for the effects of exposure to physical and chemical agents. Exposure to radiation, to such chemicals as alcohol and vinyl chloride, and to cigarette smoke causes increases in chromosomal aberra- tion.l20 Cytogenic end points of aberration are useful, but one should remember that often chemicals induce very few aberrations at concentrations that permit the end point of gene mutation to be readily observed.141 In recent comparisons of three cytogenetic tests- 4-9

induction of chromosomal aberration, induction of micronuclei, and induction of SCE--the third proved to be the most sensitive in testing with several PAHs.8 NEOPLASTIC TRANSFORMATION - Neoplastic transformation has been assayed by a variety of in vitro systems, and it is not possible to review all the pertinent literature here. The reader is directed to the recent reviews of Casto and Carver,21 Heidelberger,64 and Mishra et al.115 Specific cells that have been used for assay of in vitro chemically induced neoclassic transformation include normal rodent (di laid) cell strains,42, 29 established aneuploid rodent cell lines,36~43~64~84 cell lines derived from human tumors,80~138 and cell lines initiated from apparently healthy human tissue.50~85~113~154 Table 4-7 com- pares properties of some mammalian-transformation systems. These cell lines share the following properties to some degree: They exhibit density-dependent inhibition of cell division and reach a defined saturation density, do not form colonies on soft agar or agarose, and do not give rise to tumors when inoculated into immunosuppressed syngeneic hosts. After transformation by chemicals, they lose the density-dependent inhibition of cell division and form piled-up, cries-crossed foci; they grow on soft agar or agarose, and they form tumors when inoculated into host animals. In addition many trans- formed cells exhibit increased fibrinolytic activity, 134 altered morphology in the scanning electron microscope, 106 specific chromo- somal arrangement, 10~134 and specific DNA sequences that can be transfected into normal cells, resulting in formation of the trans- formed phenotype. 33, 152 Although each of these cell systems has been successfully used to ascertain the biologic activity of chemical agents, none appears to be capable of universally detecting all classes of chemical carcinogens, low concentrations of all such agents, and relatively weak biologic activity of some chemicals. MUTAGENESIS - As just discussed, a number of model systems are available for assessing the mutagenic activity of emission, individual PAHs, and their mixtures. These are in two categories: bacterial systems and mammalian cell-culture systems. The activity of emission and its PAR constituents is discussed below relative to both kinds of model. BACTERIAL MUTAGENESIS Particulate matter from city air has been tested for mutagenic activity with the Salmonella/microsome system.131~167~169 In all cases, a positive response was obtained. Furthermore, many of the samples exhibited direct-acting mutagenic activity, i.e., the addition of activating enzymes present in a liver S-9 fraction was not required 4-10

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