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

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                              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

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                                   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

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                              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

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                         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

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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

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          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

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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.

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          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

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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

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          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

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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

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          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.

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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

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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

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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.

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          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

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     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

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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

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      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

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               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

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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

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     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

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         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

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        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

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               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

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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

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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

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          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

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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

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                         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

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                 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

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   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

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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

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      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

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  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

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     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

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                       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

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   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

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   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

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                      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

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     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

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  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

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     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

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     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

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        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

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     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

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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

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         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

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           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

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     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

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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

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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

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(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

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                          References for Section 3.0


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Apostolescu, N.D., R.D. Matthew, and R.F. Sawyer (1977), "Effects of a Barium-
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Begeman, C.R. and J.M. Colucci (1968), "Polynuclear Aromatic Hydrocarbon Emissions
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Black, F. and L. High  (1978), "Diesel Hydrocarbon Emissions, Particulate and
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Boyer, K.W. and H.A. Laitinen (1975), "Automobile Exhaust Particulates:  Proper-
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Braddock, J. and R. Bradow (1975), "Emissions Patterns of Diesel-Powered
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Braddock, J.N. and P.A. Gabele (1977), "Emission Patterns of Diesel Powered
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Broome, D. and I.M. Khan, (1971), "Mechanisms of Soot Release from Combustion of
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Campbell, K. and P.L. Dartnell (1972), "Vehicle Particulate Emissions," Air-
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Candeli, A., G. Morozzi, A; Paolacci, and L. Zoccolillo  (1975), "Analysis
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     Hydrocarbons in the Exhaust Products from a European Car Runnning on
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     Atmos. Environ., j):843-849.

Candeli, A., V. Mastrandrea, G. Morozzi, and S. Toccaccli (1974), "Carcinogenic
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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

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Dolan, D.F., D.K. Kittelson, and K.T. Whitby (1975), "Measurement of Diesel
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Dow Chemical Co. (1970), "Effects of Fuel Additives on the Chemical and Physical
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Dravnieks, A., A. O'Donnell, R. Scholz, and J.D. Stockham (1971), "Gas
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EPA (1977), "Characterization of Exhaust Emissions from a Dual Catalyst-Equipped
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EPA (1978), Toxicological Assessment of Diesel Emissions, U.S. Environmental
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Energy and Environmental Analysis, Inc. (March 6, 1978), Draft Report to EPA,
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Frey, J.W. and M. Corn (1967), "Diesel Exhaust Particulates," Nature, 216(5115);
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Gabele, P., J. Braddock, and R. Bradow (1977), "Characterization of Exhaust
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Ganley, J.T.  (1973), "Particulate Formation in Spark Ignition Engine Exhaust Gas,"
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Greeves, G.,  I.M. Khan, and G. Onion (1977), "Effect of Water Introduction on
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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
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Grimmer, G. (1977), "Analysis of Automobile Exhaust Condensates," in Air
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Gross, G.P. (1972), "The Effect of Fuel and Vehicle Variables on Polynuclear
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     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

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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,
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Hangebrauck, R.P., D.J. von Lehmden, and J.E. Meeker (1967), "Sources of Poly-
     nuclear Hydrocarbons in the Atmosphere," Environmental Health Series,
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Henein, N.A. (1973), "Diesel Engines Combustion and Emission," in Engine
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     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

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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

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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
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                                       93

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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.),
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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
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     28, 1974.

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Vuk, C.T. and J.H. Johnson (1975), "Measurement and Analysis  of Particles
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     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
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Wang, Y.Y., S.M. Rappaport, R.F. Sawyer, R.E. Talcott, and E.T. Wei  (1978),
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     sion Experiments:  Summary of EPA Measurements," J. Air  Poll. Control
     Assoc., 27;46-51.
                                      94

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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

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          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

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     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

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               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

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                                                  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

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  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

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     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

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     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

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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

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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

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(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

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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

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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

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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

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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

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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

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          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

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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

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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

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(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

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     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

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                    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

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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

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                    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

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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

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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

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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

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               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

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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

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     and R.I. Freudenthal (eds.), Raven Press, New York.

Waxweiler, R.J., J.K. Wagoner, and W.C. Archer (1973), "Mortality of Potash
     Workers," J. Occup. Med., 15;406-409.

Wiester, M.J., R. Iltis, J.F. Swan, and W. Moore (1978), Altered Function
     and Histology in Guinea Pigs After Inhalation of Diesel Exhaust,  U.S.
     Environmental Protection Agency, unpublished report.

Wynder, E.L. and D. Hoffmann (1962), "A Study of Air Pollution Carcinogenesis.
     III. Carcinogenic Activity of Gasoline Engine Exhaust Condensate," Cancer,
     15:103-108.
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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
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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.


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          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

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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.
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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.
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 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.
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