645R78002 FINAL REPORT LITERATURE REVIEW AND EVALUATION OF THE HEALTH EFFECTS ASSOCIATED WITH DIESEL EXHAUST EMISSIONS October 1978 Prepared for: Health Effects Research Laboratory U.S. Environmental Protection Agency Research Triangle Park, N. C. 27711 EPA Project Officer: James R. Smith EPA Contract No. 68 - 02 - 2800 SRC Contract L-1348 SYRACUSE RESEARCH CORPORATION ------- Principal Authors The Syracuse Research Corporation (SRC) and its consultants developed the basic information for EPA and reviewers under Contract No. 68-02-2800. James R. Smith served as the EPA Project Officer. The major authors of this document are listed below. SRC Staff: Mr. Joseph Santodonato Dr. Dipak Basu Dr. Philip Howard SRC Consultant: Dr. Paul Sheehe Department of Preventive Medicine State University of New York College of Medicine Syracuse, New York 13210 ------- Preface Engineering tests have shown a significant improvement in fuel economy (25% or greater) in light duty vehicles equipped with diesel engines versus those equipped with gasoline engines. Automobile manufacturers are considering a major program for conversion to diesel engines in the automobile fleet by 1985. Available studies show rather large differences in emissions from diesel engine.exhausts as opposed to gasoline engine exhaust. Conversion of a major portion of. the automobile fleet to diesel engines may significantly change the ambient concentrations of both regulated and unregulated pollutants, and hence the potential human exposure pattern. Such changes may impact upon public health, and consequently require changes in air quality standards, and/or new emissions standards. An assessment of the current state of knowledge regarding the health effects from diesel exhaust emissions, and the identification of major research needs, are important factors which must be considered by the EPA under the 1977 Amendment to the Clean Air Act. In order to accomplish this objective, the following information on diesel emissions has been reviewed in this document: physical and chemical character- istics; biological effects in animals and man; epidemiologic studies; knowledge gaps; and research needs. ii ------- TABLE OF CONTENTS 1.0 Summary and Conclusions 1 1.1 Biological Effects ! 1.2 Physical and Chemical Characteristics 6 2.0 Introduction 9 3.0 Physical and Chemical Characteristics 11 3.1 Particulates 11 3.1.1 Physical Characteristics 12 3.1.2 Gasoline Exhaust 14 3.1.3 Emission Rate of Particulate Matter 17 3.1.4 Chemical Composition 22 3.1.5 Trace Metals 26 3.1.6 Inorganic Acids and Their Salts 27 3.1.7 Elemental Carbon and Unburned and Partially Burned Fuel and Lubricant 33 3.1.8 Polycyclic Aromatic Compounds 39 3.1.8.1 Dependency of PNA Emission on Vehicle Characteristics 46 3.1.8.2 Dependency of PNA Emission on Engine Operation Mode 46 3.1.8.3 Variation of PNA Emission with Engine Maintenance 48 3.1.8.4 Effect of Fuel Composition 53 3.1.8.5 Effect of Engine Mileage on PNA Emission 54 3.1.8.6 Effect of Exhaust Emission Control 54 3.2 Volatile Emissions 57 3.3 Fuel Economy 70 3.4 Smoke Results 71 3.5 Odor Rating 73 3.6 Noise 76 3.7 Engine Modification and Antipollution Devices for Diesel Cars 78 3.8 Effect of Irradiation of Automobile Exhaust 81 3.8.1 Photoreactivity of Gasoline Emissions 81 3.8.2 Photoreactivity of Diesel Emmissions 82 3.9 Research Gaps and Recommendations 85 3.9.1 Definition of Particulate Matter 85 3.9.2 Inadequate Particulate Sampling Procedure 85 3.9.3 Better Storage Method 86 3.9.4 Improvement of Analytical Methodology 86 iii ------- TABLE OF CONTENTS (Cont'd) Page 3.9.5 Identification and Quantification of New Components 86 3.9.6 Analysis of Sulfates 86 3.9.7 Effect of NO and 03 on Pollutant Formation 87 3.9.8 Quantification of Different PNA Levels 87 3.9.9 Uniformity in Data Reporting 87 3.9.10 Diesel Odor Characterization 87 3.9.11 Necessity for Using Additives 87 3.9.12 Regulation of Pollutants 88 References for Section 3.0 89 4.0 Biological Effects 95 4.1 In Vitro Studies 97 4.1.1 Mutagenicity in Bacterial Systems 97 4.2 In Vivo Studies 104 4.2.1 Absorption, Metabolism, and Excretion 104 4.2.2 Acute Toxicity 107 4.2.2.1 Inhalation Exposure 107 4.2.3 Subacute Toxicity 113 4.2.3.1 Inhalation Exposure 113 4.2.3.2 Dermal Exposure 122 4,2.3.3 Behavioral Effects 123 4.2.4 Chronic Toxicity 126 4.2.5 Bioassays for Carcinogenicity 127 4.3 Human Studies 131 4.3.1 Controlled Exposures 131 4.3.2 Epidemiologie Studies 131 4.3.2.1 Occupational Studies 131 4.3.2.2 Community Studies 140 References for Section 4.0 142 5.0 Identification of Knowledge Gaps 149 5.1 Biological Effects 149 6.0 Recommended Research 152 6.1 Biological Effects iv ------- 1.0 Summary and Conclusions 1.1 Biological Effects Human exposure to vehicular combustion products has been a matter of public health concern for many years. Increasing utilization of internal com- bustion engines in the development of industrial civilization has forced our society to live with an increased burden of air pollutants. The prospect that passenger cars equipped with diesel engines will soon represent a significant proportion of new car production raises an important question concerning pos- sible impacts on public health. Recognition of this situation allows the opportunity for evaluation of a major environmental change caused by the intro- duction of greater quantities and/or types of diesel-derived pollutants. It must be recognized, however, that the diesel engine is by no means the only (or even major) source of the pollutants of primary concern. The components of automotive emissions which are generally regarded to have greatest toxic potential include carbon monoxide, oxides of nitrogen, aldehydes, hydrocarbons, sulfur dioxide, and particulates. In comparison to the gasoline engine operating with or without a catalytic converter, the diesel produces far greater quantities of carbonaceous particulate material. These particles are of respirable size and have high surface areas, enabling them to adsorb gaseous exhaust products. Among these products are small amounts of irritant gases and, perhaps most significant, a large proportion of the polycyclic organic matter (e.g., benzo[a]pyrene) produced during combus- tion, some of which are carcinogens. This poses the potential risk of delivery of adsorbed gases into the lung by carrier particles. In turn this may lead to extensive localization of harmful materials in the lung, with the accompanying threat of emphysema and cancer development. In addition, fibrotic changes may occur leading to reduced lung compliance and/or obstruction. 1 ------- Experimental studies designed to establish whether diesel emissions represent a significant threat to human health have been conducted only infre- quently during the past 25 years. Moreover, these studies have not provided definitive and comprehensive insight to the health effects of diesel emissions. While it was recognized that the gaseous emissions from diesel engines are com- parable to or lower than for the noncatalyst-equipped gasoline engine, the toxicologic role of increased particulate production remains unclear. Just recently, however, it was reported that organic extracts of diesel particulate contained materials that were mutagenic to histidine-requiring strains of Salmonella typhimurium in the Ames assay. This positive result raises a ques- tion concerning the potential carcinogenlcity of this material, although it is not known how the effects of widely dispersed diesel exhaust in air may be related to the mutagenic effect of diesel extracts. These mutagens in diesel exhaust included, but were not limited to, the well-known polycylic aromatic carcinogens. Other positive compounds found included direct-acting (i.e., not requiring metabolic activation) frameshift mutagens; probably composed of polar compounds such as substituted polynuclear aromatics, phenols, ethers, and ketones. The strong formal relationship between mutagenesis and carcinogenesis thus may implicate extracts of diesel particulate as a carcinogenic material. It is also known, however,.that extracts of airborne particulate pollutants in urban atmospheres and gasoline engine exhaust are also mutagenic in the Ames assay. Moreover, direct-acting mutagens are found in gasoline engine exhaust (noncatalyst-treated) just as they are found in diesel emissions. In addition, a high incidence of skin cancers has been produced in mice by dermal administration with organic extracts of the particulate exhaust fraction from diesel and gasoline engines, and from extracts of ambient particulate ------- pollutants. However, quantitative differences in potentcy are likely to exist among extracts from these various sources. Investigators have for many years attempted to show that exposure to automotive emissions may lead to the development of cancer. Indeed, it was shown several decades ago that both diesel and gasoline engine exhaust contain carcinogenic polycyclic aromatic hydrocarbons such as benzo[a]pyrene. Since that time, chronic studies have been initiated which involve the inhalation of total diesel emissions by rats and hamsters. Under the conditions of exposure employed, these experiments have thus far failed to produce tumors of the respiratory tract. On the other hand, evidence of serious damage to the respiratory tissues has been obtained. Rats exposed to diesel exhaust for 20 months displayed extensive particulate accumulations in the lungs, accompanied by vesicular emphysema and beginning interstitial fibrosis. Similar observa- tions were made in hamsters, in addition to the presence of cuboidal meta- plasia. It is not known whether this tissue damage in rats and hamsters is reversible or if it may lead to significant shortening of life. A series of in vivo studies with several animal species inhaling diluted irradiated and non-irradiated diesel exhaust are being conducted by the U.S. Environmental Protection Agency (EPA). The initial subacute exposure studies using relatively high concentrations of diesel exhaust (1:12 dilution) were designed to provide preliminary data on toxic effects and target organs. Animals inhaling diesel exhaust for up to two months were found to have black granular particles in alveolar macrophages, and black pigment in the bronchial and carinal lymph nodes. These observations indicated the existence of clear- ance mechanisms for diesel particulate. ------- Among guinea pigs inhaling diesel exhaust several exposure-related changes were seen including, increased pulmonary flow resistance, increased lung weight to body weight ratios, and sinus bradycardia. Microscopic examina- tion of the lungs revealed goblet cell hypertrophy and focal hyperplasia of alveolar lining cells, possibly an early indication of damage to the alveolar wall by diesel exhaust. Neither the reversibility of these lesions, nor the degree of functional impairment which accompanies them has yet been determined. Other changes which EPA investigators observed were biochemical alterations in the lungs of rats, behavioral changes in rats, and increased susceptibility to death by respiratory infection in mice. The presently available data base does not allow for an accurate com- parison to be made between the effects of environmentally realistic concentra- tions of diesel emissions and catalyst or noncatalyst treated gasoline engine exhaust. Nevertheless, diluted gasoline exhaust produced emphysematous lesions in the lungs of dogs as well as a high incidence of bilateral renal sclerosis in rats. Evidence which is available thus far indicates that the use of an oxidation catalyst with gasoline engines will dramatically reduce the toxicity of resulting emissions. This can be attributed to the substantial reductions realized in the emission of most harmful gaseous components in the catalyst- treated exhaust. An overall assessment of the public health risks associated with diesel exhaust exposure cannot be based solely on the results of available animal studies. This is partly due to the fact that many areas of concern with respect to the toxicity of diesel emissions remain to be explored. In addition, parallel studies with diesel and gasoline engines have not been conducted which ------- would allow direct comparison of results. The alteration of the environment by increased utilization of diesel engines will probably be due to the relative abundance of particulate matter which is emitted. Protection of the public health will thus be best achieved by examining the potential adverse impact of this component of diesel exhaust. The ultimate goal in demonstrating that increased utilization of dieselized vehicles is an environmentally acceptable substitute for gasoline engines is to provide reliable epidemiologic evidence which supports this claim. Unfortunately, the previous epidemiologic research which is often used to support the safety of the diesel provides only a limited data base, which is clearly inadequate for developing sound conclusions. It is this fact more than anything else which prevents the formulation of a valid health risk assessment for diesel emissions. Among the more recent occupational mortality and morbid- ity studies which have been reported, it has not been possible to isolate diesel emissions as a singularly important factor in contributing to the excess deaths and adverse health effects occasionally observed. Several studies involving populations of workers exposed to high levels of diesel emissions are currently being conducted by NIOSH. Results of these investigations should be forthcoming within the next several years. Since large populations that have been exposed to ambient levels of light duty diesel emissions do not yet exist, the possibility of conducting community studies at this time is remote, espec- ially when the intervals necessary for the development of neoplasms in humans after exposure are considered. Thus because of the lack of a broad-based community study or well-controlled investigation of a worker population where quantitative exposure data are available, no definitive judgement regarding diesel emissions can now be made. 5 ------- There is presently no way to place into perspective the hazards of diesel emissions relative to those of automotive emissions as a whole. In the absolute sense, diesel exhaust is a noxious mixture with the potential to pro- duce serious lung disease, behavioral alterations, biochemical changes, and decrements in pulmonary function. Its risk as a human carcinogen, however, is unquantified. When looked upon in light of what we know regarding the poten- tial health effects of noncatalyst-treated gasoline exhaust, the impact of diesel emissions remains unclear. Presently, there are no data which suggest an increased carcinogenic threat from the substitution of diesel- for gasoline- powered light duty vehicles. Further epidemiologic research must be pursued and studies in laboratory animals conducted to characterize cause-and-effect relationships and exposure-response parameters. 1.2 Physical and Chemical Characteristics A comparison of well-maintained diesel cars (without emission control) and gasoline cars (with emission control) for regulated vaporous emissions shows that diesel cars emit more hydrocarbons than gasoline cars. With auto- mobiles of comparable size, diesel cars emit twice as much hydrocarbons as gasoline cars in the FTP mode. The difference between the two classes of cars becomes even greater in the SET and FET mode, with diesel cars likely to emit three times more hydrocarbons than gasoline cars. The 1977-79 Federal Standard of 1.5 g/mile for hydrocarbon emissions, however, can be met by diesel cars. With respect to CO, both gasoline and diesel cars have about the same emission rate. In the FTP mode, gasoline cars have higher CO emission rates than diesel cars, and the reverse is true in the FET and SET modes. The 1977-79 Federal Standard o£ 15 g/mile is met by diesel cars. The NO emission for gasoline A ------- cars is higher than for diesel cars in all modes. Most diesel and gasoline cars will meet the 1977-80 Standard for NO .of 2.0 g/mile. If a 0.5 g/mile A particulate emission standard is introduced for diesel cars in the future, most cars will be able to meet this standard. The fuel economy consideration is in favor of diesel cars. Based on combined city/highway estimates, the fuel economy for diesel cars is 33 to 60% better than in corresponding gasoline-powered cars. In terms of unregulated emissions, diesel cars are higher sources of carbonyls and substantially higher, sources of particulate emissions. Although there is uncertainty about benzo[a]pyrene emission rates, it appears from the work of Springer and Baines (1977) that diesel cars emit at least an order of magnitude more benzo[a]pyrene than gasoline cars. The reliability of the BaP data in this work, particularly for gasoline exhaust, can be doubted because of the unreliable sample collection technique. It has been demonstrated by Gross (1972) that an increase of 0.5% CO could cause a 45% increase of PNA emissions. Based on this result one would not expect higher PNA emissions from diesel cars. This aspect of research correlating PNA and CO emission rates should be reinvestigated with newer cars equipped with catalytic converters. Sulfur dioxide emission rates for diesel cars are substantially higher than for gasoline-powered cars. This is, however, expected because the national average diesel fuel contains 0.23 weight% sulfur compared to 0.03 weight% $ulfur for the national average gasoline fuels. Reduction of fuel sulfur will reduce the S0? emission rate from diesel cars. The sulfate emis- sion rate for gasoline-powered cars with no air pump in the catalytic system is less than for diesel cars. However, with air pumps, the sulfate emission rates become comparable. 7 ------- Diesel engines produce more visible smoke than gasoline-powered cars. However, diesel cars are capable of operation within the EPA smoke visibility limit, for the most part, with only brief excursions during rapid throttle movement. .Diesel exhaust have more odor than gasoline exhausts and the odor intensity of diesel exhaust may noticeably change during the transient cycle. Interior noise levels are slightly higher with the diesel during acceleration than in gasoline automobiles. The idle noise levels are also higher with diesels compared to gasoline cars. There is a substantial conflict in the available data base among various authors due primarily to nonuniformity of experimental conditions and uncertainty in the variable experimental parameters. In addition to these conflicts in the data base, nonuniformity of data reporting sometimes makes it difficult to compare results among various investigators. A number of new suspected carcinogenic compounds, namely, methylene- PNA's and nitro-PNA's, have been reported in gasoline exhausts. Their presence can be expected in diesel exhaust and needs confirmation. ------- 2.0 Introduction According to an EPA projection it has been estimated that automobiles equipped with diesel engines are likely to increase at a rate of 5% per year and capture up to 25% of the U.S. new car market by 1985. The major factor behind the projected increase in diesel-powered automobiles is the considerable i fuel economy for this type of car. Of the total estimated auto fuel consump- tion during the period 1976-2000, it is projected that gasoline will decrease by about 2% and diesel will increase by about 37% (EHA, 1978). At the present time, diesel-powered motor vehicles (mostly heavy duty) contribute about 1% of all motor vehicle emissions (National Academy of Sciences, 1976). With the steady increase of diesel-powered automobiles, the effect caused by the anti- cipated change in the quantities of environmental pollutants emitted to the atmosphere dictates the need for more thorough investigations. The present report is prepared for the EPA to assess the environmental health impact as a result of conversion of light duty vehicles from gasoline-powered to diesel- powered engines. However, much of the information to date is on heavy duty diesel engines and might thus lead to biassed extrapolations. Although, diesel exhaust contains relatively low levels of CO, making it suitable for use in mining operations, it is considered by some to be poten- tially a major source of air pollution due to its propensity for emitting visible smoke and obnoxious odor. Particular attention, therefore, should be given to the latter parameters in order to evaluate their significance in promoting any deleterious health effects. The exhaust emissions from gasoline- powered automobiles, on the other hand, are steadily decreasing as a result of introduction of emission control devices. With the rates expected to decrease ------- even further when the statutory emission standard becomes mandatory, the emissions from diesel-powered automobiles may become a significant factor in air pollution. Likewise, recent decreases in particulate emissions from stationary sources might make the effects of diesel emissions even more evident. It is, therefore, important to make a comparative study between diesel and gasoline exhaust with the objective of maintaining a comparable level (in terms of health effects) of environmental pollution. Although the presently available literature contains abundant information in some aspects of exhaust emission rates from diesel- and gasoline-powered automobiles, there is a lack of data in other areas. In many cases, emission rate data determined with the objective of quantitating chemical species lack accompanying details about the engine operating conditions and vice versa. This makes the comparative study of emission rates between the two fuel-powered automobiles very difficult and/or impossible. The following section undertakes the task of presenting a comparative review of the physical and chemical sig- nificance of different exhaust emission parameters from diesel- and gasoline- powered automobiles, with particular emphasis on those with suspected injurious health effects. 10 ------- 3.0 Physical and Chemical Characteristics The chemical compositions of diesel and gasoline emission have been broadly divided into two sections, one section detailing the particulate matter and the v other vaporous emissions. 3.1 Particulates The exhaust from both diesel and gasoline engines contain suspensions of microsize solid particles and liquid droplets in gas or vapor. It is, therefore, necessary to define which part of the exhaust can be considered as particulate matter. There is no general agreement on this subject. According to a commonly used definition anything other than condensed water that can be collected on Type A glass files filtering media at a temperature not to exceed 125°F (51.78C) is considered as particulate matter. The choice of the type A filter is based on the fact that it removes 98% of the particles larger than 0.05 ym diameter (Sampson and Springer, 1973) from the gas or vapor phase. The selection of collection temperature of 125°F is on the basis of a compromise between minimization of moisture condensation and maximization of particulate collection. However, there are certain limitations to this definition. When the hot exhaust from the automobiles is discharged into the atmosphere, inhala- tion of particulate matter by humans occurs at ambient temperature after air dilution and associated cooling of the exhaust stream. Far more serious limitations of this definition may arise unless the retention efficiencies of the filtering media can be demonstrated to be high for particles of size ranges below 0.05 ym. Data regarding the efficiency of particulate collection from automobile exhaust are very limited. Therefore, until a better method is available, the particulate data developed by various authors should be inter- preted in their proper perspective. 11 ------- 3.1.1 Physical Characteristics The physical characteristics of the particulate from both diesel and gasoline exhaust are discussed individually. Diesel Exhaust: X-ray spectroscopy shows soot to have a graphite structure with hexagonal basic carbon units linked into platelets giving a crystallite about 21 x 134° containing 10 to 30 mole percent of hydrogen (Millington and French, 1966). The structure has a good resemblance to poly- benzenoid substances, such as the polynuclear aromatic hydrocarbons (PNA's). The basic crystallite units agglomerate into spheres with a diameter range of 100-800A" (Vuk and Johnson, 1975). These agglomerates containing as few as one 100A° spherical particle or as many as 4000 spheres combine to form particles up to 30 vim diameter (Vuk et al., 1975). The other physical characteristics of the particulates as measured by different authors are presented in Table 3.1. Table 3.1 shows that the particulate matter has very large surface area which make it a powerful adsorptive agent. The low still air settling velocity will make it remain airborne for a long period after gener- ation. It should be recognized that several parameters, such as, fuel composition, engine design and maintenance, operating conditions and emission control devices may influence the physical characteristics of the emitted particulates. The particle size is normally expressed in terms of either aerodynamic diameter or Mass Median Equivalent Diameter (MMED: diameter of an aerodynamically equivalent sphere of unit density). The effect of engine operating parameters, such, as engine speed and load, on particle size was studied by Vuk and Johnson (1975). From their work these authors concluded 12 ------- TABLE 3.1. PHYSICAL CHARACTERISTICS OF PARTICIPATE FROM DIESEL EXHAUST Parameter Mass medium Particulate Surface area Settling velocity diameter (ym) count no/cm3 m2/m3 mm/hr. Value 0.1 - 0.3 107 2 0.25 - 40 Reference Vuk & Johnson, Frey & Corn, Frey & Corn, Frey & Corn, 1975, Dolan 1967 1967 1967 et al., 1975, and Schreck, 1978 13 ------- that the particle diameter decreases slightly with increasing engine load and temperature, Ddlan et_ &!_<, (1975), however, reported a shift in particle size shown as in Figure 3.1 from the smaller "nuclei mode" to the large "accumula- tion mode" with increasing engine load. The results of Laresgoiti e_t al. (1977) and Schreck (1978) do not show any significant variation in particle size either with engine speed or load. It can be concluded from these inves- tigations that particle size may not be strongly dependent on engine operating conditions. Although no definite explanation can be offered, it can be con- jectured that the discrepancies between the various results are due to the differences in engine design and fuel composition used in these experiments. 3.1.2 Gasoline Exhaust The size of the particulate matter emitted from gasoline engine exhaust was studied by Mueller et. aJL. (1962) and Moran and Manary (1970). Their findings were similar to that of Sampson and Springer (1973). The latter work is summarized below. The particulate size from gasoline engine exhaust depends on the fuel composition. Unleaded fuel results in particulates of larger aerodynamic diameter. For leaded fuels, approximately 90 wt% of the emitted particulates are below 0.35 urn diameter and over 98 wt% below 10.0 ym diameter. In case of unleaded fuels, approximately 40 wt% of the total particulates are below 0.35 ym diameter and 88 wt% below 10.0 ym diameter. The particle size distri- butions of the emitted particulates from leaded and unleaded fuels was studied by Sampson and Springer (1973). They concluded that the weight of the smaller particles (<0.35 ym diameter) was much higher with leaded than with unleaded fuel, 14 ------- g M H I O U w A TOTAL D NUCLEI o ACCUMULATION FULL LOAD Figure 3.1. Variation in aerosol volume concentration with load for the two size components of diesel exhaust: the accumulation mode 0.08 ^ Dp <^ 2.0 ym and the nuclei mode Dp <_ 0.08 ym (from Dolan et_ al_., 1975). Dp: diameter of particles. 15 ------- It has been estimated by Mueller (1970) that the MMED of the lead particles which can stay dispersed in the atmosphere fall in the range of 0.1 to 1.0 ym. Of the total lead particles emitted from leaded gasoline about 71-91% are respirable compared to 34-59% respirable particles in the total particulate matter in the exhaust (Mueller, 1970). The particle size of the exhaust is similarly dependent on the fuel sulfur content. In gasoline vehicles equipped with a catalytic converter, the sulfate emission rate is substantial compared to the total particulate emission rate (see Section 3.1.6). More than 70% of the sulfate emitted by the vehicles may be in the form of HLSO, with a geometric mean diameter of M).02 pm (Wilson et^ al., 1977). The rest of the suifate is primarily in the form of (NH,)2SO, and other refractory sulfates (Lee and Duffield, 1977). The mean diameter for ammonium sulfate aerosol is 0.07 ym. Therefore, the introduction of a catalytic converter to vehicles is bound to shift the emitted particulate diameter to smaller size ranges. When sulfuric acid aerosol is exhausted into the atmosphere, most of the aerosol in the smaller nuclei mode undergoes growth into the larger accumulation mode in the size range of 0.1 to 1.0 urn. When this aerosol is inhaled, the high relative humidity in the pulmonary system causes the aerosol droplets to grow further in size. As a result of water vapor absorption the acid is also diluted. Thus Wilson e£ al. (1977) estimated that a 0.35 urn diameter droplet at 50% relative humidity would grow to a 1.0 ym in diameter at 99% relative humidity and the concentration would decrease from approximately 10.5 N to less than 0.5 N. But particles in the smaller nuclei mode will experience less growth and dilution due to the decrease in vapor pressure 16 ------- caused by the high curvature of small droplets. Both size ranges will deposit appreciably in the bronchi and alveolar regions. However, the nuclei mode will give greater total, deposition and more deposition in the alveolar region. The diameter of the emitted particles not only depends on fuel composition but also on engine operating conditions. Generally, it has been found that for leaded fuels cyclic operations yield larger particles than steady state operations (Habibi, 1970). The average size of the emitted lead particles, also, increase significantly with mileage accumulation from a MMED of 1.1 ym at 6350 average mileage to 4.7 ym at 21350 average mileage (Habibi, 1970). The corresponding effects on the particle size for unleaded fuels has not yet been studied. 3.1.3 Emission Rate of Particulate Matter The emission rates of particulate matter from both diesel- and gasoline-powered vehicles are presented in Table 3.2. Several parameters affect the weight of particulates emitted from vehicles operated by both fuels. These parameters include fuel composi- tion, engine design and maintenance, operating conditions, engine mileage, and the presence or absence of emission control devices. In the case of diesel-powered vehicles, increase in fuel sulfur and aromaticity has been shown to increase particulate emissions (Braddock and Gabele, 1977). Similar increases in particulate emission with increase in fuel aromaticity has been observed by Ter Haar et al. (1972) in case of gasoline cars. The increase of particulate emission with increase in S-content of the 17 ------- TABLE 3.2. PARTICULATE EMISSIONS FROM DIESEL- AND GASOLINE-POWERED PASSENGER CARS Vehicle type Diesel vehicles: VW Rabbit1 2 Peugeot 504 3 Mercedes 240D Mercedes 300D3 Oldsmobile 3501 Gasoline vehicles: With emission control VW Rabbit1 Oldsmobile 3501 Engine displacement CID 90 129 146 183 350 90 350 Total particulates in FTP mode, mg/mile 294.0 397.0 477.0 490.0 924.0 6.8 9.1 Without emission control 4 Leaded gasoline car a 4 Unleaded.gasoline car a Advanced unleaded gasoline car c 246.0L 181.Ol 2.0 a. Various 1966-70 model cars. b. Average of low and high mileage cars. c. Data not available. 1. Ref. Springer and Baines, 1977 2. Ref. Braddock and Gabele, 1977 3. Ref. Springer and Stahman, 1977 4. Ref. TerHaar e£ al., 1972 5. EPA generated data cited in PEDCO Environ. Inc., 1978 18 ------- fuel has been observed by Stara ejt al_. (1974). Using a G.M. engine equipped with a pelletized catalyst, these authors have reported an increase of particu- late emission from 9.6 rag/mile with 0.05% S indolene fuel to a value of 30.2 mg/mile with 0.10% S indolene fuel. The effect of fuel additives with non emission-controlled cars has been studied by Ter Haar et, a!L. (1972). Addition of lead, carburator detergent, phosphorus and a commercial upper cylinder lubricant all caused increases in particulate emission. The effect of engine size and operating modes on particulate emission rates has been studied by Springer and Stahman (1977) and Springer and Baines (1977). In the case of diesel-powered automobiles, the increase in particulate weight with the increase in engine size has been demonstrated by Springer and Stahman (1977). The effect of diesel engine operating parameters on the variation of particulate mass emission has been studied by Laresgoiti et al. (1977) with a Mercedes Benz Model 240D car and the effect is shown in Figure 3.2 and Figure 3.3. From their work Laresgoiti et al. (1977) concluded that any change in engine performance parameters which affects a change in combustion temperature, combustion time, and fuel-to-air ratio in the combustion chamber will cause variation in the emitted particulates. For gasoline-powered vehicles, moderate variations in the air- to-fuel ratio and spark timing has no significant effect on particulate emis- sion rate (Ganley, 1973). However, an increase of the particulate weight by about 300% was observed as the engine speed and load was increased from 40 MPH to 70 MPH under road load conditions. 19 ------- 3IOOrpm 2900 rpm 2150 rpm 25 50 75 PERCENT Of FULL LOAD 100 Figure 3.2. Exhaust particulate concentration as a function of engine speed. (Laresgoiti et al., i 977) 20 ------- PERCENT OF FULL LOAD: 1.000 2,000 REVOLUTIONS PER MINUTE 5,000 Figure 3.3. Exhaust particulate concentration as a function of engine load. (Laresgoiti et_ al., 1977) 21 ------- The dependency of particulate emission rates for both diesel- and gasoline-powered automobiles on engine size and operating modes is shown in Table 3.3. It can be seen from Table 3.3 that the particulate emission rate for both catalyst equipped gasoline-powered cars and non-catalyst equipped diesel-powered automobiles increases with increase in engine size and that the emission rates are dependent on the engine operating modes. The emission rates are higher during cold cycle than hot cycle. The particulate matter in exhaust from a non-catalyst equipped diesel is about 47 to 102 times more than gasoline engines fitted with a catalytic converter. The use of a catalytic converter has the effect of increasing the amount of particulate from both diesel and gasoline-powered automobiles. Table 3.4 shows the effect of a catalytic converter on particulate emission rates. It is necessary to emphasize that the particulate emission rate from non-catalyst cars operating with unleaded fuel has decreased substantially (see Table 3.2) with the introduction of advanced lean-burn engines, probably due to decreases in the sulfate emission rate. The primary reason for the increase in particulate matter with catalyst equipped cars is due to conversion of SCL to particulate sulfate (see Section 3.1.6). The effect of different variables on the mode of particulate emission is qualitatively summarized in Table 3.5. 3.1.4 Chemical Composition The chemical composition of particulate matter in both gasoline and diesel exhaust is complex. The characterization of diesel exhaust 22 ------- TABLE 3.3. VARIATION OF PARTICULATE EMISSION RATES WITH CAR SIZE AND ENGINE OPERATING MODES3 Operating mode Particulate emission rate, mg/km Size of gasoline-powered car Size of' diesel-powered car V.W. Rabbit 90 CID Oldsmobile Cutlass 350 CID V.W. Rabbit 90 CID Oldsmobile Cutlass 350 CID U> 1975 Federal Test 3.34 Procedure Federal Test 4.95 Procedure cold Federal Test 3.01 Procedure hot Sulfur Emission Test 1.63 Fuel Economy Test 1.55 5.63 8.38 3.55 9.72 13.62 182.0 202.0 165.0 161.0 157.0 573.0 628.0 523.0 360.0 298.0 a. Ref. Springer and Baines, 1977. ------- TABLE 3.4. EFFECT OF CATALYTIC CONVERTER ON PARTICULATE EMISSION RATES Vehicle category Particulate emission rate, mg/mile Light-duty gasoline-powered vehicles: Catalyst3 6.0 Catalyst (excess air)a 15.0 Non-catalyst (lead fuel)a 250.0 Non-catalyst (unleaded fuel)a 2.0 Light-duty diesel-powered vehicles: Non-Catalyst3 500.0 Catalyst Some small decrease a. EPA generated data cited in FED Co. Environ. Inc., 1978. b. Ref. Seizinger, 19/8 24 ------- TABLE 3.5. EFFECT OF VARIABLES ON PARTICULATE EMISSION FROM GASOLINE- AND DIESEL-POWERED CARS Variable Engine type: Indirect injection Direct injection Turbocharglng Engine displace- ment Emission control: Exhaust gas recirculatlon (EGR) Catalyst Catalyst & water scrubber Thermal reactor Engine speed & load Engine maintenance: Engine deteriora- tion Combustion chamber deposits Fuel Composition S-content Aromatlclty Fuel Additives Lead Halogen compounds Nitromethane Ba & Nl-additives Methanol Water injected with fuel Emission Parameter Particulate mass Particulate mass Particulate mass Particulate mass Particulate mass .Particulate mass Particulate mass Particulate mass Particulate size Particulate mass Particulate mass Particulate mass Particulate mass Particulate mass Farticulate mass Particulate mass Particulate mass Particulate mass Particulate mass Particulate mass Effect Diesel increase decrease decrease decrease with decrease in parameter increase increase decrease decrease no change increase with increase in variable increase with poor maintenance increase with increase in variable increase with increase in variable increase decrease decrease but may decrease engine life decrease decrease Gasoline decrease with decrease in parameter increase decrease increase with increase in variable increase with deposits increase with increase in variable increase with increase in variable increase increase decrease Reference EEA, Inc., 1978 EEA, Inc., 1978 NIOSH, 1978 Springer & Balnes, 1977 NIOSH, 1978 Stewart et al., 1975 & Stara et at. , 1974 NIOSH, 1978 NIOSH, 1978 Laresgoiti et al . , 1977 & Ganley,~T973 NIOSH, 1978 GI-OBS, 1972 NIOSH, 1978 & Stara et al. , 1974 Braddock & Gabele, 1977 & TerHaar et al., 1972 Sampson & Springer, 1973 Broome & Khan, 1971 Broome & Khan, 1971 Broome & Khan, 1971; Apostolescu et al. , 1977 Broome & Khan, 1971 Greeves et. al. , 1977 Detergent Particulate mass Injector stays increase clean but no hard data on particu- late emission NIOSH, 1978 & TerHaar, et al., 1972 25 ------- particulates has begun only recently and the available information is limited. Complete combustion of fuel under perfect conditions should yield principally carbon dioxide and water. Because the combustion process in an actual engine is imperfect, several other products are produced. Both absolute and relative concentrations of combustion products are influenced by numerous factors. Some of the most prominent factors are: (1) air-to-fuel ratio, (2) ignition timing, (3) inlet mixture density, (4) combustion chamber geometry, (5) the variable parameters, such as speed, load, and engine temperatures, (6) fuel composition, and (7) presence of emission control devices. The particulate matter from both diesel and gasoline exhaust contains a variety of products. Some of those which have been identified are: (1) unburned carbon, (2) unburned and partially burned hydrocarbons originating primarily from fuel and oil, (3) trace amounts of metals, (A) inorganic acids and their salts, namely, sulfates and nitrates, and (5) polycyclic aromatic hydrocarbons. The exhaust emissions from diesel and gasoline cars containing each of these categories of compound are discussed individually. 3.1.5 Trace Metals The origin of metals in automobile emissions is from two dis- tinct sources, namely, fuel and lube oil, and engine and exhaust system wear. When catalytic converters are used, the third possible source could be attri- tion products from the catalyst. However, no trace metals from, the latter source have been reported. When leaded gasoline is used, obviously the pre- dominant metal content in the exhaust is lead (Campbell and Dartnell, 1973). The lead emission rates from cars under cyclic operating conditions have been studied by Ter Haar £t al. (1972); Habibi et^ al., (1970); Ninomiya e£ al. (1970) 26 ------- Typical emission factors for metals cannot be derived from baseline characterization of auto exhaust by dynamometer tests as performed by EPA, since attempts are made to keep variability of additives, oils, and lubri- cants to a minimum. Emphasis is placed rather on the effect of emissions as a function of variations in operating conditions. The data cited in Table 3.6 reflect this because the different test cycles differed significantly in the average speed and variability of the operating mode. All the metal data, except the precatalyst Cu and Fe data, given in Table 3.6 were obtained by an X-ray fluorescence method. The precatalyst Fe and Cu data were obtained by emission spectrometry. A comparison of the results given in Table 3.6 with the results obtained by Springer and Baines (1977) is interesting. With the exception of iron, the latter authors have failed to detect any other metals listed in Table 3.6 in all modes of operation with a 1976 Oldsmobile diesel Cutlass and a 1977 V.W. diesel Rabbit. Evidently, more research is needed in this field to establish the possible emissions of trace metals from both diesel- and gasoline- powered passenger cars. 3.1.6 Inorganic Acids and Their Salts The sulfate emission rates for diesel- and gasoline-powered passenger cars are .demonstrated .in Table 3.7, Comparison of the average values shows that the diesel has higher sulfur emission rates than non-catalyst gasoline cars. However, gaso- line cars equipped with a catalyst have comparable sulfate emission rates to diesel cars. These emission rates are substantially lower for advanced non- catalyst and three-way catalyst gasoline-fueled vehicles. However, addition of 27 ------- TABLE 3.6. EMISSION RATES OF SELECTED METALS FROM A VARIETY OF CARS UNDER DIFFERENT OPERATING CONDITIONS Pre-catalyst cars Metals FTP FET SET 60 mph Cruise Catalyst cars (49-State Standard) ^ 50 mph Cruise Mean Median Range Catalyst cars (Calif. Standard)4 FTP Dual catalyst FTP FET SET 4 Lean Burn Engine FTP FET SET 4 Stratified charge FTP FET SET 4 Rotary FTP Diesel (#2 Natl. Avg. Fuel) FTP FET SET Pb (rag/mi) 40.5 19.8 20.0 0.028 0.015 0-0.325 0.03 0.18 0.03 0.07 6.69 3.76 7.00 N.D. N.D. 0.12 0.40 6 2.55 2.50 2.00 Mn (mg/mi) N.A.a N.A. N.A. N.A. N.A. N.A. N.D. N.A. N.A. N.A. 0.05 0.12 0.07 N.D. N.D. 0.01 0.09 1.46 1.45 1.19 Cu (mg/mi) N.A. N.A. N.A. 0.016 0 0-0.293 0.18 0.12 0.01 0.02 0.06 0.08 0.08 N.D. N.D. N.D. 0.04 1.56 2.03 1.54 Fe (mg/mi) N.A. N.A. N.A. 0.029 0.007 0-0.341 2.28 0.56 0.03 0.07 1.17 0.07 0.15 0.13 0.23 0.05 0.70 1.56 0.12 0.08 Ni (mg/mi) N.D.b N.D. N.D. N.A. N.A. N.A. 0.01 4.12 0.27 0.50 N.D. N.D. N.D. 0.01 0.01 N.D. 0.06 N.A. N.A. N.A. ? N.A.: not available *"^ IkT "IN » u ... x. J^A^^-i-j-— .13 1 Unpublished data by R.L. Bradow cited in Lee and Duffield, 1977b. 2 Dow, 1970 3 DEC, 1976 4 Gabele ejt^ al., 1977 5 EPA, 1977 6 Braddock and Bradow, 1975 28 ------- TABLE 3.7. SULFATE EMISSION RATES (mg/mile) FROM DIESEL VERSUS GASOLINE PASSENGER CARS Vehicle type Diesel vehicles: V.W. Rabbit1 Peugeot 204D2 Peugeot 504 3 2 Mercedes 220D (comprex) Mercedes 240D2 Mercedes 300D2 Oldsmobile 3501 Gasoline vehicles: Non-catalyst, no air pump Chevy, 1972* Non-catalyst, air pump Granada, 19754 Dodge, 19 754 Catalyst, pelletized, no air Average of 1975-76 cars4 Catalyst, pelletized, air / Average of 1975-76 cars Catalyst, Monolith, no air L Average of 1975-76 cars Catalyst, Monolith, air L Average of 1975-76 cars Advanced non-catalyst A Stratified charge / Rotary, THM reactor 4 Lean burn 4 Lean burn, THM reactor Advanced catalyst 3-way, F-l4 (fuel injected) 1 3-way4 Start cat. Duel Cat.4 / Lean bum oxd. cat. Sulfate trap Eaee metal cat. Emission rate (mg/mlle) 1.7 8.2 6.5 9.2 14.2 16.6 21.0 0.2 0.7 2.7 10.1 " 12.8 * 7.7 33.5 1.9 1.5 1.0 6.3 1.5 0.6" 26.3 36.1 88.9 4.7 6.3 a. One high value rejected In averaging the result. 1. Ref. Springer and Balnes, 1977 2. Ref. Springer and Stahman, 1977 3. Ref. Braddock and Gabele, 1977 4. Ref. goners et al., 1977 29 ------- an air injected oxidation catalyst downstream of a three-way catalyst, or addition of an oxidation catalyst to a lean burn non-catalyst system, will result in higher sulfate emission rates typical of air pump equipped oxidation catalyst systems. The sulfate emission rates for both classes of cars (diesel and gasoline) are dependent on four variables. These are: (1) vehicle design and engine displacement, (2) sulfur content of the fuel, (3) vehicle operation mode, and (4) engine mileage. The emission rates tend to increase proportion- ately to vehicle size, which is reasonable because this is the order of in- creasing fuel consumption. The effect of vehicle size, and mode of operation on sulfate emission rates has been demonstrated by Springer and Baines (1977). The national average for diesel and gasoline fuel supply sulfur content are 0.23% and 0.03%, respectively (Springer and Baines, 1977). Of the total fuel sulfur, 1-3% is converted to sulfate (Braddock and Gabele, 1977) in diesel engine operation. The conversion rate is similar in gasoline engines equipped with a catalytic .converter (Springer and Baines, 1977). However, Wilson et al. (1977) have shown that the conversion rate can be as high as 13 + 3% in gasoline cars fitted with a catalyst and air pump. Since diesel fuels contain about 8 times more sulfur than gasoline fuels, the increase of sulfate emission with increase in fuel sulfur content is pronounced in diesel vehicles. This is demonstrated in Table 3.8. The effect of engine mileage on sulfate emission as noted by Lee and Duffield (1977) is evident in gasoline vehicles with catalytic converters. This is due to sulfate storage in the catalyst as shown by the reaction: A£0 + 3 S0 —' A£ 30 ------- TABLE 3.8. SULFATE EMISSION RATES WITH THE VARIATION OF FUEL SULFUR CONTENT3 Fuel Jet A No. 1 No. 2 No. 2D° High-Sulfur No. 2D Fuel % sulfur 0.04 0.13 0.23 0.29 0.49 Sulfate emission rates in SET mode, mg/mile 2.6 5.4 6.5 7.0 11.7 a. Ref. Braddock & Gabele, 1977 b. National average for No. 2 fuel oil. c. With the exception of 26.5% aromatics content versus the minimum 27% specified, this fuel conforms with the No. 2D fuel specifications given in Federal Register for certification of light duty diesel engines. 31 ------- On a fresh catalyst, much of the SC>3 that is formed is stored as AH (SO.) . However, as the catalyst nears saturation, the reverse reaction becomes prominent. The equilibrium storage/release level of a catalyst is a function of catalyst temperature, catalyst space velocities, feed gas composi- tion and time (Somers et^ ai. , 1977). Although the irate of sulfate emission is shown in Table 3.7, nothing has been said about the form of sulfate emitted from automobiles, that is, how much of it is emitted in the free acid and salt state. This could be important in relation to the study of any possible effects on health. It is not known what types of sulfate are emitted by the diesel. In the case of gasoline cars, essentially all the sulfate is in sulfuric acid form (Lee and Duffield, 1977). A striking increase in the acidity of the particulate has been observed by Stara et al. (1974) when gasoline engine exhausts are treated with a catalytic converter. Comparison of the exhaust particulate acidity has shown that the acidity of catalyst-fitted engines is 65-260 times greater than engines with no catalytic converter (Stara et ajl., 1974). The sulfuric acid mist emitted from vehicles is partly neutral- ized by ammonia to form (NH,)«SO, and NH.HSO,. A part of the acid reacts with other metallic elements or compounds in the atmosphere to form metal sulfates. However, it has been estimated by Wilson et al. (1977) that more than 70% of the sulfate emitted by the vehicles remains in the form of H9SO, at 20 meters downwind from the point of emission. The emission rates of hydrocyanic acid (HCN) as studied by Braddock and Gabele (1977) is discussed in Section 3.2. Certainly, anions other than sulfate, such as nitrate and carbonate are emitted from automobile exhaust. Campbell and Dartnell (1972) 32 ------- have estimated that the nitrate ion from non-catalyst gasoline cars comprises 7.3% by weight of the total particulate. Stara e_t ad. (1974) have reported nitrate emission rates from gasoline cars with and without a catalytic con- verter as 0.01 mg/mile and 0.04 mg/mile, respectively, at 15 MPH speed. 3.1.7 Elemental Carbon and Unburned and Partially Burned Fuel and Lubricant The combustion of hydrocarbon fuels under "non-ideal" conditions involves complex processes. Some fuel passes the combustion zone unaltered, while some cracking processes in the ignition zone produce lower molecular weight compounds. Cracking processes out of contact with Cv may produce ele- mental carbon. Some of the fuel is chemically rearranged by pyrolysis to produce fragments. Consequently, some new products can be formed by the inter- action of various fragments of the fuel molecules. A part of the fuel under- goes oxidation producing partially oxidized products. Besides the fuel, lubricating oil is partially responsible for hydrocarbon emissions from auto- mobiles. Both absolute and relative concentrations of combustion products are influenced by numerous factors. Some of the most prominant factors are: (1) fuel-to-air ratio, (2) ignition timing, (3) inlet mixture density, (4) combustion chamber geometry, and (5) the variable parameters, such as speed, load and engine temperature. The fuel-to-air ratio influences the principal combustion products more than any other factors. Although the literature has abundant data on the percent of carbon in the particulate matter from automobile emissions, the quantitative distribution of carbon into elemental and organically bound forms is not well established. One of the better methods for determining elemental carbon has 33 ------- been developed by Schreck £t al_. (1978). According to this method, the exhaust particulate matter is subjected to thermogravimetric analysis in a NZ atmos- phere from room temperature to 700°C. The particulate matter will start losing weight until all of the volatile organic matter has decomposed and/or volatil- ized and pure carbon particulates are left as residue. At 700°C, the atmos- phere is changed to air. Oxidation of the remaining carbon particles will occur. When this process is complete, the. remaining residue from the sample may be assumed to be due only to nonvolatile metallic compounds, chiefly as oxides. The residue from soxhlet extraction of particulate matter with benzene; ethanol (4:1) will also indicate the amount of unburned carbon particles and metallic compounds. These methods were applied by Schreck et_ al. (1978) for the determination of elemental carbon in diesel exhaust. With a Peugeot 504D engine, these authors found that 40% of the particulate matter consisted of unburned elemental carbon and metallic compounds. Of the 40%, 31% was elemen- tal carbon and 9% was metallic residue. The value for percent elemental carbon from unleaded gasoline cars with emission controls was determined by Springer and Baines (1977) as 0.08%. It is evident from these results that the percent of elemental carbon from emission-controlled gasoline cars is very small compared to diesel auto- mobiles. This is important to keep in mind since the PNA's usually have a tendency to remain adsorbed on the particulate phase, including the elemental carbon. Because of the absence of abundant particulate elemental carbon, the determination of PNA's in gasoline exhaust (with emission control) becomes especially difficult. 34 ------- Determination of total hydrocarbons (THC) emissions from gaso- line vehicles is usually performed by collecting the integrated cyclic emissions in a bag. Measurement of THC emissions from diesel motor vehicles is more difficult than with gasoline vehicles. The .high boiling range fuels used in diesel preclude integration of the cyclic emissions in a bag since a major portion of the. high molecular weight hydrocarbons are lost to the walls of the bag and other cool surfaces contacted. Thus, the cyclic emissions in diesel must be "real-time" integrated electronically. Filtration of particulate matter from diesel emissions for hydrocarbon determinations poses several problems. First, the particulate adsorbed form must be distinguished from the free unadsorbed form. If the particulates are filtered at ambient temperature, the potential exists for adsorption of gaseous hydrocarbons on the carbon particles during their inti- mate contact on filtration. On the other hand, heating the filters could result in desorption of hydrocarbons which would remain particulate-bound under ambient conditions. This sensitivity of the gas phase-particulate phase parti- tioning of the organics to a variety of controllable sampling parameters was examined by Black and High (1978). The findings of their investigations are summarized below. 1. Instead of sample collection on hot (375°F) or cold (85°F) filters, a turbulent flow tunnel mixing system described in this work appears to adequately simulate the important parameters of short-term ambient dilution. The small variation of filter temperature under this sampling con- dition did not affect the particulate collection efficiency. 2. The probability of organic adsorption on the retained parti- culates on the filters was extremely low under this collec- tion technique. 3. Isokinetic sampling is not important with diesel particu- lates under most conditions due to their very small aero- dynamic size. 35 ------- 4. The distribution of organics between the gas and particulate phases is not sensitive to dilution ratio (dilution factor 8.7 to 17.9). There was indication of a small shift towards somewhat small particulate size at higher dilution rates. 5. The filtration media is also important as it was found that glass fiber media acted as sorption media for some gas phase organics. Best results were obtained with Teflon-coated glass fiber filter media (Pallflex Type T60 A20). Determination of organic emissions by the above authors from diesel passenger cars driven under the cyclic patterns of the FTP showed that the hydrocarbons range from CL to about C,n. The hydrocarbons in the CL to C range result from the combustion process, that is, cracking from higher molecular weight organics. The CL to C organics are dominated by C. , CL, and C hydrocarbons. The C_n to C, organics are dominated by uncombusted fuel and lubricant and by partial combustion and rearrangement of these compounds. Some of the organics in this range (C to C, ) are particle bound and some are gas phase. Typically 15 to 20% of the THC from the vehicles are associated with the particles, but this can range to 40% with vehicles emitting significant levels of lubricant. NMR determination of the solvent extracted portion of the parti- culate matter from a Peugeot 504D car showed that 45 wt% of the extract con- sisted of aromatic compounds with two or more rings (Schreck et^ al., 1978). Only 8% of the 45% consisted of three or more rings. Liquid exclusion chroma- tography (LEG) with styragel columns showed that the particle bound organics contained compounds with carbon numbers more than CL,,. The origin of the higher carbon number compounds was probably lubricating oil (Schreck et al., 1978) The values for the hydrocarbons from automobile emissions are normally reported as total hydrocarbon (THC) and volatile hydrocarbons. These 36 ------- values are given in later sections. Quantitative concentration values for the individual compounds in the particulate adsorbed hydrocarbons are not available. Various authors have attempted to identify these compounds. Boyer and Laitenen (1975) have detected hundreds of compounds in the molecular weight range 300 to 500 in gasoline automobile exhaust particulates by extraction and fractionation of the extract. The first fraction consisted of straight chain aliphatic hydrocarbons from Cn,H0/ to C_.H,0. The second fraction contained branched lo J4 Jj Oo chain aliphatics, unsaturated aliphatics and small ring compounds. The indiv- idual components in this fraction have not been identified. The third fraction consisted of PNA's. Because of the carcinogenic properties of some of these compounds the PNA's will be discussed individually (see Section 3.1.9). The fourth fraction contained mostly oxygenates. The individual components detected in this fraction by GC-MS are: 1) diethyl phthalate, 2) di-isobutyl phthalate, 3) di-n-butyl phthalate, 4) triphenyl phosphate, 5) di-n-octyl phthalate, 6) methyl triphenyl phosphate, 7) trimethyl triphenyl phosphate, 8) dimethyl triphenyl phosphate, 9) benzanthrone, 10) suspected 8-capryophyllene, benzo[cj- cinnoline, benzoic acid, 2,6-di-tert-butyl hydroquinone or nonylphenol, and a number of other unidentifed compounds including oxygenated PNA's. The relative amounts of the classes of compounds has been estimated to be 50% saturated aliphatics, 5% PNA's and 30% oxygenated hydrocarbons (Boyer and Laitinen, 1975). Organic compounds adsorbed on diesel exhaust particulates have been studied by Mentser and Sharkey (1977). The list of compounds detected by these authors by high resolution MS with diesel fuel oil No. 1 and No. 2 is as follows: 1) crotonaldehyde, 2) g-propriolactone, 3) unresolved 2-butanone, tetrahydrofuran, 4) pentane, 5) unresolved ethylformate, 2,3-epoxy-l-propanol, 37 ------- methyl acetate, 6) carbon disulfide, 7) benzene, 8) pyridine, 9) cyclohexane, 10) cyclohexene, 11) methylacrylate, 12) 2-pentanone, 13) hexane, 14) unresolved dioxane, ethyl acetate, 15) toluene, 16) aniline, 17) phenol, 18) furfural, 19) furfuryl alcohol, 20) unresolved mesityl oxide, cyclohexanone, 21) methyl cyclohexane, 22) unresolved cyclohexanol, 2-hexanone, 23) unresolved ethyl acrylate, methyl methacrylate, 24) heptane, 25) styrene, 26) unresolved ethyl benzene, xylene, 27) unresolved monomethylaniline, 0-toluidine, 28) cresol, 29) hydroquinone, 30) methylcyclohexanone, 31) allylglycidyl ether, 32) octane, 33) unresolved vinyl toluene, a-methyl styrene, 34) cumene, 35) isophorone, 36) p- tert-butyl toluene, 37) phenylglycidyl ether, 38) camphor, 39) phenyl ether, and 40) dinitro-o-cresol. The lower molecular weight compounds in the list have not been reported by other workers. Besides the above listed compounds, sulfur containing compounds, namely benzothiophenes and dibenzothiophenes have been detected in diesel exhaust (NIOSH, 1978). The distribution of organic compounds in. particulates changes in a consistent and characteristic manner as the speed and loading of the engines are increased from the idle to rated speed and full load. The composition profiles are not largely affected by the type of diesel engine or the type of fuel used (Mentser and Sharkey, 1977). The above hydrocarbons in the presence of NO and light can be A responsible for the formation of photochemical smog. Among the oxygenates, aldehydes are extremely reactive. Low molecular weight saturated ketones, alcohols, esters, and ethers are unreactive (Seizinger and Dimitriades, 1972). No reactivity data for heavier or unsaturated ketones, alcohols, ethers, and nitroalkanes have been reported. Seizinger and Dimitriades (1972) have sugges- ted that the unsaturated oxygenates might possess significant reactivity. 38 ------- 3.1.8 Polycyclic Aromatic Compounds This class of compounds is found in the automotive exhaust mostly in the particulate adsorbed phase. These compounds are discussed separately because of the demonstrated animal carcinogenic effects of some of these compounds. One group of polycyclic aromatic compounds, the polycyclic aromatic hydrocarbons (PNA's), have been detected in both diesel and gasoline exhaust. These compounds originate from three sources: (1) PNA's present in original fuel, (2) synthesis from lower molecular weight hydrocarbons during fuel ignition, and (3) pyrolysis of lubricating oil. The mechanism of PNA formation in automotive engines has been demonstrated by Laity e_t^ al. (1973). PNA's apparently can exist in the quench zone at the surfaces of the combustion chamber. Some of these PNA's are vaporized from the walls or deposits during engine operation. Anything that increases the heat input to the combustion chamber walls, for example, advanced ignition timing, knock, use of hydrocarbon fuels, or high speed operation, leads to enhanced PNA emissions (Laity et ajl., 1973). From the examination of the soot particles obtained from a gasoline- powered passenger car and a diesel-powered omnibus, Lyons qualitatively detec- ted a series of PNA compounds shown in Table 3.9. Quantitative comparison of the PNA emission levels from diesel and gasoline exhaust requires that the vehicles at least be of similar duty category and operated under typical driving and fuel conditions. Although several publications have reported the levels of various PNA in the exhaust from gasoline- and diesel-powered vehicles, the results in most cases cannot be used for comparative purposes because either the engine, fuel, or driving 39 ------- TABLE 3. 9. PNA1 s DETECTED IN VARIOUS ATMOSPHERIC POLLUTANT SAMPLES3 Compound Gasoline Diesel soot Atmospheric SOOt 800t Naphthalene + Acenaphthylene +• + "*" Anthracene + + + Phenanthrene 4- Anthracene derivatives + + + Pyrene + + + Fluoranthene + + • + Alkyl pyrene + Benz (a) anthracene + + H" Chrysene + - + Benzo(e)pyrene + •)• + Perylene 4- + + Benzo(a)pyrene + + + Benzo(ghi)perylene + + + Benzo(b)f luoranthene 4- + + Anthranthrene H- + + Tetracene + Coronene 4-4- 4- Dibenz(a,h)anthracene + - Dibenzo(a,l)pyrene +• + Benzo(k)f luoranthene + 4- + Pentaphene 4- + Dibenzo(a,l)naphthacene + Dibenzo (a,h)pyrene • 4- Dibenzo(a,e)pyrene + Dibenzo (b.pqr)perylene 4- - Dibenzofluorene 7 - + + Tribenzo(h,rst)pentaphene 4- Indeno-1,2,3-f luoranthene ? 4- a. Re if. Lyons, 1962 b. Detected in sample c> Not detected in sample 40 ------- mode were not comparable. The average PNA emissions from typical diesel vehicles run under the 13-mode federal cycle, and typical gasoline automobiles run under European and American city driving schedules are presented in Table 3.10. The data from older cars are included since current data on detailed PNA analysis are not available. The fuels used in the tests given in Table 3.10 are as follows: Diesel-2D diesel fuel with 26% aromatics; American cars - typical regular grade gasoline fuels with 25% aromatics; European cars - a blend containing 47.7% aromatics and 52.3% paraffins. It should be pointed out that the diesel vehicles in Table 3.10 are the heavy duty variety. Due to unavailability of data from light duty vehicles, the heavy duty vehicle has been used for the purpose of comparison. A large uncertainty in PNA levels from automobile exhaust can be expected. The discrepency between reported PNA values exists primarily because of difficulties in sample collection and analytical procedures, and the depen- dence of PNA emissions on engine operating conditions. This is reflected in Table 3.11. Compounds other than those listed in Table 3.9 and Table 3.10 have also been detected in exhausts from automobiles operated on both types of fuel. For example, Grimmer (1977) has reported six PNA's, two of which are unknown compounds of molecular weight 300 and the rest are cyclopento[cd]- pyrene, methylenebenzo[a]pyrene, methylenebenzo[e]pyrene, and methylenebenzo- [ghijperylene. Grimmer (1977) felt that this group of compounds accounted for the predominant part of the carcinogenic effect observed with gasoline engine exhaust extracts in mouse skin-painting studies. 41 ------- TABLE 3.10. COMPARISON OF PNA EMISSION RATES FROM HEAVY DUTY DIESEL- AND GASOLINE-POWERED VEHICLES Compounds Anthracene Phenanthrene Phenanthrene derivatives Fluor anthene Pyrene Benz (a) anthracene Chrysene Benzo ( j+k) f luoranthene Benzo(a)pyrene Benzo (e)pyrene Indeno (1,2,3 , -cd) pyrene Benzo (ghi)perylene Anthranthrene Coronene Perylene Emission rates, pg/gal fuel Diesel vehicles3 N.D.d 6410 8280 253 349 35f 5 N.R. 22 4 N.R. 7 N.R. N.R. N.R. Typical 6 cyclinder 1956-1962 American cars (gasoline) 41 176 N.R. 872 1145 N.R. N.R. N.R. 147 205 N.R. 649 27 256 12 burned 1970 European car (gasoline) 1486 N.R.6 N.R. 891 2159 123 246 33 63 147 97 423 N.R. 197 N.R. a. Ref. Spindt, 1974 b. Ref. Hangebrauck, 1967 c. Ref. Candeli et al., 1974 d. N.D.: not detected e. N.R.: not reported f. Ref. Spindt, 1977 42 ------- TABLE 3.11. FREQUENCY OF OCCURRENCE OF PNA's IN DIESEL EXHAUST PARTICIPATES a 1 •" ' •" ..~^-~- * — . ' ' ^ ' ' Formula C18H12 C20H12 C20H14 C20H16 C21H14 C20H13N C22H12 C22H14 Compound Carcino- Mol. wt. Frequency of genicityk occurrence in 30 samples Chrysene + 228.0936 Benzo ( c) phenanthrene +++ Benz( a) anthracene + Benzo(a)pyrene +++ 252.0936 Benzo (b) f luoranthene -H- Benzo(j)fluoranthene 4+ Benz(j)aceanthrylene 4+ 254.1092 7, 12-Dimethylbenz( a) anthracene +44+ 256.1248 Dibenzo(a,g)fluorenfe 4 266.1092 Dibenzo(c,g)carbazole 444- 267.1045 Indeno(l,2,3-cd)pyrene 4 276.0936 Dibenz (a, h) anthracene 4+4 278.1092 Dibenz (a, j) anthracene + Dibenz ( a, c) anthracene + 28 16 2 1 2 1 3 2 a. Ref. Menster & Sharkey, 1977 b. Carcinogenicity: +, uncertain; +, carcinogenic; ++, H-44-, Mil, strongly carcinogenic, as per NAS notation. 43 ------- In a recent publication Wang et_ al. (1978) have speculated on the presence of 6-nitrobenzo[a]pyrene in gasoline automobile exhaust. The Ames Salmonella tjrphimurium assay of this compound has shown that this compound is a direct-acting mutagen with activity comparable to benzo[a]pyrene (Wang ejt aJL. , 1978). In fact, the formation of these direct-acting mutagens (nitro- BaP) upon exposure of PNA to gaseous pollutants in smog has been demonstrated by Pitts £t al. (1978). In simulated atmospheres containing 1 ppm NO and traces of HNO., direct-acting mutagens are readily formed from both BaP and perylene, a non-mutagen in the Ames reversion assay (Pitts e£ a!L , 1978). The nitration reaction produces 6-nitro, 1-nitro and 3-nitro-isomers of BaP and 3- nitro-isomers of perylene. These authors also suggest that the nitro-deriva- tives of PNA may eventually photooxidize to polycyclic quinone. Primarily because of its carcinogenicity and frequency of occur- rence, BaP has typically been measured as an indicator of PNA emission from automobile exhausts. Consequently, the bulk of available data is in terms of BaP, although the use of BaP data as an indicator of other PNA's is highly questionable. Polynuclear aza heterocyclics is another class of compounds in automobile exhaust which can contribute to carcinogenic activity. Sawicki et al. (1965) determined the amounts of poly aza arenes in gasoline automobile exhaust which are summarized in Table 3.12. However, these data were generated with cars not equipped with a catalyst and may be subject to change. So far, the emission levels of PNA have been discussed without any specific reference to the dependency of emissions on other parameters. In fact, the PNA emissions, like all other exhaust emissions, are dependent on a 44 ------- TABLE 3.12. CONCENTRATION OF POLY AZA ARENES IN AUTOMOTIVE EXHAUST3 Compound Cone, in ug per g exhaust particulate Benz(h)quinoline 0.2 Benz(c)acridine 0.4 Indenoquinolines 0.9 Dibenz(a,j)acridine < 0.2 Dibenz(a,h)acridine • < 0.2 Alkylbenz(c)acridines < 0.2 a. Ref. Sawicki et al., 1965 45 ------- number of parameters. These are: (1) vehicle characteristics and engine design, (2) engine operation mode, (3) engine maintenance, (4) fuel composi- tion, and (5) exhaust emission control system. The effect of each individual parameter is discussed in the following sections. 3.1.8.1 Dependency of PNA Emission on Vehicle Characteristics Since the objective of this report is to consider emissions from light duty vehicles only, emissions from heavy duty vehicles will not be discussed. Even in light duty automobiles, PNA emissions may be dependent on the engine displacement capacity of the automobile. Comparing a number of 1956-1964 V-8 and V-6 engines, Hangebrauck et_ ail. (1967) have failed tb detect any statistically significant difference in PNA emission rates between the two engines operated with gasoline. A'Similar conclusion has been reached by Springer and Baines (1977) from the comparison of two catalytically- equipped cars, one with a V-8 and the other with an 1-4 engine, and both powered with gasoline. In the case of diesel engines, BaP emission rates and their dependency on engine type are shown in Table 3.13. It can be seen from Table 3.13 that BaP emission rates may not only depend on engine displacement but also on the engine type. The Peugeot 504D engine with larger engine dis- placement showed a lower BaP emission rate per mile. However, this may be due to the fact that the Peugeot 504D results may have been subjected to sampling error. 3.1.8.2 Dependency of PNA Emission on Engine Operation Mode The dependency of PNA emission on engine speed and load for a gasoline- and diesel-powered vehicle is shown in Table 3.14 and Table 3.15. 46 ------- TABLE 3.13. DEPENDENCY OF BaP EMISSION RATES WITH ENGINE TYPE Vehicle type Engine displace- BaP emission rate, ment, CID yg/mile Oldsmobile, V-8 350 7.3a VW Rabbit, 1-4 90 4.3a Peugeot 504D 129 1.6b a. Ref. Springer & Baines, 1977 b. Ref. Braddock & Gabele, 1977 47 ------- The marked contrast between gasoline and diesel engine exhausts can be noted from Table 3.14 and Table 3.15. Increasing the engine load resulted in a rapid decrease in PNA emission in the former, and a marked increase in the latter. As the speed of the engine increased, the quantity of PNA emitted decreased for the gasoline-powered automobile. No uniform variation of PNA production with speed was noted for diesel emissions. The PNA emission rates given in Table 3.14 and Table 3.15 are for older model gasoline cars and the characteristics of the diesel engine are not identified. With new model gasoline cars equipped with a cataly- tic converter, the PNA emission rates can be expected to be substantially lower (see Section 3.1.8.6). The BaP emission rates for diesel-powered passenger cars under various recently-developed cyclic modes of operations are shown in Table 3.16. Corresponding results for gasoline cars are not available. That the BaP emission rates in the FTP mode are higher than in SET and FET modes is obvious from Table 3.16. 3.1.8.3 Variation of PNA Emission with Engine Maintenance Both deposits in the combustion chamber and fouling of the fuel injection system (improper fuel-to-air ratios) can dramatically increase PNA emissions in vehicular exhaust. With a gasoline-powered auto- mobile having combustion chamber deposits, Gross (1972) has shown that the amount of BaP emission could be as much as 6.5 times greater than for clean engines. The dramatic effect of fuel-to-air ratio, which controls the effi- ciency of diesel engine operation, on the .variation of PNA emission is shown in Table 3.17. It is evident from Table 3.17 that diesel engines with improper 48 ------- TABLE 3.14. VARIATION OF PNA EMISSION RATES WITH INCREASING LOAD AND CONSTANT SPEED OF 1000 r.p.m.3 Engine load Emission rate, yg/min. for PNA compound Pyrene t 0 1/4 1/2 3/4 full Gasoline 439 59 26 17 21 Diesel" 137 267 536 1800 2500 Benzo (a) py rene Gasoline 61 0 1 0 0 Diesel 146 465 772 1320 876 Benzo (ghi)perylene Gasoline 177 45 5 3 2 Diesel 22 42 124 640 1265 Anthranthrene Gasoline 102 17 0.3 0.3 0.3 Diesel 0 43 223 472 469 a. Ref. Kotin et al., 1955 & Kotin et al., 1954 b. All the diesel results were run under inefficient fuel injection systems. ------- TABLE 3.15. VARIATION OF PNA EMISSION RATES WITH INCREASING SPEED AND NO LOAD3 Ui o r.p.m. Emission rate, ug/min. for PNA compound Pyrene 500 1000 1200 1400 1500 2000 2500 3000 Gasoline 225 439 N.R. N.R. 507 374 346 121 Dieselb N.R.° 137 208 188 N.R. N.R. N.R. N.R. Benzo(a)pyrene Gasoline 120 61 N.R. N.R. 33 40 25 13 Diesel N.R. 146 9 80 N.R. N.R. N.R. N.R. Benzo (ghi ) p erylene Gasoline Diesel 235 177 N.R. N.R. 60 73 70 85 N.R. 22 79 0 N.R. N.R. N.R. N.R. Anthranthrene Gasoline 153 102 N.R. N.R. 36 27 31 14 Diesel N.R. 0 4.3 20 N.R. N.R. N.R. N.R. a. Ref. Kotin et al., 1955 and Kotin et al., 1954 b. All the diesel results were run under inefficient fuel injection system. c. N.R.: not reported. ------- TABLE 3.16. BENZO(a)PYRENE EMISSION RATES UNDER VARIOUS MODES OF ENGINE OPERATION BaP emission rate, yg/mile Cycle Oldsmobile V-8a V.W. Rabbit I-4a FTP • 7.3 4.3 FET , 3.1 2.4 SET 4.0 2.5 a. Springer and Baines, 1977 51 ------- TABLE 3.17. DEPENDENCY OF BaP EMISSION UNDER DIFFERENT DIESEL ENGINE MAINTENANCE CONDITIONS3 Load 0 1/4 1/2 3/4 full BaP Emission Efficient condition*3 0 0 0 0 0 rate, yg/min. Inefficient condition0 9 47 437 432 1706 a. Ref. Kotin et al., 1955 b. Clean fuel injection system and obtaining samples from completely warmed-up engine. c. Fouling of the fuel injection system and/or engine deterioration. 52 ------- maintenance can be a significantly greater source of PNA pollution. However, well maintained diesel engines may preclude PNA emission into the atmosphere to a remarkable degree. Optimization of fuel-to-air ratio, except during the warm-up period, can make a diesel engine almost completely free from PNA emissions into the atmosphere. 3.1.8.4 Effect of Fuel Composition Increased fuel aromaticity generally causes an in- crease in PNA emissions from gasoline engines (Griffing e£ al^., 1971; Candeli e£ al., 1974). Gross (1972) has shown that an increase in fuel aromaticity from 11% to 46% causes an increase of 134% in PNA emissions from uncontrolled gasoline cars. Begeman and Colucci (1970) have demonstrated that the emission of BaP and benz[a]anthracene increased by 5 and 3.5 times, respectively, by increasing the BaP content of fuel from 1.1 ppm to 4 ppm. Analogous results have been obtained by Rinehart e_t al. (1970). According to Gross (1972) fuel rich in BaP enhances the emission of the same compounds, only if there are deposits in the combustion chamber of the engine. Stichting Concawe (1974), however, has contradicted this result and has shown that PNA emission is on the average 40% lower with fuels without PNA than with fuels containing 1.3 ppm of BaP at about the same level of aromaticity. Candeli et_ al. (1975) have attempted to resolve the problem but have been unable to ascertain whether the observed increase in BaP emission is due to an increase in fuel aromaticity or to an increase in fuel PNA content. Tests with two gasoline cars by Gross (1972) have shown that fuels containing a high-boiling naphtha displayed increased PNA emissions compared to fuels without the naphtha but with the same fuel aromatics 53 ------- and PNA levels. In a third vehicle, the naphtha effect has been shown to be reversed. The immediate effect of the presence of lead in gasoline on PNA emission has been examined in several laboratories. Begeman and Colucci (1970) have shown both small increases and small decreases in PNA emission for the presence of lead in Indolene fuel. Griff ing es£ al_. (1971), employing two different 1967 vehicles, have not found any effect of lead on BaP emissions. A similar conclusion has been reached by Gross (1972) from examina- tion of later model gasoline cars. 3.1.8.5 Effect of Engine Mileage on PNA Emission The effect of engine mileage on PNA emissions from gasoline cars is evident from Table 3.18. Hoffman et al. (1965) have reported BaP emission rates at two levels of oil consumption for the same V-8 engine. BaP emission rates equivalent to 19 and 250 ng/mile have been determined for oil consumption of 1 quart per 1600 miles and 1 quart per 200 miles, respectively. The 13 times greater emission for the high-oil-consumption test suggests that the source of BaP might have been from burning of oil. 3.1.8.6 Effect of Exhaust Emission Control Table 3.19 shows the effectiveness of engine modifi- cation and emission control devices on PNA emission rates. 54 ------- TABLE 3.18. EFFECT OF GASOLINE ENGINE MILEAGE ON PNA EMISSION3 Car Mileage 19000 26000 49000 58000 BaP 5.6 4.2 3.9 21.5 Pyrene 81 70 27 119 PNA emissions, BeP 9.5 8.1 8.6 23.5 Perylene 0.28 0.78 0.57 1.38 yg/mile B(ghi)P 26.0 35.0 14.3 77.0 Anthranthrene 2.3 0.64 0.3 3.17 Coronene 9.6 10.7 4.1 32.2 a. Ref. Hagenbrauck et al., 1967 55 ------- TABLE 3,19. EFFECT OF EXHAUST EMISSION CONTROL ON PNA EMISSION Type of control BaP emission rate, % Reduction pg/gal fuel consumed Gasoline: Uncontrolled (1956-64) 170a Uncontrolled, 1966 70b 0 Engine modification, 1968 19-25 ^ 70 Air-injected RAM thermal , reactor, 1968 1.6 ^98 Catalyst equipped, 1970 1.1 ^ 98 Diesel: Catalyst treated 80-90° Water scrubber , 30C Catalyst + water scrubber 80-90° a. Hangebrauck et al., 1967 b. Gross, 1972 c. NIOSH, 1978 56 ------- 3.2 Volatile Emissions Table 3.20 summarizes the regulated gaseous emissions data from diesel-powered passenger cars. The dependence of these emissions on engine class and operating modes is obvious from this table. The corresponding values from gasoline vehicles is shown in Table 3.21. To make comparison easy, the federal light-duty emission standards are presented in Table 3.22. ,From the emission rates given in these tables it can be concluded that diesels (without emission controls) can be a higher source of hydrocarbon pollution than catalyst-equipped gasoline cars. The CO emission rates for both diesel and gasoline cars are about equal with gasoline cars emitting more CO in the FTP and less in the FET and SET modes than diesel cars'. The NO, emission X rates for the gasoline cars, on the other hand, are higher than for diesel cars in all modes of cyclic operation. The individual hydrocarbon emission rates for diesel-powered passen- ger cars are given in Table 3.23. The corresponding values for gasoline cars are presented in Table 3.24. With the exception of methane and toluene, in- dividual hydrocarbon emission levels are higher for diesel than for gasoline cars. The emission rates of earbonyl compounds for diesel cars are shown in Table 3.25. Tha emission rates for carbonyl compounds for gasoline cars are shown in Table 3.26. It is evident from these tables that with the exception of crotonaldehyde, diesel cars emit more carbonyl compounds than catalyst- equipped gasoline cars. That the emission rates for aromatic aldehydes increase with fuel aromaticity is shown in Table 3.27 for cars without emission controls. 37 ------- TABLE 3.20, GASEOUS EMISSIONS DATA FROM A VARIETY OF DIESEL CARS UNDER DIFFERENT ENGINE MODES 00 Yehicle Mercedes 220Da Mercedes 240Da Mercedes 300Da Peogeot 204Da Peugeot 504D Nissan 220C° Oldsmobile V.W. Rabbitd Engine displac( ment, lit 2. 2. 3. 1. 2. -N. 5. 1. 20 4 0 36 11 A.e 74 47 Emission rates, g/km Hydrocarbons FTP 0.11 0.18 0.10 0.69 0.29 0.25 0.47 0.23 FET 0.08 0.06 0.06 0.48 0.07 N.A. 0.21 0.08 SET 0.06 0.06 0.08 0.54 0.12 N.A. 0.27 0.09 FTP 0.81 0.60 0.53 1.06 0.88 1.10 1.24 0.49 CO FET 0.48 0.38 0.36 0.57 0.37 N.A. 0.63 0.31 SET 0.55 0.45 0.39 0.71 0.51 N.A. 0.79 0.34 PXP 0.65 0.79 1.07 0.42 1.63 1.37 0.70 0.54 NOX FET 0.56 0.80 0.99 0.34 1.20 N.A. 0.59 0.52 SET 0.57 0.78 0.98 0.33 1.33 N.A. 0.59 0.50 a. Ref. Springer and Stahman, 1977 b. Ref. Braddock and Gabele, 1977 c. Ref. EPA result cited in b d. Ref. Springer and Baines, 1977 e. N.A.: Not available ------- Ut VO TABLE 3.21. GASEOUS EMISSIONS DATA FROM A VARIETY OF GASOLINE CARS WITH AND WITHOUT CATALYST Vehicle Emission rates, Hydrocarbons CO NOX FTP FET SET FTP FET SET FTP FET SET 1977 Catalyst equipped Olds. Cutlassa 0.24 0.06 0.08 1.34 0.12 0.53 0.85 0.88 0.86 1977 Catalyst equipped V.W. Rabbit3 0.14 0.03 -0.03 2.30 0.03 0.19 0.63 1.22 1.01 1970 Mercedes (no catalyst)b 1.66 N.A.d N.A. 20.05 N.A. N.A. 2.19 N.A. N.A. 1968 Air-injected RAM thermal reactor vehicle^ 0.04 N.A; N.A. 2.60 N.A. N.A. 1.18 N.A. N.A. 1970 Catalyst equipped carc 0.25 N.A. N.A, 4.96 N.A. N.A. 0.43 N.A. N.A. a. Ref. Springer and Baines, 1977. This is a prototype automobile. b. Ref. Springer, 1971 c. Ref. Gross, 1972 d. N.A. : not available ------- TABLE 3.22. FEDERAL LIGHT-DUTY EMISSION STANDARDS3 Emission Standards, g/mile ItJcir 1977-79 1980 1981 Hydrocarbons 1.5 90% reduction from 1970 value 90% reduction from 1970 value CO 15 7 90% reduction from 1970 value NO X 2 2 1 a Ref. Public Law 95-95 issued Aug. 7, 1977. 60 ------- TABLE 3.23. DETAILED HYDROCARBONS EMISSION RATES (mg/km) FOR DIESEL CARS DURING TRANSIENT CYCLES Emission Methane Ethylene Acetylene Propylene Ethane Propane Benzene Toluene Cycle FTP SET FET FTP SET FET FTP SET FET FTP SET FET FTP SET FET FTP SET FET FTP SET FET FTP SET FET Mercedes 220D a 19.65 13.82 12.58 21.63 15.26 14.56 8.65 6.51 6.07 N.D.C N.D. N.D. N.A/ N.A. N.A. N.A. N.A. N.A. 6.07 3.26 4.99 N.A. N.A. N.A. Mercedes 24 OD a 5.57 2.75 3.66 17.74 12.07 12.14 1.31 5.02 8.94 N.D. N.D. N.D. N.A. N.A. N.A. N.A. N.A. N.A. N.D. N.D. N.D. N.A. N.A. N.A. Mercedes 300D a 3.94 3.34 4.25 14.49 9.39 8.49 2.81 trace 3.50 N.D. N.D. N.D. N.A. N.A. N.A. N.A. N.A. N.A. 2.51 N.D'. 3.10 N.A. N.A. N.A. Peugeot 204D a 9.30 4.44 4.04 38.13 27.76 24.20 7.57 5.08 4.77 19.98 10.93 9.37 N.A. N.A. N.A. N.A. N.A. .N.A. N.D. N.D. N.D. N.A. N.A. N.A. Cutlass 12.7 5.1 3.4 49.2 28.5 21.8 5.3 2.6 1.9 17.1 8.9 6.5 4.2 1.7 0.3 0.1 N.D. N.D. 11.6 6.4 4.9 2.6 N.D. 0.9 v.w.b Rabbit 6.7 3.3 4.7 28.1 15.3 15.1 1.5 1.2 1.7 9.6 4.5 4.5 0.9 0.4 0.6 N.D. N.D. N.D. 5.1 2.9 3.2 0.6 1.6 N.D. b. Ref. Springer and Baines, 1977 c. N.D. not detected d. N.A. not available 61 ------- TABLE 3.24. DETAILED HYDOCARBON EMISSION RATES (mg/km) DURING TRANSIENT CYCLES OF GASOLINE CARS3 Emission Methane Ethylene Acetylene Propylene Ethane Propane Benzene Toluene Cycle FTP SET FET FTP SET FET FTP SET FET FTP SET FET FTP SET FET FTP SET FET FTP SET FET FTP SET FET Cutlass 29.5 24.2 18.4 18.2 6.3 2.9 1.1 N.D.b N.D. 8.2 N.D. N.D. 14.8 9.2 6.7 N.D. N.D. N.D. 5.6 2.7 0.8 13.6 2.4 1.4 V.W. Rabbit 33.0 17.4 14.6 15.2 1.1 2.0 2.6 N.D. N.D. 4.0 N.D. N.D. 6.4 2.4 N.D. N.D. N.D. N.D. 9.1 'N.D. 0.4 12.3 1.2 0.9 a. Ref. Springer and Baines, 1977 b. N.D.; not detected. 62 ------- TABLE 3.25. EMISSION RATES (mg/km) FOR CARBONYL COMPOUNDS FROM DIESEL CARS DURING TRANSIENT CYCLES Emission Formaldehyde Acetaldehyde Acetone Iso-butalde- hyde Crotonalde- hyde Hexanalde- hyde Benzaldehyde Cycle FTP SET FET FTP SET FET FTP SET FET FTP SET FET FTP SET FET FTP SET FET FTP SET FET Mercedes 220Da 2.52 1.50 1.55 1.00 N.D.C N.D. 8.37 10.15 4.31 11.08 15.96 7.90 2.37 2.82 1.75 0.47 1.81 1.55 N.D. N.D. N.D. Mercedes 240Da 3.96 3.08 3.57 1.13 0.55 1.19 1.47 2.99 2.46 2.19 3.58 4.26 0.67 2.27 1.51 N.D. 0.13 0.67 N.D. 2.29 2.00 Mercedes 300D3 3.80 5.81 3.95 1.11 N.D. N.D. 9.41 6.53 1.45 N.D. N.D. 1.50 1.17 1.17 N.D. N.D. N.D. 0.45 N.D. N.D. 1.22 Peugeot 204Da 11.25 8.50 7.76 4.28 3.75 4.05 3.01 1.58 4.61 8.75 6.54 7.92 4.10 2.75 3.05 N.D. N.D. N.D. N.D. N.D. N.D. Cutlass 15.8 12.3 8.2 6.5 6.3 3.0 35.7 5.1 3.3 18.5 10.4 8.9 4.2 2.4 N.A. N.A. N.A. N.A. 1.8 1.1 N.A. V.W.b Rabbit 16.0 6.0 4.3 5.0 1.5 1.1 2.6 1.0 2.7 16.0 1.9 3.3 N.A.d N.A. N.A. N.A. N.A. N.A. 2.7 N.A. N.A. a. Ref. Springer and Baines, 1977 b. Ref. Springer and Baines, 1977 c. N.D.: not detected. d. N.A.: not available. 63 ------- TABLE 3.26. DETAILED CARBONYL EMISSION RATES (mg/km) FOR GASOLINE CARS DURING TRANSIENT CYCLES3 Emission Formaldehyde Acetaldehyde Acetone Iso-butanaldehyde Crotonaldehyde Hexanaldehyde Benzaldehyde Cycle FTP SET FET FTP SET FET FTP SET FET FTP SET FET FTP SET FET FTP SET FET FTP SET FET Cutlass 2.6 1.3 1.6 0.4 N.A. N.A. N.A. N.A. 0.5 3.8 1.8 6.5 7.2 0.6 1.2 N.A. N.A. N.A. N.A. 5.3 0.8 V.W. Rabbit 0.4 0.3 0.5 N.A.b N.A. N.A. N.A. N.A. N.A. 2.6 2.1 6.4 32.1 4.3 3.7 N.A. N.A. N.A. 2.7 2.2 1.0 a. Ref. Springer and Baines, 1977 b. N.A.: not available 64 ------- TABLE 3,27. INCREASE IN AROMATIC ALDEHYDE EMISSION RATES FOR GASOLINE CARS WITH INCREASE IN FUEL AROMATICITY3 Fuel Aromatics, mole % Unleaded Premium 46 . 6 Leaded Premium 30.8 Leaded Regular 27.3 Total aldehydes, ppm 65 72 69 Aromatic aldehyde , ppm 13.6 6.1 5.8 a. Ref. Hinkamp et al., 1971 65 ------- TABLE 3.28. PHENOL IN EXHAUST GAS Phenol emission range, mg/gal Test vehicle 11% Aromatic fuels Aromatic fuels 46% Aromatic fuels 1966, no emission control 1968, engine modification 1970, engine modication with spark retard 1968, air injected RAM thermal reactor 1970, catalyst equipped 110-179 78-165 74-123 279-435 314-406 222-287 653-776 535-691 370-485 Ref. Gross (1972). 66 ------- TABLE 3.29. SO- EMISSION RATE FROM VARIOUS CARS UNDER CYCLIC OPERATIONS3 SO,, Emission Rate mg/km Cycle Mercedes 220D Mercedes 240D Mercedes 300D Peugeot 204D FTP 350 320 . 310 260 FET 270 270 320 210 SET 250 250 260 200 o Ref. Springer and Stahman, 1977. 67 ------- TABLE 3.30. COMPARISON OF HCN AND COS HUSSIONS (mg/mlle) FROM DIESEL AND GASOLINE CARS* 00 Emission Cycle HCN FTP FET SET e COS FTP FET SET Peugeot 504D 1.32 + 0.31° 0.63 + 0.39 0.43 + 0.05 0.55 + 0.15 0.19 + 0.22 0.24 + 0.14 Honda CVCC Lean-burn Chrysler 11.5 + 2.0 7.6 + 0.5 NR 0.06 + 0.06 0.51 + 0.67 NR 4.44 + 2.67 NRd NR 0.40 + 0.35 0.26 + 0.16 NR Dual Catalyst Hornet 10.7 + 1.6 7.2 + 0.3 5.2 + 0.8 NR NR NR a Ref. Braddocfc & Gabele (1977). The tiiesel tests were run with national average diesel, and gasoline tests were run with unleaded gasoline. £» Means standard deviation from mean. The diesel tests were run with 0.46 weight% fuel sulfur, and gasoline tests were run with 0.03 weight% fuel sulfur. ------- Phenols have also been detected in exhaust gases from gasoline cars. Table 3.28 shows the phenol emission rates as the gasoline cars became more and more modified. It is evident from Table 3.28 that phenol emission increases with increase in fuel aromaticity. However, with the present catalyst equipped cars the effect may not be pronounced since the phenol emission rate is too low. Sulfur dioxide emission rates from diesel cars are dependent on fuel sulfur content. As the fuel sulfur increases, SO- emission also increases (Braddock and Gabele, 1977). The SCL emission rate from a number of cars operating with national average fuel sulfur (0.23%) is shown in Table 3.29. The emission rates of HCN and COS from both diesel and gasoline passenger cars are listed in Table 3.30. 69 ------- 3.3 Fuel Economy For comparison purposes, Springer and Baines (1977) have used one large (Oldsmobile V-8) and one small car (V.W. Rabbit 1-4) in each diesel and gasoline category. Their results are summarized as follows: fuel consumption (&/100 Km) of the diesel Cutlass is consistently 26 to 29% lower than the gasoline car regardless of the driving cycle. In terms of fuel economy (mpg), the percent increase in miles per gallon for the diesel is 35 to 40% greater than the gasoline car. In the case of the Rabbit, the fuel consumption rates for the diesel are 42%, 39% and 33% lower for FTP, SET and FET tests, respec- tively, compared to the gasoline Rabbit. In terms of fuel economy, the corres- ponding percent increase amounts to 74%, 65% and 49%, respectively. 70 ------- 3.4 Smoke Results The results of a diesel smoke test on the larger Oldsmobile Cutlass and smaller V.W. Rabbit car are presented in Table 3.31. It should be noted that 3 to 4% opacity by the EPA smokemeter is at the limit of smoke visibility. Most of the time, both cars operated in this area with brief excursions during rapid throttle movement. 71 ------- TABLE 3.31. PERCENT EXHAUST SMOKE OPACITY FOR TWO DIESEL CARS Cutlass Condition Start Idle First acceleration peak Idle at 1255 sec. Second acceleration peak Cold start cycle 16v.3 4.4 21.4 5.2 19.4 Hot start cycle 7.8 4.1 7.5 4.3 16.6 Rabbit Cold start cycle 72.9 4.5 7.4 0.5 39.4 Hot start cycle 27.4 0.4 3.0 0.3 37.7 Ref. Springer and Baines, 1977 72 ------- 3.5 Odor Rating The odor rating by the Turk Kit method includes an overall "D" odor which is comprised of burnt-smoky "B", oily "0", aromatic "A", and pungent "P" qualities as determined by an odor panel. On an odor intensity series of one through four, the last is considered the strongest odor. The odor intensity determined by this method (odor panel) for a number of diesel cars under various engine modes of operation is given in detail by Springer and Stahman (1977) and Springer and Baines (1977). Since the objective of this report is to identify the chemical components, the odor rating based on this scale will not be discussed. The reader is referred to the previously mentioned investi- gations. Another system of odor rating called the Diesel Odorant Analytical System (DOAS) which expresses odorant as Total Intensity of Aroma (TIA) has been used by Springer and Baines (1977) for diesel cars. At IIT Research Institute, Dravnieks and coworkers (Dravnieks et al., 1971; O'Donnell _et_ al., 1970) have employed two high-resolution chromatographic columns for separation of diesel exhaust components in order to identify diesel odorants. Table 3.32 lists the odorants they determined quantitatively. Another group which has been conducting odor-related research on diesel exhaust for a number of years is Arthur D. Little Co. Based on the results of their odor studies (Spicer et^ al., 1975), ADL investigators have identified a large number of aromatic compounds and their isomers which are listed in Table 3.33. 73 ------- TABLE 3.32. EXHAUST CONCENTRATIONS OF SOME ODORANTS AS DETERMINED BY IITRI WITH HIGH-RESOLUTION CHROMATOGRAPHY3 Exhaust component Concentration, ppm Acetaldehyde 0.00003 n-Butanol 0.00017 Decane 0.00344 Methyl benzene 0.000009 Cg Substituted benzene 0.000032 Allyl toluene 0.000037 Methylindan 0.000074 Benzaldehyde 0.000345 Naphthalene 0.00038 Methyl naphthalene 0.00034 Ref. Dravnieks et^ al_. (1971), O'Donnell e£ al. (1970). It is not clear from the original reference whether these estimates refer to actual exhaust concentrations or to exhaust which has been diluted 11 to 1. 74 ------- TABLE 3.33. DIESEL EXHAUST ODORANTS IDENTIFIED BY ADL Compound Methylindan Tetralin Dimethylindan Methyltetralin Dimethyltetralin Trimettiylindan Alkyltetralin Trimethyltetralin Alkyltetralin Alkylindene Alkylindene Monomethyl napthalene Composition C- _H _ 10 12 C10H12 C11H14 C11H14 C12H16 C12tt16 C12H16 C13H18 C13H18 C12H14 C13H16 C11H16 Odor note Irritation Rubbery sulfide Kerosene Naphthenate Kerosene Kerosene, irritation Kerosene Irritation Kerosene, pungent, acid Heavy oil Heavy oil Mothball, irritation Ref. Spicer e£al. (1975) 75 ------- 3.6 Noise A summary of sound levels from diesel and gasoline cars under differ- ent driving conditions is shown in Table 3.34. The driveby exterior rating for a diesel Cutlass has been found to be 5 dBA higher than for a gasoline Cutlass, while the Rabbit has shown the same dBA level under this driving condition. Interior noise levels are slightly higher with diesels of both makes during acceleration. The exterior driveby at a constant 48.3 Km/hr speed has shown slightly higher interior and exterior noise for the Cutlass, while the opposite is true for the gasoline Rabbit. Idle noise levels are noticeably higher with the diesel Rabbit. 76 ------- TABLE 3.34. SUMMARY OF SOUND LEVEL MEASUREMENTS Noise at Exterior Interior Interior Exterior Interior Interior Exterior Interior Interior Driving mode Accel, driveby Blower on Blower off 48.3 km/hr, driveby Blower on Blower off Idle Blower on Blower off Oldsmobile Gasoline 68.8 73.2 68.8 58.8 71.5 60.5 64.5 71.5 48.5 Noise on Cutlass Diesel 73.8 74.2 70,5 61.2 72.2 64.0 70.0 71.0 51.5 dBA scale V.W. Rabbit Gasoline 71.0 78.2 76.5 60.5 73.5 70.5 65.0 69.5 58.0 Diesel 71.5 80.0 79.5 58.5 71.8 68.0 67.0 69.5 62.5 Ref. Springer & Baines (1977). 77 ------- 3.7 Engine Modification and Antipollution Devices for Diesel Cars Diesel powered cars discussed so far do not include automobiles equipped with antipollution devices. However, for diesel cars, the variation of combustion systems may result in different pollution characteristics and fuel economy. Table 3.35 shows qualitatively the characteristics of the two combustion systems without any other emission control system. With the introduction of further emission control device(s), the pollution level can be further decreased in diesel cars. This is indicated in Table 3.36. Although the emission rates given in this table are for diesel vehicles run during mining operations, the results can be qualitatively applied towards diesel passenger cars. The effects of catalytic reactors, certain types of traps, and a combination of these, on diesel exhaust composition have been studied in detail by Marshall e_t al. (1978) and Seizinger (1978). 78 ------- TABLE 3.35. FUEL ECONOMY AND EMISSION CHARACTERISTICS OF TWO DIESEL CARS WITH DIFFERENT COMBUSTION SYSTEMS3 Characteristics Direct Injection Indirect Injection Fuel economy Favorable Less favorable CO Less favorable Favorable Hydrocarbons Less favorable Favorable NO Less favorable Favorable Aldehydes Less favorable Favorable SO- Approximately same Approximately same a. Ref. NIOSH, 1978 79 ------- TABLE 3.36. DIESEL EMISSION FACTORS WITH AND WITHOUT EMISSION CONTROL3 Pollutant CO Hydrocarbons NO N02 Carbon Phenols Aldehydes so2 H2S°4 Trace metals PNA Odor Irritancy co2 Noise, dBA Emission level, grams/brake horsepower-hour Untreated engine 0.6-2.7 0.03-0.17 1.25-4.1 0.3-0.7 0.17-0.67 Trace 0.02-0. ,2 0.5 Trace 510-600 96-104 Catalyst treated 0.6-0.3 0.003-0.017 1.25-3.5 0.15-1.1 0.17-0.67 80-90% reduction 0.005 0.25 0.37 0.025 max 80-90% reduction substantial reduction — no reduction no reduction Water scrubber 0.6-2.7 0.02-0.12 1.25-4.1 0.3-0.7 0.12-0.47 30% reduc- tion 0.01 0.096 30% reduc- tion — some reduc- tion no reduction no reduction Catalyst and water scrubber 0.6-0.3 0.003-0.017 1.25-3.5 0.15-1.1 0.08-0.33 80-90% reduction 0.005 <0.09 <0.24 80-90% reduction — — no reduction no reduction a. Ref. NIOSH, 1978 80 ------- 3.8 Effect of Irradiation of Automobile Exhaust It has been long known that nitrogen oxides and hydrocarbons present in automobile exhaust can react photochemically in the presence of sunlight to produce 'photochemical smog.1 The primary source of Los Angeles smog has been attributed to automobile emissions arising from evaporative fuel losses and exhaust discharges. Substantial research efforts have been devoted on this subject. No attempt has been made in this report to describe all these inves- tigations. Instead, only a few investigations which demonstrate the altera- tions of major components as a result of photoreaction of exhaust emissions are presented below. 3.8.1 Photoreactivity of Gasoline Emissions Light irradiation of gasoline emissions usually results in oxi- dation of products which are present in the original emissions. The reactivity criteria expressed in terms of rate of formation of 0 , N09, peroxyacetyl nitrate (PAN), peroxypropionyl nitrate, peroxybenzoyl nitrate (PBzN), formalde- hyde and increase in eye irritation. In the case of gasoline cars, the effects of increased fuel aromaticity on photoreactivity of exhaust emissions have been studied by Heuss et_ aJL. (1974). This study is particularly important since unleaded gasoline used for catalytically equipped cars contains a higher per- centage of aromatics in order to maintain, the equivalent octane rating. The study by Heuss et al. (1974) has shown that the presence or absence of tetra- ethyl lead (TEL) in gasoline does not affect the photochemical reactivity of the exhaust hydrocarbons produced from the gasoline. Certain aromatics, when added to a low-aromatic gasoline, greatly increase the eye irritation and PBzN yield of the exhaust, although they do not increase other reactivity criteria. 81 ------- The six aromatics tested by Heuss et al. (1974) have been ranked in the follow- ing order for their effect on eye irritation: isopropylbenzene > (o-xylene, n_- propylbenzene, and ethylbenzene) > toluene > benzene. These authors concluded that the specific aromatics in gasoline, not the total, is the important factor affecting eye irritation. Similar results on photochemical reactivity of gasoline exhaust in relation to increased fuel aromaticity have been estimated by Altshuller (1972). His results are summarized in Table 3.37. 3.8.2 Photoreactivity of Diesel Emissions The photoreactivity of diesel emissions has been studied by EPA (1978). Their results show small but positive differences in the measured values of component concentrations between irradiated and non-irradiated diesel emissions. These differences exist between NO , S09, hydrocarbon and X £• particulate matter in both atmospheres. Low molecular weight aliphatic hydro- carbons and solvent extractables do not show any significant differences. The EPA (1978) studies are summarized in Table 3.38. 82 ------- TABLE 3.37. EFFECT OF PHOTOCHEMICAL REACTIVITY RESULTING FROM 10% INCREASE IN FUEL AROMATICITY3 Photochemical Reactivity Probable Results Ozone or oxldant Peroxyacyl nitrate Formaldehyde and other aldehydes Eye irritation Aerosol formation Plant damage No increase overall and decrease for evaporative loss contribution No increase overall and decrease for evaporative loss contribution Decrease with increase in fuel arpmaticity 2 to 5% increase 10% increase No change a. Ref. Altschuller, 1972 83 ------- TABLE 3.38. EFFECT OF IRRADIATION OF DIESEL EMISSIONS' Component Concentration in exposure chamber Non-irradiated Irradiated co2% CO, ppm Total hydrocarbons, ppm C 75°F 350°F NO, ppm N02, ppm S02, ppm 03, ppm o Total particulate, mg/m 3 Sulfate, mg/m 0.252 15.7 15.6 31.2 5.85 2.19 2.13 6.32 0.57 0.255 15.4 15.0 26.0 4.94 2.73 1.91 <0.01 6.83 0.57 a. Ref. EPA, 1978 84 ------- 3.9 Research Gaps and Recommendations The present review of the state-of-the-art knowledge on light duty vehicular emissions has detected the following areas of research gaps with regard to physical and chemical characterization. 3.9.1 Definition of Particulate Matter There is no general agreement about the specific fraction of exhaust emissions which constitutes the particulate matter. Certainly, the nature and quantity of the particulate matter will depend on both the temper- ature of .sample collection and the nature of the filtering medium. Therefore, a universally acceptable definition of particulate matter requires a standard- ization of these parameters. 3.9.2 Inadequate Particulate Sampling Procedure This is perhaps one of the major reasons for both inter- and intralaboratory inconsistencies between the reported particulate matter con- centrations from automobile exhausts. The turbulent flow tunnel mixing system described by Black and High (1978) seems promising. Although the filter paper and the cooling system for hot exhaust is optimized to accomplish consistent quantitative collection of particulates, hard data showing the actual collec- tion efficiency are not available. Data by Spindt (1977) have shown that the collection efficiency for BaP can be less than 10%. In their experiments with gasoline exhausts, Springer and Baines (1977) point out the difficulty of collecting BaP present in particulate matter. Use of radioactive, tracer to establish the recovery of particulate matter by the collection method used may be helpful. The possibility of interactions among pollutants during collec- tion (namely oxidants with PNA's) and during storage should be further 85 ------- investigated. This interaction may be responsible for the production of arti- facts during these processes. 3.9.3 Better Storage Method In cases where real time analyses are not possible, a better storage method for HLSO, and other reactive components is needed. 3.9.4 Improvement of Analytical Methodology For certain components where quantifications are hindered by interferences, namely, aldehydes, PNA's and phenols, better analytical method- ologies need to be developed. There is a need for an instrument which will specifically measure NO concentration. Better analytical procedures are also needed for the reasonable recovery of adsorbed components in the particulate matter during the solvent extraction procedure (perhaps ultrasonic extraction). Recovery during eva- porative concentration of the extract can be improved by such well-established procedures as Kuderna-Danish evaporation. 3.9.5 Identification and Quantification of New Components More research is required to identify and quantify suspected new carcinogenic components in the exhaust, namely, methylene-PNA's, (Grimmer, 1977) and nitro-PNA's, (Pitts e£ al., 1978), and hitherto undetected nitro- soamines. Fractionation of the extractables in the particulate matter into acid, base, and neutral fractions and the subsequent separation of each indivi- dual fraction may be helpful for this purpose. EPA has ongoing programs on the latter subject. 3.9.6 Analysis of Sulfates A better method for the analysis of H-SO, and other neutral sulfates from automobile exhaust is needed. Ion chromatography may be helpful 86 ------- for the detection of these and other ionic components. The time scale for neutralization of H-SO, in ambient air has to be established. 3.9.7 Effect of NO and 0_ on Pollutant Formation The effect of NO and 0_ on PNA and other compounds formed through free radical mechanisms should be investigated. Since NO and 0, are well-known free radical quenchers, a relationship establishing NO and 0- concentration and rate of PNA formation in automobile exhaust should be estab- lished. 3.9.8 Quantification of Different PNA Levels More research effort should be directed towards establishing different PNA levels and measuring the effects of variables on PNA's emitted from light duty vehicles. 3.9.9 Uniformity in Data Reporting EPA should establish a uniform method for data reporting. Com- parison between various results sometimes becomes impossible because of the various units used to express the data. 3.9.10 Diesel Odor Characterization Diesel odor characteristics as measured by DOAS and total "D" odor ratings by a human odor panel needs further evaluation because of their inherent inadequacies. Identification of odor components by chemical methods and rating odor on the basis of analytical quantification of a few representa- tive odorants may be a solution to this problem. 3.9.11 Necessity for Using Additives Use of a smoke suppresant for diesel exhaust is thought to be neither widespread nor essential. The use of MMT (C&EN News, 1978) or Ce(thd) 87 ------- (Sievers and Sadlowski, 1978) to increase the anti-knock value for gasoline fuels needs careful examination. The best ways to control emission of pollu- tants from automobiles may be: (1) control of fuel parameters, (2) introduc- tion of anti-pollution devices, and (3) engine modification. 3.9.12 Regulation of Pollutants Finally, decisions have to be made regarding the necessity of regulation of some of the components in automobile emissions of possible interest in relation to health effects. The presently regulated gaseous emissions may be toxic and photochemically reactive, but are not principally mutagenic/carcinogenic. The regulation of vaporous components has uninten- tionally reduced the emission of some carcinogenic compounds (PNA's) in gaso- line exhaust. Whether the presence of residual trace amounts of carcinogenic compounds poses any long term health hazards has to be assessed both by in vitro and long term in vivo biological studies. 88 ------- References for Section 3.0 Altshuller, A.P. (1972), "Effects of Reduced Use of Lead in Gasoline on Vehicle Emissions and Photochemical Reactivity," EPA National Environmental Research Center, Research Triangle Park, N.C., February, 1972. Apostolescu, N.D., R.D. Matthew, and R.F. Sawyer (1977), "Effects of a Barium- Based Fuel Additive on Particulate Emissions from Diesel Engines," SAE Paper No. 770828. Begeman, C.R. and J.M. Colucci (1968), "Polynuclear Aromatic Hydrocarbon Emissions from Automotive Engines," SAE Transactions, Vol. 79, Paper 700469, p. 1682- 1698. Black, F. and L. High (1978), "Diesel Hydrocarbon Emissions, Particulate and Gas Phase," Symposium on Diesel Particulate Emissions Measurement Char- acterization, Ann Arbor, Michigan, May 17-19. Boyer, K.W. and H.A. Laitinen (1975), "Automobile Exhaust Particulates: Proper- ties of Environmental Significance," Environ. Sci. Technol., £:457-469. Braddock, J. and R. Bradow (1975), "Emissions Patterns of Diesel-Powered Passenger Cars, Part I," SAE Paper No. 750682. Braddock, J.N. and P.A. Gabele (1977), "Emission Patterns of Diesel Powered Passenger Cars. Part II," SAE (Tech. Pap.) 770168, 11 pp. Broome, D. and I.M. Khan, (1971), "Mechanisms of Soot Release from Combustion of Hydrocarbon Fuels with Particular Reference to the Diesel Engine," Insti- tutipn of Mechanical Engineers Symposium on Air Pollution in Transport Engines, Paper C140/71, Nov. 1971. Campbell, K. and P.L. Dartnell (1972), "Vehicle Particulate Emissions," Air- Pollut. Control Transp. Engines, Symp., pp. 14-20. Candeli, A., G. Morozzi, A; Paolacci, and L. Zoccolillo (1975), "Analysis Using Thin Layer and Gas-Liquid Chromatography of Polycyclic Aromatic Hydrocarbons in the Exhaust Products from a European Car Runnning on Fuels Containing a Range of Concentrations of These Hydrocarbons," Atmos. Environ., j):843-849. Candeli, A., V. Mastrandrea, G. Morozzi, and S. Toccaccli (1974), "Carcinogenic Air Pollutants in the Exhaust from a European Car Operating on Various Fuels," Atmos. Environ., JJ:693-705. Chemical and Engineering News, (1978), .56(28), 24 pp. DEC, New York State (1976), "Sulfate and Particulate Emissions from In-Use Catalyst Vehicles," EPA Grant No. R803520. 89 ------- Dolan, D.F., D.K. Kittelson, and K.T. Whitby (1975), "Measurement of Diesel Exhaust Particle Size Distributions," ASME Publication 75-WA/APC-5. Dow Chemical Co. (1970), "Effects of Fuel Additives on the Chemical and Physical Characteristics of Particulate Emissions in Automotive Exhaust," EPA Contract No. EPA-22-69-145. Dravnieks, A., A. O'Donnell, R. Scholz, and J.D. Stockham (1971), "Gas Chromatographic Study of Diesel Exhaust Using a Two-Column System," Presented at A.C.S. Meeting, Los Angeles, California. EPA (1977), "Characterization of Exhaust Emissions from a Dual Catalyst-Equipped Vehicle," Report No. 600/2-77-068. EPA (1978), Toxicological Assessment of Diesel Emissions, U.S. Environmental Protection Agency, HERL, Cincinnati, Ohio, April, 1978. Energy and Environmental Analysis, Inc. (March 6, 1978), Draft Report to EPA, Atmospheric POM: Source and Population Exposure Estimate. Frey, J.W. and M. Corn (1967), "Diesel Exhaust Particulates," Nature, 216(5115); 615-616. Gabele, P., J. Braddock, and R. Bradow (1977), "Characterization of Exhaust Emissions from Lean Burn, Rotary, and Stratified Charge Engines," SAE Paper No. 770301. Ganley, J.T. (1973), "Particulate Formation in Spark Ignition Engine Exhaust Gas," Dissertation Work, University of Michigan, available from Univ. Microfilms, Ann Arbor, Mich., Order No. 73-24,565, 148 pages. Greeves, G., I.M. Khan, and G. Onion (1977), "Effect of Water Introduction on Diesel Engine Combustion and Emissions," Symposium (Int.) Combust. (Proc.), Vol. 16, p. 321-336. Griffing, M.E., A.R. Maler, J.E. Borland, and R.R. Decker (1971), "Applying a New Method for Measuring Benzo[a]pyrene in Vehicle Exhaust to the Study of Fuel Factors," presented at Div. Petrol. Chem., Inc., ACS, Los Angeles Meeting, March 28 - April 2, 1971. Grimmer, G. (1977), "Analysis of Automobile Exhaust Condensates," in Air Pollution and Cancer in Man, IARC Sci. Publ. No. 16. Gross, G.P. (1972), "The Effect of Fuel and Vehicle Variables on Polynuclear Aromatic Hydrocarbons and Phenol Emissions," Paper No. 720210. Presented at the SAE Automotive Engineering Congress and Exposition. Detroit, Michigan. Habibi, K. (1970), "Characterization of Particulate Lead in Vehicle Exhaust - Experimental Techniques," Environ. Sci. Technol., 4_:239-248. 90 ------- Habibi, K., E.S. Jacobs, W.G. Kunz, Jr., and D.L. Pastell (1970), Characteriza- tion and Control of Gaseous and Particulate Emissions from Vehicles, Presented at the Air Pollution Control Association, Fifth Technical Meet- ing, San Francisco, October, 1970, available from E.I. DuPont de Nemours & Co., Wilmington, Delaware. Hangebrauck, R.P., D.J. von Lehmden, and J.E. Meeker (1967), "Sources of Poly- nuclear Hydrocarbons in the Atmosphere," Environmental Health Series, U.S. Dept. of HEW, Cincinnati, Ohio. Henein, N.A. (1973), "Diesel Engines Combustion and Emission," in Engine Emissions. Chapter 6, G.S. Springer and D.J. Patterson (eds.), Plenum Press, New York. Heuss, J.M., G.J. Nebel, and B.A. D'Alleva (1974) "Effects of Gasoline Aromatic and Lead Content on Exhaust Hydrocarbon Reactivity," Environ Sci. Technol., £: 641-647. Hinkamp, J.B., M.E. Griffing, and D.W. Zutut," Aromatic Aldehydes and Phenols in the Exhaust from Leaded and Unleaded Fuels," Presented at Div. Pet. Chem., Inc., ACS, Los Angeles Meeting, March 28 - April 2, 1971. Hoffman, D., E. Theisz, and E.L. Wynder (1965), "Studies on the Carcinogenicity of Gasoline Exhaust," J. Air Poll. Control Assoc., 15;162-165. Kotin, P., H.L. Falk, and M. Thomas (1955), "Aromatic Hydrocarbons III. Presence in the Particulate Phase of Diesel-Engine Exhausts and the Carcinogenicity of Exhaust Extracts," AMA Arch. Ind. Health, 11:113-120. Kotin, P., H.L. Falk, and M. Thomas (1954), "Aromatic Hydrocarbons II. Presence in the Particulate Phase of Gasoline-Engine Exhausts and the Carcinogenicity of Exhaust Extracts," AMA Arch. Ind. Hygiene and Occup. Med., J3:164-177. Laity, J.L., M.D. Malbin, W.W. Haskell, and W.I. Doty (1973), "Mechanisms of Polynuclear Aromatic Hydrocarbon Emissions from Automotive Engines," SAE Paper No. 730835. Laresgoiti, A, A.C. Loos, and G.S. Springer (1977), "Particulate and Smoke Emission from a Light Duty Diesel Engine," Environ. Sci. Technol., 11:973- 978. Lee, R.E., Jr. and F.V. Duffield (1977), "EPA's Catalyst Research Program: Environmental Impact of Sulfuric Acid Emissions," J. Air Poll. Control Assoc., 2^:631-635. Lee, R.E. and F.V. Duffield (1977b), "Sources of Environmentally Important Metals in the Atmosphere," Presented at ACS National Meeting, August 29- September 2, Chicago, Illinois. 91 ------- Lyons, M.J. (1962), "Comparison of Aromatic Polycyclic Hydrocarbons from Gaso- line Engine and Diesel Engine Exhausts, General Atmospheric Dust, and Cigarette-Smoke Condensate," NCI Monogr. No. 9, p. 193-199. Marshall, W.F., D.E. Seizinger, and R.W. Freedman (1978), "Effects of Catalytic Reactors on Diesel Exhaust Composition," Bureau of Mines Technical Progress Report No. 105, U.S. Dept. of the Interior. Menster, M. and A.G. Sharkey, Jr. (1977), Chemical Characterization of Diesel Exhaust Particulates, NTIS, PERC/RI-77/5. Millington, B.W. and C.C.J. French (1966), "Diesel Exhaust - A European View- point," SAE Paper No. 660549. Moran, J.B. and O.J. Manary (1970), Effect of Fuel Additive on the Chemical and Physical Characteristics of Particulate Emissions in Automotive Exhaust, Interim Technical Report to the National Air Pollution Control Administration, submitted by the Dow Chemical Co., Midland, Michigan, July, 1970. Mueller, P.K. (1970), "Characterization of Particulate Lead in Vehicle Exhaust - Experimental Techniques," Environ. Sci. Technol., 4.:248-251. Mueller, P.K., H.L. Helwig, A.E. Alcocer, W.K. Gong, and E.E. Jones (1962), "Concentration of Fine Particles and Lead in Car Exhaust," in Symposium on Air Pollution Measurement Methods, ASTM Special Technical Publication 352, Philadelphia, A.S.T.M., p. 60-77. National Academy of Sciences (1976), "Medical and Biologic Effects of Environ- mental Pollutantss Vapor-Phase Organic Pollutants," NRC, Washington, D.C. NIOSH (1978), "The Use of Diesel Equipment in Underground Coal Mines," Work Group Reports from a NIOSH Workshop, Morgantown, W.Va., Sept. 19-23, NIOSH Publication Feb., 1978. Ninomiya, J.S., W. Bergman, and B.H. Simpson (1970), "Automotive Particulate Emissions," Presented at the Second International Clean Air Congress, International Union of Air Pollution Prevention Association, Washington, D.C., Dec., 1970, available from Automotive Emissions Office, Ford Motor Co., Dearborn, Michigan. O'Donnell, A. and A. Dravnieks (1970), "Chemical Species in Engine Exhaust and Their Contributions to Exhaust Odors," Report No. IITRI C6183-5, for NAPCA and CRC, Nov., 1970. PEDCO Environmental, Inc. (1978), Report on Air Quality Assessment of Particulate Emissions from Diesel-Powered Vehicles, prepared for Pollutant Strategies Branch, U.S. Environmental Protection Agency, Research Triangle Park N C March, 1978. ' 92 ------- Pitts, J.N., Jr., K.A. Van Cauwenberghe, D. Grosjean, J.P. Schmid, D.R. Fitz, W.L. Belser, Jr., G.B. Knudson, and P.M. Hynds (1978), "Atmospheric Reac- tions of Polycyclic Aromatic Hydrocarbons!: Facite Formation of Mutagenic Nitro-Derivatives," Science (in press). Reinhart, W.E., S.A. Gendermalik, and L.F. Gilbert (1970), "Fuel Factors in Automobile Tailpipe Emissions," presented at American Industrial Hygiene Conference, Detroit, Michigan, Paper No. 127, 15 pp. Sampson, R.E. and G.S. Springer (1973), "Effects of Exhaust Gas Temperature and Fuel Composition on Particulate Emission from Spark Ignition Engines," Environ. Sci. Technol., j^:55-60. Sawicki, E., J.E. Meeker, and M. Morgan (1965), "Polynuclear Aza Compounds in Automotive Exhaust," Arch. Environ. Health, 11:773-775. Schreck, R.M. (1978), "Health Effects of Diesel Exhaust," Biomedical Sciences Dept., General Motors Research Laboratories, Warren, Michigan. Schreck, R.M., J.J. McGrath, S.J. Swarin, W.E. Bering, P.J. Groblicki, and J.S. MacDonald (1978), "Characterization of Diesel Exhaust Particulate for Mutagenic Testing," G.M. Research Report No. 78-33.5, General Motors Research Labs., Warren, Michigan. Seizinger, D.E. (1978), "Analysis of Carbonaceous Diesel Emissions," Presented at the Conference on Carbonaceous Particles in'the Atmosphere, March 20- 22, Berkeley, California. Seizinger, D.E. and B. Dimitriades (1972), Oxygenates in Automotive Exhaust Gas; Estimation of Levels of Carbonyls and Noncarbonyls in Exhaust from Gasoline Fuels, NTIS, PB-212 600, Springfield, Virginia. Sievers, R.E. and J.E. Sadlowski (1978), "Volatile Metal Complexes: Certain Chelates Are Useful as Fuel Additives, as Metal Vapor Sources, and in Trace Metal Analysis," Science, 201:217-223. Somers, J.H., R.C. Garbe, R.D. Lawrence, and T.M. Baines (1977), "Automotive Sulfate Emissions - A Baseline Study," SAE Paper No.770166, 20 pp. Spicer, C.W. and A. Levy (1975), The Photochemical Reactivity of Diesel Exhaust Organics. Battelle Columbus Laboratories, NTIS, PB-244 166, Springfield, Virginia. Spindt, R.S. (1977), Polynuclear Aromatic Content of Heavy Duty Diesel Engine Exhaust Gases, prepared for Coordinating Research Council, Inc., CRC APRAC Contract CAPE-24-72, NTIS, PB-267 774. Spindt, R.S. (1974), First Annual Report on Polynuclear Aromatic Content of Heavy Duty Diesel Engine Exhaust Gases, Gulf Research and Development Co., prepared for Coordinating Research Council, Inc., EPA Contract No. 68-01-' 2116. 93 ------- Springer, K.J. and T.M. Baines (1977), "Emissions from Diesel Versions of Production Passenger Cars," SAE Paper No. 770818. Springer, K.J. and R.C. Stahman (1977), "Diesel Car Emissions - Emphasis on Particulate and Sulfate," SAE Tech. Paper, Vol. 770254, 29 pp. Springer, G.S. (1973), "Particulate Emission from Spark-Ignition Engine," in Engine Emissions, Chapter 6, G.S. Springer and D.J. Patterson (eds.), Plenum Press, New York. Springer, K.J. (1971), Emissions From Gasoline- and Diesel-Powered Mercedes 220 Passenger Cars, report to EPA, Contract No. CPA-70-44, June, 1971. Stara, J.F., W. Moore, and A.W. Breidenbach (1974), "Toxicology of Atmospheric Pollutants Resulting from Fuel Additives and Emissions Associated with the Use of Automobile Catalytic Converters," Recent Advances in the Assessment of the Health Effects of Environmental Pollutants, Vol. II., pp. 751-772. Proceedings of an International Symposium, Paris, June 24- 28, 1974. Stichting Concawe (1974), Effect of Gasoline Aromatic Content on Polynuclear Aromatic Exhaust Emissions, Report 6-74, 60 Von Hogenhouckleaan, The Hague, Sept., 1974. Ter Haar, G.L., D.L. Lenane, J.N. Hu, and M. Brandt (1972), "Composition, Size, and Control of Automotive Exhaust Particulates," J. Air Poll. Control Assoc., 22:39-46. Vuk, C.T. and J.H. Johnson (1975), "Measurement and Analysis of Particles Emitted from a Diesel Combustion Process." Paper presented at the Combustion Institute, Central States - Western States, 1975 Spring Technical Meeting, San Antonio, Texas, April 20-21, 1975. Vuk, C.T., M.A. Jones, and J.H. Johnson (1975), "The Measurement and Analysis of the Physical Characteristics of Diesel Particulate Emissions," SAE Paper No. 760131. Wang, Y.Y., S.M. Rappaport, R.F. Sawyer, R.E. Talcott, and E.T. Wei (1978), "Direct-Acting Mutagens in Automobile Exhaust," Cancer Letters (in press). Wilson, W.E., L.L. Spiller, T.G. Ellestad, P.J. Lamothe, T.G. Dzubay, R.K. Stevens, E.S. Macias, R.A. Fletcher, J.D. Husar, R.B. Husar, K.T. Whitby, D.B. Kittelson, and B.K. Cantrell (1977), "General Motors Sulfate Disper- sion Experiments: Summary of EPA Measurements," J. Air Poll. Control Assoc., 27;46-51. 94 ------- 4.0 Biological Effects It has been known for many years that the exhaust emissions from both gasoline- and diesel-powered vehicles contain a variety of potentially toxic materials. Most prominent among these are several gaseous emissions: carbon monoxide, sulfur dioxide, oxides of nitrogen, aldehydes, and hydrocarbons. In * addition, the presence of sulfates, metals, particulates, and polycyclic organic matter (POM) can be detected in varying amounts depending upon the type of fuel, engine load, and efficiency of operation (see Section 3.0). The major public health concern regarding the use of diesel engines presently involves the particulate fraction of diesel exhaust. Recent analy- tical studies have shown that particulate emissions in diesel exhaust can be up to 82 times as much as in gasoline exhaust using paired vehicles (Springer and Baines, 1977). Emissions of carbon monoxide and volatile hydrocarbons are lower from diesel than from gasoline engines, although the use of an oxidation catalyst can substantially reduce most of these emissions from gasoline engines (Stara e£ _al_., 1974; Lee et_ _al., 1976). There are several important reasons why increased exposure to particulates derived from diesel engines may con- stitute a potential health hazard (Schreck, 1978): 1) Carbonaceous particles from diesel exhaust are reportedly composed in part of high molecular weight polycyclic aromatic hydrocarbons. 2) These particles have high surface areas, theoretically enabling them to adsorb large quantities of gaseous exhaust products, most importantly the carcinogenic POM's such as benzo[a]pyrene. 3) The particles themselves may be degraded by atmospheric oxidation to yield lower molecular weight POM's which are potentially carcinogenic. 95 ------- 4) Diesel particulates are primarily in a size range (0.2-0.3 ym mean diameter) which would allow for deposition in the deep lung compartments, and possible retention in the lung. The discussions presented in the following sections of this report summar- ize the major studies conducted thus far which indicate potential toxic reac- tions to diesel exhaust mixtures, particulate extracts, and fuel additives. Significant related studies using gasoline exhaust are included for comparison and clarification of toxicologic hazards resulting from combustion processes. Extensive health effects reviews have recently been published for many of the individual components of diesel exhaust such as carbon monoxide (National Academy of Sciences, 1977a), oxides of nitrogen (National Academy of Sciences, 1977b), particulates (National Academy of Sciences, 1977c), and polycyclic organic matter (Santodonato jst: a^., 1978). Selected individual toxicants will be considered which make a particularly significant contribution to the overall toxic potential of the diesel exhaust mixture. 96 ------- 4.1 In Vitro Studies 4.1.1 Mutagenicity in Bacterial Systems It has been shown recently that organic extracts of airborne particulate matter are mutagenic to histidine-requiring strains of Salmonella typhimurium (Teranishi eit al. , 1978; Dehnen £t al., 1977). Because of the strong formal relationship between molecular events involved in mutagenesis and carcinogenesis (Miller, 1978), the demonstration of mutagenic activity for a substance is generally taken as strong presumptive evidence for the existence of carcinogenic activity as well. Therefore, it is believed that an investi- gation of the mutagenicity of foreign substances: (1) may be predictive of carcinogenic potential, (2) may be used to identify the most biologically active fractions of complex organic pollutants (e.g., diesel exhaust), and (3) may serve as an early warning of a possible threat to human health in cases where positive results are obtained. The Ames Salmonella mutagenicity assay incorporating a mammalian microsomal preparation for activation of promutagens has received widespread use in environmental research. Studies sponsored by the U.S. Environmental Protection Agency have applied this assay to guide the fractionization of heavy-duty diesel exhaust by identifying biologically active components of the particulate fraction (Huisingh ejt al., 1978). Five histidine-requiring tester strains of Salmonella typhimurium were employed: TA 1535, TA 1537, TA 1538, TA 98, and TA 100. Strains TA 1537 and TA 1538 are reverted to histidine-inde- pendence by frameshift mutagens, while TA 1535 is reverted by mutagens causing base-pair substitutions. Strains TA 98 and TA 100, which contain a plasmid to increase sensitivity, respond to mutagens acting either by frameshift mutation or base-pair substitution. 97 ------- Studies were carried out on fractions of a dichloromethane (DCM) extract of diesel exhaust particulate collected from two different engines on glass fiber filters. The DCM extract was divided into ether insoluble (INT), acidic (ACD), basic (BAS), and neutral (NUT) fractions; the NUT fraction being by far the largest and was further subdivided into paraffins (PRF), aromatics (ARM), a transitional (TEN) fraction, and a polar oxygenated (OXY) fraction (Figures 4.1 and 4.2). Some mutagenic activity was demonstrated in the insoluble, basic, and acidic fractions extracted from both particulate samples. However, the neutral fraction showed most of the mutagenic activity. Within the neutral fraction, the paraffins subfraction was not mutagenic, whereas the transitional and oxygenated subfractions were highly active. Both direct-acting components and components requiring metabolic activation were apparent, although most of the mutagens were of the direct-acting frameshift type. These results are summarized in Figure 4.3. The observation of direct-acting mutagens is signi- ficant in that it excludes unsubstituted polycyclic hydrocarbons (e.g., benzo- [a]pyrene) as causative agents, since they require metabolic activation for expression of mutagenic effects. Analysis of the specific components of the TRN and OXY subfractions was difficult, however, it was suggested that polar neutral compounds such as substituted polynuclear aromatics, phenols, ethers, and ketones were the major components. Caution must be exercised before implicating polar neutral compounds in diesel particulate fractions as major health hazards to man. The human body, when confronted with airborne particulate pollutants, has no physiologic means to chemically fractionate these complex organic mixtures. 98 ------- FILTERS SOXHLET EXTRACTION CH2CI2 (DCM) DCM EXTRACT 1. EVAPORATES WEIGH RESIDUE I 2. REDISSOLVE IN ETHER ETHER SOLUTION WITH SOME INSOLUBLES EXTRACT WITH BASE vo VO BASIC FRACTION BAS FILTERS 1 SOXHLET EXTRACTION CH3CN (ACN| ACN EXTRACT * 1 AQUEOUS PHASE ETHE 1. ACIDITY 2. EXTRACT ETHER 1 ACID FRACTION AQUEOUS PHASE (ACD) (DISCARD) R SOLUTION EXTRACT H3P04 .1-2.08-5.15% AQUEOUS PHASE 11. ADD BASE 2. EXTRACT ETHER f ETHER INSOLUBLES (INT) I -0.12-0.008 II - 1.18-0.700 ~1 ETHER SOLUTIONS NEUTRALS (NUT) 1 -53.38-51.81 II . Id •>-? . 17 Tfl AQUEOUS PHASE (DISCARD) I - 0.03 - II -0.09 0.03 0.05 Figure 4.1. Isolation and fractionation organics from diesel exhaust particulates (Huisingh e£ al., 1978) ------- NEUTRALS SILICA GEL CHROMATOGRAPHY HEXANE ELUTION NO FLUORESCENCE 1% ETHER/HEXANE INCIPIENT FLUORESCENCE CONTINUED 1% ETHER HEXANE STRONG FLUORESCENCE 50/50 ACETONE/METHANOL ELUTION MODERATE FLUORESCENCE N-PRF I - 36.26 II - 8.89 34.35% 8.94% 7.51% 1.61% 2.96% 1.22% I - 7.40 II - 7.43 6.31% 5.64% Figure 4.2. Silica gel chromatography fractionation of the neutral organics from diesel exhaust particulate (Huisingh e_t^ al., 1978) 100 ------- 800 120 240 CONCENTRATION OF COMPOUND ADDED TO PLATE IN MICROGRAMS DOSES ARE 10, 33. 100. 333. 1000 1000 (+) = with metabolic activation; (-) = without metabolic activation Figure 4.3. Comparison of the mutagenic response of various organic fractions from the 4-stroke cycle diesel truck exhaust particulate in Salmonella typhimurium strain TA 1538. ------- Target organs are thus simultaneously exposed to large numbers of environmental chemicals. It is well-established that various chemical components of polluted air, automobile exhaust, and tobacco smoke may interact with each other to either increase or decrease the carcinogenic response (Falk &t_ al_., 1964; Pfeiffer £t al., 1973; 1977; Van Duuren jet al., 1976). Therefore, the biologi- cal activity of chemical mixtures cannot be reliably predicted based on the specific actions of individual components. Furthermore, factors governing ease of absorption and biotransformation are important determinants of carcinogenic potency. These factors cannot be accounted for in bacterial systems. The apparent lack of correlation between potency in the Ames assay under certain conditions with carcinogenic potency in animals (Ashby and Styles, 1978a,b) further emphasizes the need for restraint in extrapolation of results. The formation of direct-acting mutagenic compounds by combustion processes was confirmed in studies involving non-catalyst treated automobile exhaust (Wang e£ al., 1978). Acetone extracts of particulates collected from six different gasoline engines showed direct-acting mutagenic activity to Salmonella typhimurium strains TA 98, TA 100, and TA 1537. In contrast, unused motor oil and various fuels (leaded, unleaded, diesel) were not muta- genic. The postulated formation of nitro-substituted polycyclic aromatic hydrocarbons during combustion led to the synthesis and examination of 6- nitrobenzo[a]pyrene as a potential mutagen. This compound was found to be a direct-acting mutagen in strains TA 98, TA 100, and TA 1537. Mutagenic activity of 6-nitrobenzo[a]pyrene was comparable to that obtained with benzo[a]pyrene in the presence of a liver enzyme activating system. Since the mutagenic activity of particulate fractions of city air was correlated to the lead content of air 102 ------- it was suggested that automobile emissions may be a primary source of direct- acting mutagens in the ambient atmosphere. However, nitro-substituted poly- cyclic compounds per se have not been monitored in the urban atmosphere. Taken together, the results of bacterial mutagenicity assays on diesel and gasoline engine exhaust indicate that direct-acting mutagens are formed during combustion. The chemical identity of these substances is un- known, although substituted polycyclic aromatic hydrocarbons seem to be likely candidates in both cases. Presently there is no way to compare the mutagenic potency of gasoline versus diesel particulates since different collection and chemical fractionation schemes have been employed. Even if results were avail- able from parallel Ames bioassays, the extrapolation of these data to support a health risk assessment would be limited to a qualitative judgement concerning cancer risk. 103 ------- 4.2 In Vivo Studies 4.2.1 Absorption, Metabolism, and Excretion Exposure to diesel and gasoline engine exhaust occurs primarily by inhalation of gaseous and particulate emissions. Whereas highly water- soluble vapor phase organic emissions are generally absorbed across the moist surfaces of the upper respiratory tract, particulate material (depending upon size), water-insoluble compounds, and gases adsorbed to particulates may pene- trate to the deeper lung compartments. Studies on the deposition and retention of diesel particulate have considerable significance in light of the preponderance of this emission in comparison to that produced by the gasoline engine. Moreover, the likeli- hood that diesel particulate will contain adsorbed oxidants and POM presents a further dimension to the problem of potential toxic interaction with, or absorption across, the respiratory epithelium. In the absence of adsorbed substances with toxic potential, pure carbon particles as are formed during the diesel combustion process may not present a significant health threat. Preliminary results are available concerning the physical characterization and clearance of diesel particulate from lungs of rats exposed to a 1:13 dilution of automotive diesel exhaust (Moore e_t. aJL., 1978). The nature of the diesel particulate when collected on nucleopore membranes was examined by scanning electron microscopy. Particles smaller than 0.01 ym resembled spherical cotton balls while the larger respirable particulate had a flaky appearance, presumably due to the presence of adsorbed and condensed organic matter. Daily eight-hour exposures of rats to diesel exhaust lasting from one to 54 days produced a grey to black pigmentation of the lungs which 104 ------- varied in intensity with the duration of exposure. Black granular particulate material was observed histologically in the cytoplasm of the alveolar macro- phages from all exposed animals. The diesel particulate could no longer be found in alveolar macrophages examined 28 days after a single eight-hour exposure, Phagocytosis has been found to occur following the inhalation of diesel particulates. Examination of macrophages containing the phagocytosed particles has recently been conducted by transmission electron microscopy (Orthoefer £t al., 1978). At 5000 times magnification, diesel particulate appears in the macrophage as an aggregation of small particles. Macrophages containing the particulate aggregates were also distinguished by the lack of primary vacuoles. The quantitative aspects of particle clearance by macrophage ingestion are not well understood (NAS, 1977). It is generally believed that phagocytosed particles are transported by macrophages to the pharynx where they are subsequently swallowed. Thus, exposure to adsorbed chemicals may also occur via the gastrointestinal tract. In addition, it is suggested that ; clearance of macrophages from the lung may also lead to localization in various organs and tissues (Moore £t al_., 1978; Lauweryns and Baert, 1977). This process may have important implications for toxic effects in non-respiratory tissues. Insoluble particles, and presumably diesel particulate as well, can actually be partially digested by lysosomal hydrolases in the macrophage or remain trapped for the life of the cell. It is likely that the chemical nature of the diesel particulate will be the critical factor in determining its fate within the macrophage. Examination of the physical and chemical characteristics of diesel particulate, however, are complicated by the fact that particles and 105 ------- their agglomerates may be altered during the collection process prior to analysis. The fate of POM adsorbed to diesel particulate can be inferred from studies involving BaP-coated carbon particles intratracheally instilled in mice (Creasia et_ al., 1976). When radiolabelled BaP was adsorbed to large carbon particles (15-30 ym) and instilled in the lungs, 50 percent of both the BaP and the carrier particles were cleared from the lungs in four to five days. Little carcinogen was released from the carbon particles in this case, and therefore, contact with the respiratory epithelium (and carcinogenicity) was low. With smaller carbon particles (0.5-1.0 urn),. however, 50 percent particle clearance was not achieved until seven days after instillation. In this case, 15 percent of the adsorbed BaP was eluted from the particles and left free to react with the respiratory tissues. No measurements were made in this study of the phagocytic uptake of the particles by alveolar macrophages. In the complete absence of carrier particles, however, BaP was cleared from the lungs at 20 times the rate of adsorbed BaP. In addition to mucociliary clearance and phagocytosis by alveo- lar macrophages, processes occurring in the lung which also determine the fate of adsorbed POM include metabolism by the respiratory tissues, and systemic absorption across the respiratory epithelium. It is known that BaP when administered intratracheally to rats appears in the body tissues with the same pattern of distribution as when given parenterally (Kotin e_t al., 1959). Similarly, Vainio and coworkers (1976) reported that unchanged BaP quickly appears in the perfusion fluid of isolated perfused rat lungs following intra- tracheal administration of a 200 nmole dose. The presence of particulate 106 ------- matter, however, can profoundly affect the rate and pathways of BaP metabolism in the isolated perfused lung (Warshawsky, 1978). When BaP and crude air particulate or ferric oxide were administered together, the rate of BaP meta- bolism was inhibited (Table 4.2). Pretreatment with particulate, on the other hand, caused a significant increase in the subsequent rate of BaP metabolism (Table 4.3). The enhancement of BaP metabolism by pretreatment with parti- culate apparently resulted from increased enzyme activity. Particulate-induced inhibition of the metabolism of co-administered BaP may have been due to the sequestering of adsorbed BaP in macrophages. 4.2.2 Acute Toxicity 4.2.2.1 Inhalation Exposure The first comprehensive examination of the acute inhalation toxicity of diesel exhaust was conducted by Pattle and coworkers (1957). Their objective was to determine the principle toxic constituents of diesel exhaust generated under four conditions of engine operation: light load; moderate load; moderate load with "worn" fuel injector; light load with high fuel-to-air ratio. Mice, rabbits, and guinea pigs were severely exposed for five hours to the undiluted diesel exhaust. Under a light load, a highly acrid exhaust was produced which caused no mortality and minimal damage to the lungs. Exposures of greater duration (7 to 14 hours) under light load conditions produced nearly complete mortality in all species, accompanied by mild pathologic alterations in the trachea and lungs. Aldehydes (16 ppm) and oxides of nitrogen (46 ppm) were presumed to be the primary toxic agents in this case. Under moderate load conditions, a less irritating but more lethal exhaust was produced. Only slight alterations were seen in the trachea, but severe lung damage occurred, 107 ------- g Table 4.1 Influence of Particulates Administered to Isolated Perfused Lung on BaP Metabolism* (Warshawsky et al., 1978) Pretreatment : IPL: No. of animals: Total rate of appearance of metabolites in blood (ng/hr/g lung + SE) Metabolic pattern in blood (%+SE)b 7,8-Dihydrodiol 9,10-Dihydrodiol 4 , 5-Dihydrodiol Monohydroxylated Diones Nonextractable All three columns compared 1 mg/kg. BaP 9 256+38 6.6+0.9 15.4+4.0 3.3+0.6 9.7+1.1 10.6+1.8 54.4+5.4 to each other. All metabolites BaP + Fe 0 a 5 * 165+51 14.0+2.9° 20.4+1.9 6.0+3.1 5.4+1.66 5.6+1.5- 48.0+4.5 separated by TLC. BaP + CAP3 5 156+42 19.1+4.4d 28.3+7.9 3.0+1.3 5.1+1.4e 5.2+2.6 39.3+13.8 Metabolite pattern values expressed as percent of total rate of appearance of metabolite in blood +SE. ° p = 0.05. ° p = 0.01. ^ p = 0.1 (by Student-Newman-Keuls test). abbreviations: IPL, isolated perfused lung; CAP, crude air particulate* BaP benzo[a]pyrene ------- Table 4.2. Influence of Particulate Pretreatment on BaP Metabolism" (Modified from Warshawsky et_ al., 1978) o VO Pretreatment : IPL: No. of animals Total rate of appearance of metabolites in blood (ng/hr/g lung + SE) : Metabolite pattern in blood (Z + SE)d 7,8-Dihydrodiol 9,10-Dihydrodiol 4,5-Dihydrodiol Monohydr oxy lated Diones Nonextractable BaP 9 256+37 6.640.9 15.4+4.0 3.3+0.6 9.7+1.1 10.6+1.8 54.4+5.4 Fe2°3ITa BaP 5 637+203 13.3+2.3 26.3+5.6 2.9+2.0 4.9+0.7c 14.3+4.4 37.7+5.8 CAPITa BaP 5 830+100° I. 18.2+5.6° 32.6+4.3 0.9+0.5 3.4+0.6c 5.5+1.8 39.4+8.0 CAPIT* BaP+CAP 5 143+29C 23.6+7.6 17.0+7.2 1.9+0.7 6.5+2.3 10.4+2.3 40.6+6.6 All three columns compared to each other. All metabolites separated by TLC. ? 10 mg/kg, once/week x 5. p = 0.05 (by Student-Newman-Keuls test). ": p = 0.01. a Metabolite pattern values expressed as percent of total rate of appearance of metabolite in blood +SE. abbreviations: IPL, isolated perfused lung; CAP, crud air particulate; BaP, benzo[a]pyrene ------- probably resulting from the high levels of nitrogen oxides (174-209 ppm) present in the exhaust. A rich combustion mixture produced the most lethal exhaust, killing all animals within five hours. The exhaust was high in aldehydes (154 ppm) and carbon monoxide (0.17%) and produced extreme irritation, only mild lung damage, but severe tracheal damage in rabbits and guinea pigs. Death was most likely due to carbon monoxide poisoning. Hydrocarbon levels were not determined in these experiments, and thus it is not known to what extent they may have contributed to the effects observed. The acute effects of irradiated and nonirradiated gasoline engine exhaust in rats and hamsters were qualitatively similar to those pro- duced by diesel exhaust as described above (Stara et al., 1974). After seven days of continuous inhalation exposure to gasoline exhaust (diluted at a ratio of 10:1), mortality in groups of infant rats reached 100% for irradiated exhaust and 77% for nonirradiated exhaust. The specific toxicant(s) responsible for the lethal effect was not determined, although death apparently did not result from carbon monoxide poisoning. In adult rats and hamsters exposed continuously for five days, various changes in lung morphology were noted, as well as vacuolar changes in hepatic parenchymal cells (irradiated and nonirradiated exhaust) and renal tubular cells (irradiated exhaust) of hamsters. In marked contrast to these results, gasoline exhaust from engines equipped with an oxidation catalyst produced virtually no mortality in infant rats or pathologic alterations in the tissues of adult rats and hamsters. The importance of the particulate fraction in contributing to the acute effects of inhaled diesel exhaust was suggested in studies by 110 ------- Battigelli and coworkers (1966). The effect of diluted diesel exhaust on tracheal clearance by mucociliary action was examined in rats exposed for cumulative periods of 4 to 100 hours. It has been previously established that noxious irritants and such gases as NO and SO can inhibit ciliary clearance and thereby render an organism more susceptible to respiratory infection and the actions of inhaled carcinogens (e.g., benzo[a]pyrene). As might be expected, inhalation of diluted diesel exhaust produced varying degrees of mucociliary inhibition which appeared to correlate with levels of N0? (1.9 •* 15.0 ppm) and S0~ (0.1 - 3.0 ppm) in the exhaust. Even more noteworthy, however, was the observation that the inhibition of clearance was markedly less in animals inhaling particle-free (filtered) exhaust. The particulate material was a complex mixture composed primarily of inorganic carbon (55-60%) and normal paraffins with chain lengths greater than four carbon atoms (35-38%). The authors concluded that the particulates in diesel exhaust may contribute directly to an adverse effect on host defenses, even in the absence of other gaseous emissions. The authors demonstrated that the inhibitory effect of a single exposure to diesel exhaust on mucociliary clearance was completely reversible within a few days. Recent tests have now shown that female mice (CD-I, Charles River) inhaling diesel exhaust displayed enhanced mortality from respiratory infection by Streptococcus pyogenes (Campbell et^ al., 1978). Mice inhaled either irradiated or nonirradiated diesel exhaust, diluted with clean air at a ratio of 1:13, for a six hour period. Following the diesel exhaust exposure (within 1-2 hours), animals were briefly exposed to an aerosal of a broth culture of the test pathogen. Enhanced susceptibility to lethal infection was 111 ------- observed in all exhaust-treated groups, with those animals exposed to irradi- ated exhaust apparently being more severely affected. Enhanced susceptibility was not displayed when animals were challenged 22 hours after acute exposure. The contribution of N0_ exposure to the observed increase in mortality is not known. Both catalyst- and noncatalyst-treated gasoline engine exhaust can also enhance infective susceptibility in mice. Coffin and Blommer (1967) reported that mice exposed to diluted irradiated gasoline exhaust (no oxidation catalyst) for four hours experienced increased mortality from sub- sequent immediate exposure to streptococci. Exhaust diluted to yield carbon monoxide levels as low as 25 ppm and oxidant levels as low as .15 ppm was effective in increasing mortality to infectious pneumonia. In related studies using catalyst-treated gasoline engine exhaust (average dilution 1:14.1), irradiated exhaust caused a consistent and significantly greater susceptibility to infection than non-irradiated exhaust (Campbell e£ al., 1978). It was concluded, however, that relative to mortalities produced in clean air-treated controls, diesel exhaust was somewhat more effective than catalyst-treated gasoline engine exhaust in producing increased infection mortality. Several studies have been concerned with the health effects of potential diesel fuel additives. Gutwein and coworkers (1972, 1974) con- ducted distribution and retention studies in rats acutely exposed to exhaust generated from diesel fuel containing a radiolabelled barium-based antismoke additive. Barium contained in the diesel exhaust (average concentration 3 1.39 mg/m ) was transferred to the lungs, gastrointestinal tract, and bone during a 10 hour exposure. Whole body levels of barium reached 0.1 yg/g of 112 ------- tissue; clearance of barium from the lungs and gastrointestinal tract was rapid, whereas accumulation of the compound occurred in the bone. No observa- tions were made for toxic symptoms resulting from absorption of barium or other components of the diesel exhaust. 4.2.3 Subacute Toxicity 4.2.3.1 Inhalation Exposure A series of extensive studies has been initiated by the U.S. Environmental Protection Agency (EPA) regarding the effects of repeat- ed inhalation of automotive diesel exhaust in animals. Preliminary results are available from several of these investigations where biological effects on selected parameters were measured at various intervals following initiation of exposure. Diesel exhaust used for these studies was generated with a Nissan CN6-33 engine coupled to a Chrysler Torque-flite automatic transmission. The engine was operated in a modified "California Cycle" using number 2 diesel fuel. A summary of exhaust component concentrations measured in the animal exposure chambers is presented in Table 4.3. Moore and coworkers at EPA (1978a) exposed infant rats for 54 days (8 hours per day) to irradiated and non-irradiated diesel exhaust diluted at a ratio of 1:13. Clinical laboratory determinations were made during the study and selected animals were sacrificed for histologic examina- tion of tissues at the termination of exposure. During the exposure period there was no mortality or adverse effects on body weight gain and general appearance of the animals. No significant differences in hematologic para- meters or plasma electrolyte values could be shown between treated and control groups. However, reduced levels of alkaline phosphatase, serum glutamic- oxaloacetic transaminase (SCOT), and lactate dehydrogenase were evident in rats 113 ------- TABLE 4.3 . EXHAUST CONSTITUENTS AND CONDITIONS IN EXPOSURE CHAMBERS3 (LEE et al., 1978) Atmosphere Constituent or Condition Carbon monoxide (CO), ppmb Total hydrocarbons (THC)C, ppm (as carbon) Nitric oxide (NO), ppm Nitrogen dioxide, (N02), ppm Sulfur dioxide (S02), ppm Total suspended particulates (TSP), mg/m3 Sulfate , SO- mg/ni Ozone ppm Carbon dioxide, (C02), mol % Temperature, °C Relative humidity, per cent Exposure Chamber Atmosphere Pur.ified Air Nonirradiated Irradiated (Control Diesel Exhaust Diesel Exhaust atmosphere) 2.0 15.7 15.4 2.0 15.6 15.0 0.11 5.85 4.94 0.07 2.19 2.73 NAd 2.13 1.91 NA 6.32 6.83 0.0 0.57 0.57 <0.01 0.040 0.252 0.255 24.0 23.7 24.1 51.8 51.3 48.2 , Averages of weekly means ppm values are v/v By ambient-temperature probe flame ionization detector. Values using heated (350°F) probe are higher and may be approximated by . multiplying by 1.9 Data not yet available; values should be much lower than in exhaust chambers. 114 ------- exposed to irradiated and non-irradiated diesel exhaust. Tissue damage gener- ally results in increased serum levels of these enzymes, thus the toxicologic relevance of these observations is not known. Upon necropsy, minor histo- pathologic lesions of the respiratory tract were found. These included an accumulation of black pigmented alveolar macrophages throughout the lung. Black pigment found in the bronchial lymph nodes of one animal suggested clear- ance of particulate-laden macrophages. In the absence of any observed func- tional impairment, it is not possible to make a definitive statement regarding the severity of these pathologic changes. On the other hand, the presence of diesel particulate in .the alveolar region and their clearance via the lymphatics indicates that adsorbed carcinogens are also delivered to these sites. In further studies at EPA conducted with rats, the effect of a 28-day exposure to diesel exhaust on pulmonary function and arterial blood gases was evaluated (Pepelko et al., 1978). Groups of rats were exposed to diluted, irradiated and non-irradiated, diesel exhaust 20 hours per day, seven days per week. The slope of the static lung compliance curve and resi- dual lung volume, both indicators of emphysematous change, were not affected by exposure to either irradiated or non-irradiated exhaust. Vital capacity and total lung capacity, which are non-specific indicators of change in pul- monary function, were both significantly increased in the group exposed to non-irradiated exhaust. This observation is consistent with previous results from studies with catalyst-treated automotive gasoline engine exhaust. It was not considered a serious effect in light of the duration of exposure. However, since these studies did not allow adequate time for the development of chronic lung disease, definitive conclusions cannot yet be drawn. Likewise, a lack of 115 ------- significant treatment effects on arterial blood gases may have reflected func- tional integrity only under conditions of short-term exposure. In addition, most clinical measures of pulmonary function are not ideally suited for the detection of very early lung damage. More extensive studies on pulmonary function were conducted at EPA with cats exposed for 28 days to a 1:13 dilution of diesel exhaust (Pepelko e£ a_l. , 1978a). Following completion of exposure, measure- ments were made of expiratory flow-volume curves, dynamic compliance, resis- tance, and pulmonary diffusing capacity. In addition, hematologic parameters were recorded and pathologic tissue evaluations conducted. No exposure-related physiologic effects were found other than a decrease in maximum expiratory flow rate at 10% of vital capacity; probably resulting from a slight increase in small airway resistance. This change can result from airway constriction under conditions such as smoking, chronic exposure to coal dust, or subclinical emphysema. However, pathologic examination of the respiratory tissues did not reveal emphysematous changes. The most prominent finding was the presence of focal alveolitis characterized by an accumulation of black pigmented clusters of one to 50 alveolar macrophages. These results support the conclusion that diesel exhaust particulate may penetrate to deep lung compartments and produce histopathologic changes, but do not allow for the prediction of possible chronic effects. More serious physiologic and pathologic effects were found in infant guinea pigs exposed continuously (20 hours/day) to the diluted diesel exhaust for 28 or 56 days (Wiester e£ al., 1978). After four weeks of exposure to irradiated diesel exhaust, pulmonary flow resistance was substantially 116 ------- increased while dynamic compliance, minute volume, breathing rate, and tidal volume did not differ between exposed and control groups. The reason for the paradoxical increase only in pulmonary flow resistance was not evident. Expo- sure to either irradiated or nonirradiated exhaust caused increased lung weight to body weight ratios. In addition, guinea pigs exposed to irradiated exhaust displayed a slight but significant sinus bradycardia on electrocardiogram tracings. Other parameters of cardiac function and histopathology were normal. Thus the significance of the observed sinus bradycardia may have been more statistical than clinical. Animals sacrificed after 56 days of exposure re- vealed a characteristic focal alveolitis accompanied by pigmented macrophage accumulation, as was observed in cats and rats similarly exposed to diesel exhaust. The presence of black pigment in draining bronchial and carinal lymph nodes indicated a similar clearance mechanism for inhaled diesel particulate as was seen in the rat. Tissue response to diesel exhaust irritation was mani- fested by hypertrophy of goblet cells in the tracheobronchial tree; possible tissue damage was suggested by the presence of focal hyperplasia of alveolar lining cells, presumably Type II granular pneumocytes. There was no evidence of other changes such as squamous metaplasia, emphysema, peribronchitis, or peribronchiolitis. It is apparent that the irritant effects produced by inhalation of diesel exhaust cannot be attributed solely to the action of carbonaceous particles, even though it is apparent that diesel particulate becomes widely distributed throughout the lung. At least some of the tissue damage produced by inhalation of diesel exhaust may be attributable to oxides of nitrogen, and particularly N02- On the other hand, water-soluble gases such as S02, as well as sulfate aerosols may contribute to functional disturbances 117 ------- (i.e., increased pulmonary flow resistance) but probably do not act in the alveolar region (NAS, 1977). The intervention of carrier particles having the proper size, however, can deliver irritant substances to the deepest lung compartments. Thus, diesel exhaust contains particulate which can adsorb irritant gases which are responsible for producing histopathologic damage that may lead to the development of emphysema. Moreover, the relative abundance of NO and particulates produced by diesel engines in comparison to gasoline X engines suggests that the risk for chronic respiratory disease may be increased due to the greater potential for carrying adsorbed oxidants into the parenchymal region. The participation of adsorbed POM in eliciting irritation of the alveolar tissue is probably minimal (Santodonato et^ a.^., 1978). Lee and coworkers at EPA (1978) have examined several biochemical parameters relevant to pulmonary fibrosis/emphysema and carcino- genesis that are influenced by exposure to diesel exhaust. In the rat, sub- chronic exposure to diesel exhaust produced a doubling in aryl hydrocarbon hydroxylase (AHH) activity, a measure of mixed-function oxidation, in the prostate and lung, and a 30% increase in the liver. Epoxide hydrase activity in these tissues was not increased by the diesel exposure. These microsomal enzyme systems are normally involved with detoxification of xenobiotics in conjunction with various P-450 type cytochromes. However, this system is also directly involved with the metabolism of carcinogenic polycyclic hydrocarbons to their active species (epoxides and diol-epoxides). Epoxide hydrase, also a microsomal enzyme, converts epoxides into vicinal glycols. Since some glycols are further metabolized by the mixed-function oxidases to form ultimate carcino- genic forms (i.e., diol-epoxides). this enzyme would likely affect both carcino- genesis and detoxification. Figure 4.4 presents a schematic representation of 118 ------- 3 l S CM CO (ENDOPLASMIC RETICULUM) GLUTATHIONE CYTOCHROME P-450 MIXED-FUNCTION OXIDASE (MFO) MFC BaP- -SG (DETOXIFICATION TRANSFERASE PRODUCTS) (CYTOSOL) BaP OXIDES EPOXIDE HYDRASE (ENDOPLASMIC RETICULUM) BaP PHENOLS MFO BaP QUINONES MFO BaP DIOL EPOXIDES (PROPOSED ULTIMATE CARCINOGENS) BaP DIHYDRODIOLS (PROPOSED PROXIMATE CARCINOGENS) UDP-GLUCURONOSYL TRANSFERASE (ENDOPLASMIC RETICULUM) H2O-SOLUBLE CONJUGATES (DETOXIFICATION PRODUCTS) Figure 4.4. Enzymatic pathways involved in the activation and detoxification of BaP. 119 ------- the various enzymes involved in activation and detoxification pathways for BaP, that is also representative of the known mechanisms of POM metabolism in general. Further biochemical aspects of the subacute toxicity of diesel exhaust concerned early changes produced in the lung tissue (Lee £t al_. , 1978). Inhalation of a 1:13 dilution of diesel exhaust by rats caused increases in the rate of collagen and protein synthesis, and enhanced prolyl- hydroxylase activity in the lungs. These alterations were indicative of fibrogenic changes, consistent with a large increase in connective tissue proliferation and continuous scar formation in response to injury. Such dis- turbances in the integrity of lung structure, although not necessarily linked, are important indicators of potential emphysema development. Accompanying these biochemical alterations were noticeable changes in the appearance of the diesel-exposed lungs. These lungs were rubbery to the touch, charcoal grey in color, and much more difficult to homogenize than control lungs. Subacute exposure studies with gasoline engine exhaust have clearly shown the difference in toxicity between catalyst- and noncatalyst- treated exhaust (EPA, 1978). Infant guinea pigs exposed continuously for 35 days to diluted (1:10) catalyst-treated exhaust displayed reduced growth rate (0-20%), increased airway resistance (3-47%), and no change in lung compliance. Removal of the catalyst, however, resulted in growth rate reductions of 34-36%, increased airway resistance by 63-68%, and a significant decrease in lung compliance (35-39%). A severe increase in bronchial constriction was indicated in the non-catalyst group, which might represent a simple defense mechanism. Pathologic changes in the lungs of clean air controls and catalyst-treated exhaust groups included inflammatory lesions, focal thickening of the alveolar 120 ------- walls, and a focal pneumocytic hyperplasia. Similar, but more severe, changes were seen in the lungs of guinea pigs inhaling noncatalyst-treated exhaust. The changes observed in the control animals complicates the analysis of these results. Lactating female rats and their newborn offspring exposed to catalyst- treated gasoline exhaust for four and 12 weeks, respectively, displayed no treatment-related effects on mortality, body weight, hematology, or histo- pathology (EPA, 1978). The ability of an oxidation catalyst to reduce carbon monoxide levels in gasoline exhaust is credited with preventing the cardiac hypertrophy, and polycythemia which results from subchronic (4 week) exposure of rats to noncatalyst-treated exhaust. In addition, damage to the lung and/or kidney as shown by increased serum lactate dehydrogenase levels is also pre- vented by the catalyst. Overall it is apparent that health-related benefits are derived from the use of an oxidation catalyst with gasoline engines. The prevention of significant subchronic effects by a catalytic converter can almost certainly be attributed to the substantial reductions which are realized in the emission of gaseous exhaust components. Subchronic exposure to diesel exhaust, on the other hand, produces damage which is apparently more severe than that produced by catalyst-treated gasoline exhaust, but somewhat less than that resulting from exposure with the catalyst removed. Fuel additives have the potential to alter the chemi- cal composition of engine emissions and possibly modify the biological effects produced by inhalation of exhaust. Moore and coworkers (1975) studied the biological effects of automotive emissions containing Mn particulate introduced by the fuel additive, methylcyclopentadienyl manganese tricarbonyl (MMT). MMT is used in unleaded gasoline as an antiknock additive, and is marketed as a 121 ------- smoke suppressant for diesel engines and stationary jet fuel power sources. Rats and hamsters were exposed eight hours per day for 56 consecutive days to gasoline engine exhaust (1:25 dilution) derived from fuel containing MMT at 0.25 g (as Mn) per gallon. Although increased tissue concentrations of Mh were produced by the exposure, no gross changes or histopathologic lesions could be attributed to the presence of MMT in the fuel. The primary lesion produced was a thickening of the cuboidal epithelium in the terminal bronchioles of the lung; an effect which was not considered particularly severe. Lesions did not become more severe with length of exposure, but occurred in 21% of the animals exposed to irradiated exhaust, 14% exposed to non-irradiated exhaust, and 60% of the clean air controls. It is noteworthy that the incidence of lesions in control animals costs doubts on the entire experiment. 4.2.3.2 Dermal Exposure An early study has demonstrated that an organic extract of diesel exhaust particulates can produce severe systemic toxicity when applied to the skin of mice (Kotin et_ akL., 1955). Extracts of exhaust from a grossly inefficiently operating diesel engine when applied to the inter- scapular area of C57 black mice produced immediate tremors, followed by a reversible lethargy and loss of neuromuscular responses. Deaths began to result after about ten weeks of treatment (3 applications per week). Post- mortem examination revealed a combined hepatotoxic and nephrotoxic effect. This was characterized by liver cord cell degeneration, and tubular degenera- tion in the lower nephron of the kidneys. The immediate cause of death in exhaust-treated mice was pneumonia, which was taken as evidence of decreased host resistance, although a mechanism was not postulated. When mice of the same strain were treated with extracts from gasoline engine exhaust (no oxidation 122 ------- catalyst) in the same manner as in the diesel studies, severe toxicity was not encountered (Kotin e_t al., 1954). The effect of the solvent employed in these experiments must be carefully considered, however. 4.2.3.3 Behavioral Effects Behavioral alterations in rats have been produced by exposure to catalyst- and noncatalyst-treated gasoline engine exhaust (Cooper et ajL. , 1977) as well as diluted diesel exhaust (Laurie e£ al., 1978). Con- centrations of the various exhaust components are summarized in Table 4.4. Exposure of adult rats to diesel exhaust for 20 hours per day for six weeks caused a significant reduction in spontaneous locomotor activity measured at the end of the treatment period (Figure 4.5). In addition, decrements in forced activity performance resulted from the diesel exhaust exposure. During a four week recovery period, however, the difference in spontaneous locomotor activity between exhaust-treated and control rats was reduced. In related studies, neonatal rats were exposed to diesel exhaust from day one after birth, 20 hours per day, for 17 days (Laurie je_t al.., 1978). Measurements of surface righting and ear detachment taken after one or two days of exposure showed no differences from control values. Like- wise., air righting, measured on days 14, 15, and 16, was not affected by the treatment. However, significant reductions were observed for both pivoting (measured on days 6 and 7) and eye opening (measured on days 14, 15, and 16) behavior when compared to controls. If data collected on female rats were considered alone, eye opening behavior was not significantly delayed. It was concluded from these studies that spontaneous locomotor activity in adult rats was depressed further by exposure to diluted 123 ------- CD (M o 30^ 26- ~ 22-\ o if «H £ W | 141 tt 10- • Control o Exposed I 1 I I 2 I I 3 4 I I I I I I 561 2 3 t Weeks Figure 4.5. Effect of diesel exhaust on spontaneous locomotor activity in rats (Laurie et_ al., 1978) 124 ------- diesel exhaust than by exposure to catalyst- and noncatalyst-treated gasoline engine exhaust (1:11 dilution). The causative agent(s) which affects rat behavior cannot be specified. It was postulated, however, that hydrocarbon components of diesel exhaust most likely accounted for the behavioral altera- tions observed. 125 ------- 4.2.4 Chronic Toxicity The preliminary results of only two studies have been published thus far concerning the pulmonary damage resulting from chronic inhalation of diesel exhaust. These have employed high concentrations of emission products. Stuart and coworkers (1978) have exposed male rats (48 per group) to the fumes 3 of an inefficiently operating diesel engine (50 ppm carbon monoxide, 10 mg/m 3 soot) alone and in combination with bituminous coal mine dust (6 mg/m ) for six hours daily, five days per week for periods up to 20 months. Serial sacrifice and histopathologic examination of the lungs in rats inhaling diesel exhaust revealed particulate accumulations, vesicular emphysema, and beginning inter*- stitial fibrosis. Inhalation of diesel exhaust together with coal dust pro- duced similar alterations in the lungs as well as bronchiolar epithelial pro- liferation and inflammatory reaction. Carboxyhemoglobin levels were elevated in both treatment groups. Parallel studies have also been conducted by Stuart and co- workers with Syrian golden hamsters exposed to diesel exhaust, and their results were summarized at a recent workshop (NIOSH, 1978). Exposures to diesel exhaust 3 containing 4-6 ppm NO^ and respirable particulates at 6-10 mg/m were conducted five hours daily, five days per week, for up to 20 months. Histopathologic changes which resulted in the lungs included marked particulate aggregation in alveoli or macrophages, pulmonary consolidation, vesicular emphysema4 inter- stitial fibrosis, and cuboidal metaplasia. Very few studies have been conducted which involve chronic inhalation exposure to gasoline exhaust, usually because the carbon monoxide exposures involved are too great. Thus, direct comparison of histopathologic damage with that produced by diesel exhaust cannot be validly performed. In 126 ------- early reports of studies where mice were chronically exposed (>2 years) to diluted gasoline exhaust, most toxicologic observations were negative (Campbell, 1936). No adverse effects were noted on death rate, body weight, or rate of growth. When death occurred, it apparently involved heart failure accompanied by lung congestion. Pneumonia and pathologic alterations in the liver (con- gestion, atrophy with fibrosis or necrosis) were more common in exhaust-treated mice than in controls. More recent studies involving life-long exposure of rats to diluted (1:100) gasoline exhaust (containing 58 ppm CO and 23 ppm of total nitrogen oxides) have yielded several significant results (Stupfel et al., 1973). The most important finding was the presence of bilateral renal sclerosis in more than half of the animals autopsied. In addition, a greater number of emphysematous lesions and spontaneous tumors of various organs were observed in exhaust-treated rats than in controls. However, no tumors of the respiratory tract were found. It is noteworthy that the levels of nitrogen oxides were very high in this study. Most recently, a chronic study has been completed which involved the exposure of beagle dogs to raw or photochemically reacted gasoline engine exhaust 16 hours daily for 68 months (Hyde e_t^ aJ^., 1978). In all exposure groups, reversible lung damage was encountered. Dogs inhaling raw exhaust dis- played hyperplasia of nonciliated bronchiolar cells, which apparently persisted long after cessation of exposure. With irradiated exhaust, incipient emphysema was produced, which was thought to result from exposure to nitrogen oxides (1.77 + 0.68 mg/m3 N02; 0.23 + 0.36 mg/m3 NO) and ozone (0.39 + 0.18 mg/m3). 4.2.5 Bioassays for Carcinogenicity Pioneering work by Kotin and coworkers (1955) established that the particulate fraction of exhaust from an inefficiently operating diesel 127 ------- engine contains carcinogenic POM which are capable of producing tumors in experimental animals. Although the production of polycyclic hydrocarbons in an efficiently running diesel engine was extremely low, the exhaust from an in- efficient diesel engine contained significant amounts of pyrene, benzo[a]- pyrene, benzo[e]pyrene, benzo[ghi]perylene, anthanthrene, coronene, and an unidentified "compound X." Acetone solutions of benzene extracts from the particulate exhaust fraction from an inefficiently operating diesel engine were repeatedly applied (3 times weekly for more than 60 weeks) to the skin of mice (C57 black and A strain). A high incidence of skin cancers resulted in A strain mice when they were pa,inted with particulate extracts obtained during full-load engine operation. These results corresponded with chemical analyses showing that polycyclic hydrocarbon emissions are greatest under conditions of full load and inefficient engine operation. Kotin and coworkers noted that the diesel engine can be a greater source of polycyclic hydrocarbons than the gasoline engine (without oxidation catalyst) depending on engine operating conditions. However, pre- vious studies by these same investigators demonstrated that benzene extracts of gasoline exhaust particulates are also capable of producing large numbers of skin cancers using C57 black mice (Kotin eit^ a3L , 1954). Subsequent studies conducted on the potential carcinogenicity of diesel exhaust fractions have reportedly produced negative results. Clemo and Miller (1955) briefly mentioned that two fractions from diesel bus smoke yielded no carcinomas in mice, but experimental details were not reported. Mittler and Nicholson (1957) collected diesel and gasoline engine exhaust condensates (without using filters) and applied benzene extracts of this material twice weekly for eleven months to mice. They obtained a 76% incidence of skin tumors 128 ------- (presumably papillomas) in mice receiving a 4.0% gasoline exhaust extract, and no tumors in mice receiving a 2.26% diesel exhaust extract. These results are difficult to interpret, however, for several reasons: a) conditions of engine operation were not reported, b) the collection efficiency for the exhaust particulate fraction by the method employed is not known, and c) no chemical analyses were conducted on the engine exhaust condensates. Thus far, attempts to produce tumors of the respiratory tract by the inhalation of either diesel exhaust (Stuart ejt al., 1978) or gasoline exhaust (Campbell, 1936; Stupfel et_ al., 1973) have not been successful. Nevertheless, the carcinogenicity of gasoline exhaust fractions by dermal application or subcutaneous injection in mice has been repeatedly confirmed (Wynder and Hoffmann, 1962; Brune, 1977; Pott et^ al_., 1977). Most investigators agree that the demonstrated carcinogenicity of particulate diesel and gasoline exhaust fractions, as well as particulate air pollutants from fossil fuel combustion, is largely (but not entirely) due to the presence of POM. Consequently, an intensive research effort has been mounted over the past several decades to thoroughly characterize the biological activity of chemicals in this class. A recent review of the published litera- ture on POM indicated that benzo[a]pyrene is the most well-studied of all these compounds (Santodonato ^t al., 1978). Attention has focused on benzo[a]pyrene primarily because: a) it is an ubiquitous contaminant in atmospheric emissions from the combustion of fossil fuels, b) it is easily detected, and c) it is a potent animal carcinogen. It is evident that POM's in general and benzo[a]- pyrene in particular, when present in air, are nearly always found as adsorbed material on particulate matter. Thus, the inhalation of particulate matter 129 ------- from combustion processes can deliver a number of carcinogenic POM's, including benzo[a]pyrene, into direct contact with the respiratory tissues. Furthermore, numerous studies have indicated that the ability of suspensions of benzo[a]- pyrene to induce experimental lung tumors can be considerably enhanced by concomitant exposure to particulate matter. It is suggested that particulates increase the carcinogenic response to benzo[a]pyrene by providing increased retention in the lung. In addition, simultaneous exposure to ciliastatic gases (e.g., SO , N0«) can further enhance the respiratory tumor reponse to benzo[a]- pyrene administration, possibly by inhibiting normal lung clearance mechanisms. Consequently, both gasoline and diesel exhaust are rightfully suspect as carcinogenic mixtures, and the amount of particulate material and POM's con- tained in them might be regarded as critical determinants of carcinogenic potential. Nevertheless, in the absence of positive bioassay data involving chronic inhalation exposures, a direct comparison cannot be made between the carcinogenic potential of diesel versus gasoline exhaust. Based on the limited number of animal studies which have thus far been conducted, there are no data which suggest an increased carcinogenic threat from the substitution of diesel for gasoline exhaust. 130 ------- 4.3 Human Studies 4.3.1 Controlled Exposures Little is known concerning the specific effects of diesel ex- haust on various physiologic parameters in humans. Battigelli (1965) exposed volunteers to several dilutions of diesel exhaust containing 0.2-7.0 ppm NO^, 0.2-2.8 ppm SO , 20-80 ppm CO, 900-15,000 ppm CO , 19.5-20% 0 , total aldehydes £* £* £• less than 1-2 ppm, and total hydrocarbons less than 5-6 ppm. Inhalation of the diluted exhaust for periods up to one hour had no effect on pulmonary resistance and produced no complaints of respiratory distress from the experimental sub- jects. Although the diesel exhaust produced no complaints when inhaled, the same subjects found that eye exposure to the diesel exhaust dilutions produced conjunctival irritation which often became intolerable. 4.3.2 Epidemiologic Studies Attempts to establish an association between exposure to speci- fic pollutants and adverse non-occupational health effects, especially cancer, are seldom successful. However, in occupational situations the effects of long-term exposure to high levels of a toxicant are more easily quantified; thus allowing for extrapolation back to the effect of small doses present in the ambient atmosphere. Unfortunately, only a few occupational studies in- volving diesel exhaust exposure have been published, and in none of these could the exposure be considered particularly- intense in terms of concentration and/or duration. 4.3.2.1 Occupational Studies Raffle (1957) authored a general review paper which made use of a number of examples to argue for the mutual benefits which can accrue 131 ------- to industry, medicine and the worker through the study of occupational and health records of employees. Absences from work because of sickness were shown to vary in frequency, duration and type depending upon the age, sex and occupa- tional category of the worker. While acknowledging the diagnostic inaccuracy of individual absence records, Raffle emphasized the validity of comparisons between large groups. Using records of the London Transport staff, he recalled the classical studies of coronary heart disease in conductors and drivers, in which uniform sizes at the times of initial employment provided critical infor- mation for the interpretation of self-selection. Raffle used health records of the conductors and drivers to show differences in their rates of absence attri- buted to "bronchitis" (undefined). Lastly, he reported on the incidence of cancer of the lung in relation to occupational exposure to the exhausts of diesel engine buses. When the London Transport staff, aged 45-64, were grouped according to expected low to high exposure there was no discernible gradient in the rates of death, retirement or transfer to alternative work during the period 1950 to 1954 due to lung cancer. There was an observed tendency for lung cancer death rates to follow the workers' residential patterns with respect to urban density and air pollution carried by prevailing winds. This is in agree- ment with the concept that "the amount of carcinogen in town air depends on the density of the population (possibly the number of coal fires) and that it is also driven by the prevailing wind." Thus, diesel exhaust could not be speci- fically implicated as a serious contributing factor. This clearly does not rule out possible health hazards of diesel engine exhausts, especially if diesel-powered urban vehicles were to predominate at some time in the future. 132 ------- It could be argued, in connection with the London Transport staff work, that the period 1950 to 1954 was too early for any possible effects of diesel emissions to have become evident; diesel buses having been introduced gradually over a period from about 1935 to 1952. Therefore, the collection of lung cancer data has continued for this same group of workers, and by now a 25 year series is available (Raffle and Waller, to be published). The findings broadly support those for the first five years, and overall the lung cancer incidence rates are slightly lower than expected in the general population of London. This feature is common to other studies among occupational groups (Kaplan, 1959), and to some extent is may reflect the selection of relatively fit people for employment. At about the same time as the paper by Raffle, air sampling data for two London Transport garages were reported by Commins and coworkers (1957). The Merton garage housed about 200 diesel buses and Dalston housed 120. Each garage was monitored from 6:00 P.M. to 7:00 A.M. on two nights: Merton in April and again in June, 1956; Dalston in October, 1956, and in June, 1957. Each 13 hour session was divided into 4 periods typified by fueling, down-time, departures and returns. Smoke samples for analysis of polycyclic hydrocarbons were taken at one site in each garage, and one outside (on the roof) as a control. A long-term smoke record (one week at Dalton and two weeks at Merton) was also taken at each garage. On each occasion in every period, the average concentration of smoke was higher inside than outside each garage, though only slightly so during the down periods. Typically, the concentrations of hydrocarbons (pyrene, fluoranthene, 1:2- and 3:4- and l:12-benzpyrene) were greater inside than out, but by a lower value than would be indicated by the inside to outside smoke 133 ------- concentration ratio. No marked excess of inside over outside sulfur dioxide concentration was observed. Variations in nitrogen dioxide concentrations followed the same pattern as smoke concentrations. Thus all pollutants were at their lowest levels in the down periods. In their introductory remarks and at the conclusion of the report, the authors underscore the limited usefulness of their data in attempt- ing to generalize: "The results are not to be applied without qualification to air pollution under the different conditions obtained in streets in the open air." Kaplan (1959) analyzed the records of 154 lung cancer deaths among employees of the relief department of the Baltimore and Ohio Railroad from January 1, 1953 to December 31, 1958. Three groups, in order from greatest to least putative exposure, were compared: (1) those with direct occupational exposure to diesel or steam engine exhaust; (2) service workers or laborers in shops or roundhouses; (3) clerks and others rarely occupationally exposed. 96% of the employees were males and the few females belonged mainly to group (3) with low exposure. Group 3 was found to have a slightly greater age-adjusted rate of lung cancer deaths than group 1, while the rate for group 2 was considerably lower than for the others. Thus, the pattern did not con- form well with the concept of exposure to diesel fuel or coal engine exhausts. Overall, the age-adjusted lung cancer death rate fell somewhat below that estimated for the United States male population. Kaplan pointed out that these results were in strong con- flict with those of a similar study by Heuper in 1955, i.e., that, while only 25% were operating employees (group 1), they accounted for 75% of the lung cancer cases. One of the reasons advanced for the relatively high lung cancer 134 ------- rate in group 3 was its greater proportion of urban dwellers. This factor was as least partly offset, however, by its higher proportion of females. Not mentioned by the author, but clearly of concern is the limited character of the data. Selection in comparing local railway employees with the United States as a whole may operate through variations in the coding of causes of death due to lung cancer. In addition, the extent to which selec- tion operated to retire ill employees was not evaluable. Lastly, it would have been desirable to consider causes of death which compete with lung cancer as well as to analyze inedical records of the occurrences of chronic bronchitis and other illnesses, both of long and short-term character. In a later review article Battigelli (1963) reported that none of the several measured components of air samples taken over several months in various studies of confined areas polluted by diesel engine exhausts (e.g., roundhouses, railway tunnels, bus garages) exceeded threshold limits established by the American Conference of Governmental Industrial Hygienists. He recognized, however, that in every major episode of air pollution with adverse effects to humans, none of the measured contaminants had exceeded accepted maximum concentrations. Diesel exhaust was characterized as being distinct from the two major types of health-threatening polluted atmospheres typified by London and Los Angeles. Air polluted by diesel engine exhausts contains relatively low levels of carbon monoxide and of carcinogenic polycyclic hydrocarbons, as compared with gasoline engine polluted air. Diesel engines produce higher levels of objectionable odorants, conjunctival irritants and smoke, but Battigelli expressed the opinion that diesel exhausts were no more harmful than alternative forms of pollution. 135 ------- The author pointed out that diesel engines discharge more nitrogen oxides and aldehydes per hour than comparable gasoline engines. This disadvantage was tempered by noting that the concentration of both of these gases in diesel exhaust is lower because of a greater air-to-fuel ratio in diesel motors. However, the air-to-fuel dilution factor is valuable only with respect to localized sources of pollution in confined spaces. When considering the environmental effects of a predominance of diesel powered vehicles, hourly discharges of nitrogen oxides and aldehydes would seem to be the more relevant issue. In 1964, Battigelli teamed with two colleagues to report a cross-sectional study involving physical examinations and medical histories of 210 workers occupationally exposed for an average of 10 years to diesel exhausts in three Pittsburgh railroad engine houses. These workers were compared to 154 yard workers comparably distributed with respect to age, cigarette smoking histories, and extrapulmonary medical problems. The internal air was sampled systematically at locomotive roof levels and at head-high "floor" levels at locations near to and distant from the locomotives. While NCL, SCL, total aldehydes, acrolein and hydro- carbons from C- to Cfi varied somewhat according to type of location, the gen- eral pattern indicated an extensive dilution of exhaust products. For example, the average concentration of total hydrocarbons was nearly identical for all three types of sample locations (engine roof, near floor and distant floor levels). Winter concentrations consistently exceeded those in summer. The medical data were based on a physical examination, chest X-ray, electrocardiogram, spirometr.y, a standardized medical history with special focus on chronic respiratory diseases, and other standardized pulmonary 136 ------- function tests. The investigators reported that no significant differences were discernible between the 210 exposed workers and the 154 controls. In order to allay suspicions of insensitivity to existing major differences, they presented parallel comparative analyses of the workers who smoked versus those who did not smoke cigarettes within the previous 10 years. These analyses revealed consistently higher relative frequencies of dyspnea, cough and measures of bronchitis together with lower pulmonary function levels in cigarette smokers than in non-smokers. Nonetheless, this study has shortcomings which resulted from an inability to pursue the original study plan. A low number of examinees was obtained, and participation was strictly on a volumtary basis. While the exposed workers were processed with a participation of better than 90% of the specific employed population, the non-exposed group showed a much smaller participation frequency. Thus, any attempt to carry out a formal analysis of statistical significance on a group of this composition is useless. However, based on their collected observations, particularly considering a mean exposure of 10 years, the fact that no major adverse effects were found should not be considered as trivial. Several cohort mortality studies have been conducted with workers from underground mines in which diesel equipment was routinely used (Waxweiler e_t al_., 1973; NIOSH, 1978). Although deaths attributed to malignant and non-malignant respiratory disease were elevated in certain instances, it was not possible to determine the potential contribution of diesel exhaust to this result. It was concluded that, "no excess mortality was attributable to the presence of diesel engines in some mines; however, there has probably been too little elapsed time for this observation to be definitive" (Waxweiler et al. 137 ------- 1973). Further epidemiologic studies involving metal and non-metal miners exposed to diesel exhaust are in progress (NIOSH, 1978) and may provide further clarification of the risk for lung cancer and respiratory disease. A preliminary analysis of ventilatory function among 60 coal miners exposed to diesel emissions has recently been performed (Reger, 1978). Decrements in lung function over the period of a work shift could be demonstrated among miners exposed to coal dust either with or without concomi- tant exposure to diesel emissions. The decrements shown were no greater in the presence of diesel emissions than for exposure to ordinary mine atmospheres in the absence of diesel emissions. The combustion of fossil fuels, resulting in exposure to POM, has long been associated with an increased cancer risk. More recently, however, inhalation of vehicular emissions has received attention as a specific factor in the etiology of malignant disease. In this regard it was reported that moderately elevated relative risks for cancers of the nose, pancreas, and prostate were observed in mechanics and repairmen (Viadana et^ al^., 1976). In addition, bus, taxi, and truck drivers showed increases in cancer of the pan- creas; locomotive engineers were at increased risk for lymphomas and cancers of the buccal cavity and pharynx. Other investigators observed an elevated lung cancer rate in Los Angeles County for workers in the auto repair industry (Menck and Henderson, 1976). Occupational exposure to gasoline engine emissions have also been of interest to epidemiologists for the development of non-malignant disease. One recent report concerns a retrospective cohort study of mortality among approximately 1600 motor vehicle examiners employed in New Jersey during the period 1938 through 1973 (Stern and Lemen, 1978). Because previous studies 138 ------- had shown that chronic low-level exposures to carbon monoxide may exacerbate coronary heart disease, measurements were made of carbon monoxide levels (average concentration 22 ppm) and heart disease mortality was specifically pursued. The study, however, failed to show a significant excess of heart disease deaths, but instead revealed a significant excess of cancer deaths (13 observed vs. 6.69 expected) for individuals with greater than 30 years since onset of employment. The excess of cancers was not associated with a particu- lar organ site. Since cause-specific mortality rates for the general United States white male population were used for comparisons in this study, the consistently higher New Jersey cancer death rate was not taken into considera- tion. Thus, it is not possible to conclusively attribute the excess of cancer deaths in this study to occupational exposure to automotive exhaust. A study of 386 children who died of malignant disease in the province of Quebec during the years 1965 through 1970 has suggested a correlation with specific types of occupation of the father (Fabia and Thuy, 1974). Prior to undertaking the study it had been postulated that the risk of malignant disease may be greater among children whose fathers are occupation- ally exposed to petroleum products. The study revealed that excess cases of cancer existed among the children of motor vehicle mechanics, machinists, miners, and painters. These striking results do not provide an explanation of the mechanism by which such a phenomenon might occur. Nevertheless, in other studies involving occupational exposure to known carcinogens (e.g., vinyl chloride) it has been reported that fetal deaths and congenital defects may be increased in the offspring of exposed fathers (Infante eit al., 1976; U.S. Public Health Service, 1976). 139 ------- 4.3.2.2 Community Studies A suitable community population has not yet been studied which might reveal the impact of diesel emissions in the ambient atmosphere on human health. However., the effect of diesel emissions on the general population may be too small to be accurately detected and separated from other variables. Similarly, the question of whether gasoline engine emissions represent a signi- ficant carcinogenic threat to man has not yet been resolved (Lawther and Waller, 1976). This is primarily due to the diversity of pollutants in the environment, and the inability to identify a suitable population having significant exposure to a specific pollutant type. Nevertheless, a report implicating emissions from automobiles (presumably gasoline-powered) as an important cause of cancer has been published in Switzerland (Blumer et_ al_., 1972). In this study of a very small population, deaths due to cancer of various sites were nine times more frequent (11% vs. 1.2%) among residents of a Swiss mountain town living near a highway as compared to residents living in an area remote from traffic. The authors concluded that differences in age, occupation, exposure to non- automotive combustion products, sex, and smoking habits could not entirely account for the increased cancer mortality rate. However, the population studied was too small to allow for determination of age/sex/site specific cancer rates. Therefore, the reported observations may have'little overall significance In a follow-up study to clarify these observations, it was found that soil content of polycyclic aromatic hydrocarbons in this region showed a correlation with proximity to a highway (Blumer ejt a!L., 1977). The compounds identified were present as a complex mixture of unsubstituted three- to eight-membered rings and heavily alkyl-substituted derivatives, which the 140 ------- author concluded had originated primarily from automobile exhaust. Thus it was believed that the observed mortality from cancer in this area might indeed be associated with exposure to automotive exhaust. Little can be said, however, concerning the levels of exposure to automobile-derived carcinogens among those residents living near the highway. Since the Swiss town was situated in a deep valley with frequent thermal inversions, it is likely that these persons had unusually high exposures to exhaust emissions. On the other hand, deaths due to non-malignant disease (heart and circulatory) did not seem to vary greatly between roadside and non-roadside residents. 141 ------- References for Section 4.0 Ashby, J. and J.A. Styles (1978), "Does Carcinogenic Potency Correlate with Mutagenic Potency in the Ames Assay?" Nature, 271(5644);452-455. Ashby, J. and J.A. Styles (1978a), "Factors Influencing Mutagenic Potency In Vitro," Nature, 274;20-22. Battigelli, M.C. (1963), "Air Pollution from Diesel Exhaust," J. Occup. Med., 5:54. Battigelli, M.C. (1965), "Effects of Diesel Exhaust," Arch. Environ. Health, 10:165-167. Battigelli, M.C., F. Hengstenberg, R.J. Mannella, and A.P. Thomas (1966), "Mucociliary Activity," Arch. Environ. Health, JL2_:460-466. Battigelli, M.C., R.J. Mannella, and T.F. Hatch (1964), "Environmental and Clinical Investigation of Workmen Exposed to Diesel Exhaust in Railroad Engine Houses," Ind. Med. Surg., 33:121-124. Blumer, M., W. Blumer, and T. Reich (1977), "Polycyclic Aromatic Hydrocarbons in Soils of a Mountain Valley: Correlation with Highway Traffic and Cancer Incidence," Environ. Sci. Technol., 11:1082-1084. Blumer, W., R. Jauman, and T. Reich (1972), "Automobile Exhausts - The Most Important Cause of Cancer?" Schweiz. Rundsch. Med. Prax., 61:514-518. Brune, H.F.K. (1977), "Experimental Results with Percutaneous Applications of Automobile Exhaust Condensates in Mice," in Air Pollution and Cancer in Man, IARC Sci. Publ. No. 16:41-47. Campbell, K., E. George, I. Washington, and Y. Yang (1978), Enhanced Suscepti- bility to Respiratory Infection in Mice Exposed to Automotive Diesel Emissions, U.S. Environmental Protection Agency, unpublished report. Campbell, J.A. (1936), "The Effects of Exhaust Gases from Internal Combustion Engines and of Tobacco Smoke Upon Mice, with Special Reference to Inci- dence of Tumours of the Lung," Brit. J. Exper. Pathol., 17:146-158. Candeli, A., G. Morozzi, A. Paolacci, and L. 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Meeker (1967), "Sources of Poly- nuclear Hydrocarbons in the Atmosphere," Environmental Health Series, U.S. Dept. of HEW, Cincinnati, Ohio. Hoffmann, D., E. Theisz, and E.L. Wynder (1965), "Studies on the Carcinogenicity of Gasoline Exhaust," J. Air Pollut. Control Assoc., 15;162-165. Hueper, W.C. (1955), "A Quest Into the Environmental Causes of Cancer of the Lung," Public Health Monograph No. 36, U.S. Dept. of Health, Education, and Welfare, Public Health Service. Huisingh, J., R. Bradow, R. Jungers, L. Claxton, R. Zweidinger, S. Tejada, J. Bumgarner, F. Duffield, and M. Waters (1978), "Application of Bioassay to Characterization of Diesel Particle Emissions," Symposium on Application of Short-term Bioassays in the Fractionation and Analysis of Complex Environmental Mixtures, Feb. 21-23, Williamsburg, VA. Hyde, D., J. Orthoefer, D. Dungworth, W. Tyler, R. Carter, and H. 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Presence in the Particulate Phase of Gasoline-Engine Exhausts and the Carcinogeni- city of Exhaust Extracts," AMA Arch. Ind. Health, 9^:164-177. Laresgoiti, A., A.C. Loos, and G.S. Springer (1977), "Particulate and Smoke Emission from a Light Duty Diesel Engine," Environ. Sci. Technol., 11:973. Laurie, R.D., J.P. Lewkowski, G.P. Cooper, and L. Hastings (1978), Effects of Diesel Exhaust on Behavior of the Rat, U.S. Environmental Protection Agency, unpublished report. Lauweryns, J.M. and J.H. Baert (1977), "Alveolar Clearance and the Role of Pulmonary Lymphatics," Am. Rev. Resp. Dir., 115:625-683. Lawther, P.J. and R. Waller (1976), "Coal Fires, Industrial Emissions and Motor Vehicles as Sources of Environmental Carcinogens," in Environmental Pollution and Carcinogenic Risks, IARC Sci. Publ. No. 13, pp. 27-40. 144 ------- Lee, S.D., K.I. Campbell, D. Laurie, R.G. Hinners, M. Malanchuk, W. Moore, R.J. Bhatnagar, and I. Lee (1978), "lexicological Assessment of Diesel Emissions," Presentation at the 71st Annual Meeting of the Air Pollution Control Association, Houston, Texas, June 25-30, 1978. Lee, S.D., M. Malanchuk, and V.N. Finelli (1976), "Biologic Effects of Auto Emissions. I. Exhaust from Engine With and Without Catalytic Converter," J. Toxicol. Environ. Health, l.:705-712. Menck, H.R. and B.E. Henderson (1976), "Occupational Differences in Rates of Lung Cancer," J. Occup. Med., 18(12):797-801. Miller, E.G. (1978), "Some Current Perspectives on Chemical Carcinogenesis in Humans and Experimental Animals: Presidential Address," Cancer Res., 3_8:1479-1496. Mittler, S. and S. Nicholson (1957), "Carcinogenicity of Atmospheric Pollutants, Ind. Med. Surg., 26^:135-138. Moore, W., J. Orthoefer, J. Burkart, and M. Malanchuk (1978), "Preliminary Findings on the Deposition and Retention of Automotive Diesel Particulate in Rat Lungs," Presentation at the 71st Annual Meeting of the Air Pollu- tion Control Association, Houston, Texas, June 25-30, 1978. Moore, W., J. Orthoefer, and P. Berez (1978a), Subchronic Exposure of. Infant Rats to Irradiated and Non-Irradiated Diesel Exhaust, U.S. Environmental Protection Agency, unpublished report. Moore, W., D. Hysell, R. Miller, M. Malanchuk, R. Hinners, Y. Yang, and J.F. Stara (1975), "Exposure of Laboratory Animals to Atmospheric Mangan- ese from Automotive Emissions," Environ. Res., £:274-284. Mustafa, M.G., A.D. Hacker, J.J. Ospital, M.Z. Hussain, and S.D. Lee (1977), "Biochemical Effects of Environmental Oxidant Pollutants in Animal Lungs," in Biochemical Effects of Environmental Pollutants, Chapter 6, S.D. Lee (ed.), Ann Arbor Science Pub., Ann Arbor, Michigan. 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Ball (1978), Electron Microscopic Observations of Macrophages Containing Diesel Emission Particulate, U.S. Environmental Protection Agency, unpublished report. Pattle, R.E., H. Stretch, F. Burgess, K. Sinclair, and J.A.G. Edginton (1957), "The Toxicity of Fumes from a Diesel Engine Under Four Different Running Conditions," Brit. J. Ind. Med., 14_:47-55. Pepelko, W., J. Mattox, Y.Y. Yang, and W. Moore (1978), Effects of 28 Days Exposure to Diesel Exhaust Emissions Upon Arterial Blood Gases and Pul- monary Function in Rats, U.S. Environmental Protection Agency, unpub- lished report. Pepelko, W.E., J.K. Mattox, Y.Y. Yang, and W. Moore, Jr. (1978a), Pulmonary Function and Pathology in Cats Exposed 28 Days to Diesel Exhaust, U.S. Environmental Protection Agency, unpublished report. Pfeiffer, E.H. (1977), "Oncogenic Interaction of Carcinogenic and Non-Carcino- genic Polycyclic Aromatic Hydrocarbons in Mice," in Air Pollution and Cancer in Man, V. Mohr, D. SchmMhl, L. 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Carcinogenic Activity of Gasoline Engine Exhaust Condensate," Cancer, 15:103-108. 148 ------- 5.0 Identification of Knowledge Gaps 5.1 Biological Effects There are no areas concerning the biological activity of diesel emissions in which complete information is available. These gaps in the health effects data base are a reflection of the limited number of studies which have been conducted, rather than an indication that the data are not obtainable. Nevertheless, this lack of information is sufficient to prevent the formulation of any definitive health risk assessment at this time. Recognizing that data in certain areas are more valuable than in others for the purpose of risk assessment, selected gaps in our body of knowledge are discussed (but not nec- essarily in order of priority) below. A population study has not yet been conducted in which a diverse human group has been studied with respect to chronic low-level exposure to diesel emissions. Therefore, nothing can be said regarding the existence of susceptible groups, effects on mental and physical development, interference with reproductive success, exacerbation of pre-existing disease, or interaction with other common environmental pollutants. Data derived from human exposure studies are of paramount importance in establishing a chemical threat to health. Unfortunately, the available epi- demiologic evidence is insufficient to define the effect of diesel emissions on human populations. The historical epidemiologic literature regarding morbidity and mortality has not adequately addressed the factors of exposure intensity and duration, contial populations, and possible bias in reporting of results. The comparative analysis of diesel emissions health effects is further com- plicated by uncertainty over the consequences of human exposure to gasoline 149 ------- engine exhaust. Moreover, the impact of catalyst-treated gasoline engine exhaust on human health is virtually unknown. Thus far only one investigator has examined the clinical symptoms and metabolic alterations produced by controlled human exposures to diesel exhaust. Numerous questions still remain to be answered including: lung deposition, retention and clearance of diesel particulate; alterations in enzyme activity; effects on hematologic parameters; and correlation of physiologic effects with concentration of specific components in the diesel exhaust mixture. Animal bioassays conducted with diesel exhaust have provided important data regarding the production of histopathologic lesions and biochemical altera- i tions in the lung, behavioral disturbances, susceptibility to infection, effects on the heart, and decrements in pulmonary function. However, little is known concerning the reversibility of this damage or the correlation between extent of tissue damage and degree of functional impairment. In addition, dose- response studies have not been conducted, nor is it known whether the toxic effects produced by subchronic exposures are indeed life-shortening. Recognizing that the lung is the primary organ which contacts air- borne diesel emissions, several parameters of its interaction with diesel exhaust components should be classified. Furthermore, it is difficult to re- late morphologic alterations to biochemical events produced in response to toxic insult. Since the respiratory epithelium is a major site for the sys- temic absorption of airborne chemicals, we should also know the extent to which diesel particulate and its adsorbed materials (e.g., carcinogenic POM) reach the systemic circulation via the lung. This is especially relevant in light of studies implicating automobile exhaust as a contributing factor in cancers of various internal organs. 150 ------- Thus far it has not been possible to attribute most of the toxic effects of diesel exhaust to the action of specific components in the mixture. Likewise, a similar problem exists with most studies involving exposure to gasoline engine exhaust, and thus comparisons between the two systems are difficult. The behavior of environmental pollutants in isolated organs and individual cells often provides critical data concerning mechanisms of toxic action. Numerous _in vitro studies with extracts.of airborne particulate pol- lutants and their individual components (e.g., POM) have revealed the basis by which damage is produced. With diesel emissions, however, nothing is known regarding cytotoxicity, interaction with critical cellular macromolecules, cell transformation, or cytogenetic damage. 15.1 ------- 6.0 Recommended Research 6.1 Biological Effects Animal studies conducted with diesel exhaust have revealed a diver- sity of toxic effects in several species. These results are sufficient to warrant further investigations in several areas. A list of suggested bio- logical research projects is presented below which would fill many of the information gaps identified in Section 5.1. This, however, is not a list of research priorities. 1. Conduct of occupational and community-based epidemiologic studies to provide morbidity and mortality data regarding diesel exhaust exposure - Cancer as a biologic endpoint should be of primary interest, but chronic respiratory disease such as emphysema must also be carefully evalua- ted. Whenever possible, information should be obtained regarding current and past employment, respiratory symp- toms, smoking histories, and other health information such as genetic factors. For morbidity studies, a battery of tests which includes pulmonary function measurements and sputum cytology should be conducted. In addition, comparison of the health status of persons exposed to gasoline engine emissions with those exposed to diesel emissions is highly desirable. Furthermore, a means to quantitate observed exposures to diesel exhaust will be necessary for the formulation of valid health risk exposure criteria. It must be recognized, however, that there are few opportunities for separating diesel and gasoline exposure. 2. Cytogenetic testing of workers having high occupational exposures to diesel emissions - Analysis, should be made for chromosomal aberrations in cultured lymphocytes taken from exposed workers. These determinations are felt by many scientists to provide an indication of increased cancer risk and potential for transmission of birth defects and mutations. The use of somatic cells to predict a muta- genic effect that may occur in germinal cells is not entirely valid. Nevertheless, numerous examples of the positive correlation between a chemical's ability to pro- duce chromosome aberrations in somatic cells and its car- cinogenic/mutagenic activity indicate that cytogenetic data should be carefully evaluated. Moreover, the widely held view that cancer arises as a result of somatic muta- tion emphasizes the need for cytogenetic testing. 152 ------- 3. Conduct of inhalation exposure studies in animals using various dose levels - These studies should be designed to detect dose-response parameters and ascertain the reversibility of treatment-induced damage. Included in the experimental protocols should be means to detect neurotoxicity, reproductive effects, cardiovascular function, effects on host defenses and threshold dose levels for toxic response. 4. Evaluation of diesel exhaust mutagenicity in vivo and in vitro - For the detection of gene mutations the use of mammalian somatic cells in culture (with and without metabolic activation) should be employed. Chromosomal aberrations should be measured by in vivo cytogenetic tests in animals, dominant lethal effects in rodents, and heritable translocation tests in rodents. Primary DNA damage should be detected using tests for unsched- uled DNA repair synthesis and sister chromatid exchange in mammalian cells (with and without metabolic activa- tion), DNA repair in bacteria, and mitotic recombina- tion and/or gene conversion in yeast. 5. Evaluation of in vitro carcinogenesis by diesel emissions - Previous studies have shown that organic extracts of certain samples of airborne particulate matter can transform mammalian cells in culture. To establish the presence of carcinogenic materials in diesel exhaust particulate, various systems could be employed such as early passage hamster embryo cells, baby hamster kidney cells, C3H10T 1/2 mouse fibroblasts, and several organ culture systems using respiratory tract epithelium. Results from such tests would provide important data to support the observed mutagenic effect of diesel particulate extracts in the Ames assay. 6. Evaluation of in vivo carcinogenesis by diesel emissions - Studies using various fractions of diesel exhaust and employing various routes of administration should be pursued. In addition, an evaluation of the potential involvement of cocarcinogens should be conducted. 7. Evaluation of the pulmonary deposition, clearance, and transport of diesel particulate - Animal models should be employed to ascertain the fate of inhaled diesel particulate matter. 8. Evaluation of the toxicity of the vapor phase components of diesel exhaust emissions - Standard inhalation experi- ments in animals using reconstituted mixtures of gaseous components at ratios found in raw exhaust should be con- ducted. 153 ------- 9« Evaluation of the effect of variation in fuels and engine operating parameters on the resultant toxicity of diesel exhaust emissions - These parameters can be incorporated into nearly all of the suggested research studies listed above. 10. Conduct of parallel toxicity studies with diesel and gasoline engine exhaust - Using identical test conditions, a comparison should be made between the relative hazards to health of diesel versus gasoline engine exhaust. These studies would provide important data concerning the ulti- mate environmental impact and public health implications of a major changeover to the use of diesel vehicles. 154 ------- |