UNITED NATIONS ENVIRONMENT PROGRAMME 

 INTERNATIONAL LABOUR ORGANISATION 

 WORLD HEALTH ORGANIZATION 

 INTERNATIONAL PROGRAMME ON CHEMICAL SAFETY 

 ENVIRONMENTAL HEALTH CRITERIA 171

 DIESEL FUEL AND EXHAUST EMISSIONS

 This report contains the collective views of an international group of 

 experts and does not necessarily represent the decisions or the stated 

 policy of the United Nations Environment Programme, the International 

 Labour Organisation, or the World Health Organization. 

 Environmental Health Criteria 171 

 DIESEL FUEL AND EXHAUST EMISSIONS 

 First draft prepared by the staff members of the Fraunhofer Institute 

 of Toxicology and Aerosol Research, Germany, under the coordination of 

 Dr. G. Rosner 

 Published under the joint sponsorship of the United Nations 

 Environment Programme, the International Labour Organisation, and the 

 World Health Organization, and produced within the framework if the 

 Inter-Organization Programme for the Sound Management of Chemicals. 

 World Health Organization 

 Geneva, 1996 

 The International Programme on Chemical Safety (IPCS) is a joint 

 venture of the United Nations Environment Programme, the International 

 Labour Organisation, and the World Health Organization. The main 

 objective of the IPCS is to carry out and disseminate evaluations of 

 the effects of chemicals on human health and the quality of the 

 environment. Supporting activities include the development of 

 epidemiological, experimental laboratory, and risk-assessment methods 

 that could produce internationally comparable results, and the 

 development of manpower in the field of toxicology. Other activities 

 carried out by the IPCS include the development of know-how for coping 

 with chemical accidents, coordination of laboratory testing and 

 epidemiological studies, and promotion of research on the mechanisms 

 of the biological action of chemicals. 

 WHO Library Cataloguing in Publication Data 

 Diesel Fuel and exhaust emission 

 (Environmental health criteria ; 171) 

 1.Air pollutants, Enviromental 2.Air pollution 3.Fueloils 

 I.International Programme on Chemical Safety II.Series 

 ISBN 92 4 157171 3 (NLM Classification: WA 754) 

 ISSN 0250-863X 

 The World Health Organization welcomes requests for permission to 

 reproduce or translate its publications, in part or in full. 

 Applications and enquiries should be addressed to the Office of 

 Publications, World Health Organization, Geneva, Switzerland, which 

 will be glad to provide the latest information on any changes made to 

 the text, plans for new editions, and reprints and translations 

 already available. 

 (c) World Health Organization 1996 

 Publications of the World Health Organization enjoy copyright 

 protection in accordance with the provisions of Protocol 2 of the 

 Universal Copyright Convention. All rights reserved. The designations 

 employed and the presentation of the material in this publication do 

 not imply the expression of any opinion whatsoever on the part of the 

 Secretariat of the World Health Organization concerning the legal 

 status of any country, territory, city or area or of its authorities, 

 or concerning the delimitation of its frontiers or boundaries. The 

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 mention of specific companies or of certain manufacturers' products 

 does not imply that they are endorsed or recommended by the World 

 Health Organization in preference to others of a similar nature that 

 are not mentioned. Errors and omissions excepted, the names of 

 proprietary products are distinguished by initial capital letters. 

 CONTENTS

 NOTE TO READERS OF THE CRITERIA MONOGRAPHS 

 PREAMBLE 

 ENVIRONMENTAL HEALTH CRITERIA FOR DIESEL FUEL AND EXHAUST EMISSIONS 

 WHO DRAFTING GROUP ON ENVIRONMENTAL HEALTH CRITERIA FOR DIESEL FUEL 

 AND EXHAUST EMISSIONS 

 WHO TASK GROUP ON ENVIRONMENTAL HEALTH CRITERIA FOR DIESEL FUEL AND 

 EXHAUST EMISSIONS 

 PART A: DIESEL FUEL 

 A1. SUMMARY 

 A1.1 Identity, physical and chemical properties, and 

 analytical methods 

 A1.2 Sources of human and environmental exposure 

 A1.3 Environmental transport, distribution, and 

 transformation 

 A1.4 Environmental levels and human exposure 

 A1.5 Effects on laboratory mammals and in vitro test 

 systems 

 A1.6 Effects on humans 

 A1.7 Effects on other organisms in the laboratory and the 

 field 

 A1.8 Evaluation of human health risks 

 A1.9 Evaluation of effects on the environment 

 A2. IDENTITY, PHYSICAL AND CHEMICAL PROPERTIES, AND ANALYTICAL 

 METHODS 

 A2.1 Identity 

 A2.1.1 Fuel components 

 A2.1.1.1 Alkanes 

 A2.1.1.2 Alkenes 

 A2.1.1.3 Aromatic compounds 

 A2.1.1.4 Sulfur 

 A2.1.2 Fuel additives 

 A2.1.2.1 Cetane number improvers 

 A2.1.2.2 Smoke suppressors 

 A2.1.2.3 Flow improvers 

 A2.1.2.4 Cloud-point depressors 

 A2.1.2.5 Wax anti-settling additives 

 A2.1.2.6 Other additives 

 A2.1.3 Quality aspects of diesel fuels 

 A2.1.3.1 Ignition performance and cetane 

 number 

 A2.1.3.2 Density 

 A2.1.3.3 Sulfur content 

 A2.1.3.4 Viscosity 

 A2.1.3.5 Cold-flow properties 

 A2.2 Physical and chemical properties 

 A2.3 Analytical methods 

 A2.4 Conversion factors 

 A3. SOURCES OF HUMAN AND ENVIRONMENTAL EXPOSURE 

 A3.1 Natural occurrence 

 A3.2 Anthropogenic sources 

 A3.2.1 Production and use 

 A3.2.1.1 Production process 

 A3.2.1.2 Use 

 A3.2.1.3 Production and consumption 

 levels 

 A3.2.2 Emissions during production and use 

 A3.2.2.1 Air 

 A3.2.2.2 Water 

 A3.2.2.3 Soil 

 A3.2.3 Accidental releases to the environment 

 A4. ENVIRONMENTAL TRANSPORT, DISTRIBUTION, AND TRANSFORMATION 

 A4.1 Transport and distribution between media 

 A4.1.1 Evaporation from and dissolution in the 

 aqueous phase 

 A4.1.2 Transport in and adsorption onto soil and 

 sediment 

 A4.1.2.1 Soil 

 A4.1.2.2 Sediment 

 A4.2 Transformation and removal 

 A4.2.1 Photooxidation 

 A4.2.2 Biodegradation 

 A4.2.2.1 Microbial degradation 

 A4.2.2.2 Phytoplankton and marine algae 

 A4.2.2.3 Invertebrates and vertebrates 

 A4.2.3 Bioaccumulation 

 A4.2.4 Tainting 

 A4.2.5 Entry into the food chain 

 A4.3 Ultimate fate after use 

 A4.3.1 Use in motor vehicles 

 A4.3.2 Spills 

 A4.3.3 Disposal 

 A5. ENVIRONMENTAL LEVELS AND HUMAN EXPOSURE 

 A5.1 Environmental levels 

 A5.2 Exposure of the general population 

 A5.3 Occupational exposure during manufacture, 

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 formulation, or use 

 A6. KINETICS AND METABOLISM IN LABORATORY ANIMALS AND HUMANS 

 A7. EFFECTS ON LABORATORY MAMMALS AND IN VITRO TEST SYSTEMS 

 A7.1 Single exposure 

 A7.2 Short-term exposure 

 A7.2.1 Subacute exposure 

 A7.2.1.1 Dermal exposure 

 A7.2.1.2 Inhalation 

 A7.2.2 Subchronic exposure 

 A7.2.2.1 Dermal exposure 

 A7.2.2.2 Inhalation 

 A7.3 Long-term exposure 

 A7.3.1 Dermal exposure 

 A7.3.2 Inhalation 

 A7.4 Dermal and ocular irritation; dermal sensitization 

 A7.4.1 Dermal irritation 

 A7.4.2 Ocular irritation 

 A7.4.3 Sensitization 

 A7.5 Reproductive toxicity, embryotoxicity, and 

 teratogenicity 

 A7.6 Mutagenicity and related end-points 

 A7.6.1 In vitro 

 A7.6.2 In vivo 

 A7.7 Carcinogenicity 

 A7.7.1 Dermal exposure 

 A7.7.2 Inhalation 

 A8. EFFECTS ON HUMANS 

 A8.1 Exposure of the general population 

 A8.2 Occupational exposure 

 A9. EFFECTS ON OTHER ORGANISMS IN THE LABORATORY AND THE FIELD 

 A9.1 Laboratory experiments 

 A9.1.1 Microorganisms 

 A9.1.1.1 Water 

 A9.1.1.2 Soil 

 A9.1.2 Aquatic organisms 

 A9.1.2.1 Plants (phytoplankton) 

 A9.1.2.2 Invertebrates 

 A9.1.3 Terrestrial organisms 

 A9.1.3.1 Plants 

 A9.1.3.2 Invertebrates 

 A9.1.3.3 Vertebrates 

 A9.2 Field observations 

 A9.2.1 Microorganisms. 

 A9.2.1.1 Water 

 A9.2.1.2 Soil 

 A9.2.2 Aquatic organism 

 A9.2.3 Terrestrial organisms 

 A9.2.3.1 Plants 

 A9.2.3.2 Invertebrates 

 A9.2.3.3 Vertebrates 

 A10. EVALUATION OF HUMAN HEALTH RISKS AND EFFECTS ON THE 

 ENVIRONMENT 

 A10.1 Evaluation of human health risks 

 A10.1.1 Exposure of the general population 

 A10.1.2 Occupational exposure 

 A10.1.3 Non-neoplastic effects 

 A10.1.4 Neoplastic effects 

 A10.2 Evaluation of effects on the environment 

 A11. RECOMMENDATIONS 

 A11.1 Recommendations for the protection of human health 

 A11.2 Recommendation for the protection of the environment 

 A11.3 Recommendations for further research 

 A12. PREVIOUS EVALUATIONS BY INTERNATIONAL BODIES 

 PART B: DIESEL EXHAUST EMISSIONS 

 B1. SUMMARY 

 B1.1 Identity, physical and chemical properties, and 

 analytical methods 

 B1.2 Sources of human and environmental exposure 

 B1.3 Environmental transport, distribution, and 

 transformation 

 B1.4 Environmental levels and human exposure 

 B1.5 Kinetics and metabolism in laboratory animals and 

 humans 

 B1.5.1 Deposition 

 B1.5.2 Retention and clearance of particles 

 B1.5.3 Retention and clearance of polycyclic 

 aromatic hydrocarbons adsorbed onto diesel 

 soot 

 B1.5.4 Metabolism 

 B1.6 Effects on laboratory mammals and in vitro test 

 systems 

 B1.7 Effects on humans 

 B1.8 Effects on other organisms in the laboratory and the 

 field 

 B1.9 Evaluation of human health risks 

 B1.9.1 Non-neoplastic effects 

 B1.9.2 Neoplastic effects 

 B1.10 Evaluation of effects on the environment 

 B2. IDENTITY AND ANALYTICAL METHODS 

 B2.1 Identity 

 B2.1.1 Chemical composition of diesel exhaust 

 gases 

 B2.1.2 Type and composition of emitted particulate 

 matter 

 B2.2 Analytical methods 

 B2.2.1 Sampling 

 B2.2.1.1 Sampling from undiluted exhaust 

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 gas (raw gas sampling) 

 B2.2.1.2 Sampling from diluted exhaust 

 (dilution tube sampling) 

 B2.2.2 Extraction from particles 

 B2.2.3 Clean-up and fractionation 

 B2.2.4 Chemical analysis 

 B2.3 Conversion factors 

 B3. SOURCES OF HUMAN AND ENVIRONMENTAL EXPOSURE 

 B3.1 Anthropogenic sources 

 B3.1.1 Diesel exhaust emissions 

 B3.1.1.1 Emission of chemical 

 constituents with the gaseous 

 portion of diesel exhaust 

 B3.1.1.2 Emission of particulate matter 

 and adsorbed components in 

 diesel exhaust gases 

 B3.1.2 Parameters that influence diesel exhaust 

 emissions 

 B3.1.2.1 Engine conditions 

 B3.1.2.2 Fuel specification 

 B3.1.2.3 Malfunction 

 B3.1.3 Total emissions by diesel engines 

 B3.1.4 Control of emissions 

 B3.1.4.1 Particle traps 

 B3.1.4.2 Catalytic converters 

 B3.2 Regulatory approaches 

 B4. ENVIRONMENTAL TRANSPORT, DISTRIBUTION, AND TRANSFORMATION 

 B4.1 Transport and distribution between media 

 B4.2 Transformation and removal 

 B5. ENVIRONMENTAL LEVELS AND HUMAN EXPOSURE 

 B5.1 Exposure of the general population 

 B5.2 Occupational exposure 

 B5.2.1 Truck drivers and mechanics 

 B5.2.2 Bus garage and other bus workers 

 B5.2.3 Fork-lift truck operators 

 B5.2.4 Railroad workers 

 B5.2.5 Mine workers 

 B5.2.6 Fire fighters 

 B5.3 Biomonitoring 

 B5.3.1 Urinary mutagenicity 

 B5.3.2 Other analyses 

 B6. KINETICS AND METABOLISM IN LABORATORY ANIMALS AND HUMANS 

 B6.1 Deposition 

 B6.2 Retention and clearance of particles 

 B6.3 Retention and clearance of polycyclic aromatic 

 hydrocarbons adsorbed onto diesel soot 

 B6.4 Metabolism 

 B7. EFFECTS ON LABORATORY MAMMALS AND IN VITRO TEST SYSTEMS 

 B7.1 Single exposure 

 B7.2 Short-term exposure 

 B7.3 Long-term exposure and studies of carcinogenicity 

 B7.3.1 Non-neoplastic effects 

 B7.3.2 Carcinogenicity 

 B7.3.2.1 Inhalation 

 B7.3.2.2 Other routes of exposure 

 B7.4 Dermal and ocular irritation; dermal sensitization 

 B7.5 Reproductive toxicity, embryotoxicity, and 

 teratogenicity 

 B7.5.1 Reproductive toxicity 

 B7.5.2 Embryotoxicity 

 B7.5.3 Teratogenicity 

 B7.6 Mutagenicity and related end-points 

 B7.6.1 In vitro 

 B7.6.2 In vivo 

 B7.6.3 DNA adduct formation 

 B7.7 Special studies 

 B7.7.1 Immunotoxicity 

 B7.7.2 Behavioural effects 

 B7.8 Factors that modify toxicity; toxicity of 

 metabolites 

 B7.9 Mechanisms of toxicity; mode of action 

 B7.9.1 Carcinogenic effects 

 B7.9.1.1 DNA-reactive mechanisms 

 B7.9.1.2 Cytotoxicity with regenerative 

 cell proliferation 

 B7.9.1.3 Effects of particles 

 B7.9.1.4 Effects of polycyclic aromatic 

 hydrocarbons 

 B7.9.2 Noncarcinogenic effects 

 B8. EFFECTS ON HUMANS 

 B8.1 General population 

 B8.1.1 Acute exposure: olfactory, nasal, and 

 ocular irritation 

 B8.1.2 Air pollution 

 B8.2 Occupational exposure 

 B8.2.1 Effects on the respiratory system 

 B8.2.1.1 Symptoms 

 B8.2.1.2 Acute changes in pulmonary 

 function 

 B8.2.1.3 Pulmonary effects 

 B8.2.2 Epidemiological studies (noncarcinogenic 

 effects) 

 B8.2.2.1 Effects on the respiratory 

 system 

 B8.2.2.2 Effects on the circulatory 

 system 

 B8.2.3 Epidemiological studies (carcinogenic 

 effects) 

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 B8.2.3.1 Lung cancer 

 B8.2.3.2 Urinary bladder cancer 

 B9. EFFECTS ON OTHER ORGANISMS IN THE LABORATORY AND THE FIELD 

 B10. EVALUATION OF HUMAN HEALTH RISKS AND EFFECTS ON THE 

 ENVIRONMENT 

 B10.1 Exposure of the general population 

 B10.2 Occupational exposure 

 B10.3 Non-neoplastic effects 

 B10.3.1 Hazard identification 

 B10.3.1.1 Humans 

 B10.3.1.1 Experimental animals 

 B10.3.2 Dose-response assessment 

 B10.3.2.1 Epidemiological studies 

 B10.3.2.2 Studies in experimental animals 

 B10.3.3 Exposure assessment 

 B10.3.4 Risk characterization 

 B10.3.4.1 Humans 

 B10.3.4.2 Experimental animals 

 B10.4 Neoplastic effects 

 B10.4.1 Hazard identification 

 B10.4.1.1 Lung cancer: occupational 

 exposure 

 B10.4.1.2 Urinary bladder cancer: 

 occupational exposure 

 B10.4.2 Dose-response assessment 

 B10.4.2.1 Lung cancer 

 B10.4.2.2 Urinary bladder cancer 

 B10.4.3 Exposure assessment 

 B10.4.4 Risk characterization 

 B10.4.4.1 Human lung cancer 

 B10.4.4.2 Human urinary bladder cancer 

 B10.4.4.3 Risk characterization based on 

 studies in experimental animals 

 Appendix B10.1 Construction of a biologically 

 based (alternative) model 

 Appendix B10.2 E-M algorithm 

 Appendix B10.3 A tumour growth model 

 B11. RECOMMENDATIONS 

 B11.1 Recommendations for the protection of human health 

 B11.2 Recommendation for the protection of the environment 

 B11.3 Recommendations for further research 

 B12. PREVIOUS EVALUATIONS BY INTERNATIONAL BODIES 

 REFERENCES 

 RESUMÉ 

 RESUMEN 

 

 NOTE TO READERS OF THE CRITERIA MONOGRAPHS 

 Every effort has been made to present information in the Criteria 

 monographs as accurately as possible without unduly delaying their 

 publication. In the interest of all users of the Environmental Health 

 Criteria monographs, readers are requested to communicate any errors 

 that may have occurred to the Director of the International Programme 

 on Chemical Safety, World Health Organization, Geneva, Switzerland, in 

 order that they may be included in corrigenda. 

 * * * 

 A detailed data profile and a legal file can be obtained from the 

 International Register of Potentially Toxic Chemicals, Case postale 

 356, 1219 Châtelaine, Geneva, Switzerland (Telephone No. 979 9111). 

 * * * 

 This publication was made possible by grant number 5 U01 

 ES02617-15 from the National Institute of Environmental Health 

 Sciences, National Institutes of Health, USA, and by financial support 

 from the European Commission. 

 Environmental Health Criteria 

 PREAMBLE 

 Objectives 

 The WHO Environmental Health Criteria Programme was initiated in 

 1973, with the following objectives: 

 (i) to assess information on the relationship between exposure to 

 environmental pollutants and human health and to provide 

 guidelines for setting exposure limits; 

 (ii) to identify new or potential pollutants; 

 (iii) to identify gaps in knowledge concerning the health effects of 

 pollutants; 

 (iv) to promote the harmonization of toxicological and 

 epidemiological methods in order to have internationally 

 comparable results. 

 The first Environmental Health Criteria (EHC) monograph, on 

 mercury, was published in 1976; numerous assessments of chemicals and 

 of physical effects have since been produced. Many EHC monographs have 

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 been devoted to toxicological methods, e.g. for genetic, neurotoxic, 

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 Since the time of its inauguration, the EHC Programme has widened 

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 addition to their health effects. 

 The original impetus for the Programme came from resolutions of 

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 Scope 

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 Content 

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 the chemical 

 * Identity: physical and chemical properties, analytical methods 

 * Sources of exposure 

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 * Kinetics and metabolism in laboratory animals and humans 

 * Effects on laboratory mammals and in-vitro test systems 

 * Effects on humans 

 * Effects on other organisms in the laboratory and the field 

 * Evaluation of human health risks and effects on the environment 

 * Conclusions and recommendations for protection of human health 

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 on Pesticide Residues 

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 the hazards. 

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 All participating institutions are informed, through the EHC 

 progress report, of the authors and institutions proposed for the 

 drafting exhaust emissions of the documents. A comprehensive file of 

 all comments received on drafts of each EHC monograph is maintained 

 and is available on request. The chairpersons of task groups are 

 briefed before each meeting on their role and responsibility in 

 ensuring that these rules are followed. 

 WHO DRAFTING GROUP ON ENVIRONMENTAL HEALTH CRITERIA FOR DIESEL FUEL 

 AND EXHAUST EMISSIONS 

 WHO, Geneva, 6-9 December 1993 

 Members

 Dr J.A. Bond, Chemical Industry Institute of Toxicology, Research 

 Triangle Park, NC, United State 

 Dr R.P. Bos, University of Nijmegen, Nijmegen, Netherlands 

 Dr R. Brown, Medical Research Council Toxicology Unit, University of 

 Leicester, Leicester, United Kingdom (Joint Rapporteur)

 Dr Chao Chen, Human Health Assessment Group, United States 

 Environmental Protection Agency, Washington DC, United States 

 Dr I. Farkas, National Institute of Hygiene, Budapest, Hungary 

 Dr E. Garshick, Pulmonary Section, Brockton/West Roxbury VA Medical 

 Center, West Roxbury, MA, United States 

 Dr P. Gustavsson, North Western Health Board, Stockholm, Sweden 

 Dr D. Guth, United States Environmental Protection Agency, Research 

 Triangle Park, NC, United States 

 Dr U. Heinrich, Department of Experimental Hygiene, Fraunhofer 

 Institute of Toxicology and Aerosol Research, Hanover, Germany 

 Dr R.F. Hertel, Federal Health Office, Bundesgesundheitsamt, Berlin, 

 Germany 

 Professor G. Oberdörster, Department of Environmental Medicine, 

 University of Rochester Medical Center, Rochester, NY, United States 

 Dr W. Pepelko, United States Environmental Protection Agency, 

 Washington DC, United States 

 Dr P.J.A. Rombout, Laboratory of Toxicology, National Institute of 

 Public Health and Environmental Protection, Bilthoven, Netherlands 

 (Vice-Chairman)

 Dr G. Rosner, Hazardous Substances Documentation Group, Fraunhofer 

 Institute of Toxicology and Aerosol Research, Hanover, Germany 

 Dr J. Roycroft, National Institute of Environmental Health Sciences, 

 Research Triangle Park, NC, United States 

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 Dr A. Sivak, Environmental Health Sciences, Saint Augustine, FL, 

 United States (Chairman)

 Dr B.H. Thomas, Environmental Health Directorate, Ottawa, Canada 

 Dr L. Turrio, Istituto Superiore di Sanita, Laboratorio Tossicologia 

 Comparata e Ecotossicologia, Rome, Italy 

 Mr. R. Waller, Department of Health, London, United Kingdom 

 Secretariat

 Dr P. Boffetta, International Agency for Research on Cancer, Lyon, 

 France (6-7 December 1993) 

 Dr E. Smith, International Programme on Chemical Safety, World Health 

 Organization, Geneva, Switzerland 

 Representatives/Observers

 CONCAWE 

 Dr R.H. McKee, Exxon Biomedical Sciences, East Millstone, NJ, 

 United States 

 UNITED KINGDOM DEPARTMENT OF THE ENVIRONMENT 

 Dr P.T.C. Harrison, MRC Institute of Environment & Health, 

 Leicester, United Kingdom 

 WHO TASK GROUP ON ENVIRONMENTAL HEALTH CRITERIA FOR DIESEL FUEL AND 

 EXHAUST EMISSIONS 

 Fraunhofer Institute of Toxicology & Aerosol Research, Hanover 

 27 June-1 July 1994 

 Members

 Dr J.A. Bond, Chemical Industry Institute of Toxicology, Research 

 Triangle Park, NC, United States 

 Dr R. Brown, Medical Research Council Toxicology Unit, University of 

 Leicester, Leicester, United Kingdom 

 Dr Chao Chen, Human Health Assessment Group, United States 

 Environmental Protection Agency, Washington DC, United States 

 Dr E. Garshick, Pulmonary Section, Brockton/West Roxbury VA Medical 

 Center, West Roxbury, MA, United States 

 Dr U. Heinrich, Department of Experimental Hygiene, Fraunhofer 

 Institute of Toxicology and Aerosol Research, Hanover, Germany 

 Dr R.F. Hertel, Federal Health Office, Bundesgesundheitsamt, Berlin, 

 Germany 

 Dr Jun Kagawa, Tokyo Women's Medical College, Tokyo, Japan 

 Professor G. Oberdörster, Department of Environmental Medicine, 

 University of Rochester Medical Center, Rochester, NY, United States 

 Dr P.J.A. Rombout, Laboratory of Toxicology, National Institute of 

 Public Health and Environmental Protection, Bilthoven, Netherlands 

 Dr M. Roller, Medizinishes Institut für Umwelthyglene an der 

 Universität Düsseldorf, Düsseldorf, Germany Dr G. Rosner, Hazardous 

 Substances Documentation Group, Fraunhofer Institute of Toxicology and 

 Aerosol Research, Hanover, Germany 

 Dr A. Sivak, Environmental Health Sciences, Saint Augustine, FL, 

 United States 

 Dr L. Turrio, Istituto Superiore di Sanita, Laboratorio Tossicologia 

 Comparata e Ecotossicologia, Rome, Italy 

 Mr R. Waller, Department of Health, London, United Kingdom 

 Secretariat

 Dr H. Moller, International Agency for Research on Cancer, Lyon, 

 France 

 Dr E. Smith, International Programme on Chemical Safety, World Health 

 Organization, Geneva, Switzerland 

 Dr M. Younes, European Centre for Environment and Health, Bilthoven, 

 Netherlands 

 Representatives/Observers

 Dr Lutz Von Meyerinck, BP Oil Europe, Brussels, Belgium 

 GERMAN AUTOMOBILE ASSOCIATION 

 Dr N. Pelz, Mercedes-Benz AG, Stuttgart, Germany 

 ILSI 

 Dr I.T. Salmeen, Chemistry Department, Ford Motor Company, 

 Dearborn, MI, United States 

 IUTOX 

 Dr P. Montuschi, Department of Pharmacology, School of Medicine, 

 Catholic University of the Sacred Heart, Rome, Italy 

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 ENVIRONMENTAL HEALTH CRIETERIA FOR DIESEL FUEL AND EXHAUST EMISSIONS 

 A WHO Task Group on Environmental Health Criteria for Diesel Fuel 

 and Exhaust Emissions met at the Fraunhofer Institute of Toxicology 

 and Aerosol Research, Hanover, Germany from 27 June to 1 July 1994. 

 Dr G. Rosner, Fraunhofer Institute, welcomed the participants on 

 behalf of the Institute and its Director, Professor U. Mohr, and 

 Dr E.M. Smith, IPCS, welcomed the participants on behalf of 

 Dr M. Mercier, Director of the IPCS, and on behalf of the heads of the 

 three IPCS cooperating organizations (UNEP, ILO, and WHO). The Task 

 Group reviewed and revised the draft and evaluated the risks for human 

 health and the environment from exposure to diesel fuel and exhaust 

 emissions. 

 The first draft of the monograph was prepared at the Fraunhofer 

 Institute. After international circulation for comment, this draft was 

 extensively revised by a Working/Drafting Group, convened at WHO, 

 Geneva, from 6 to 9 December 1993, and a second draft was prepared for 

 further international circulation for comment. The membership of the 

 drafting group is shown previously. A final draft, incorporating 

 comments received from the IPCS contact points for Environmental 

 Health Criteria monographs and new material, was completed at the 

 Fraunhofer Institute under the coordination of Dr G. Rosner, with 

 important contributions to the text from the following Institute staff 

 members: 

 Dr B. Bellman 

 Dr A. Boehnke 

 Dr O. Creutzenberg 

 Dr J. Kielhorn 

 Dr E.M. Smith of the IPCS Central Unit was responsible for the 

 scientific content of the monograph and Mrs E. Heseltine, Lajarthe, 

 France, for the editing. 

 The efforts of all who helped in the preparation and finalization 

 of the monograph are gratefully acknowledged. 

 PART A DIESEL FUEL

 A1. SUMMARY

 A1.1 Identity, physical and chemical properties, and analytical 

 methods 

 Diesel fuel is a complex mixture of normal, branched, and cyclic 

 alkanes (60 to > 90% by volume; hydrocarbon chain length, usually 

 between C9 and C30); aromatic compounds, especially alkylbenzenes 

 (5-40% by volume); and small amounts of alkenes (0-10% by volume) 

 obtained from the middle-distillate, gas-oil fraction during petroleum 

 separation. Benzene, toluene, ethylbenzene, and xylenes and polycyclic 

 aromatic hydrocarbons (PAHs), especially naphthalene and its 

 methyl-substituted derivatives, may be present at levels of parts per 

 million in diesel fuel. The sulfur content of diesel fuels depends on 

 the source of crude oil and the refinery process. It is regulated by 

 law in a number of countries and is usually between 0.05 and 0.5 

 weight percent. Additives are used to influence the flow, storage, and 

 combustion of diesel fuel, to differentiate products, and to meet 

 trademark specifications. At room temperature, diesel fuels are 

 generally moderately volatile, slightly viscous, flammable, brown 

 liquids with a kerosene-like odour. The boiling ranges are usually 

 between 140 and 385°C (> 588°C for marine diesel fuel); at 20°C, the 

 density is 0.87-1.0 g/cm3 and the water solubility is 

 0.2-5 mg/litre. The quality and composition of diesel fuel influence 

 the emissions of pollutants from diesel engines considerably. 

 Important variables are ignition behaviour (expressed in terms of 

 cetane number), density, viscosity, and sulfur content. The 

 specifications of commercial diesel fuel differ considerably in 

 different countries. 

 Heating fuels and some kerosene jet fuels produced during the 

 refining process may have a composition similar to that of diesel 

 fuel, although with different additives. Biological data on these 

 mixtures have therefore also been taken into account in the 

 assessments of toxicity and ecotoxicity. 

 Owing to the complexity of the diesel fuel mixture, there is no 

 specific analytical method, and the analytical techniques used in most 

 environmental assessments are suitable only for measuring the total 

 petroleum hydrocarbon mixture. The methods consist of preliminary 

 solvent extraction, a clean-up procedure to remove naturally occurring 

 hydrocarbons, and subsequent detection by gravimetry, infrared 

 spectroscopy or gas chromatography. Neither the gravimetric nor the 

 infrared technique provides useful qualitative or quantitative 

 information on contaminants and can thus be used only for screening. 

 Gas chromatography combined with detection techniques such as flame 

 ionization and mass spectrometry is the standard procedure for 

 analysing environmental samples. Many other methods are available for 

 the analysis of individual hydrocarbons in diesel fuels. 

 A1.2 Sources of human and environmental exposure 

 Diesel fuels are produced by refining crude oils. In order to 

 meet technical specifications for performance, diesel fuels are 

 generally blended; further formulation with additives improves their 

 properties for specific uses. Diesel fuels are widely used as 

 transportation fuels. The more volatile fuels, with low viscosity, are 

 required for high-speed engines and the heavier grades for railroad 

 and ship diesel engines. Much heavy-duty road transport is powered by 

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 diesel engines. Passenger cars powered by diesel engines are becoming 

 increasingly more common in Europe and Japan (10-25%), whereas in 

 North America the percentage of diesel-fuelled passenger cars is about 

 1-2%, with a slightly decreasing tendency. Diesel fuel is used in 

 stationary engines and in boilers, e.g. reciprocating engines, gas 

 turbines, pipeline pumps, gas compressors, steam processing units in 

 electric power plants, burner installations, and industrial space and 

 water heating facilities. 

 Over the last five years, the worldwide demand for diesel fuels 

 has increased steadily. In 1985, the following amounts of diesel fuel 

 were consumed: about 170 000 kt per year in North America; about 

 160 000 kt per year, including gas oils, in the European Union; and 

 about 46 000 kt per year in Australia, Japan, and New Zealand, 

 equivalent to a total of 1062 kt per day. In 1990, world demand was 

 reported to be about 1110 kt per day. 

 No information is available on emissions during the production of 

 diesel fuels; however, this source would seem to be of minor 

 importance, because the refining process is carried out in closed 

 systems. Emissions may occur principally during storage and 

 transportation. Diesel fuels are released as a result of spills and at 

 filling stations during the refuelling of vehicles. The atmosphere and 

 the hydrosphere are the most heavily affected environmental 

 compartments. Soil contamination with diesel fuels may occur during 

 accidents and is also a problem in railroad yards. The numerous 

 techniques for cleaning soils contaminated with diesel fuel include 

 excavation, biological methods, and containment. 

 A1.3 Environmental transport, distribution, and transformation 

 Very few data are avilable on the environmental fate of diesel 

 fuels, but the mechanisms of their distribution and transformation are 

 considered to be comparable to those of heating fuels, such as No. 2 

 fuel oil, which have been well studied. Spills of diesel fuel on water 

 spread almost immediately to form a 'slick'. The polar and 

 low-relative-molecular-mass components dissolve and leach out of the 

 slick, and the volatile components evaporate from the surface; 

 microbial degradation also begins. Chemical and biological weathering 

 alter the composition of the spill. These processes are dependent on 

 temperature; spills that occur in Arctic conditions are more 

 persistent than those that occur in temperate climates. In marine 

 environments, most of the low-relative-molecular-mass aromatic species 

 are dissolved into the water phase, but the primary branched alkanes, 

 cycloalkanes, and remaining aromatic compounds may remain in sediments 

 for more than a year. 

 Although no information is available on the photooxidation of 

 diesel fuels in water and air, evaporated oil components are degraded 

 photochemically. No. 2 fuel oil has been shown to be photooxidized 

 rapidly in water under environmental conditions. 

 The individual constituents of diesel fuel are inherently 

 biodegradable, to varying degrees and at different rates. The 

 n-alkane, n-alkylaromatic, and simple aromatic molecules in the C10-C22

 range are the most readily degradable. Smaller molecules are generally 

 rapidly metabolized. Long-chain n-alkanes are more slowly degraded, 

 owing to their hydrophobicity and because they are viscous or solid at 

 ambient temperatures. Branched alkanes and cycloalkanes are relatively 

 resistant to biological breakdown, and PAHs are resistant. The overall 

 rates of degradation of hydrocarbons are limited by temperature, water 

 content, oxygen, pH, inorganic nutrients, and microbial metabolic 

 versatility. 

 Unicellular algae can take up and metabolize both aliphatic and 

 aromatic hydrocarbons, but the extent to which this actually occurs in 

 nature is poorly understood. Unlike microorganisms that use petroleum 

 carbons as a carbon source, animals generally oxidize and conjugate 

 products, rendering end-products that are more soluble and therefore 

 easier to excrete. All animal species tested can take up petroleum 

 hydrocarbons. PAHs, crude oil, and refined petroleum products are 

 known to induce cytochrome P450 enzymes and to increase the levels of 

 hydrocarbon metabolism in numerous marine and freshwater fish species. 

 Few data are available on the bioaccumulation of diesel fuel in 

 the laboratory, but there is plentiful evidence from studies of spills 

 and laboratory studies on other oils, particularly No. 2 fuel oil, 

 that aquatic organisms bioconcentrate hydrocarbons. The 

 n-octanol-water partition coefficient for diesel fuel is 3.3-7.06, 

 which suggests high potential bioaccumulation; however, many of the 

 lower-relative-molecular-mass compounds are readily metabolized, and 

 the actual bioaccumulation of higher-relative-molecular-mass compounds 

 is limited by their low water solubility and large molecular size. 

 Thus, actual bioaccumulation may be low. 

 Fish have been tainted by diesel fuel after spills. No data are 

 available on the biomagnification of diesel fuel. 

 No experimental data are available on the movement of diesel fuel 

 through the soil, although a direct correlation between the movement 

 and kinematic viscosity has been proposed. The movement of kerosene 

 through soil depends on the moisture content and nature of the soil. 

 A1.4 Environmental levels and human exposure 

 As diesel fuels are complex mixtures, the environmental levels 

 have not been measured. The individual constituents of diesel fuels 

 can be detected in almost all compartments of the environment, 

 although their source cannot be verified. The general population may 

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 be exposed to diesel fuel at filling stations and as a result of 

 spills. 

 Occupational exposure to diesel fuel occurs in a large number of 

 activities. Because of their low volatility, diesel fuels should 

 generate only low concentrations of vapours at normal temperatures, 

 but high operating temperatures can result in significant 

 concentrations. 

 A1.5 Effects on laboratory mammals and in-vitro test systems 

 The acute toxicity of diesel fuels is low after oral or dermal 

 exposure or after inhalation. The oral LD50 value was > 5000 mg/kg 

 body weight in all species tested (mouse, rabbit, rat, guinea-pig). 

 Dermal application resulted in an LD50 value of > 5000 mg/kg body 

 weight in mice and rabbits, although values of > 2000 mg/kg body 

 weight were reported for some kerosenes and middle distillates, with 

 different protocols and lower limit doses. The LC0 value in rats 

 exposed by inhalation was about 5 mg/litre, except for one 

 straight-run middle distillate for which a value of 1.8 mg/litre was 

 seen. 

 In rabbits treated dermally with up to 8000 μl/kg body weight per 

 day and mice with up to 40 000 mg/kg body weight per day, acanthosis 

 and hyperkeratosis due to severe irritation were seen. Rabbits were 

 more sensitive than mice. Inhalation of diesel fuel was neuro- 

 depressive in mice at concentrations up to 0.2 mg/litre but not 

 in rats exposed to up to 6 mg/litre. Body and liver weights were 

 reduced in rats. 

 Mice, rats, and dogs did not show significant cumulative toxicity 

 after inhalation of up to 1.5 mg/litre subchronically. The specific 

 nephropathy syndrome seen in male rats is linked to an inherent 

 accumulation of hyalin droplets in the renal tubules. 

 The only effects of long-term exposures were ulceration after 

 dermal application to mice (250 or 500 mg/kg body weight per day) and 

 significant alterations in organ weight after inhalation of 1 or 

 5 mg/litre by rats. In both studies the mean body weights were 

 reduced. 

 Various types of diesel fuels were slightly to severely 

 irritating to the skin of rabbits. Diesel fuels do not irritate the 

 eye, but some kerosenes have been reported to have a slight irritating 

 effect. Diesel fuels do not cause skin sensitization. 

 Diesel and jet fuels (kerosene) were neither embryotoxic nor 

 teratogenic in two studies in rats exposed by inhalation to 100 or 

 400 ppm and in one study in which rats were given up to 2000 mg/kg 

 body weight per day by gavage. In the last study, reduced fetal weight 

 was observed. 

 Tests in Salmonella typhimurium did not provide clear evidence 

 of mutagenicity. Some positive findings in S. typhimurium and in 

 mouse lymphoma cells were considered to be equivocal owing to the 

 inconsistency of the results. Tests for genotoxicity in mice in vivo

 (induction of micronuclei or chromosomal aberrations) also gave 

 equivocal or negative responses. 

 Diesel fuels induced a low level of dermal carcinogenicity. In 

 the present state of research, it cannot be concluded whether the 

 carcinogenic potency of diesel fuels is mediated by a genotoxic 

 mechanism or by chronic dermal damage. 

 A1.6 Effects on humans 

 Non-occupational exposure to diesel fuel can occur during manual 

 filling of fuel tanks. The primary source of dermal exposure is 

 accidental spills, which result in immediate high levels of exposure 

 but are of short duration. 

 After accidental dermal contact, anuria, renal failure, gastro- 

 intestinal symptoms, and cutaneous hyperkeratosis have been reported. 

 Toxic lung disease has been observed after accidental ingestion of 

 diesel fuel and subsequent aspiration. Persistent productive cough has 

 been reported after inhalation. In a case-control study of men exposed 

 to diesel fuel, an increased risk for cancer of the lung other than 

 adenocarcinoma was found; a positive association was also seen with 

 prostatic cancer, although a higher risk was noted for the group with 

 'nonsubstantial' exposure than for that with 'substantial' exposure. 

 In a cross-sectional study of factory workers exposed to kerosene jet 

 fuels, dizziness, headache, nausea, palpitation, pressure in the 

 chest, and eye irritation were found to be more prevalent than in 

 unexposed controls. The time-weighted average concentration of 

 vapour from the fuel in the breathing zone was estimated to be 

 128-423 mg/m3. 

 A1.7 Effects on other organisms in the laboratory and the field 

 Diesel fuel is more toxic than crude oil to aquatic organisms and 

 plants. The ecotoxicity of diesel fuel is generally attributed to 

 soluble aromatic compounds, but insoluble aliphatic hydrocarbons may 

 also be implicated. Of the aromatic compounds, monoaromatics are the 

 least toxic, their acute toxicity increasing with molecular mass up to 

 the four- to five-ring compounds, although these are poorly soluble in 

 seawater. In some animals, e.g. fish and birds, physical coating of 

 the body surface by the fuel can produce toxicity and mortality. 

 Laboratory experiments have been carried out on diesel fuel, 

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 water-soluble fractions, oil-water dispersions, and microencapsulated 

 oil. Diesel fuel did not significantly reduce the growth in culture of 

 the green alga Euglena gracilis, whereas a low concentration (0.1%) 

 almost completely inhibited the growth of Scenedesmus quadricauda.

 Light diesel fuel (0.05%) stimulated the growth, photosynthesis, and 

 chlorophyll asynthesis of Chlorella salina but slightly inhibited 

 respiration; at higher concentrations, the growth rate and 

 photosynthesis were greatly reduced. Long-term exposure inhibited the 

 growth of the benthic algae Ascophyllum nodosum and Laminaria

 digitata. In blue-green algae, photosynthesis was reduced by the 

 aromatic and asphaltic fractions but not by the aliphatic fraction. 

 Diesel fuel was acutely toxic to Daphnia spp., chironomid 

 larvae, and the mollusc Viviparus bengalensis (Gastropoda). A 

 concentration of 0.1 ml/litre caused the death of tidepool copepods, 

 Tigriopus californicus, within five days. 

 Mytilus edulismussels accumulate diesel fuel, have markedly 

 reduced feeding and growth rates, and show reproductive toxicity after 

 chronic exposure to diesel fuel. The EC50 for spawning in mussels 

 exposed for 30 days was about 800 μg/litre. The LC50 of micro- 

 encapsulated diesel oil after exposure of maturing mussels for 

 30 days was about 5000 μg/litre. Diesel oil was more toxic to larvae 

 than to juveniles: 10 μg/litre had adverse effects on the growth of 

 larvae. 

 Freshwater crabs (Barytelphusa cunicularis) exposed to sublethal 

 concentrations of diesel fuel for up to 96 h generally reduced their 

 oxygen consumption, particularly at lower exposures up to 8 h. With 

 longer exposures, the oxygen consumption was equal to or higher than 

 that of the controls. 

 In 96-h tests of acute toxicity in juvenile salmonids under 

 static conditions, diesel fuel was more toxic to pink salmon, 

 Onchorhychus gorbuscha (LC50: 32-123 mg/litre), than to cohosalmon, 

 O. kisutch (LC50: 2186-3017 mg/litre), or rainbow trout, 

 O. mykiss (LC50: 3333-33 216 mg/litre), irrespective of water type. 

 The threshold for detection of behavioural responses of cod 

 ( Gadus morhua L.) exposed to diesel fuel in seawater was within 

 100-400 ng/litre. The Antarctic fish Pagothenia borchgrevinki

 withstood an undiluted water-soluble fraction of diesel fuel oil for 

 up to 72 h but showed signs of stress. 

 Birds are affected externally and internally by oil 

 contamination. Diesel fuel destroys the waterproof nature of the 

 birds' plumage and is ingested during preening. Diesel and fuel oil 

 fed by gavage at 2 ml/kg body weight to ducks caused lipid pneumonia, 

 extreme inflammation of the lungs, fatty infiltration of the liver, 

 and hepatic degeneration after 24 h. Administration of diesel or fuel 

 oil at 1 ml/kg caused severe irritation of the digestive tract and 

 toxic nephrosis. Higher doses resulted in adrenal enlargement (mainly 

 due to hyperplasia of cortical tissue), depression of plasma 

 cholinesterase levels, ataxia, and tremors. Doses up to 20 ml/kg body 

 weight were not fatal to healthy birds, but the LD50 for diesel and 

 fuel oil administered to birds under stress was 3-4 ml/kg body weight. 

 After spills of diesel fuel, zooplankton appear to be highly 

 vulnerable to dispersed and dissolved petroleum constituents but less 

 so to floating oils. Aquatic organisms may be affected in a number of 

 ways, including direct mortality (fish eggs, copepods, and mixed 

 plankton), external contamination by oil (chorions of fish eggs and 

 cuticles and feeding appendages of crustaceans), tissue contamination 

 by aromatic constituents, abnormal development of fish embryos, and 

 altered metabolic rates. 

 A1.8 Evaluation of human health risks 

 The general population can be exposed to diesel fuel and other 

 middle distillates at filling stations, as a result of accidental 

 spills, during the handling of such fuels, and during use of kerosene 

 for domestic cooking or heating. Workers can be exposed to diesel fuel 

 and other middle distillates while handling and discharging the fuel 

 at terminals, storage tanks, and filling stations; during the 

 manufacture, repair, maintenance, and testing of diesel engines and 

 other equipment; during use of diesel fuel as a cleaning agent or 

 solvent; and in handling and routine sampling of diesel fuel in the 

 laboratory. Owing to the low volatility of diesel fuel, only low 

 concentrations of vapour are likely to occur at room temperature, 

 although in confined spaces at high temperatures significant levels 

 may be found. 

 Exposure to vapour is minimal during the normal handling of 

 diesel fuel. The most likely effect on human health is dermatitis 

 after skin contact. Diesel fuel is a skin irritant but does not appear 

 to irritate the eye. Acute toxic effects on the kidney can occur after 

 dermal exposure, but the effects of long-term dermal absorption of low 

 concentrations are unknown. 

 Diesel fuels are toxic when ingested, sometimes resulting in 

 regurgitation and aspiration, which can cause chemical pneumonia; the 

 same is true for any hydrocarbon in a particular range of viscosity. 

 In rodents exposed by inhalation to diesel fuel at concentrations 

 up to 0.2 mg/litre, a neurodepressive effect was seen in mice but not 

 in rats at the higher concentrations. Subchronic exposure by 

 inhalation to various distillate fuels induced specific 

 alpha2-microglobulin nephropathy in male rats; this effect is 

 considered irrelevant for humans. 

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 Diesel fuels were neither embryotoxic nor teratogenic in animals 

 exposed orally or by inhalation. 

 There is no clear evidence of mutagenic activity in bacteria, and 

 the results of other tests for genotoxicity in vitro and in vivo were 

 equivocal. 

 A case-control study of workers exposed to diesel fuel suggested 

 an increased risk for cancer of the lung other than adenocarcinoma and 

 for prostatic cancer. In neither case was there an exposure-response 

 relationship. In view of the small number of studies available, the 

 small number of cases, and the correspondingly wide confidence 

 intervals, no conclusion can be drawn about the carcinogenicity to 

 humans of diesel fuel. 

 In mice, dermally administered diesel fuels had weak carcinogenic 

 potential. In view of the absence of clear genotoxicity, cancer could 

 be induced by nongenotoxic mechanisms, e.g. by chronic dermal 

 irritation characterized by repeated cycles of skin lesions, causing 

 epidermal hyperplasia. 

 A1.9 Evaluation of effects on the environment 

 The environment can be polluted by accidental release of diesel 

 fuel on a large scale, such as during tanker disasters and pipeline 

 leaks, or on a smaller scale from contamination of soil around 

 factories or garages. In water, diesel fuel spreads almost 

 immediately, polar and low-relative-molecular-mass components dissolve 

 and leach out, volatile components evaporate from the water surface, 

 and microbial degradation begins. The extent to which 'weathering' 

 takes place depends on the temperature and on climatic conditions. The 

 chemical composition of spills changes with time: after spillage on 

 water, some fractions evaporate, and the evaporated diesel components 

 are degraded photochemically; in sediment, diesel fuel appears 

 generally to be delivered to bottom sediments by settling particles; 

 in soil, the components of diesel fuel migrate at different rates, 

 depending on the soil type. 

 The individual constituents of diesel fuel are inherently 

 biodegradable, but the rates of biodegradation depend heavily on 

 physical and climatic conditions and on microbial composition. 

 Aquatic organisms, in particular molluscs, bioaccumulate 

 hydro-carbons to varying extents, but the hydrocarbons are depurated 

 on transfer to clean water. Diesel fuel may be bioaccumulated; no data 

 are available about biomagnification. 

 Spills of diesel fuel have an immediate detrimental effect on the 

 environment, causing substantial mortality of biota. Recolonization 

 may occur after about one year, depending on the animal or plant 

 species and the chemical and physical content of the spill residues. 

 Aquatic organisms that survive diesel fuel spills can be affected by 

 external oil contamination and tissue accumulation: abnormal 

 development and altered metabolic rates are signs of the resulting 

 stress. 

 A2. IDENTITY, PHYSICAL AND CHEMICAL PROPERTIES, AND ANALYTICAL 

 METHODS

 A2.1 Identity 

 Diesel fuels are a gas-oil fraction occurring during petroleum 

 separation and commonly known as middle distillates (International 

 Agency for Research on Cancer, 1989a). Gas oils are generally blended 

 materials formulated to meet technical specifications (CONCAWE, in 

 press). Commercial diesel fuels contain aliphatic, olefinic, 

 cycloparaffinic, and aromatic hydrocarbons (see section A2.1.1), and 

 additives (see section A2.1.2) to improve their fuelling properties 

 (Sandmeyer, 1981). 

 Four qualities of diesel fuel are available commercially: diesel 

 fuel (general), diesel fuel No. 1, diesel fuel No. 2, and diesel fuel 

 No. 4 (see Table 1). The composition of diesel fuels is comparable to 

 that of heating oils (e.g. No. 1 and No. 2 fuel oils), except for the 

 additives (International Agency for Research on Cancer, 1989a; Agency 

 for Toxic Substances and Disease Registry, 1995). 

 Diesel fuel No. 2 is used mainly as automobile fuel and 

 corresponds to diesel fuel (general). In Europe (countries of the 

 European Union (EU) and European Free Trade Area (EFTA)), the 

 specifications for diesel fuel for transportation purposes are given 

 in European standard EN 590 (European Committee for Standardization, 

 1993), which also provides for changes in the specifications to meet 

 the requirements of different climatic conditions. In Sweden, two 

 further qualities of on-road diesel fuel are available: environmental 

 class 1 and class 2 (city diesel), with sulfur contents of 0.05% and 

 0.001%, respectively (Standardization Board in Sweden, 1991). The 

 sulfur content of city diesel corresponds to that of kerosene. Diesel 

 fuel for ship engines is covered by the International Standards 

 Organization (ISO) standard 8217 (International Standards 

 Organization, 1987). In the United States of America, three grades of 

 diesel fuel are available: diesel fuel No. 1 (relatively high 

 volatility) for road vehicle engines subject to frequent speed and 

 load changes; diesel fuel No. 2 (lower volatility) for industrial or 

 heavy-duty, high-load engines running at uniform speed; and diesel 

 fuel No. 4 (viscous) for low- and medium-speed engines such as those 

 used in ships (American Society for Testing and Materials, 1988, 

 1992). 

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 Several types of kerosene, also derived from the gas-oil fraction 

 of petroleum separation, are used as aviation turbine fuels (JP fuels, 

 jet fuels). Their hydrocarbon composition is comparable to that of 

 diesel fuels. 

 A2.1.1 Fuel components 

 A2.1.1.1 Alkanes 

 Normal, branched, and cyclic alkanes (paraffins) are the most 

 abundant components (about 65-85%) of diesel fuels. Pristane 

 (2,6,10,14-tetramethylpentadecane) and phytane (2,6,10,14- 

 tetramethyl-hexadecane) are of particular interest environmentally, as 

 the ratios of pristane to heptadecane and of phytane to octadecane 

 make it possible to identify the source of a fuel spill; furthermore, 

 as these ratios increase during biological degradation, they can be 

 used to estimate the age of an environmental contamination and the 

 degree of elimination. Cycloalkanes and bicycloalkanes constitute a 

 significant portion of the mixture, but individual compounds are 

 present only at low levels and are difficult to analyse. Alkyl 

 derivatives of cyclopentane, cyclohexane, and cycloheptane are common 

 components (Block et al., 1991; Table 2). 

 A2.1.1.2 Alkenes 

 Alkenes are not common components of crude oil but may be 

 present in diesel fuel if converted products are added after cracking. 

 These alkenes have predominantly branched and cyclic structures (Block 

 et al., 1991). The total alkene content of diesel fuels is up to 10% 

 (CONCAWE, 1985) (see also Table 2). 

 A2.1.1.3 Aromatic compounds 

 Aromatic compounds constitute 5-30% of automotive diesel fuel, 

 5-40% of marine diesel fuel (CONCAWE, 1985), and 10-30% of diesel 

 fuel No. 2 (Block et al., 1991). Table 2 shows the specifications of 

 commercial diesel fuels in this regard. 

 Table 1. Synonyms and trade names of commercial diesel fuels 

 

 Name CAS CAS Registry Range of Synonyms 

 name number carbon 

 numbers 

 Diesel fuel Diesel oil 68334-30-5 C9-C20a Auto diesel, automotive 

 (general) C10-C28b diesel oil, DERV, diesel, 

 diesel fuel oil, diesel 

 oil, gas oil 

 Diesel fuel Not assigned C9-C16c Diesel fuel oil No. 1, 

 No. 1 (essentially C4-C16 (for diesel oil No. 1, No. 1 

 equivalent to wide-cut dieseld

 kerosene, aviation)c

 8008-20-6) 

 Diesel fuel No. 2 68476-34-6 Diesel fuel, diesel fuel 

 No. 2 diesel (applicable for oil No. 2, diesel oil 

 fuel specific No. 2, No. 2 diesele

 viscosity 

 limits) 

 Diesel fuel 68476-31-3 C10-C30f Marine diesel fuel, 

 No. 4 distillate marine diesel 

 fuel 

 

 Adapted from International Agency for Research on Cancer (1989a) and supplemented 

 a From CONCAWE (in press) 

 b From CONCAWE (1985); automotive gas oil (automotive diesel fuel, DERV) 

 c From CONCAWE (1985, 1995) 

 d In Europe, fuels similar to US diesel No. 1 are commonly referred to as 

 'kerosene' or 'Arctic diesel' 

 e Term uncommon in Europe. In the United Kingdom, distillate fuels are frequently 

 categorized as Class A1 (road diesel) and A2 (off-highway diesel) 

 f From CONCAWE (1985); distillate marine diesel 

 

 Only trace quantities of toxicologically relevant benzene, 

 toluene, ethyl benzene, and xylene compounds (for physicochemical 

 properties, see Table 6) are present in diesel fuel No. 2, but 

 significant levels are found in diesel fuel No. 1 (Arctic diesel), 

 which has lower flash-point specifications (Block et al., 1991); the 

 International Agency for Research on Cancer (1989a) cites a 

 flash-point of 0.25-0.5%. The concentration of benzene in kerosenes is 

 < 0.01% by volume; wide-cut aviation kerosenes may have higher 

 levels, but they are usually < 1% by volume (IPCS, 1986; CONCAWE, 

 1995; IPCS, 1993). 

 Table 2. Hydrocarbon specifications of some commercial diesel fuel oils 

 

 Specification Diesel Keroseneb Distillate Diesel 

 fuela marine fueld

 dieselc

 

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 Paraffins/naphthenes 65-95e 78-96 60-90 

 (volume %) (wide-cut 

 aviation, < 1) 

 n-Hexane (volume %) < 0.01 

 (wide-cut 

 aviation, < 1) 

 Saturates (volume %) 59.4-76.6 

 Olefins (volume %) 0-10 0-5 0-10 0.0-1.0 

 Aromatics (volume %) 5-30 4-25 5-40 23.4-39.6 

 (wide-cut 

 aviation, 

 6-25) 

 Aromaticity (weight %) 11-15 

 

 See also Table 1 

 a From CONCAWE (1985, in press); fuel oil similar to diesel fuel (general) 

 b From CONCAWE (1985, 1995); fuel oil similar to diesel fuel No. 1 

 c From CONCAWE (1985, in press); fuel oil similar to diesel fuel No. 4 

 d From German Scientific Association for Petroleum, Natural Gas, and Coal (1991); 

 three samples of diesel fuel (general) 

 e Depending on origin of crude oil 

 

 Alkyl benzenes (particularly C3 and C4) are common components of 

 diesel fuel. Polycyclic aromatic hydrocarbons (PAHs), e.g. 

 naphthalene, phenanthrene, acenaphthene, acenaphthylene, fluorene, 

 fluoranthene, and pyrene, are also present, as are alkyl- and 

 cycloalkyl-substituted homologues of these substances, the predominant 

 ones being naphthalene and its methyl-substituted derivatives (see 

 Table 6 for physicochemical properties) (Block et al., 1991). 

 As some PAHs and the benzene, toluene, ethyl benzene, and xylene 

 components have been shown to be toxic and ecotoxic, these classes of 

 compounds are usually included in analytical procedures for 

 environmental contamination by diesel fuel. The PAH content of diesel 

 fuels varies widely, the highest levels being found in low-quality 

 fuel blended for large users (frequently railroad companies). The 

 mid-range aromatic (and PAH) content of diesel blends is limited by 

 the cetane number specification (Block et al., 1991) (see section 

 A2.1.3). 

 The concentrations of total PAHs in diesel fuel are < 5% by 

 volume, although some marine diesel fuels may contain > 10% by volume 

 (CONCAWE, 1985; International Agency for Research on Cancer, 1989a). 

 In straight-run gas-oil components, which are the major blending 

 material of diesel fuel (see section A3.2.1.1), three-ring PAHs 

 predominate; use of heavier atmospheric vacuum or cracker gas oils in 

 a diesel-fuel mixture leads to an increasing content of four- to 

 six-ring PAHs (CONCAWE, in press). 

 The concentrations of these constituents in a commercial diesel 

 fuel (unspecified) and, for comparison, in No. 2 fuel oil are shown in 

 Table 3. It should be noted that the PAH content of No. 2 fuel oil is 

 not limited by cetane number specification, so that it may include a 

 larger proportion of these hydrocarbons (Block et al., 1991). Table 3 

 also gives the composition of the water-soluble fractions of diesel 

 and No. 2 fuel oils and indicates how the solubility of a compound 

 affects the composition of the fraction and of the whole oil. 

 A2.1.1.4 Sulfur 

 The sulfur content of middle distillates depends on the source of 

 crude oil (Booth & Reglitzky, 1991; CONCAWE, 1995). The sulfur content 

 of most diesel fuels is 0.1-0.5% by weight; it is higher than that of 

 gasoline, which is about 0.02% by weight (Scheepers & Bos, 1992a). 

 Only diesel fuel No. 4 (distillate marine diesel) has a sulfur level 

 > 1% by weight (CONCAWE, 1985, in press). ISO standard 8217 

 (International Standards Organization, 1987) specifies a sulfur 

 content of marine diesel fuel of 1.0-2.0% by weight. 

 The sulfur content of some diesel fuels ranges from 0.01 to > 3% 

 by weight. In Europe (countries of EU and EFTA), the sulfur content is 

 restricted to a maximum of 0.2-0.3% by weight, and, as of 1996, it 

 will be further reduced to 0.05% by weight (European Commission, 

 1993). In the United States in 1988, the maximal sulfur content 

 permitted was 0.5% by weight for diesel fuels No. 1 and 2 and 2.0% by 

 weight for diesel fuel No. 4 (American Society for Testing and 

 Table 3. Concentrations of toxicologically relevant aromatic hydrocarbons in diesel fuel and No. 2 fuel oil and in 10% water-soluble

 fractions prepared from them 

 

 Compound Diesel fuela Diesel fuelb No. 2 fuelc No. 2 fueld Water-soluble fractions (μg/litre) 

 (% by wt) (% by wt) (% by wt) (% by wt) 

 No. 2 Diesel 

 fueld fuela

 

 Benzene 0.1 > 0.02 0.006-0.008 NR 550 344 

 Toluene 0.7 0.25-0.5 0.01-0.08 NR 1040 777 

 Alkylbenzenese 970 

 Ethylbenzene 0.2 0.25-0.5 0.01-0.08 NR 139 

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 Xylene 0.5 0.25-0.5 0.01-0.08 NR 875 

 Polycyclic aromatic hydrocarbons 

 Naphthalene 0.4 0.273 0.4 840 6.6 

 1-Methylnaphthalene NR NR 0.82 340 66.2 

 2-Methylnaphthalene NR 0.67 1.89 480 108 

 Dimethylnaphalenese NR NR 3.11 240 NR 

 Trimethylnaphthalenese NR NR 1.84 30 NR 

 Fluorenese NR NR 0.36 20 NR 

 Phenanthrenese NR 0.15 0.53 20 NR 

 

 NR, not reported 

 a From Dunlap & Beckmann (1988); the analytical method is not described in detail; the concentration of benzene seems to be 

 unusually high. 

 b From International Agency for Research on Cancer (1989a); according to CONCAWE (1985), some marine diesel fuels may contain 

 more than 10% polycyclic aromatic hydrocarbons. 

 c From Stone (1991); summary of several reports 

 d From Anderson et al. (1974); US National Research Council (1985) 

 e Total of several isomers 

 Materials, 1988); in October 1993, the maximum was reduced to 0.05% by 

 weight (US Environmental Protection Agency, 1992a; American Society 

 for Testing and Materials, 1992). The permitted sulfur level in Brazil 

 is > 3% by weight (A. Sivak, personal communication, 1993). In Japan, 

 the sulfur content of diesel fuels was reduced to 0.2% by weight in 

 1994, and a further reduction, to 0.05% by weight, is under discussion 

 (CONCAWE, 1990a). Blended marine diesel fuel may also contain up to 

 about 15% residual components, i.e. material with an initial 

 boiling-point above about 350°C (CONCAWE, in press). 

 A2.1.2 Fuel additives 

 Only agents that are added to fuels at a concentration < 1% are 

 described as 'additives'. A more appropriate term for substances 

 present at higher concentrations is 'fuel components'. Fuels are 

 treated with additives for a number of reasons (see Table 4 and 

 below); they also differentiate products and determine the trademark 

 quality of commercial fuels (Fabri et al., 1990). 

 A2.1.2.1 Cetane number improvers 

 Cetane number improvers upgrade the ignition characteristics of a 

 base fuel more economically than refinery processes (Fabri et al., 

 1990) (see section A2.1.3). Primary alkyl nitrates (e.g. isooctyl 

 nitrate) are often used to improve cetane number. Polyethyleneglycol 

 dinitrates, although effective at much lower concentrations, have a 

 number of disadvantages, including their price and the fact that they 

 may not improve the performance of fuel in low-compression engines 

 (Russell, 1989). 

 A2.1.2.2 Smoke suppressors 

 Organometallic compounds containing barium, calcium, manganese, 

 or iron have been used to reduce diesel smoke. With barium-based 

 products, 85-95% of the metal is emitted as particulates in the 

 exhaust (Russell, 1989); however, barium and calcium compounds are no 

 longer used. 

 A2.1.2.3 Flow improvers 

 Cold-flow improvers increase the fluidity of the fuel by 

 modifying the growth of wax crystals formed by higher homologues of 

 paraffins at low temperatures. The wax content of diesel fuels is 

 influenced by the origin of the crude oil, the distillation range of 

 the fuel, and the source of blend components (Coley, 1989). 

 Table 4. Diesel fuel additives 

 

 Additive Material Concentration Effect 

 (ppm) 

 

 Ignition improvers, Organic nitratesa Enhancement of self-ignition qualitiesa

 cetane enhancersa

 Smoke suppressors, Organic compounds of Ca, Ba, Reduction of soot; increase in metal 

 combustion enhancersa or (sometimes)Mga sulfate emissionsa

 Detergentsa Amines, imidazolines, Prevention and removal of coke deposits 

 succinimides, etc.b on fuel injector tips, etc.a

 Flow improvers Olefin-ester copolymers 50-500 Interaction with wax crystals and 

 modification of their growth; prevention

 of formation of agglomerates 

 Cloud-point depressors Olefin-ester copolymers About 1000 Depression of cloud-point; prevention of

 formation of agglomerates 

 Wax anti-settlers Modified ethylene-vinyl 100-500c Reduction of crystal size and rate of 

 acetate copolymersc settling; prevention of formation of agglomerates 

 Anti-static agents Not reported Not reported Reduction of building up of charges of 

 static electricity 

 Anti-corrosion chemicals Alkenyl succinic acids and 5-50 Prevention of corrosion or rusting of 

 esters, dimer acids, amine storage tanks, pipelines, and metal fuel

 salts system components 

 

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 Table 4 (contd) 

 

 Additive Material Concentration Effect 

 (ppm) 

 

 Antioxidants Hindered phenols or amines 25-200 Prevention of aging processes 

 Anti-foam agents Silicones Up to 20 Reduction of foaming tendency; reduction

 of risk of ground pollution from oil spills 

 Dehazers Quaternary amine salts 5-50 Reduction of formation of hazes; 

 acceleration of haze clearance 

 Biocides Imines, amines, About 200 Prevention of growth of bacteria and 

 imidazolines, etc. fungi in storage tank bottoms 

 Lubricants Surface-active agents such 50-500 Compensation of lower viscosity of fuels

 as polyfunctional acids and in low-temperature regions 

 derivatives 

 Odour maskers Natural, identical substances, 10-100 Reduction or elimination of smell 

 such as vanillin and terpenesc

 

 From Coley (1989), except as noted 

 a From Organisation for Economic Co-operation and Development (1993) 

 b From Russell (1989) 

 c From Fabri et al. (1990) 

 A2.1.2.4 Cloud-point depressors 

 Diesel fuels must be easily filterable, as wax crystals formed at 

 low temperatures can clog fuel filters. Cloud-point depressors are 

 therefore added (Fabri et al., 1990) which consist of substances with 

 lower cloud-points, e.g. kerosene. Addition of 10% kerosene lowers the 

 cloud-point of diesel fuel by about 2°C. Olefin-ester copolymers 

 depress the cloud-point by 3-4°C but are not currently in commercial 

 use (Coley, 1989). 

 A2.1.2.5 Wax anti-settling additives 

 These additives inhibit the tendency of wax to settle by reducing 

 the crystal size and slowing the settling rate. A five-fold reduction 

 in wax crystal size slows the settling rate by one-twenty-fifth. With 

 increasing temperature, small dispersed crystals redissolve more 

 readily than settled wax (Coley, 1989). 

 A2.1.2.6 Other additives 

 Detergents, including amines, amides, imidazolines, and 

 succinates, are used to reduce injector nozzle fouling. Detergents 

 such as polyalkenyl succinimides also improve fuel stability, 

 resistance to corrosion, and combustion efficiency (Russell, 1989). 

 Antistatic agents lower the risk of building up a charge of static 

 electricity during pumping at high rates at bulk terminals or in 

 large-capacity truck fuel tanks. 

 Other additives used are anti-oxidants (phenols, amines), 

 anti-corrosion chemicals (alkenyl succinic acids, esters, dimer acids, 

 amine salts), anti-foam agents (silicones), dehazers (anti-emulsion 

 agents) (quaternary ammonium salts), biocides, lubricants for cold 

 regions (surface-active polyfunctional acid derivatives), and odour 

 maskers (vanillin, terpenes) (Coley, 1989; Fabri et al., 1990). 

 A2.1.3 Quality of diesel fuels 

 A2.1.3.1 Ignition performance and cetane number 

 The cetane number determines the ignition performance of 

 transport fuels relative to a scale on which methyl naphthalene 

 corresponds to a combustion rate of 0 and cetane to one of 100 

 (Scheepers & Bos, 1992a). The cetane number is calculated by comparing 

 the ignition quality of a fuel with that of two reference fuel blends 

 of known cetane numbers under standard operating conditions (American 

 Society for Testing and Materials method D 613 CFR). A high cetane 

 number improves cold starting and engine durability and reduces noise, 

 fuel consumption, smoke emissions during warm-up, and exhaust 

 emissions (Russell, 1989). In Europe (countries of the EU and EFTA), 

 the minimal cetane number must be in the range 45-49, depending on the 

 climatic conditions (European Committee for Standardization, 1993); 

 cetane numbers are usually 49-53 (CONCAWE, 1987). In the United 

 States, the cetane number must be at least 30 for diesel fuel No. 4 

 and 40 for diesel fuels No. 1 and 2 (American Society for Testing and 

 Materials, 1988, 1992). 

 A2.1.3.2 Density 

 The density of diesel fuel influences engine performance: higher 

 density leads to enrichment of the fuel:air mixture, which results in 

 greater engine power output. Enrichment may, however, increase the 

 particulate content of exhaust gas emissions (Fabri et al., 1990) (see 

 section B3.1.2.2). A density range is specified in fuel standards in 

 some countries (American Society for Testing and Materials, 1992; 

 European Committee for Standardization, 1993). 

 A2.1.3.3 Sulfur content 

 Gas and particle emissions in diesel engine exhaust are 

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 influenced by the sulfur content of the fuel; there is a direct 

 relationship between particle production and sulfur content (Hare, 

 1986) (see section B3.1.2.2). 

 A2.1.3.4 Viscosity 

 Too low a viscosity can lead to wear in the injection pump; too 

 high a viscosity impairs fuel injection and mixture formation (Fabri 

 et al., 1990). In Europe (countries of the EU and EFTA), the viscosity 

 of commercial diesel fuels at a temperature of 40°C must be 

 1.5-4.5 mm2/s (European Committee for Standardization, 1993). In the 

 United States, the permitted ranges of viscosity at 40°C are 

 1.3-2.4 mm2/s for diesel fuel No. 1, 1.9-4.1 mm2/s for diesel fuel 

 No. 2, and 5.5-45.0 mm2/s for diesel fuel No. 4 (American Society 

 for Testing and Materials, 1988, 1992). 

 A2.1.3.5 Cold-flow properties 

 Cloud-point and cold filter plugging point characterize the 

 behaviour of diesel fuels at low temperatures (Fabri et al., 1990). 

 These points are lowered by the addition of cloud-point depressors and 

 by special blending techniques, e.g. increasing the kerosene content 

 of the fuel (see section A2.1.2). 

 Changes in diesel fuel quality have been assessed. Wade & Jones 

 (1984) reported a deterioration in fuel quality with decreasing cetane 

 number and found that a 90% increase in boiling-point led to greater 

 emissions of particulates, nitrogen oxides and PAHs. A decline in 

 diesel fuel quality on the European market was predicted, as the 

 rising demand would lead to greater use of fuels from catalytic or 

 thermal cracking processes (CONCAWE, 1987) (see section A3.2.1.1). A 

 study by the Organisation for Economic Co-operation and Development 

 (1993) indicated an improvement in the quality of diesel fuel in the 

 United States due to a decline in aromaticity. 

 A2.2 Physical and chemical properties 

 Diesel fuel is a brown, slightly viscous, flammable liquid at 

 room temperature (Sandmeyer, 1981). It generally has a kerosene-like 

 odour (Agency for Toxic Substances and Disease Registry, 1995). Its 

 physical and chemical properties are listed in Table 5. 

 The water solubility of diesel fuels varies. The aqueous 

 solubility of crude and fuel oils in the environment is clearly 

 dependent on the salinity of the water and the age of the oil slick 

 (see section A4.1.1) and is of the same order of magnitude as the 

 solubility of fuel oils: at room temperature, 0.37-0.53 mg/litre in 

 sea water (Boehm & Quinn, 1974) and 0.7-11 mg/litre in tap water 

 (Lysyj & Russell, 1974). The solubility of a fuel slick decreases with 

 its age as the concentration of long-chain hydrocarbons increases; the 

 solubility of fresh crude oil is 29.3-32.3 mg/litre, whereas that of 

 weathered crude oil is 0.06-23.2 mg/litre at 25°C (Mackay & Shiu, 

 1976). 

 The physicochemical properties of the toxicologically relevant 

 benzene, toluene, ethyl benzene, xylene and PAH components are given 

 in Table 6. 

 A2.3 Analytical methods 

 Exhaustive identification and quantification of the individual 

 constituents of commercial diesel fuel (see section A2.1) is almost 

 impossible owing to their number and complexity. In most environmental 

 assessments, therefore, the mixture is analysed as total petroleum 

 hydrocarbon (Block et al., 1991). All such methods involve preliminary 

 solvent extraction of the matrix, with e.g. trichlorotrifluoroethane. 

 This step may also extract naturally occurring hydrocarbons, which 

 interfere with the analysis; however, some of these compounds are 

 polar and can be removed on silica gel. Three analytical methods are 

 available: 

 Table 5. Physicochemical properties of diesel fuels 

 

 Property Diesel fuel Diesel fuel Diesel fuel Diesel fuel 

 (general) No. 1 No. 2 No. 4 

 

 Melting-point (°C) - 34a 18a - 29-9a

 Boiling range (°C) 160-190b 145-300 (wide-cut 282-338a 170-420d

 143-384e aviation, 45-280)c 101- > 588a

 193-293a

 Flash-point (°C) > 56b > 21 - < 55 52 (closed cup)a > 56d

 58-66e (wide-cut aviation, > 54 (closed cup)a

 (Pensky-Martens) < 21)c

 38 (closed cup)a

 Autoignition temperature (°C) 177-329a 254-285a 263a

 Density (g/cm3) 0.81-0.90 (15°C)b 0.805 (wide-cut 0.87-0.95 0.87-0.92 (15°C)d

 0.82-0.84 (15°C)e aviation, 0.75-0.801) (20°C) 0.81-0.94 (15°C) 

 (15°C)c 0.81-0.94 1 (20°C) 

 (15°C) 

 Kinematic viscosity (mm2/s) 2-7.4 (40°C)b 1.5-2.5 (wide-cut 2-7.4 (40°C)d

 2.20-3.25 (40°C)e aviation, about 1.1 

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 (20°C)c

 Vapour pressure (kPa) About 40 (40°C)b About 10 (wide-cut 2.83-35.2 2.83-35.2 (21°C)a

 0.04f aviation, 140-210) (21°C)a

 (Reid, 37.8°C)c

 2.83-35.2 (21°C)a

 

 Table 5 (contd) 

 

 Prpoerty Diesel fuel Diesel fuel Diesel fuel Diesel fuel 

 (general) No. 1 No. 2 No. 4 

 

 Water solubility (mg/litre) 1f About 5 (20°C)a About 5 (20°C)a About 5 (20°C)a

 0.2f

 Henry's law constant 4.3 × 103f 6.03-7.5 × 105a 6.03-7.5 × 105a 6.03-7.5 × 105a

 (Pa × m3/mol) (20°C) 

 n-Octanol-water partition 3.3-7.06a 3.3-7.06a 3.3-7.06a

 coefficient (log Kow) 

 Soil sorption coefficient 3.04f 3.0-6.7a 3.0-6.7a 3.0-6.7a

 (log Koc) 

 Diffusion coefficient in air 4.63 × 10-2f

 (cm2/s) 

 Odour threshold (ppm) 0.7a 0.5g

 

 a From Agency for Toxic Substances and Disease Registry (1995) 

 b From CONCAWE (in press); automotive gas oil 

 c From CONCAWE (1985, 1995); kerosenes 

 d From CONCAWE (in press); distillate marine diesel 

 e From German Scientific Association for Petroleum, Natural Gas, and Coal (1991); average of three samples 

 f From Custance et al. (1993); water solubility measured, other data from literature; no further details 

 g From Fraser Williams (Scientific Systems) Ltd (1985) 

 -- Gravimetric detection: determination of the weight of residue 

 remaining after solvent evaporation. Although this method is 

 useful for measuring gross contamination, it cannot be used in 

 trace analysis. 

 -- Infrared detection: the absorbance of petroleum hydrocarbons is 

 detected in a solvent matrix at the maximal value, near 

 2930 cm-1. This carbon-hydrogen bond stretching absorbance is 

 directly related to the hydrocarbon concentration in the extract. 

 The results are dependent on the hydrocarbon standard used for 

 quantification. 

 -- Gas chromatographic detection: capillary gas chromatography 

 combined with flame ionization or mass spectrometric detection. 

 The gravimetric and infrared techniques are fast, relatively 

 simple and widely accepted by regulatory authorities; however, they do 

 not provide sufficient qualitative and quantitative information on 

 composition. Gas chromatography is therefore the standard procedure 

 used to identify and quantify fuel constituents in environmental 

 samples. Different distribution and degradation processes in 

 environmental compartments (see section A4) mean that the composition 

 of petroleum hydrocarbons in air, water, soil, and biota may differ 

 considerably from that of the original fuel. Newton et al. (1991) 

 developed an analytical method for identifying and quantifying traces 

 of diesel contamination in tinned fish products on the basis of the 

 n-alkane pattern. 

 Because of the suspected toxicity of aromatic components in 

 diesel fuel, a detailed analysis is often necessary. Two groups of 

 compounds are detected: 

 -- volatile aromatic compounds: Analysis of these minor components 

 of diesel fuel requires special enrichment techniques, such as 

 purge-trap gas chromatography, and methods of detection including 

 flame ionization and mass spectrometry. 

 -- PAHs: Gas chromatography with flame ionization or mass 

 spectrometric detection, or liquid chromatography, is used after 

 solvent extraction. As PAHs are poorly resolved from the diesel 

 fuel matrix, gas chromatography-mass spectrometry is necessary in 

 most cases to quantify the components. The target analytes of 

 commonly used analytical methods do not, however, include C3

 and C4 alkyl-substituted benzenes or most alkyl-substituted 

 PAHs in diesel fuels. 

 Table 6. Physicochemical properties of aromatic components of diesel fuel 

 

 Aromatic compound Water solubility Henry's law constant Diffusion coefficient (cm2/s) Octanol-water partition 

 (mg/litre) (Pa × m3/mol) In air In water coefficient (log Pow) 

 

 Benzene 1791 550 0.087 9.8 × 10-6 1.99 

 Toluene 534.8 602 0.083 8.6 × 10-6 2.52 

 Ethylbenzene 161.0 855 0.076 7.8 × 10-6 2.94 

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 Xylene 156.0 778 0.076 1 × 10-5 2.94 

 Polycyclic aromatic 0.067 0.007 0.067 2.12 × 10-6 5.30 

 hydrocarbons 

 

 Adapted from Custance et al. (1993) 

 A2.4 Conversion factors 

 As diesel fuel vapour is a complex mixture of gases, it is 

 impossible to give a conversion factor for converting parts per 

 million in the gaseous phase to SI units. 

 A3. SOURCES OF HUMAN AND ENVIRONMENTAL EXPOSURE

 A3.1 Natural occurrence 

 Diesel fuels are derived from crude oil, which can be considered 

 a 'natural product'. Nevertheless, human and environmental exposure 

 results almost exclusively from anthropogenic activities. 

 A3.2 Anthropogenic sources 

 A3.2.1 Production and use 

 A3.2.1.1 Production process 

 Diesel fuel is produced during the refining of crude oils but is 

 generally blended to meet the specifications for technical 

 performance. The blending components may be produced by atmospheric 

 distillation of crude oil (straight-run atmospheric gas oil), vacuum 

 distillation of atmospheric residue (vacuum gas oil), thermal cracking 

 (thermally cracked gas oil), or catalytic cracking processes (e.g. 

 light catalytically cracked gas oil; cycle oil). The main components 

 are straight-run gas oils: 80% of European automotive diesel fuel is 

 made up of these components (Booth & Reglitzky, 1991). Secondary 

 processing of heavier fractions is increasingly necessary in order to 

 meet product demand (CONCAWE, in press). 

 Diesel fuel No. 1 is manufactured by a straight-run distillate 

 process (Agency for Toxic Substances and Disease Registry, 1995); 

 diesel fuel No. 2 is generally made by mixing straight-run and 

 catalytically cracked distillates; and diesel fuel No. 4 is produced 

 by adding blending stocks to distillation residues in order to meet 

 viscosity specifications (International Agency for Research on Cancer, 

 1989a). Further variations are introduced by formulation with 

 additives to improve fuel properties (see section A2.1.2). 

 A3.2.1.2 Use 

 Diesel fuel is widely used as a transport fuel for light- and 

 heavy-duty vehicles; the Organisation for Economic Co-operation and 

 Development (1993) classifies vehicles weighing < 3.5 t as light-duty 

 and those weighing > 3.5 or, occasionally, > 5 t as heavy-duty. 

 Diesel fuel No. 1 is suitable for engines that undergo frequent 

 changes in speed and load (Agency for Toxic Substances and Disease 

 Registry, 1995). Heavier grades (diesel fuels No. 2 and 4) are used 

 for trucks, railroad and marine diesel engines, and stationary engines 

 in continuous high-load service (Sandmeyer, 1981; International Agency 

 for Research on Cancer, 1989a). Diesel fuels are also used in 

 stationary gas turbines, e.g. to generate electric power during 

 peak-load periods. Residual fuel oils, such as diesel fuel No. 4, are 

 used to generate steam in electric power plants (International Agency 

 for Research on Cancer, 1989a), in commercial and industrial burner 

 installations without preheating facilities, in plants and factories 

 for space and water heating, for pipeline pumping, and in gas 

 compression; they are also sprayed on unmade roads to compact the 

 surface and are used in the manufacture of asphalt cement (Agency for 

 Toxic Substances and Disease Registry, 1995). 

 A3.2.1.3 Production and consumption levels 

 The demand for diesel fuel has increased worldwide over time. In 

 1990, world demand was about 1100 kt/day (Booth & Reglitzky, 1991). 

 The production and consumption of diesel fuel in different regions 

 over time are shown in Table 7. 

 Diesel-fuelled passenger cars are relatively common in western 

 Europe. The percentages of passenger cars with diesel engines in 

 various European countries over time are shown in Table 8. In many 

 European countries, taxi-cabs are equipped almost exclusively with 

 diesel engines. In 1985, diesel-fuelled heavy-duty trucks comprised 

 about 86% of the fleet in Norway, 89% in Denmark, 95% in Sweden, and 

 100% in the former Federal Republic of Germany. In some countries of 

 Europe, diesel fuel consumption has increased steadily over the last 

 decade, and consumption for heavy-duty vehicles is predicted to more 

 than double between 1980 and 2005 (Organisation for Economic 

 Co-operation and Development, 1993). In western Germany, diesel fuel 

 consumption was almost 60% higher in 1990 (about 5100 kt) than in 1984 

 (about 3200 kt) (Federal Ministry for Transport, 1992). 

 Diesel-fuelled passenger cars are less common in North America. 

 In the United States in 1986, about 1.6% of passenger cars were 

 diesel-fuelled, and the tendency was predicted to decrease slightly 

 (US Department of Energy, 1988). In contrast, 82% of heavy-duty trucks 

 were diesel-fuelled in 1985 (Organisation for Economic Co-operation 

 and Development, 1993), and 59300 kt of diesel fuel were consumed by 

 highway traffic in 1986, representing 14.8% of all the highway fuel 

 used and about one-half of United States diesel fuel consumption. 

 On-road use of diesel fuel was predicted to increase to 15.5% of all 

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 highway fuel (66600 kt) in 1995. A difference in fuel use patterns is 

 seen between light- and heavy-duty vehicles. In 1986, about 4000 kt 

 were used by passenger cars and light trucks, with an estimate of 

 about 2300 kt for 1995, whereas in 1986 about 55300 kt were used by 

 heavy-duty trucks, with an estimate of 64300 kt for 1995 (US 

 Department of Energy, 1988). In Canada, only about 1% of passenger 

 cars are equipped with diesel engines. In 1992, 14126 kt of diesel 

 fuel were produced; 13508 kt were sold for domestic purposes (heating) 

 and about 10849 kt for on-road use (Thomas, personal communication, 

 1994). 

 The percentage of diesel-fuelled vehicles is increasing in Japan 

 (Table 9). 

 Table 7. Production and use of diesel fuel (including gas oils in 

 Europe) in different regions, and development over time 

 

 Region Production/ 1975 (kt) 1980 (kt) 1985 (kt) 

 Use 

 United States Production 134 967 138 323 135 181 

 Use 133 300 136 161 130 297 

 Canada Production 19 187 

 Use 19 130 

 OECD (all 24 Production 370 240 408 848 372 728 

 countries) Use 380 181 403 642 386 081 

 OECD (Europe) Production 173 474 

 Use 190 960 

 European Union Production 152 091 

 Use 163 132 

 Australia, Japan, Production 44 886 

 New Zealand Use 45 694 

 

 Adapted from International Agency for Research on Cancer (1989a); 

 OECD, Organisation for Economic Co-operation and Development 

 A3.2.2 Emissions during production and use 

 A3.2.2.1 Air 

 No data are available on emissions during the production and use 

 of diesel fuel. Release to the atmosphere during production in the 

 refining process is unlikely, as closed systems are used, but 

 volatilization may occur during storage and transport. Diesel fuel may 

 be released into the atmosphere as a result of spills during storage 

 and transport and at filling stations during bulk storage and vehicle 

 tank filling. The low-relative-molecular-mass constituents 

 (short-chain alkanes, benzene, toluene, ethyl benzene, and xylene 

 compounds) are the most likely to evaporate under environmental 

 conditions. 

 Table 8. Percentage of diesel passenger cars in western Europe, and 

 development over time 

 

 Country Diesel passenger cars (%) 

 1984 1988 1991 1992a

 

 France 15.8 21.1 25.5 38 

 Germany (without former 16.9 15.1 15.3 14.9 

 German Democratic Republic) (1993)b

 Germany (without former About 8 13.6 13 

 German Democratic Republic)c

 Italy 18.7 11.9 7.4 NR 

 Spain (without station wagons) 15.3 10.5 14.6 NR 

 United Kingdom 1.1 4.5 11.3 12.5 

 United Kingdomd NR 5 9 19 (1993) 

 

 Adapted from American Automobile Manufacturers Association (1993), 

 unless otherwise stated; NR, not reported 

 a From Menne et al. (1994) 

 b With the former German Democratic Republic 

 c From German Institute for Scientific Research (1993) 

 d From Quality of Urban Air Review Group (1993) 

 Table 9. Percentage of diesel-fuelled vehicles in Japan and 

 development over time 

 

 Year Passenger cars (%) Trucks (%) Buses (%) 

 1984 3.8 23.7 49.5 

 1988 5.8 28.5 63.2 

 1991 8.3 40.7 81.7 

 

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 Adapted from American Automobile Manufacturers Association (1993) 

 A3.2.2.2 Water 

 No data are available on effluents and emissions during diesel 

 fuel production. Diesel fuel oils may be released to surface waters as 

 a result of leakage from storage tanks or tankers (see section 

 A3.2.3). In the United States, the total volumes of spills of diesel 

 fuel oils in 1991 were (Agency for Toxic Substances and Disease 

 Registry, 1993): diesel fuel No. 1, 10.6 t (20 notations); diesel fuel 

 No. 2, 8.9 t (28 notations); and diesel fuel No. 4, 39.3 t (35 

 notations). 

 Groundwater can be contaminated with diesel fuel constituents by 

 leakage from underground bulk storage tanks, but quantitative data are 

 lacking. In the Province of New Brunswick, Canada (Thomas, personal 

 communication, 1993), of a total of 671 gasoline, diesel, and fuel oil 

 tanks examined in 1987, 11% leaked diesel or fuel oil; in 1989, 6% of 

 1085 tanks had leaks; and in 1991, 13% of 539 tanks leaked fuel. No 

 data were available about the amounts leaked, and diesel contamination 

 was determined on the basis of a cluster of 'middle-range peaks' 

 detected by gas chromatography. 

 On the basis of chronic petroleum inputs to sediments of 

 Narragansett Bay and Rhode Island Sound, United States, Van Vleet & 

 Quinn (1978) estimated that about 200 kt of petroleum hydrocarbons may 

 be released to surface waters worldwide from municipal treatment 

 plants. The precise source of the inputs cannot be verified in most 

 cases, but they are due, for example, to accidental discharge to sewer 

 systems, disposal of used crankcase and lubricating oils, oil washed 

 from roads, and atmospheric deposition of hydrocarbons. 

 No data were available from other countries. 

 A3.2.2.3 Soil 

 Diesel fuels may be released to soil as a result of accidental 

 spills (see section A3.2.3) and leakage from storage tanks or 

 pipelines. Diesel-contaminated soil is a major problem in railroad 

 yards, where diesel fuel is used in locomotives and as a solvent to 

 clean moving metal parts (the remaining paraffins give a waxy 

 anti-corrosive coat). Spillage during refuelling, engine maintenance, 

 and steam cleaning, leakage from fuel storage tanks, and absorption of 

 diesel fuel on sand used for traction are other possible sources of 

 soil contamination (Dineen, 1991); however, no quantitative data are 

 available. 

 A3.2.3 Accidental releases to the environment 

 Data on the accidental release of diesel fuels are summarized in 

 Table 10. The effects on the environment depend on both the amount and 

 environmental conditions. 

 Table 10. Diesel fuel spills and their effects on the environment (see also section A9.2) 

 

 Year Place Amount (t); type Effects Reference 

 of diesel fuela

 

 Aquatic environment 

 1972 North of Puget Sound, > 600; diesel fuel Substantial mortality of some intertidal taxa; Woodin et al. (1972) 

 Washington State, USA No. 2 larval recruitment within six months 

 1973 East Lamma Channel 2000-3000; Almost total kill of meiofauna within four days; Wormald (1976); 

 near Hong Kong diesel fuel No. 4 heavy mortality among bivalves and molluscs, Stirling (1977) 

 Nerita albicilla and Monodonta labio, and in 

 marine fish farms; almost no effect on 

 Clypeomorus humilis or Planaxis sulcatus 

 1978 Svea, Mijenfjord, Norway 111 Most fuel trapped in ice; transport out of fjord Carstens & 

 during break-up; heavy mortality among shoreline Sendstad (1979) 

 invertebrates in some regions of fjord 

 1983 Yaquina Bay, Oregon, About 240 (with Decline in population of Rhepoxynius abronius Kemp et al. (1986) 

 USA Bunker C oil) by 75%; influence of spill not clear 

 1984 Queen Charlotte 130 (plus 30 t Low fuel levels in water during flood tide, high McLaren (1985) 

 Islands, Canada gasoline) levels during ebb as diesel was retained in 

 sediment; high mortality among barnacles 

 

 Table 10 (contd) 

 

 Year Place Amount (t); type Effects Reference 

 of diesel fuela

 

 1987 Macquarie Island, 230; diesel fuel High mortality among one species of holothuroid, Pople et al. (1990) 

 Australia No. 4 one of isopod, one of limpet, and one of chiton; 

 decreased populations of crab, two species of 

 starfish, and gastropod; small number of dead 

 algae; slow recovery of organisms 

 1989 Arthur Harbor, 510; diesel fuel High mortality among limpets; partial recovery one Kennicutt et al. 

 Antarctica No. 1 year after spill; small effect on macroalgae (1991a,b,1992a,b) 

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 Terrestrial environment 

 1983 San Bernadino County, 3 Hydrocarbon contamination up to 1500 mg/kg; Frankenberger et al. 

 CA, USA plume migrating towards surface water; in-situ (1989) 

 bioremediation (see also section A3.2.4) 

 NR Califonia, USA 193; diesel fuel Contamination at 6-34 m below surface; Peters et al. (1992) 

 No. 2 hydrocarbon levels at 18.3, about 1500 mg/kg; 

 remediation by flooding with surfactants 

 (see also section A3.2.4) 

 

 aWhen available 

 A4. ENVIRONMENTAL TRANSPORT, DISTRIBUTION, AND TRANSFORMATION

 Few data are available on the environmental fate of diesel 

 fuels, but there are adequate data on the environmental behaviour of 

 individual hydrocarbon components. The transport, distribution, and 

 transformation of crude oils and some fuel oils (e.g. heating oils 

 No. 1 and 2) have been studied, and the mechanisms of distribution and 

 transformation are considered to be comparable to those of diesel 

 fuel. 

 The calculated half-lives for the toxicologically relevant PAH 

 components are listed in Table 11. 

 A4.1 Transport and distribution between media 

 Diesel fuels are released into the environment mainly during 

 storage, transport, and use (see section A3.2.3). The hydrosphere and 

 geosphere are the affected compartments. 

 A4.1.1 Evaporation from and dissolution in the aqueous phase 

 Oils and fuels spilled on water spread out almost immediately; 

 polar and low-relative-molecular-mass components dissolve and leach 

 out of the slick; and volatile components evaporate from the water 

 surface. With the start of microbial degradation the pattern of 

 substances changes, as was observed, for example, after a major oil 

 spill off the French coast (Atlas et al., 1981). The sum of these 

 processes is known as chemical and biological 'weathering'. At the 

 same time, the oil is emulsified to oil-in-water and water-in-oil 

 ('mousse') emulsions (Atlas & Bartha, 1973). In laboratory experiments 

 with several diesel fuels, however, stable mousses were not formed at 

 any temperature (US National Research Council, 1985). Experiments 

 with South Louisiana crude oil showed that the evaporation rate was 

 more than twice the dissolution rate (Harrison et al., 1975). The loss 

 by evaporation of oil spread on water, which in oil spills amounts to 

 about 25% of the total released mass, is generally dependent on the 

 following factors (US National Research Council, 1985): 

 -- the exposed area, which increases with time as the film spreads; 

 -- the oil-phase vapour pressures, which decrease with time as the 

 low-relative-molecular-mass components evaporate. Components 

 with vapour pressures higher than that of n-octane evaporate 

 rapidly from the surface of spilled fuel oil, while those with 

 vapour pressures lower than that of n-octadecane persist and 

 form a viscous residue that retards the volatilization of other 

 constituents (Regnier & Scott, 1975); 

 -- the oil-air mass transfer coefficient, which depends on wind 

 speed and hydrocarbon diffusivity (for the diffusion coefficient 

 in air, see section A2.2, Table 5); 

 -- diffusion barriers, such as emulsions, or formation of a 'skin' 

 on the surface. Many surface waters have a thin layer of organic 

 material of natural origin on the surface, and these films may 

 reduce spread and volatilization, altering the persistence and 

 concentration of the oil in water (Edgerton et al., 1987). 

 Table 11. Calculated half-lives of polycyclic aromatic hydrocarbon 

 components in environmental compartments 

 

 Component Air Water Soil Sediment 

 Naphthalene 1 day 1 week 2 months 8 months 

 Acenaphthalene 2 days 3 weeks 8 months 2 years 

 Fluorene 2 days 3 weeks 8 months 2 years 

 Phenanthrene 2 days 3 weeks 8 months 2 years 

 Anthracene 2 days 3 weeks 8 months 2 years 

 Pyrene 1 week 2 months 2 years 6 years 

 Fluoranthene 1 week 2 months 2 years 6 years 

 Chrysene 1 week 2 months 2 years 6 years 

 Benz[a]anthracene 1 week 2 months 2 years 6 years 

 Benzo[a]fluoranthene 1 week 2 months 2 years 6 years 

 Benzo[a]pyrene 1 week 2 months 2 years 6 years 

 Perylene 1 week 2 months 2 years 6 years 

 Dibenz[a,h]anthracene 1 week 2 months 2 years 6 years 

 

 Adapted from Mackay et al. (1992) 

 On the basis of the constant of Henry's law (see section A2.2, 

 Table 5) and the classification of Thomas (1990), diesel fuels can be 

 considered to volatilize significantly from the aqueous phase. The 

 constant may change during volatilization, as the composition of the 

 mixture changes with time. Lockhart et al. (1987) observed a clear 

 decrease in the hydrocarbon composition of the 50% water-soluble 

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 fraction of diesel fuel in open-aerated test cylinders. Within 48 h, 

 the concentration of hydrocarbons with a very low boiling-point 

 (< 115°C) decreased from 0.73 to 0.04 mg/litre and that of 

 hydrocarbons with a low boiling-point (115-270°C) from 3.2 to 

 0.17 mg/litre. Under sealed or open non-aerated conditions, there were 

 only minor changes. Regnier & Scott (1975) showed that n-decane 

 volatilizes from diesel fuel with a half-life of 1.65 h at 30°C, 

 whereas the half-life was 9.67 h at 5°C in a darkened chamber with a 

 constant wind speed of 21 km/h. Edgerton et al. (1987) reported that 

 diesel fuel spilled on ice had lost only 2-4% of its lightest fraction 

 after 10 days. 

 Dissolution of spilled oils and fuels in water is less important 

 from the viewpoint of mass loss than the ecotoxic effects of the 

 mixture. Lysyj & Russell (1974) conducted long-term experiments (42 

 days) on the dissolution of different fuel oils and gasoline in water. 

 After a period of stable concentration, during which physical 

 dissolution was probably the main mechanism for oil-to-water transfer, 

 the dissolution of organic compounds accelerated, probably because of 

 chemical modification by oxidation or microbial action of the 

 water-insoluble petroleum fraction. 

 Under equilibrium mass-transfer conditions, the levels of PAHs 

 (naphthalene and its methyl derivatives, acenaphthene, fluorene, 

 phenanthrene, anthracene, and fluoranthene) in the water phase in 

 contact with commercial automobile diesel fuel were about four to six 

 orders of magnitude lower than those in the diesel fuel itself, i.e. 

 in the low microgram per litre range. The concentrations of these 

 constituents were likely to be smaller under non-equilibrium 

 conditions but might be higher in the presence of surfactants, 

 emulsifiers, or co-solvents (Lee et al., 1992). When No. 2 fuel oil 

 and kerosene were placed in contact with drinking-water for 17 h, 

 although each fuel contained about 50% by weight of aliphatic 

 hydrocarbons, the water-soluble fractions contained primarily aromatic 

 compounds: total, > 93% by weight; proportion of benzene and 

 substituted derivatives, 19.4% by weight in No. 2 fuel oil and 53.2% 

 by weight in kerosene (Coleman et al., 1984). The chemical composition 

 of the water-soluble fractions of No. 2 fuel oil is compared with that 

 of the whole oil in Table 3. 

 During chemical weathering, other changes in composition (e.g. 

 autoxidation of n-alkanes) may occur that are not necessarily 

 associated with a net mass loss (Davis & Gibbs, 1975). 

 A4.1.2 Transport in and adsorption onto soil and sediment 

 A4.1.2.1 Soil 

 The movement of diesel fuel through soil is directly correlated 

 with its kinematic viscosity (see section A2.2, Table 5). As the 

 viscosity is about one-half that of water and about one-fourth to 

 one-fifth that of gasoline, the rate of percolation of water into soil 

 is about twice and that of gasoline about four to five times that of 

 diesel fuel (Stone, 1991). The retardation coefficient (Rd) is an 

 indicator of the migration of substances into groundwater. In the 

 aqueous phase, the maximal rate of movement of dissolved compounds is 

 that of groundwater, which is represented by an Rd of 1. Stone (1991) 

 calculated the Rd from the adsorption isotherms of individual diesel 

 constituents, and derived the following classification: 

 -- low mobility (Rd > 100): fluorene, phenanthrene, pyrene, 

 benzanthracene, benzo[ a]pyrene, fluoranthene; 

 -- medium mobility (100 > Rd > 10): naphthalene, dimethylbenzenes, 

 ethylbenzene, toluene; 

 -- high mobility (Rd < 10): benzene, quinoline, cresols, phenol. 

 In effect, soil contaminated with diesel fuel acts like a 

 chromatographic column, separating individual constituents by their 

 adsorption. Experimental data on the adsorption of diesel fuels on 

 soils and their transport are not available; however, the movement of 

 a synthetic kerosene through a clay-sand soil was dependent on the 

 moisture content. With increasing moisture content, the penetration 

 rate of nonvolatile components through the soil increased and the 

 adsorption of more volatile components decreased. In contrast, upward 

 mobility of the individual constituents (both volatile and 

 nonvolatile) of the fuel decreased with increasing moisture content. 

 In fully water-saturated soil, upward transport of kerosene was 

 completely inhibited (Acher et al., 1989). Desorption of a simulated 

 kerosene applied to three types of soil with the same moisture content 

 but different contents of organic matter was found to be complete 

 after 30 days under environmental conditions. The slowest desorption 

 was from the soil with the highest level of organic matter (Yaron et 

 al., 1989). Transport of kerosene through three types of sand was 

 influenced mainly by volatilization of C9-C13 hydrocarbon 

 constituents; the increase in the viscosity of the kerosene residue 

 was followed by a decrease in the infiltration rate (Galin et al., 

 1990). 

 A4.1.2.2 Sediment 

 In marine environments, oils and fuels are generally delivered to 

 bottom sediments on settling particles. In areas with low 

 concentrations of suspended material (i.e. terrigenous minerals, 

 plankton, detrital particles, resuspended bottom sediments), the rates 

 of hydrocarbon sedimentation would be low (US National Research 

 Council, 1985). 

 No experimental data are available on diesel fuels in sediments. 

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 In laboratory experiments with fuel oil, binding of the hydrocarbon 

 components to clay minerals of marine sediments was shown to be due to 

 physical adsorption of the van der Waals type. The compounds are 

 associated firmly because, once they are incorporated into sediments, 

 desorption to the overlying water is slow. Saturated hydrocarbon 

 constituents of fuel oils were transported slowly to the sediment 

 (Meyers & Quinn, 1973). In studies of a laboratory marine ecosystem to 

 which No. 2 fuel oil was added for 24 weeks, the concentrations in the 

 sediment remained low until 135 days after the start of the 

 experiment. Then, a steep increase was seen, leading to a level of 9% 

 by weight of the total fuel added (i.e. 12% by weight of the total 

 saturated hydrocarbons). The highest concentrations of saturated 

 hydrocarbons were found in the surface flocculent layer; 2-3 cm below 

 the sediment surface, the levels were below the detection limit. The 

 smaller particles (< 45 μm) of water-suspended material seemed to 

 adsorb about twice as much fuel oil as larger particles (> 45 μm) 

 (Wade & Quinn, 1980). In a comparable study in a model marine 

 ecosystem with No. 2 fuel oil, the particulate matter contained 40-50% 

 of the total amount of aliphatic hydrocarbons added and only 3-21% of 

 the aromatic fraction, indicating that most of the aromatic 

 hydrocarbons were dissolved in the water phase (see section A4.1.1) 

 (Gearing et al., 1980). Although biodegradation may remove many of the 

 soluble aromatic hydrocarbons (see section A4.2.2), 10-20% by weight 

 of the fuel oil, consisting primarily of branched alkanes, 

 cycloalkanes, and aromatics, may remain in the upper 2 cm of sediment 

 for over a year (Gearing et al., 1980; Oviatt et al., 1982). 

 A4.2 Transformation and removal 

 A4.2.1 Photooxidation 

 No data were available on the photooxidation of diesel fuel in 

 air or water. In the atmosphere, all evaporated oil components are 

 degraded photochemically by hydroxy radicals and other species within 

 hours or days to carbon monoxide, carbon dioxide, and oxygenated 

 compounds (US National Research Council, 1985; IPCS, 1986, 1993). 

 Under laboratory conditions, No. 2 fuel oil was rapidly photo-oxidized 

 in water. Two photooxidant pools were identified: hydrogen peroxide 

 and a mixture of indane and tetralin hydrogen peroxides, the first 

 being the faster acting (Herbes & Whitley, 1983). Peroxides are formed 

 by two mechanisms: the first is the reaction of free radicals with 

 triplet oxygen to produce peroxy radicals and hydroperoxides, which 

 continue the chain reaction; the second is addition of excited singlet 

 oxygen to reactive acceptors such as olefins. The photodegradation 

 products of fuel oils are phenols, naphthols, and carboxylic acids 

 (Larson et al., 1977, 1979). 

 A4.2.2 Biodegradation 

 A4.2.2.1 Microbial degradation 

 The individual constituents of spilled oil are inherently 

 degradable to varying degrees and at different rates. The n-alkane, 

 n-alkylaromatic, and simple aromatic molecules in the C10-C22

 and the most readily degradable. Smaller molecules are generally range 

 are the least toxic rapidly metabolized, although they tend to be more 

 toxic. Long-chain n-alkanes are more slowly degraded because of 

 their hydrophobicity and also because they are viscous or solid at 

 ambient temperatures. Branched alkanes and cycloalkanes are relatively 

 resistant to attack. PAHs are the compounds most recalcitrant to 

 microbial degradation (Morgan & Watkinson, 1988). 

 A study of the breakdown of heating oils and diesel fuels in a 

 sub-soil demonstrated breakdown rates of 0.014-0.022 g/kg per day, 

 which were slower than the rates of topsoil degradation (Flowers et 

 al., 1984). The mineralization rates for heavy oils, sludges, and 

 crude oils were 0.02-0.6 gram of hydrocarbon per kilogram of soil per 

 day. Under Arctic conditions, the rates were considerably slower. 

 The relative contribution of bacteria and fungi to hydrocarbon 

 degradation is unclear. At acid pH, fungi are clearly more important, 

 but closer to neutrality hydrocarbon contamination tends to enhance 

 bacterial growth. 

 The overall rates of hydrocarbon degradation are limited by: 

 -- temperature (optimal temperature for biodegradation, 30-40°C); 

 -- water content (in soils, water contents of 50-80% capacity are 

 optimal for microbial activity); 

 -- oxygen (the metabolism of both aliphatic and aromatic 

 hydro-carbons normally requires oxygen); 

 -- pH (hydrocarbons are mineralized most rapidly at 6.5-8.0); 

 -- inorganic nutrients (as petroleum contaminants are extremely 

 deficient in nitrogen and phosphorus, a large quantity of carbon 

 sources tends to result in rapid depletion of the available pools 

 of major nutrients, i.e. enhancement of degradation in fertilized 

 soils); 

 -- microbial metabolic versatility (topsoils generally contain many 

 hydrogen-degrading bacteria, typically 105 - 106 per gram, but the 

 content of subsoils is unclear) (Morgan & Watkinson, 1988). 

 A remedial treatment consisting of liming, fertilization, and 

 tilling was evaluated on a laboratory scale for its effectiveness in 

 cleaning up a sand, a loam, and a clay-loam soil contaminated at 

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 50-135 mg/g of soil by diesel and other oils. The disappearance of 

 hydrocarbons was maximal at 27°C (Song et al., 1990). 

 In sandy soils, 50-85% of the hydrocarbons were degraded within a 

 few weeks, depending on the experimental conditions. Degradation 

 efficiency increased with additional soil inoculation (Grundmann & 

 Rehm, 1991). 

 Frehland et al. (1992) examined the substrate specificity and 

 growth conditions of nine bacterial strains on samples of 

 diesel-contaminated soil under different conditions. The 

 biodegradative properties of Pseudomonas spp. were superior (59, 60, 

 and 80% in three samples) than those of Micrococcus, Bacillus, 

 Acinetobacter, and other species tested. 

 A4.2.2.2 Phytoplankton and marine algae 

 Unicellular algae can take up and metabolize both aliphatic and 

 aromatic hydrocarbons, but the extent to which this occurs in nature 

 is poorly understood. The ability to metabolize naphthalene is 

 widespread (US National Research Council, 1985). 

 A4.2.2.3 Invertebrates and vertebrates 

 Unlike microorganisms, which use petroleum as a source of carbon, 

 animals generally oxidize and conjugate products to render them more 

 soluble and therefore easier to excrete. All animal groups tested can 

 take up petroleum hydrocarbons, either through the body surface, 

 across respiratory surfaces, or via the gut, the route varying with 

 the organism and its feeding habits. In copepods (Calanus

 helgolandicus), dietary uptake was more important than that from 

 water (Corner et al., 1976), but aromatic hydrocarbons accumulated by 

 the polychaete Neanthes arenaceodentata were derived from water and 

 not from sediment (Rossi, 1977). Hydrocarbons are stored in lipid-rich 

 tissues. The principal route of metabolism of hydrocarbons by 

 metazoans is conversion of lipophilic compounds by cytochrome 

 P450-dependent monooxygenases or mixed-function oxidases to 

 derivatives that are more water-soluble. Mixed-function oxygenase 

 activity has been found in all fish species studied. Lee (1981) 

 reported 18 marine invertebrate species belonging to four phyla 

 (Annelida, Arthropoda, Echinodermata, and Mollusca) that are known to 

 contain mixed-function oxidase activity in the hepatopancreas, 

 digestive gland, and other tissues. Sea birds and some other waterfowl 

 also have cytochrome P450 systems, but few estimates have been made of 

 their capacity for hydrocarbon metabolism. Some crude oils, PAHs, and 

 refined petroleum products are known to induce cytochrome P450 enzymes 

 and to increase the levels of hydrocarbon metabolism in marine and 

 freshwater fish, including embryonic and larval forms and polychaetes 

 (US National Research Council, 1985). Induction is usually described 

 in terms of the rate of metabolism of benzo[a]pyrene in vitro.

 A4.2.3 Bioaccumulation 

 Few data are available on the bioaccumulation of diesel fuel 

 itself, although there is adequate evidence from studies on other oils 

 that aquatic organisms bioconcentrate hydrocarbons. The 

 n-octanol-water partition coefficient (log Pow) for diesel fuel is 

 3.3-7.1 (see section A2.2, Table 5). Although a higher bioaccumulation 

 potential might be expected from these log Pow values, the measured 

 bioconcentration factors are lower than predicted because many 

 compounds of low relative molecular mass, such as substituted 

 benzenes, are readily metabolized, and the actual bioaccumulation of 

 compounds of higher relative molecular mass is limited by their low 

 water solubility and large molecular size. 

 In a continuous-flow system, diesel fuel was taken up by 

 Mytilus edulis mussels exposed for 41 days to a concentration of 

 200-400 μg/litre. The hydrocarbon levels in tissue were about 1000 

 times higher after exposure than before. Depuration was rapid during 

 the first 15-20 days and then decreased rapidly to a minimum (Fossato 

 & Canzonier, 1976). 

 The accumulation of No. 2 fuel oil has been studied in a number 

 of organisms (Lee, 1977). When No. 2 fuel oil (38% aromatics) was 

 added to a commercial shrimp pond, the concentration of naphthalenes 

 in shrimps, clams, and oysters exceeded the level in ambient water 

 after 38 days. Depuration in clean water was complete after 10 days 

 for shrimps and after 47-96 days for oysters (Cox et al., 1975). In a 

 flow-through system to study accumulation of a No. 2 fuel oil-water 

 dispersion, aromatic petroleum hydrocarbons were accumulated at a rate 

 of 89.6 mg/kg tissue by Rangia cuneata (clams) and 311.7 mg/kg by 

 Crassostrea virginica (oysters) during 8 h of exposure. The 

 bioaccumulation factor for methyl naphthalenes in clams was 2.3-26.7 

 and increased with increasing alkylation of the naphthalene ring. 

 Depuration in clean water was complete after 28 days (Neff et al., 

 1976a). The fuel components of a small spill of No. 2 fuel oil had the 

 following biological half-lives in mussels (Mytilus edulis): aliphatic 

 hydrocarbons (C16 and C23), 0.2 and 0.8 days; alkyl naphthalenes 

 (C2 and C3), 0.9 and 1.5 days; phenanthrene, 2.1 days (Farrington 

 et al., 1982). Lobsters exposed to a simulated small spill of No. 2. 

 fuel oil bioconcentrated PAH constituents in the hepato-pancreas and 

 muscle within three to four days after exposure. The levels remained 

 elevated for up to 10-11 days, and depuration was complete after 20-21 

 days. 

 The polychaetous annelid Neanthes arenaceodentata rapidly 

 accumulated 14C-naphthalene (to a biomagnification of 40 times) from 

 solution during exposure for 24 h and slowly released the accumulated 

 hydrocarbons within 300 h after return to clean sea water (Rossi, 

 1977). 

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 Oral administration of South Louisiana crude oil to mallard ducks 

 (Anas platyrhynchus) at a dose of 5 ml daily led to detectable 

 aromatic petroleum hydrocarbon levels in each of the tissues examined: 

 liver, breast muscle, heart muscle, skin, brain, uropygial gland, and 

 blood. The skin and the underlying adipose tissue had accumulated far 

 more aromatic hydrocarbons than other tissues. The individual 

 components did not accumulate in the same relative concentrations as 

 in the crude oil, suggesting different uptake and/or metabolism; two- 

 and three-membered, condensed ring aromatic compounds were accumulated 

 to a greater extent than alkylbenzenes (Lawler et al., 1978). 

 A4.2.4 Tainting 

 Tainting (unpleasant off-flavours) of various aquatic organisms 

 by petroleum hydrocarbons has been reported, and diesel fuel has been 

 suspected of tainting fish in freshwater rivers. Mackie et al. (1972) 

 reported tainted rainbow trout up to at least nine days after a spill 

 of diesel fuel into water (Six Mile Water, Ireland). Ackman & Noble 

 (1973) described tainting of whitefish in the Athabaska River, Canada, 

 which was attributed to diesel fuel from a railroad yard. 

 A4.2.5 Entry into the food chain 

 No data are available on the effect of diesel fuel on the food 

 chain. The effects of petroleum compounds on the marine food web have 

 been studied, e.g. on zooplankton Calanus helgolandicus (Corner et 

 al., 1976), on phytoplankton (Mahoney & Haskin, 1980), and on 

 freshwater crayfish, one of the primary foods of waterfowl (Tarshis, 

 1981). In a study in situ on the distribution, biotransformation, and 

 flux of PAHs in the aquatic food chain (seston --> mussel [ Mytilus

 edulis] --> eider duck [ Somateria molissima]), the PAH composition 

 changed significantly (Broman et al., 1990). The theoretical 

 inhalation of atmospheric PAHs was insignificant in comparison with 

 exposure from food. PAHs were biotransformed relatively rapidly. Their 

 concentrations did not increase with increasing trophic level. 

 A4.3 Ultimate fate after use 

 A4.3.1 Use in motor vehicles 

 Diesel fuel is combusted in motor vehicles and stationary engines 

 (see section A3.2.1.2). The resulting exhaust is discussed in Part B. 

 A4.3.2 Spills 

 The fate of diesel fuel after accidental spills is eventual 

 degradation by abiotic and biotic processes (see section A3.2.3) 

 A4.3.3 Disposal 

 In general, incineration is recommended for fuel oils (Fraser 

 Williams (Scientific Systems) Ltd, 1985). This procedure is also 

 useful for disposing of fuel production wastes. 

 Because diesel fuel is released during use, mainly accidentally 

 into water or onto soil (see sections A3.2.2.2, A3.2.2.3, and A3.2.3), 

 the affected compartments may have to be remediated. In general, oil 

 spills on beaches and into surface waters can be treated by burning 

 off; absorption onto straw, polyurethane foam, activated carbon, or 

 peat; or addition of sinking agents, gelling agents, or dispersants. 

 Mechanical systems can also be used (Fraser Williams (Scientific 

 Systems) Ltd, 1985). Various operations for treating soil affected by 

 diesel fuel have been reviewed (Dineen, 1991) and are as follows: 

 -- Disposal: excavation of contaminated soil and disposal at a 

 regulated landfill; the treatment used most commonly during the 

 last decade; advantageous for small volumes. 

 -- Biodegradation: The natural process of soil microorganisms, 

 which is stopped by a spill as a result of depletion of oxygen or 

 nutrients (mostly nitrogen and phosphorus), is restored by 

 providing sufficient amounts of the depleted substances. The 

 process can be carried out in situ (Frankenberger et al., 1989) 

 (see section A3.2.3, Table 10) or after excavation. 

 Biodegradation is the most widely applicable alternative to 

 landfill disposal, although its duration is uncertain and may be 

 relatively long and a large space is required (see sections 

 A9.1.1.2 and A9.1.3.1). 

 -- Thermal treatment: incineration of contaminated soil e.g. in 

 cement kilns or in specially designed thermal units, where the 

 soil is baked to remove the fuel, which is subsequently oxidized 

 (thermal desorption). The thermal desorption process is also 

 feasible in situ. In cement kilns, the desorbed diesel fuel is 

 used for heating the kiln, and the soil is incorporated into the 

 cement mixture. 

 -- Road base: The contaminated soil is spread on roads under 

 construction and is compacted and oiled before paving. If the 

 affected soil has a high proportion of expandable clays, it may 

 not be suitable as a road base. 

 -- Asphalt batching: The contaminated soil replaces part of the 

 sand and gravel component of asphalt; this is possible only if 

 the content of expandable clays is not too high. 

 -- Chemical oxidation: A strong oxidant, usually hydrogen 

 peroxide, in combination with a silica polymer stabilizer to 

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 control the reaction is used to oxidize diesel hydrocarbons to 

 carbon dioxide and water. The reaction is highly exothermic, and 

 uncontrolled volatilization and leaching of some constituents may 

 occur. 

 -- Fixation: addition of a strong base to convert diesel 

 hydrocarbons to organic acids and subsequent treatment with a 

 dissolved silica polymer to effectively encapsulate the acids in 

 amorphous silica; immobilizes diesel fuel in situ and prevents 

 migration into surface or groundwater. The long-term stability of 

 the immobilized chemicals is, however, unknown. 

 -- Soil washing: Diesel fuel is washed out of soil by a 

 biodegradable, non-toxic surfactant (Peters et al., 1992). The 

 operation is feasible in situ and after excavation and is 

 particularly effective on materials with a low surface:volume 

 ratio (e.g. gravels and coarse sands). The major disadvantage is 

 the need to collect and treat or dispose of the 

 surfactant-diesel mixture after washing. 

 -- Containment: construction of a low-permeability surface 

 structure ('cap') that prevents infiltration of rain, snow, and 

 other moisture that could lead to leaching of diesel constituents 

 into groundwater. Long-term monitoring of the area of the spill 

 is necessary. 

 A5. ENVIRONMENTAL LEVELS AND HUMAN EXPOSURE

 A5.1 Environmental levels 

 As diesel fuels are complex mixtures of a great variety of 

 hydrocarbons (see section A2.1), general 'environmental levels' cannot 

 be described. The individual constituents of diesel fuels should be 

 detectable in almost all compartments of the environment, but the 

 sources cannot be verified. 

 A5.2 Exposure of the general population 

 Nonoccupational exposure to diesel fuel occurs when fuel tanks 

 are filled manually. The primary source of dermal exposure is 

 accidental spills, although these exposures to high levels are of 

 short duration. Drinking-water can be contaminated by components of 

 petroleum products, including diesel fuel, after leakage into 

 groundwater from underground storage tanks. Specific data are not 

 available on the contribution of diesel fuel components to groundwater 

 contamination. Owing to the low volatility of diesel fuels at normal 

 temperatures, there is little exposure to vapours (International 

 Agency for Research on Cancer, 1989a). 

 A5.3 Occupational exposure during manufacture, formulation, or use 

 Workers are exposed to diesel fuel in a number of occupations, 

 including manual handling and discharge of fuels; loading and 

 unloading of diesel fuel; retailing at filling stations; manufacture, 

 repair, maintenance, and testing of diesel engines and other 

 equipment; use of diesel fuel as a cleaning agent or solvent; and 

 laboratory handling and routine sampling of diesel fuel (CONCAWE, 

 1985). 

 At normal temperatures, low concentrations of vapours are likely 

 to be generated from diesel fuels, owing to their low volatility. Only 

 in confined spaces or at high operating temperatures do significant 

 levels of vapour occur. Hydrogen sulfide gas may evolve from residual 

 fuel oils (CONCAWE, 1985). 

 A6. KINETICS AND METABOLISM IN LABORATORY ANIMALS AND HUMANS

 No quantitative data are available; however, the systemic and 

 local effects observed after exposure to diesel fuels by various 

 routes indicate that they are absorbed dermally, orally, and by 

 inhalation. 

 A7. EFFECTS ON LABORATORY MAMMALS AND IN-VITRO TEST SYSTEMS

 A7.1 Single exposure 

 Diesel fuels have a low order of acute toxicity after 

 administration orally, dermally, or by inhalation. Acute LD50 Table 

 12. In rats and mice, the values after oral or dermal exposure were 

 values are summarized in generally > 5000 mg/kg body weight, and the 

 values in rabbits after dermal exposure were > 2000 mg/kg body 

 weight. Since the physicochemical properties of kerosenes are similar 

 to those of diesel fuels (see also section A2.1), the LD50 values 

 for various types of kerosene are included. 

 Beck et al. (1984) reported an oral LD50 value of 7500 mg/kg 

 body weight (9 ml/kg body weight) for a market-place sample of diesel 

 fuel in male and female rats. Gross necropsy of animals that died 

 during the test showed haemorrhagic gastroenteritis, gastrointestinal 

 tympani, and pneumonia with abscess formation. No deaths were seen 

 among rabbits treated dermally with 5000 mg/kg body weight under an 

 occlusive covering for 24 h. 

 After oral administration of 12 000 mg/kg body weight kerosene to 

 rats, no change was seen in heart weight or in the relative weights of 

 lung, spleen, and kidney. There were no histopathological changes 

 (Muralidhara et al., 1982). Exposure of rats for 8 h by inhalation to 

 about 0.1 mg/litre deodorized kerosene did not induce adverse effects. 

 Four male cats that inhaled 6.4 mg/litre for 6 h showed no toxic 

 effects on the central nervous system or body weight during the 

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 exposure or during a subsequent 14-day observation period (Carpenter 

 et al., 1976). 

 Male Sprague-Dawley rats given JP-5 jet fuel at a dose of 

 18 912 mg/kg body weight (24 ml/kg body weight) orally had 

 vacuolization of periportal hepatocytes and serum enzyme alterations, 

 indicating hepatic damage, within two days (Parker et al., 1981). All 

 male and female B6C3F1 mice treated dermally with 5000-40000 mg/kg 

 body weight marine diesel fuel survived a 14-day observation period 

 (US National Toxicology Program, 1986). 

 Table 12. Acute toxicity (LD50 and LC50 values) of diesel and other fuels 

 

 Fuel Species Route LD50 or Dose Reference 

 LC50

 

 Diesel fuels 

 Diesel fuel (market-place sample) Rat Oral LD50 7500 mg/kg bw Beck et al. (1984) 

 Diesel fuel (market-place sample) Rabbit Dermal LD50 > 5000 mg/kg bw Beck et al. (1984) 

 Home heating oil No. 2a Rat Oral LD50 14 500-21 100 μg/kg bw American Petroleum 

 Institute (1980a,b,c) 

 Home heating oil No. 2a Rabbit Dermal LD50 > 5000 μg/kg bw American Petroleum 

 Institute (1980a,b,c) 

 Marine diesel fuel, JP-5, JP-8 Mouse Oral LD50 > 16 000 mg/kg bw Schultz et al. (1981) 

 shale, or petroleum oila

 Marine diesel fuel, shale, or Mouse Dermal LD50 > 16 000 mg/kg bw Schultz et al. (1981) 

 petroleum oila

 Other fuels 

 Straight-run middle distillateb Rat Oral LD50 > 5000 mg/kg bw American Petroleum 

 Institute (1985a) 

 Hydrodesulfurized middle distillateb Rat Oral LD50 > 5000 mg/kg bw American Petroleum 

 Institute (1982a,b) 

 Straight-run middle distillateb Rabbit Dermal LD50 > 2000 mg/kg bw American Petroleum 

 Institute (1985a) 

 Hydrodesulfurized middle distillateb Rabbit Dermal LD50 > 2000 mg/kg bw American Petroleum 

 Institute (1982a,b) 

 Straight-run middle distillateb Rat Inhalation LC50 1.8 mg/litre American Petroleum 

 Institute (1987a) 

 

 Table 12 (contd) 

 

 Fuel Species Route LD50 or Dose Reference 

 LC50

 

 Hydrodesulfurized middle distillateb Rat Inhalation LC50 4.6 mg/litre American Petroleum 

 Institute (1983a) 

 Light catalytically cracked distillatec Rat Oral LD50 4660 mg/kg bw (m) American Petroleum 

 3200 mg/kg bw (f) Institute (1985b) 

 Light catalytically cracked distillatec Rabbit Dermal LD50 > 2000 mg/kg bw American Petroleum 

 Institute (1985b) 

 Light catalytically cracked distillatec Rat Inhalation LC50 4.7-5.4 mg/litre American Petroleum 

 Institute (1986a,b) 

 Jet fuel Aa Rat Oral LD50 > 25 000 μl/kg bw American Petroleum 

 Institute (1980d) 

 JP-5 shale oild Mouse Dermal LD50 8000 mg/kg bw Schultz et al. (1981) 

 JP-5 petroleum oild Mouse Dermal LD50 11 200 mg/kg bw Schultz et al. (1981) 

 JP-8 shale oila Mouse Dermal LD50 6400 mg/kg bw Schultz et al. (1981) 

 JP-8 petroleum oila Mouse Dermal LD50 8000 mg/kg bw Schultz et al. (1981) 

 Jet fuel Aa Rabbit Dermal LD50 > 5000 μl/kg bw American Petroleum 

 Institute (1980d) 

 Kerosenea Rat Oral LD50 50 000 mg/kg bw Parker et al. (1981) 

 Kerosenea Guinea-pig Oral LD50 16 320 mg/kg bw Deichmann et al. (1944)

 Kerosenea Rabbit Oral LD50 22 720 mg/kg bw Deichmann et al. (1944)

 Straight-run kerosenea Rat Oral LD50 > 5000 mg/kg bw American Petroleum 

 Institute (1985c) 

 Hydrodesulfurized kerosenea Rat Oral LD50 > 5000 mg/kg bw American Petroleum 

 Institute (1982b) 

 

 Table 12 (contd) 

 

 Fuel Species Route LD50 or Dose Reference 

 LC50

 

 Straight-run kerosenea Rabbit Dermal LD50 > 2000 mg/kg bw American Petroleum 

 Institute (1985c) 

 Hydrodesulfurized kerosenea Rabbit Dermal LD50 > 2000 mg/kg bw American Petroleum 

 Institute (1982c) 

 Petroleum-derived hydrocarbona Rat Inhalation LC50 > 5.3 mg/litre American Petroleum 

 Institute (1987b) 

 Petroleum-derived hydrocarbona Rat Inhalation LC50 > 5.2 mg/litre American Petroleum 

 Institute (1983c) 

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 Deodorized kerosenee Rat Inhalation LC50 > 0.1 mg/litre Carpenter et al. (1976)

 (saturation) 

 

 a Hydrocarbon fraction similar to that of diesel fuel (see section A2.1) 

 b Hydrocarbon fractions from which also diesel fuels are gained during petroleum separation (see section A3.2.1.1) 

 c Blending component of diesel fuel 

 d Narrow boiling range 

 e Used as a solvent, not a fuel; very low aromaticity 

 Exposure of Sprague-Dawley rats to an aerosol of diesel fuel at a 

 concentration × time product of 8 mg.h/litre caused less than 1% 

 mortality and was estimated to represent the maximal tolerated 

 exposure. On this basis, 12 mg.h/litre was chosen as the highest 

 concentration in a study of repeated exposure (see section A7.2). 

 After exposure to 0.5 mg/litre for 2 h, a transient depression of the 

 startle reflex was observed. Further findings were a dose-related 

 decrease in respiratory frequency and influx of polymorphonuclear 

 cells into the lungs for several days. In a 6-h inhalation test, the 

 no-observed-adverse-effect level (NOAEL) was 2.7 mg/litre (Dalbey et 

 al., 1982, 1987). 

 A7.2 Short-term exposure 

 A7.2.1 Subacute exposure 

 A7.2.1.1 Dermal exposure 

 Dermal exposure to 0.1 ml/kg body weight per day kerosene for one 

 week was not lethal to male mice. Significant decreases in the 

 relative weights of thymus, spleen, adrenals, and abdominal lymph 

 nodes were observed (Upreti et al., 1989). 

 Eight rabbits (weighing 2.5-3.5 kg) were exposed dermally 

 (occlusive covering, 24 h/day, five days per week, two weeks) to 4 or 

 8 ml/kg body weight per day of a market-place sample of diesel fuel. 

 None of the animals given the low dose died, although there was a 

 weight loss of 0.3 kg, while five animals given the high dose died 

 with a weight loss of 0.5 kg; the control group had a weight gain of 

 0.2 kg. Severe chronic dermal irritation and anorexia were seen, which 

 were followed by cachexia and death (Beck et al., 1984). 

 Three doses between 1 and 10 ml/kg body weight per day of 10, 30, 

 or 50% fuel oil No. 2 were applied to the skin of New Zealand white 

 rabbits. After a 12-day treatment including a two-day rest, acute 

 dermal corrosion was seen in all animals treated with the 10% oil and 

 in animals given 10 ml/kg body weight per day of the 30 or 50% oil. 

 There was histopathological evidence of dermal toxicity in all treated 

 groups (American Petroleum Institute, 1980a,b,c). 

 Application of 8000 μl/kg body weight per day of jet fuel A to 

 four male and four female New Zealand white rabbits for 12 days, 

 including a two-day rest, induced acute dermal corrosion. 

 Histopathological evidence of dermal and hepatic toxicity and 

 hyperplastic changes in the urinary bladder transitional epithelium 

 were seen (American Petroleum Institute, 1980d). 

 Groups of five male and five female New Zealand white rabbits 

 were treated with 200, 1000, or 2000 mg/kg body weight per day of a 

 straight-run distillate, a light catalytically cracked distillate, or 

 two hydrodesulfurized distillates, three times per week for four 

 weeks. Moderate to severe irritation was seen, the degree of skin 

 irritation being directly related to the number of doses applied. 

 Microscopic examination of the skin at the application sites revealed 

 the presence of acanthosis and hyperkeratosis (American Petroleum 

 Institute, 1983a, 1984, 1985a,b). 

 In a study of marine diesel fuel containing 12.7% paraffins, 

 43.7% naphthalenes, and 43.6% aromatic compounds, groups of male and 

 female B6C3F1 mice received dermal applications (with an occlusive 

 covering) of 2000, 8000, 20000, or 40000 mg/kg body weight per day for 

 14 consecutive days. None of the animals at 20000 or 40000 mg/kg body 

 weight per day survived. Skin lesions were observed in all treated 

 groups, which consisted of moderate acanthosis, parakeratosis, and 

 hyperkeratosis. These findings were accompanied by a mixed cellular 

 inflammatory infiltrate in the upper dermis. The NOAEL was 8000 mg/kg 

 body weight per day. In the same study, JP-5 navy fuel containing 

 52.8% cycloparaffins, 30.8% paraffins, 15.9% aromatics, and 0.5% 

 olefins (see also Table 2) was applied at doses of 5000-40000 mg/kg 

 body weight per day for 14 days. All animals at 40000 mg/kg body 

 weight per day and females at 30000 mg/kg body weight per day group 

 died before the end of the study. Body weight loss was observed at 

 doses > 10 000 mg/kg body weight per day. The dermal findings were 

 similar to those in the study of marine diesel fuel. The NOAEL was 

 5000 mg/kg body weight per day (US National Toxicology Program, 1986). 

 A7.2.1.2 Inhalation 

 Rats (strain, age, and sex not specified) were exposed for 

 6 h/day to a droplet aerosol of deodorized kerosene at a mean 

 concentration of 7.7 mg/litre for four days. After a day with no 

 treatment, the skin of the extremities was dry and flakes had formed. 

 The body weight remained unchanged (Carpenter et al., 1976). 

 CD-1 mice were exposed for 8 h/day for five days to uncombusted 

 diesel vapour at concentrations of 0.065, 0.135, or 0.204 mg/litre. 

 The dose-response for neurotoxicity (measured by square-box activity) 

 was 50% of the control level at the high dose, 100% at the medium 

 dose, and 150% at the low dose. A drastic deterioration of motor 

 coordination was seen at the high dose in the rotarod test. In the hot 

 plate test, increased sensitivity followed by tolerance was seen at 

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 the high dose, a slight increase at the medium dose, and a substantial 

 increase at the low dose; normalization occurred in all groups within 

 24 h. No effects were seen in the inclined plane test or the corneal 

 reflex test. Vasodilatation, poor grooming, and tremors were 

 described. In general, the most obvious effects were on the nervous 

 system, diesel fuel acting as a neurodepressant (Kainz & White, 1982, 

 1984). 

 Dalbey et al. (1982, 1987) investigated the toxic effects of 

 diesel fuel aerosols to assess the health risks of their military use 

 as smoke screens. Groups of male and female Sprague-Dawley rats were 

 exposed to concentrations of 1.3-6 mg/litre for 2 or 6 h, one or three 

 times per week, for a total of nine exposures; 12 mg.h/litre was 

 chosen as the highest concentration-time product that caused 6.25% 

 mortality. A significant depression of body weight and a slower growth 

 rate were seen initially, and liver weights were significantly 

 decreased. No neurotoxicity was seen. Histologically, there was focal 

 accumulation of free pulmonary cells and increased numbers of 

 leukocytes in bronchial lavage fluid. In pulmonary function tests, a 

 non-dose-dependent change in lung volume was seen, involving a 

 decrease in total and vital capacity and increases in functional 

 residual capacity and residual volume. No other organs were affected. 

 Groups of 20 male and 20 female Sprague-Dawley rats exposed by 

 inhalation to 0.025 mg/litre of one of three hydrodesulfurized middle 

 distillates for 6 h/day on five days per week for four weeks showed no 

 treatment-related changes. Mild subacute inflammatory changes were 

 observed in the nasal respiratory mucosa of the animals in one group 

 that had been exposed to distillate API 81-09 (American Petroleum 

 Institute, 1986c). 

 A7.2.2 Subchronic exposure 

 A7.2.2.1 Dermal exposure 

 Groups of 10 male and 10 female B6C3F1 mice received dermal 

 applications under an occlusive covering of 250 or 4000 mg/kg body 

 weight per day marine diesel fuel or 500-8000 mg/kg body weight per 

 day JP-5 navy fuel for five days per week for 13 weeks. The marine 

 diesel fuel caused no treatment-related deaths. Males had reduced body 

 weight gain; mild chronic active dermatitis at the site of application 

 was observed at the highest dose. At 1000 mg/kg body weight per day, 

 all animals survived and had weight gains similar to those of the 

 controls. Exposure to JP-5 navy fuel killed five males at the 

 high-dose group and caused dermatosis, splenic extramedullary 

 haematopoiesis, and liver karyomegaly in all groups (US National 

 Toxicology Program, 1986). 

 A7.2.2.2 Inhalation 

 The results of studies of subchronic inhalation of various 

 distillate fuels are summarized in Table 13. 

 Table 13. Studies of subchronic exposure to distillate fuels by inhalation 

 

 Fuel Species Exposure (high dose) Results Reference 

 

 Diesel fuels 

 Diesel fuel Rat 4 h/d, 2 d/week, 13 weeks + Reversible loss of body weight; Lock et al. (1984) 

 8 weeks' recovery (1.5 mg/litre) no other apparent effect 

 Marine diesel fuela Mouse, rat 90 d, continuous (0.05 and Nephrotoxic effects specific to Bruner (1984) 

 0.3 mg/litre) male rats 

 Other fuels 

 JP-8 jet fuelb Mouse, rat 24 h/d, 7 d/week,90 d + 24 Nephrotoxic effects specific to Mattie et al. (1991) 

 months' recovery (1 mg/litre) male rats 

 JP-5 jet fuelb Rat, dog 24 h/d, 7 d/week,90 d Nephrotoxic effects specific to Gaworski et al. (1984) 

 (0.75 mg/litre) male rats 

 JP-4 jet fuelb Mouse, rat 6 h/d, 5 d/week,12 months Nephrotoxic effects specific to Bruner et al. (1993) 

 (5 mg/litre) male rats; increased incidence 

 of hepatocellular adenomas in 

 female mice 

 Deodorized Rat, dog 6 h/d, 5 d/week,13 weeks No apparent effects Carpenter et al. (1976) 

 kerosenec (0.1 mg/litre) 

 

 a Hydrocarbon fraction similar to that of diesel fuel 

 b Narrow boiling range 

 c Not a fuel; very low aromaticity 

 Groups of 25 male rats and four male dogs were exposed to 

 deodorized kerosene at concentrations up to 0.1 mg/litre, 

 approximately the saturation limit at 25°C, for 6 h/day on five days 

 per week for about 13 weeks. Although dose-related changes were 

 observed in survival, body weight gain, organ weights, and 

 haematological and clinical chemical parameters, none of the findings 

 was statistically significantly different from those in controls. No 

 pathological change was seen in any of the organs examined (Carpenter 

 et al., 1976). 

 Groups of 12 male and 12 female Sprague-Dawley rats were exposed 

 in whole-body chambers for 4 h/day on two days per week for 13 weeks 

 to 0.25, 0.75, or 1.5 mg/litre aerosolized diesel fuel, followed by an 

 eight-week recovery period. There were no deaths. All treated animals 

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 lost weight, indicating slight toxicity, during the first four weeks 

 of exposure, but the effect was reversed during the recovery period in 

 most cases. A slight depression of the startle reflex was seen at the 

 start of the study, and the number of macrophages in bronchial lavage 

 fluid was slightly elevated in all treated animals immediately after 

 cessation of exposure. Further tests of pulmonary function, gas 

 exchange, and dynamic lung function did not reveal any significant, 

 dose-related change. Overall, no significant cumulative toxicity was 

 seen (Lock et al., 1984). 

 A specific effect of diesel fuel in male rats, the hyaline 

 droplet nephropathy syndrome, was seen in several studies. Gaworski et 

 al. (1984) studied the effects of a 90-day exposure to 0.15 or 

 0.75 mg/litre JP-5 jet fuel derived from either petroleum or shale oil 

 for 24 h/day, in groups of three male and three female beagle dogs, 75 

 male and 75 female Fischer 344 rats, and 111-150 female C57Bl/6 mice. 

 The toxicity of the two types of fuel was not significantly different. 

 The only substantial effect at both concentrations was a renal tubular 

 lesion in male rats, probably caused by hyaline droplet accumulation 

 and unique to male rats. Other signs of toxicity were mild liver-cell 

 changes and mild nasal inflammation in rats. Cowan & Jenkins (1980) 

 studied petroleum and shale-oil marine diesel fuel using an identical 

 study design. Reduced body weight gain and hyaline droplet nephropathy 

 were reported in male rats. In another study, groups of 95 male and 75 

 female Fischer 344 rats and 100 male and 100 female C57Bl/6 mice were 

 exposed for 24 h/day on seven days per week to JP-8 jet fuel at 

 concentrations up to 1 mg/litre for 90 days, and then held for 20-21 

 months in order to assess the long-term consequences of exposure. The 

 main finding was accumulation of hyaline droplets in the kidneys of 

 male rats (Mattie et al., 1991). In a 90-day study, groups of 75 male 

 and 75 female Fischer 344 rats were exposed continuously to 0.05 or 

 0.3 mg/litre of marine diesel fuel. The main finding was again hyaline 

 droplet nephropathy in males at both levels (Bruner, 1984). In a study 

 of the carcinogenicity of JP-4 jet fuel vapour, hyaline droplet 

 nephropathy was observed in groups of 100 male Fischer 344 rats 

 exposed for 6 h/day, five days per week for 12 months to 

 concentrations up to 5 mg/litre (Bruner et al., 1993) (see also 

 section A7.7). 

 The hyaline droplet nephropathy syndrome is not considered to be 

 relevant for humans. It is linked to an inherent peculiarity of renal 

 protein. The histopathological sequence is: accumulation in the renal 

 proximal tubules of an excessive amount of hyaline droplets containing 

 alpha2-microglobulin, a special protein of male rats which is 

 synthesized in the liver; cytotoxicity and single-cell necrosis of the 

 tubular epithelium; sustained regenerative tubule-cell proliferation; 

 development of intraluminar granular casts from sloughed cell debris; 

 tubular dilatation and papillary mineralization; foci of tubule 

 hyperplasia; and renal tubule tumours (US Environmental Protection 

 Agency, 1991). Mechanistically, a globulin-substance complex that is 

 resistant to hydrolytic degradation is responsible for the protein 

 overload in kidneys. 

 A7.3 Long-term exposure 

 A7.3.1 Dermal exposure 

 Groups of 50 male and 50 female B6C3F1 mice received dermal 

 administrations of 250 or 500 mg/kg body weight per day marine diesel 

 fuel or JP-5 navy fuel on the clipped dorsal interscapular region on 

 five days per week for 103 weeks. (The doses were derived from studies 

 reported in section A7.2.) The high dose of marine diesel fuel caused 

 a dose- and time-dependent reduction in mean body weight in animals of 

 each sex, by up to 23% after week 40 in males and up to 20% after week 

 72 in females. Survival of treated females was decreased, and exposure 

 to the high dose was stopped at week 84 owing to severe ulceration. 

 Application of 500 mg/kg body weight per day JP-5 navy fuel resulted 

 in a time-dependent reduction in mean body weight in animals of each 

 sex: by up to 22% after week 76 in males and up to 25% after week 60 

 in females. Treatment of females with the high dose had to be 

 terminated at week 90. Overall, JP-5 navy fuel caused a lesser chronic 

 inflammatory response than marine diesel fuel (US National Toxicology 

 Program, 1986). 

 A7.3.2 Inhalation 

 Groups of 100 male and 100 female Fischer 344 rats and C57Bl/6 

 mice were exposed to JP-4 jet fuel vapour for 6 h/day on five days per 

 week for 12 months at concentrations of 1 or 5 mg/litre (see section 

 A7.7). The sex-specific alpha2-microglobulin nephropathy syndrome was 

 observed in 21% of male controls and in 20% of males at the low dose, 

 and 77% at the high dose (see also section A7.2). No significant, 

 dose-related alteration was seen in clinical findings, mortality, 

 haematological parameters, or clinical chemistry. All treated male 

 rats had a significant reduction in mean body weight. At the high 

 dose, male rats had significantly increased relative liver and kidney 

 weights and females had a significant decrease in relative spleen 

 weight. These alterations were not significant in comparison with 

 absolute organ weights (Bruner et al., 1993). 

 A7.4 Dermal and ocular irritation; dermal sensitization 

 A7.4.1 Dermal irritation 

 The results of studies of dermal irritation (Table 14) must be 

 interpreted critically, as different protocols were used, e.g. in 

 Europe and the United States. The main difference is in exposure time: 

 24 h in the American protocols and 4 h in those of the European Union 

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 and the Organisation for Economic Co-operation and Development, which 

 may pose a problem when only mild irritation is observed, leading to a 

 classification of 'non-irritant' according to protocols of the latter 

 organizations. 

 A market-place sample of diesel fuel, tested at a dose of 0.5 ml 

 for 24 h in rabbits, was assessed as 'extremely irritating', 

 corresponding to a Draize score of 6.81 (Beck et al., 1984). 

 Topical applications three times a week to mice of various types 

 of kerosene and gas oil with boiling ranges similar to that of diesel 

 fuel produced degenerative changes in the skin surface, including 

 necrosis and hyperplasia (CONCAWE, 1991). 

 Four types of American military fuels were investigated: 

 petroleum JP-5 fuel, shale JP-5 fuel, petroleum marine diesel fuel, 

 and shale marine diesel fuel. None was active in the Draize test, in 

 which six female New Zealand white rabbits received 0.5 ml of 

 undiluted fuel on intact and abraded skin under an occlusive covering 

 for 24 h (Cowan & Jenkins, 1980). Applications to rabbit skin of 

 0.5 ml of various shale oil- and petroleum-derived fuels under 

 occlusive dressings for 4 h were not irritating (Schultz et al., 

 1981). 

 Various modifications of fuel oil No. 2 (10, 30, and 50%) were 

 found to be moderately irritating to rabbit skin (American Petroleum 

 Institute, 1980a,b,c), and two hydrodesulfurized middle distillates 

 resulted in primary irritation indices of 4.3 and 5.9 (American 

 Petroleum Institute, 1982a,b). A straight-run middle distillate had a 

 moderately irritating effect, with an irritation index of 3.2 

 (American Petroleum Institute, 1985d). Jet fuel A was classified as 

 mildly irritating, with an irritation score of 1.96 (American 

 Petroleum Institute, 1980d). A hydrosulfurized kerosene was moderately 

 irritating, with an index of 4 (American Petroleum Institute, 1982c). 

 A light catalytically cracked distillate (American Petroleum 

 Institute, 1985d) and a straight-run kerosene (American Petroleum 

 Institute, 1985e) had severely irritating effects, with irritation 

 indexes of 5.5 and 5.6. 

 Table 14. Studies of dermal irritation in rabbits exposed for 24 h to various fuels 

 

 Fuel Classification of Reference 

 irritationa

 

 Diesel fuel Extremely irritating Beck et al. 

 (1984) 

 Marine diesel fuel or marine Not irritating Cowan & Jenkins 

 shale fuel (1980) 

 Hydrodesulfurized middle Moderately irritating American Petroleum 

 distillate Institute (1982a,b) 

 Straight-run middle distillate Moderately irritating American Petroleum 

 Institute (1985d) 

 Light catalytically cracked Severely irritating American Petroleum 

 distillate Institute (1985d) 

 Heating oil No. 2 Moderately irritating American Petroleum 

 Institute (1980a,b,c) 

 Jet fuel A Mildly irritating American Petroleum 

 Institute (1980d) 

 Various kerosenes Slightly to severely CONCAWE (1995) 

 irritating 

 Shale oil- and Not irritating Schultz et al. (1981) 

 petroleum-derived fuels 

 Hydrodesulfurized kerosene Moderately irritating American Petroleum 

 Institute (1982c) 

 Straight-run kerosene Severely irritating American Petroleum 

 Institute (1985e) 

 

 a Note differences in protocols between regulations of the United States and 

 the Organisation for Economic Co-operation and Development (see section A7.4.1) 

 

 A7.4.2 Ocular irritation 

 All of the available reports indicate no or, at the most, a 

 slight irritating effect of diesel fuels and kerosenes on the rabbit 

 eye. 

 Four types of American military fuels (petroleum JP-5 fuel, shale 

 JP-5 fuel, petroleum marine diesel fuel, and shale marine diesel fuel) 

 gave generally negative responses in the Draize test, in which nine 

 female New Zealand white rabbits were given 0.1 ml of undiluted 

 substance (Cowan & Jenkins, 1980). A market-place sample of diesel 

 fuel (0.1 ml, undiluted) was also not irritating in the Draize test 

 (Beck et al., 1984). None of several kerosenes tested was more than 

 slightly irritating to the eye (CONCAWE, 1995), and none of the shale 

 oil- and petroleum-derived fuels tested caused visible irritation in 

 the rabbit eye (0.1 ml, undiluted) (Schultz et al., 1981). 

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 Three modifications of fuel oil No. 2 (10, 30, and 50%) were 

 classified as mildly irritating in rabbits (American Petroleum 

 Institute, 1980a,b,c). Two hydrodesulfurized middle distillates did 

 not cause primary irritation in the Draize test (American Petroleum 

 Institute, 1982a,b); a straight-run middle distillate (American 

 Petroleum Institute, 1985d) and a straight-run kerosene also gave 

 negative results (American Petroleum Institute, 1985e). Jet fuel A was 

 classified as mildly irritating, with an average score of 2.67 after 

 one day and 0 after seven days (American Petroleum Institute, 1980d). 

 A hydrodesulfurized kerosene was not irritating (American Petroleum 

 Institute, 1982c). 

 A7.4.3 Sensitization 

 Three modifications of fuel oil No. 2 (10, 30, and 50%) were were 

 classified as non-sensitizing for the skin of guinea-pigs (American 

 Petroleum Institute, 1980a,b,c). A straight-run middle distillate 

 (American Petroleum Institute, 1985d), a straight-run kerosene 

 (American Petroleum Institute, 1985e), jet fuel A (American Petroleum 

 Institute, 1980d), a hydrodesulfurized middle distillate (American 

 Petroleum Institute, 1984), and a light catalytically cracked 

 distillate (American Petroleum Institute, 1985c) were also not 

 sensitizing. 

 Four types of fuels used in the United States Army, petroleum 

 JP-5 fuel, shale JP-5c fuel, petroleum marine diesel fuel, and shale 

 marine diesel fuel, were not sensitizing in a modified Landsteiner 

 test in groups of 24 guinea-pigs (Cowan & Jenkins, 1980). A 

 straight-run kerosene, hydrosulfurized kerosene, jet fuel A (CONCAWE, 

 1995), and shale oil- and petroleum-derived jet and diesel fuels 

 (Schultz et al., 1981) were also not sensitizing. 

 A7.5 Reproductive toxicity, embryotoxicity, and teratogenicity 

 Groups of 20 pregnant CRL:COBS rats were exposed by inhalation on 

 days 6-15 of gestation to 100 or 400 ppm of diesel fuel for 6 h/day 

 (American Petroleum Institute, 1979). A significant reduction in 

 maternal food consumption was seen at the high concentration, and 

 maternal body weight gain and fetal weights were reduced, although not 

 statistically significantly. Overall, no significant, dose-related 

 effects were observed in dams, and the compound had no teratogenic or 

 embryotoxic effect and no effect on fetal growth or development. 

 No signs of developmental or maternal toxicity were seen when 

 groups of 20 pregnant rats were exposed to jet fuel A or fuel oil for 

 6 h/day on days 6-15 of gestation (Beliles & Mecler, 1982). 

 Sprague-Dawley rats were fed 500, 1000, 1500, or 2000 mg/kg body 

 weight per day of JP-8 aviation fuel by gavage on days 6-15 of 

 gestation, and fetuses were examined on day 20. Significantly reduced 

 body weights were seen in dams at the two higher doses and in fetuses 

 at 1000-2000 mg/kg body weight per day, but the number of 

 malformations was not altered. The investigators concluded that JP-8 

 aviation fuel is a developmental toxin at doses > 1000 mg/kg body 

 weight per day but is not teratogenic (Cooper & Mattie, 1993). 

 A7.6 Mutagenicity and related end-points 

 A7.6.1 In vitro 

 Various samples of diesel and related fuels have been tested for 

 mutagenicity in Salmonella typhimurium (Henderson et al., 1981; 

 Conaway et al., 1984; Vandermeulen et al., 1985; US National 

 Toxicology Program, 1986; McKee et al., 1994). Negative results were 

 obtained in direct, unmodified Ames' assays (Conaway et al., 1984; 

 Vandermeulen et al., 1985; US National Toxicology Program, 1986). In 

 one study, refined shale oil, jet fuel, and shale oil- and 

 petroleum-derived marine diesel fuel were not mutagenic (Schultz et 

 al., 1981). Negative results were also found in studies of aliphatic 

 and aromatic fractions of diesel fuel in S. typhimurium TA98, TA100, 

 and TA1535 in the presence of an exogenous metabolic system (Henderson 

 et al., 1981). 

 The number of revertants of TA98 increased to 2.3-2.5 times the 

 background levels in a suspension assay (Conaway et al., 1984), but 

 increases were found at a limited number of doses. In a modified 

 Salmonella assay with an extraction step to concentrate the 

 mutagenic aromatic compounds, addition of an exogenous metabolic 

 system from Aroclor-induced hamster liver, and use of TA98 as the most 

 responsive strain, increased numbers of revertants were seen (McKee et 

 al., 1994); but the number never exceeded twice the background 

 response, and the results were considered to be equivocal. 

 A dimethyl sulfoxide extract of an intermediate, catalytically 

 cracked distillate (CAS No. 644741-60-2) was mutagenic in 

 S. typhimurium TA98 with an increased concentration of exogenous 

 metabolic system to optimize detection. Of two dimethyl sulfoxide 

 extracts of light hydrocracked distillate (CAS-No. 64741-77-7) tested 

 in the same system, one induced a weak, non-dose-dependent response, 

 while the other induced a clear dose-dependent positive response 

 (Blackburn et al., 1984). Under the same assay conditions, five 

 samples of cracked middle distillates also gave positive results 

 (German Scientific Association for Petroleum, Natural Gas, and Coal, 

 1991). These results in a series of assays in Salmonella with a number 

 of variations provide no clear evidence of mutagenic activity. In the 

 unicellular alga Chlamydomonas reinhardtii (streptomycin resistant) 

 tested in a natural aquatic environment, water-soluble fractions of 

 two crude and two refined oils did not induce forward mutations 

 (Vandermeulen & Lee, 1986). Neither aliphatic nor aromatic dimethyl 

 sulfoxide fractions of diesel fuel No. 7911 induced mutation in 

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 S. typhimurium. After reaction with nitrogen dioxide, which may 

 activate the mutagenicity of diesel exhaust, it was mutagenic in 

 strain TA100, the aromatic fraction being 40-fold more active than the 

 aliphatic fraction (Henderson et al., 1981). 

 A market-place sample of diesel fuel did not induce mutation in 

 L5178Y tk+/- mouse lymphoma cells with or without metabolic 

 activation (Conaway et al., 1984). A hydrodesulfurized middle 

 distillate (CAS 64742-80-9) was active in the presence of metabolic 

 activation, but the concentrations were cytotoxic (American Petroleum 

 Institute, 1987c). 

 A7.6.2 In vivo 

 Undiluted diesel fuel No. 2 increased the frequency of 

 chromosomal aberrations in the bone marrow of Sprague-Dawley rats 

 given single or repeated (five days; 125, 417, or 1250 mg/kg body 

 weight) oral doses. Diesel fuel given intraperitoneally for one or 

 five days at 0.6, 2, or 6ml/kg body weight significantly increased the 

 number of aberrant cells at the highest dose (Conaway et al., 1984). 

 In order to assess these findings further, McKee et al. (1994) 

 evaluated micronucleus induction by diesel fuel No. 2 and related 

 materials in male and female CD-1 mice treated by gavage at up to 

 5 g/kg body weight. No effect was seen. 

 No effect was seen on the frequency of dominant lethal mutations 

 in male CD-1 mice exposed to 100 or 400 ppm of either diesel fuel or 

 jet fuel A for 6 h/day, five days per week for eight weeks (American 

 Petroleum Institute, 1980e, 1981). 

 A7.7 Carcinogenicity 

 A7.7.1 Dermal exposure 

 Diesel fuel has been shown to have at least weak carcinogenic 

 potency after dermal administration in a number of studies. As some of 

 the test samples contained low concentrations of carcinogenic PAHs, it 

 has been suggested (Biles et al., 1988) that the tumours induced may 

 have been a consequence of the dermal damage produced by repeated 

 treatment with these materials. The available studies are summarized 

 in Table 15. 

 Doses of 25 mg per animal of petroleum and shale fuels were 

 applied to groups of 25 male and 25 female C3H/HeN mice three times a 

 week, for 62 weeks for jet fuel A with subsequent observation up to 

 105 weeks, and for 104 weeks for JP-4 fuel. Controls received mineral 

 oil. The shale and petroleum diesel fuels were characterized for 

 boiling range (jet A, 171-271°C; JP-4, 60-249°C) and sulfur content 

 (jet A: petroleum, 3510 ppm; shale, 89 ppm; JP-4: petroleum, 1830 ppm; 

 shale, 199 ppm). After 60 weeks, increased incidences of squamous-cell 

 carcinomas and fibrosarcomas were reported (jet A: petroleum, 26%; 

 shale, 28%; JP-4: petroleum, 26%; shale, 50%; controls, 0-2%), but no 

 statistical analysis was reported (Clark et al., 1988). 

 Groups of 50 male and 50 female B6C3F1 mice were given 250 or 

 500 mg/kg body weight per day marine diesel fuel dermally, on five 

 days per week for 103 or 84 weeks (see section A7.3.). A control group 

 received the vehicle, acetone, only. The survival rates were 26/50 

 males and 29/50 females at the high dose at 84 weeks, 20/49 males and 

 12/50 females at the low dose at 104 weeks, and 30/50 male and 40/50 

 female controls. Males at the high dose had a significantly increased 

 number of hepatocellular adenomas or carcinomas (29%; control, 18%). 

 The total incidences of squamous-cell papillomas and carcinomas at the 

 application site and the adjacent inguinal site were: control, 1/50; 

 low dose, 2/49; high dose, 3/50 in males; and control, 0/50; low dose, 

 1/45; and high dose, 2/48 in females. No information was available on 

 historical frequencies in acetone-treated mice; the incidence of 

 papillomas and carcinomas in 3500 observations in untreated mice was 

 0.3-0.4%. In a parallel study with JP-5 navy fuel, 1/50 papillomas 

 were seen at the low dose and 4/49 carcinomas at the high dose in 

 males, and 0/49 carcinomas were seen at the low dose and 1/47 at the 

 high dose in females. The investigators concluded that there was 

 equivocal evidence for the carcinogenicity of marine diesel fuel and 

 no evidence for the carcinogenicity of JP-5 navy fuel (US National 

 Toxicology Program, 1986). 

 Two middle-distillate fractions of each of two crude oils 

 (boiling range, 170-370°C) were painted at a dose of 50 mg onto the 

 skin of male C3H mice twice a week for 18 months. The yield of benign 

 and malignant tumours (details not specified) was 2-19 % (Lewis, 

 1983). 

 Table 15. Studies of chronic dermal exposure of mice (usually 50 mice/group) to distillate fuels 

 

 Fuel Exposure Results Reference 

 

 Marine diesel fuel 0, 250, and 500 mg/kg bw, 1/50, 2/49, and 3/50 (m) and 0/50, 1/45, and 2/48 (f) US National Toxicology

 5 d/week, 103 weeks with squamous-cell papillomas and carcinomas after Program (1986) 

 104 weeks 

 Straight-run gas oil 25 mg/animal, twice/week, Occasional ulcerations, scarring, epidermal dysplasia; American Petroleum 

 (laboratory sample)a up to 2 years after 2 years, 17/50 with tumours; controls, 0% Institute (1985c) 

 Straight-run middle 50 μl/animal, twice/week, Mild to moderate irritation (mild desquamation, American Petroleum 

 distillatea up to 2 years occasional scabbing); after 2 years, 10/50 with Institute (1989a) 

 squamous-cell carcinomas or fibrosarcomas; 

 controls, 0% 

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 Straight-run 50 μl/animal, twice/week, 29/50 with malignant and 1/50 with benign tumours; American Petroleum 

 keroseneb > 2 years latency, 76 weeks; controls, 0% Institute (1989a) 

 Two cracked 50 μl/animal, twice/week, Mild to moderate irritation; after 24 months, 39/50 American Petroleum 

 distillatesc up to 2 years and 26/50 with tumours Institute (1989a) 

 Intermediate 50 mg/animal, twice/week, 42/43 with tumours; mean latency, 17 weeks; Blackburn et al. (1984

 catalytically cracked 80 weeks controls, 0/50 

 distillatec

 Two hydrodesulfurized 50 μl/animal, twice/week, Acanthosis, fibrosis, hyperkeratosis, crusting; at end American Petroleum 

 middle distillatesa lifetime of study, 24/50 and 27/50 with tumours (no controls Institute (1989b) 

 reported) 

 

 Table 15 (contd) 

 

 Fuel Exposure Results Reference 

 

 Hydrodesulfurized 50 μl/animal, twice/week, 26 malignant and 1 benign tumours; latency, 77 American Petroleum 

 keroseneb > 2 years weeks (no controls reported) Institute (1989b) 

 Jet A and JP-4 fuels 25 mg/animal, three After 60 weeks, increased skin tumour rate; jet A, Clark et al. (1988) 

 from shale or times/ week, 62 weeks 26% petroleum, 28% shale; JP-4, 26% petroleum, 

 petroleum oilsb + observation (jet A) 50% shale 

 or 104 weeks (JP-4) 

 Two middle-distillate 50 mg/animal, twice/week, 2-19% tumour rate (no further information) Lewis (1983) 

 fractions 18 months 

 No. 2 fuel oilb 12, 25, or 50 μl/animal, Overall tumour rate, 10%; control, 0% Witschi et al. (1987)

 three times/week, up to 

 100 weeks 

 Two heating oilsa 25 μl/animal, three 7/50 and 9/50 with tumours; control, 0/50 Biles et al. (1988) 

 times/week, lifetime 

 

 a Hydrocarbon fractions similar to that of diesel fuel (see section A2.1) 

 b Hydrocarbon fractions from which also diesel fuels are gained during petroleum separation (see section A3.2.1.1) 

 c Blending component of diesel fuel 

 Application of American Petroleum Institute No. 2 fuel oil 

 dermally to C3H mice at 12, 25, or 50 μl per animal, three times 

 weekly for up to 100 weeks induced an overall tumour incidence (type 

 not specified) of 10% (15/150 in the three treatment groups; controls, 

 0/100) (Witschi et al., 1987). 

 Ten samples of middle-distillate fuels were applied dermally to 

 C3H/HeJ mice at a dose of 25 μl, three times a week for life. A virgin 

 heating oil blending base (142-307°C) and a commercial No. 2 heating 

 oil (156-352°C) had aromatic contents closest to that of diesel fuel. 

 The blending base induced five skin carcinomas and two papillomas in 

 50 animals, and the commercial heating oil produced eight skin 

 carcinomas and one papilloma in 50 animals. There were no tumours in 

 the respective control groups (Biles et al., 1988). 

 A7.7.2 Inhalation 

 Fischer 344 rats and C57Bl/6 mice were exposed for 6 h/day on 

 five days per week for 12 months to 1 or 5 mg/litre of fuel vapours 

 (see section A7.3), followed by a 12-month recovery period. No 

 significant pulmonary neoplastic changes were seen. Female mice at the 

 high dose had a slightly but significantly increased incidence of 

 benign hepatocellular adenomas (10%; controls, 2%); however, the trend 

 was reversed in male mice. No conclusions about carcinogenic potency 

 were drawn from this study (Bruner et al., 1993). 

 A8. EFFECTS ON HUMANS

 A8.1 Exposure of the general population 

 Like similar petroleum distillates, such as kerosene, diesel fuel 

 can cause dermal irritation and defatting after dermal exposure 

 (Sandmeyer, 1981). Considerable exposure and subsequent absorption may 

 also result in acute renal failure secondary to acute renal tubular 

 necrosis. A 28-year-old man developed progressive oliguria one day 

 after washing his hair with diesel fuel and had acute tubular necrosis 

 on renal biopsy (Barrientos et al., 1977). A 47-year-old man developed 

 acute tubular necrosis after cleaning his arms and hands with diesel 

 oil for several weeks (Crisp et al., 1979). Both recovered renal 

 function. 

 Accidental aspiration of diesel fuel resulted in immediate 

 coughing, followed by dyspnoea, cyanosis, and loss of consciousness 

 (Perez Rodriguez et al., 1976). X-Ray examination revealed diffuse 

 alveolar infiltrates. Mildly elevated levels of alkaline phosphatase, 

 serum glutamic-oxaloacetic transaminase, and serum glutamic-pyruvic 

 transaminase were also seen. After 37 days, residual infiltrates 

 remained, but the patient had improved. In another case, abdominal 

 pain and vomiting followed ingestion of a reported 1.5 litres of 

 diesel fuel. Pulmonary infiltrates were noted, presumably from 

 subsequent aspiration of diesel fuel (Boudet et al., 1983). 

 A8.2 Occupational exposure 

 The odour threshold values for diesel fuels No. 1 and 4 are 

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 reported to be 0.7 and 0.5 ppm, respectively (see section A2.2, Table 

 5). Six volunteers exposed to 140 mg/m3 of deodorized kerosene for 

 15 min did not experience throat irritation. Olfactory fatigue was 

 induced in three subjects, and one reported taste sensation. The 

 investigators suggested that this concentration was the sensory 

 threshold for kerosene and estimated the odour threshold at 

 0.6 mg/m3 (Carpenter et al., 1976). 

 Acne and folliculitis developed on the arms and thighs of a man 

 who had worked in various automobile workshops for 15 years. He had 

 handled diesel oil with his bare hands and then wiped them on his 

 trousers (Das & Misra, 1988). Hyperkeratosis was noted in 320 drivers 

 working in Russian oil fields with regular dermal contact with diesel 

 fuel (Gusein-Zade, 1974). A 33-year-old man was exposed to diesel fuel 

 vapour (concentration not reported) for 10 days while driving a truck 

 with a fuel injector leak. He developed abdominal cramps, nausea, 

 vomiting, and then acute renal failure with anaemia and 

 thrombocytopenia (Reidenberg et al., 1964). Two aviators who were 

 exposed to JP-5 fuel vapour for 1 h while flying a small airplane 

 experienced eye irritation, difficulties in coordination and 

 concentration, and fatigue (Porter, 1990). 

 Siemiatycki et al. (1987) conducted a case-control study in 

 Montreal, Canada, and found an increased risk for squamous-cell 

 carcinoma of the lung in men exposed to diesel fuel. When all types of 

 lung cancer except adenocarcinoma were combined, an odds ratio 

 (adjusted for smoking) of 1.6 (90% confidence interval (CI), 1.0-2.4; 

 n = 39) was found for 'any' exposure. In four subcategories, the odds 

 ratios were 1.9 (short-low), 2.0 (short-high), 1.1 (long-low), and 2.0 

 (long-high). The possible effects of exposure to combustion products 

 were not taken into consideration. An association with prostatic 

 cancer was also observed, although there was no dose-response 

 relationship, with odds ratios of 2.3 (CI, 1.3-4.0; n = 17) for the 

 subgroup with nonsubstantial exposure and 1.4 (0.7-2.9; n = 8) in 

 the subgroup with substantial exposure. 

 In another case-control study, no association was found between 

 the occurrence of renal-cell cancer and occupational exposure to fuel 

 oils, including diesel fuel (levels and duration not quantified) 

 (Partanen et al., 1991). 

 In a cross-sectional epidemiological study, the effects of 

 long-term exposure of factory workers to jet fuels (not specified) was 

 investigated. Dizziness, headache, nausea, palpitation, pressure in 

 the chest, and eye irritation were found to be more prevalent than in 

 unexposed controls. The time-weighted average concentration of jet 

 fuel vapour in the breathing zone was estimated to be 128-423 mg/m3

 (Knave et al., 1978). 

 A9. EFFECTS ON OTHER ORGANISMS IN THE LABORATORY AND THE FIELD

 Comparison and evaluation of studies of the ecotoxicological 

 effects of diesel fuel are complicated by a number of factors: 

 (1) There are comparatively few ecotoxicological studies on 

 diesel fuel, and most work in the 1970s was concentrated on the 

 effects of No.2 fuel oil, which has a similar but not identical 

 chemical composition to diesel fuel No. 2 (see section A2). The 

 composition of marine diesel fuel differs greatly from both (see 

 Table 1). As described in the same section, diesel fuel itself has 

 various specifications in different countries; in particular, the 

 composition of non-hydrocarbon compounds from e.g. catalytic processes 

 or additives may vary widely. There may also be differences between 

 batches of the same oil (Hedtke & Puglisi, 1982) (see Table 20). The 

 amount of the chemical actually in solution is also pertinent to 

 ecotoxicological studies. Table 3 gives the concentration ranges of 

 toxicologically relevant constituents of diesel and No. 2 fuel oil as 

 a whole and as 10% water-soluble fractions. 

 (2) The chemical composition of fuel oils and, as a consequence, 

 their toxicity change with time, as oil can be modified by 

 biodegradation, photooxidation, and volatilization (see section A4). 

 Their toxicity also depends on whether they are mixed with water (sea 

 water or freshwater), sediment, or soil, the temperature (tropical or 

 Arctic), and physical conditions (e.g. storm conditions with continual 

 mixing and breaking up of oil). Oil modified by these processes is 

 usually less toxic than fresh oil (Baker, 1970; Morrow, 1973). 

 (3) A variety of methods have been used in ecotoxicological 

 studies on fuel oils. There is an obvious difference between 

 conditions in the laboratory and the field. Most of the field studies 

 that have been reported are related to fuel spills. In laboratory 

 studies, either water-soluble fractions (see below) or oil-water 

 dispersions have been used, and the methods of preparing them vary 

 among laboratories. Oil films and, more recently, microencapsulated 

 diesel oil have also been tested. In none of the laboratory studies 

 reported were test media prepared with 'water accommodated fractions', 

 as described and recommended by CONCAWE (1993) in laboratory protocols 

 for petroleum products. Thus, the amount of product that must be added 

 to a given volume of medium to produce the effects reported cannot be 

 derived from the results of these studies, making comparison of data 

 on ecotoxicity from different studies practically impossible. 

 Hedtke & Puglisi (1982) tested the lethality of No. 2 fuel oil in 

 two species of freshwater fish and two species of amphibians and found 

 variable LC50 values (see Table 20). Oil-water dispersions were very 

 toxic to fish. It is thought that these tiny oil droplets make contact 

 with the gills and directly damage the respiratory epithelium 

 (Engelhardt et al., 1981; Poirier et al., 1986). With floating oils, 

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 the relationship between toxicity and oil-water contact is a function 

 of the equilibrium time for the soluble components of the oil and 

 water, death occurring more rapidly when the oil is added 96 h before 

 the organisms are exposed. Flow-through tests were more sensitive than 

 static tests, as, in the latter, the chemical nature and toxicity of 

 the oil change with time (Hedtke & Puglisi, 1982). Lockhart et al. 

 (1987) showed that the results of static tests in fish varied 

 considerably with aeration of test containers. Although flow-through 

 techniques give a better estimate of real exposure conditions, many of 

 the results reported in the literature are of static tests. 

 (4) The susceptibility of organisms to fuel oils and their 

 components depends not only on the species and strain but also on the 

 biological stage and the time of development within stages (Kühnhold, 

 1977; Winters et al., 1977). As the effects of No. 2 fuel oil and 

 diesel oil have been tested in a wide variety of organisms and life 

 stages under various conditions, direct comparison is difficult. 

 In spite of these difficulties, it can be concluded that diesel 

 oil is generally more toxic than crude oil, as seen, for example, in 

 barnacle nauplii (Winters et al., 1977), Daphnia (Cladocera), 

 chironomid larvae, and the mollusc Viviparus bengalensis (Gastropoda) 

 (Das & Konar, 1988). Crude oils themselves differ in toxicity, 

 depending on their source (Anderson, 1977a; Winters et al., 1977), as 

 do their corresponding products. 

 Rice et al. (1977a) concluded that the toxicity of fuel oil is 

 due to the chemical toxicity of soluble aromatic compounds rather than 

 to the physical toxicity of dispersed oil droplets. Physical coating 

 by oil of the gills of fish and the feathers of birds is also a cause 

 of toxicity. Monoaromatic compounds seem to be the least toxic, their 

 acute toxicity increasing with molecular size up to the four- to 

 five-ring compounds (e.g. chrysene and benzo[ a]pyrene) (Neff et al., 

 1976b; Rice et al., 1977a), but they are not very soluble in sea water 

 (see Table 6). The toxicity of one-, two-, and three-ring compounds 

 (benzenes, naphthalenes, and phenanthrenes, respectively), seemed to 

 increase with increasing degrees of alkylation of the aromatic 

 nucleus. Neff et al. (1976b) reported 96-h LC50 values of 0.3-0.6 ppm 

 for 1-methylphenanthrene, fluoranthrene, and phenanthrene, indicating 

 the high toxicity of these polynuclear aromatic compounds for the 

 polychaete, Neanthes arenaceodentata. Of the pure compounds tested 

 by Winters et al. (1977), the most toxic to barnacle nauplii were 

 indan, naphthalene, xylene, and substituted benzenes and naphthalenes. 

 In four freshwater species, the water-soluble fraction was again 

 associated with the substituted benzenes, and naphthalenes were found 

 to be associated with the observed toxicity (Lockhart et al., 1987). 

 The concentrations of naphthalenes, methylnaphthalenes, and 

 dimethylnaphthalenes are particularly high in fuel oils (see Table 3), 

 and these compounds have been used as analytical markers in several 

 studies. 

 Experiments involving microencapsulated oil fractions have shown 

 that insoluble fractions also inhibit growth, e.g. of juvenile mussels 

 (Stromgren & Nielsen, 1991). Anderson (1979) indicated that the larval 

 stage might be the most sensitive to No. 2 fuel oil. Eggs of fish and 

 invertebrates were often tolerant, and adults were sometimes more 

 sensitive than juveniles. 

 Extensive studies have been carried out on lethal toxicity to 

 marine organisms under the same conditions. The 96-h LC50 values for 

 a wide range of invertebrates in static exposure conditions 

 (temperature, 18-22°C) were 1-20 ppm for crude oil in water and 

 0.4-6 ppm for No. 2 fuel oil (Anderson et al., 1974; Neff et al., 

 1976b; Rossi et al., 1976). At 4-10°C, the 96-h LC50 values appeared 

 to be lower (Rice et al., 1976, 1977a). Table 16 gives the results of 

 lethality studies reported from several laboratories. 

 Table 16. Lethality (median lethal concentrations) to marine 

 zooplankton of physically dispersed and water-soluble 

 fractions of No. 2 fuel oil 

 

 Zooplankton Oil-water dispersions Water-soluble 

 (mg/litre) fractions (mg/litre) 

 Ctenophora 0.59 (1 day) 

 Mollusca 

 Clams 

 Embryos 0.43 (2 days) 

 Larvae 1.3 (2 days) 

 Larvae 0.53 (10 days) 

 Pteropods < 0.2 (2 days) 

 Crustacea 

 Barnacles 2.6 (1-h LC50) 

 Copepods 1.0 (3 days) 

 Amphipods 0.3 (2 days) 2.5 (3 days) 

 Decapods 

 Shrimp post-larvae 1.7; 9.4 

 Lobsters 1.2-6.6 

 Teleosts 1.5 

 

 Adapted from US National Research Council (1985). Values are for total 

 measured (extractable) hydrocarbons, calculated from initial 

 concentrations measured by spectroscopy and chromatography 

 No. 2 fuel oil (mostly the water-soluble fraction) has been found 

 to have sublethal effects in all phyla examined (Anderson, 1977a,b, 

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 1979; US National Research Council, 1985). With increasing 

 concentrations, alterations were seen in the respiratory rate of the 

 fish Cyprinodon variegatus (Anderson et al., 1974) and Oncorhynchusm

 gorbuscha (pink salmon) (Rice et al., 1977b), the crustaceans 

 Mysidopsis almyra and Penaeus aztecus, and the glass shrimp 

 Palaemoetes pugio (Anderson, 1979); and changes were found in the 

 pulse rate in embryonic estuarine fish, C. variegatus and Fundulus

 heteroclitus (Anderson, 1977a) These effects have been used as a 

 measure of stress caused by exposure. Dysregulation of the ability to 

 regulate internal concentrations of solutes (osmotic and ionic 

 regulation) was demonstrated in the brown shrimp Penaeus aztecus

 (Anderson et al., 1974; Cox, 1974; Anderson, 1979). The behaviour of 

 F. similus exposed to a 100% water-soluble fraction of No. 2 fuel 

 oil was correlated with the content of naphthalene in four organs 

 (Dixit & Anderson, 1977). Sublethal studies on No. 2. fuel oil showed 

 reduced growth rates, survival, and reproduction in a range of 

 organisms (Anderson, 1979; Table 17), including the annelid Neanthes 

 arenaceodentata (Rossi & Anderson, 1978) and the estuarine fish 

 F. grandis (Ernst et al., 1977). 

 A9.1 Laboratory experiments 

 Diesel fuel is a complex mixture of substances with a range of 

 solubilities in water (see section A2.2). In testing for aquatic 

 toxicity, it is important that the constituents in the medium be 

 characterized (Bennett et al., 1990), but these are seldom reported. 

 The results described in this section refer to diesel fuel, unless 

 otherwise stated. 

 As the solubility of diesel fuel in sea and freshwater is low, 

 investigations of the effects of diesel fuel on organisms in the 

 laboratory often involve preparation of a water-soluble fraction or an 

 oil-water dispersion. Water-soluble fractions can be prepared by 

 stirring one part of diesel fuel into nine parts of (sea) water for 

 20 h (Anderson et al., 1974) or one part of diesel fuel into eight 

 parts of sea water for 24 h (Pulich et al., 1974), and then extracting 

 the water phase. The resulting water phases contain 6-20 μg/ml of 

 total hydrocarbons; the 100% water-soluble fraction of No. 2 fuel oil 

 contains about 7 μg/ml of total hydrocarbons. Results are expressed as 

 the concentration (percent dilution of the water-soluble fraction) 

 and/or as the measured hydrocarbon concentration that causes the 

 specified level of effect. The results cannot, however, be correlated 

 with the original amount of fuel oil that was added to produce the 

 water-soluble fraction or oil-water dispersion (CONCAWE, 1993). 

 Table 17. Effects of No. 2 fuel oil on the growth and reproduction of marine animals 

 

 Species Exposure Concentration (ppm) Growth or reproduction Reference 

 (days) 

 TH TN TA 

 

 Fish 

 Cyprinodon variegatus 7 2.0 0.6 1.7 0% of eggs hatched Anderson et al. (1976) 

 Decapods 

 Rithropanopeus harrasii 27 1.0 0.3 0.9 Reduced survival and Neff et al. (1976b) 

 extended development to 

 megalopa 

 Palaemonetes pugio 12 0.9 0.3 0.8 Reduced growth rate of Tatem (1977) 

 larvae 

 3 1.4 0.6 Reduced viability of eggs 

 from exposed gravid females 

 Polychaetes 

 Neanthes arenaceodentata 22 1.0 0.3 0.9 Reduced growth of larvae Rossi & Anderson (1976) 

 28 0.3 0.1 Reduced growth of Anderson (1977a) 

 juveniles by 30% 

 Ctenodrilus serratus 28 2.2 0.5 1.4 Reduced survival and Carr & Reish (1977) 

 reproduction 

 Ophryotrocha sp. 28 1.3 0.3 0.9 Reduced survival and Carr & Reish (1977) 

 reproduction 

 

 From Anderson (1977b) 

 TH, total hydrocarbons; TN, total naphthalenes; TA, total aromatic compounds 

 Oil-water dispersions are produced by shaking a measured quantity 

 of oil in water for 5 min (Anderson et al., 1974) or 30 min (Pulich et 

 al., 1974). In some cases, the oil-water dispersion is maintained by 

 continuous mixing, but more usually it is allowed to settle, and the 

 aquatic organisms are exposed to the material in the water and to a 

 surface film. The effects seen in such tests can be due to both 

 physical action and toxicity, especially in small invertebrates such 

 as Daphnia.

 Insoluble fractions of crude oil and other hydrocarbon 

 formulations strongly inhibited growth when they were 

 microencapsulated and ingested by juvenile mussels (Stromgren et al., 

 1986; Stromgren & Reiersen, 1988) and larvae (Stromgren & Nielsen, 

 1991). In microcapsules with a thin acacia-gelatine structure, the 

 total oil is dispersed into particles of 1-10 μm, which are suitable 

 for ingestion by Mytilus larvae. The water-soluble components leak 

 through the wall, providing a low concentration, and are ingested by 

 the molluscs. 

 None of the studies involved use of the 'water accommodated 

 fractions' recommended by CONCAWE (1993), which allows the results to 

 be expressed as 'loading rate', defined as the amount of product that 

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 must be equilibrated with the aqueous test medium in order to produce 

 a specified level of effect. 

 A9.1.1 Microorganisms 

 A9.1.1.1 Water 

 Marcus & Scott (1989) tested the effects of 0, 10, 20, and 40% 

 water-soluble fractions of a shale-diesel fuel mixture and a 

 petroleum-diesel fuel mixture on the growth of faecal coliform 

 bacteria. The 20 and 40% fractions of the petroleum-diesel fuel 

 mixture resulted in significantly lower bacterial densities than the 

 shale-diesel fuel mixture. The latter appeared to biostimulate or 

 mediate against toxicity, suggesting a difference in the chemical 

 characteristics of the two fuels. 

 The effects of diesel and furnace oils, petrol, kerosene, and 

 Assam crude oil and their paraffinic, aromatic, and asphaltic 

 fractions (higher relative molecular mass, poorly defined) on the 

 photosynthesis and respiration of blue-green algae (Cyanobacteria), in 

 particular Anabaena doliolum were investigated by Singh & Gaur (1990). 

 The chemical composition of the diesel and furnace oils was almost 

 identical, with 37 and 36% paraffins, 51 and 54% aromatic compounds, 

 and 6 and 0.6% asphaltic compounds, respectively. The aromatic 

 fractions of these oils were the most toxic, followed by the asphaltic 

 fractions; photosynthesis was reduced to 40% by the aromatic fractions 

 and to 50% by the asphaltic fractions of both oils at a concentration 

 of 5.0 mg/litre. The effects were dependent on concentration up to 

 10 mg/litre. Photosynthesis was stimulated 160% by 5 mg/litre of the 

 paraffinic fractions of crude oil , but only 100% by those of diesel 

 oil and 110% by those of furnace oil. In general, crude oil inhibited 

 photosynthesis and respiration by A. doliolum least and diesel and 

 furnace oils the most. 

 A9.1.1.2 Soil 

 In outdoor lysimeters, the toxicity of spills of 2.3 ml/cm2

 diesel and heating fuels was investigated in soil microbes, using 

 Microtox(R) measurements (Wang & Bartha, 1990). (For parallel assays 

 of seed germination and plant growth, see section A9.1.3.1.) At time 

 0, both fuels were moderately toxic (EC50 = 80-90 mg of contaminated 

 soil); this was followed by a period of increased toxicity, which 

 started to decrease after 6-12 weeks. The values in soils treated by 

 biodegradation returned to background within 20 weeks, although diesel 

 fuel had significant residual toxicity in untreated soil. Seed 

 germination and plant growth were inhibited in a similar manner, and 

 diesel oil was more toxic and persistent than heating oil (section 

 A9.1.3.1). Biodegradation treatment, in which the conditions for 

 hydrocarbon degradation by microbes were optimized by mixing, 

 aeration, pH control, and addition of mineral nutrients (fertilizers), 

 strongly decreased fuel persistence and toxicity. 

 A9.1.2 Aquatic organisms 

 A9.1.2.1 Plants (phytoplankton) 

 Experiments in both the laboratory and the field have shown that 

 hydrocarbons can inhibit algal growth, although enhancement is 

 occasionally noted at lower concentrations of oil (US National 

 Research Council, 1985). 

 After 12 days of exposure to 10% diesel oil, the growth of cells 

 of Euglena gracilis was not significantly reduced, whereas a 

 concentration of 0.1% almost completely inhibited the growth of 

 Scenedesmus quadricauda. Cells of S. quadricauda grown in culture 

 media containing diesel fuel (concentration not given) became 

 chlorotic, suggesting damage to the photosynthesizing system 

 (Dennington et al., 1975). 

 A concentration of 0.05% light diesel fuel was found to stimulate 

 growth rate, growth yield, photosynthesis, and chlorophyll a 

 synthesis, while at the same time slightly inhibiting the respiration 

 of Chlorella salina CU-1 (Chan & Chiu, 1985). At higher 

 concentrations (0.5 or 5%), the growth rate, growth yield, and 

 photosynthesis were greatly reduced (to 50, 50, and 62% and 43, 32, 

 and 41% of the control levels, respectively), but the effect on algal 

 respiration was less severe (81% with 0.5% diesel and 86% with 5%). 

 Diesel fuel containing dispersants caused greater inhibition than did 

 the compounds separately. 

 The lengthwise growth of the benthic algae Ascophyllum nodosum

 and Laminaria digitata and other rocky-shore communities was 

 measured while they were kept in 50-m3 concrete basins and exposed 

 continuously to diesel fuel for two years (Bokn, 1987). An average 

 hydrocarbon concentration of 130 μg/litre continuously inhibited 

 growth in both species, while a concentration of 30 μg/litre caused 

 periodic inhibition. Under oil-free conditions during the subsequent 

 season, the plants recovered completely. 

 Boiler fuel was more toxic than diesel fuel to the kelp 

 Macrocystis; both fuels reduced photosynthesis (Baker, 1970). 

 A9.1.2.2 Invertebrates 

 (a) Several species 

 The acute toxicity of diesel fuel to Daphnia (Cladocera), 

 chironomid (insect) larvae, and the mollusc Viviparus bengalensis

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 (Gastropoda) was tested after the organisms were acclimatized to 

 laboratory conditions for four, two, and four days, respectively. The 

 bioassays were conducted at 28 ± 2°C with unchlorinated borehole water 

 (pH 7.0 ± 0.2; oxygen, 8 mg/litre; free carbon dioxide, 1.2 mg/litre; 

 total alkalinity as calcium carbonate, 240 mg/litre; hardness, 

 260 mg/litre). The results are shown in Table 18. Plankton and insect 

 larvae exhibited erratic, uncoordinated movements before becoming 

 lethargic. In the mollusc, active avoidance and heavy secretion of 

 mucus were observed. The concentrations at which these behavioural 

 changes occurred were not specified (Das & Konar, 1988). 

 Fourteen species of five phyla (Echinodermeta, Mollusca, 

 Annelida, Arthropoda, and Urochordata) were exposed to 0.5% No. 2 

 diesel fuel in sea water. Only the larvae of the echinoderm 

 Crossaster, which were also the largest, survived up to eight days; 

 all of the other larvae died 3-72 h after being placed in the 

 fuel-water mixture (Chia, 1973). 

 The periwinkles Pachymelania aurita (Muller) and Tympanotonus

 fuscatus (Linne) were exposed to refined diesel fuel films for 24 

 and 48h at concentrations of 2.5, 5.0, 7.0, or 10.0% and to emulsions 

 for 24 h at concentrations of 0.5, 1.5, 2.5, or 3.5%; they were then 

 shaken for 2 min with brackish water. After exposure to the emulsion, 

 the periwinkles were washed and reintroduced into oil-free, brackish 

 water for 24 h and their activity recorded. Both surface films and 

 emulsions were harmful to both gastropods, the emulsions being the 

 more toxic. T. fuscatus was less susceptible than P. aurita,

 possibly because the former can retract further into its shell. The 

 mean percentage survival in the presence of oil film (7.5% diesel 

 fuel) was 100% at 24 h and 80% at 48 h for T. fuscatus and 80% at 24 h 

 and 50% at 48 h for P. aurita. The mean percentage survival in the 

 presence of 3.5% diesel fuel-water emulsion was 90% for T. fuscatus

 and 80% for P. aurita (Dambo, 1993). 

 Table 18. Acute toxicity of diesel fuel to Daphnia (Cladocera), 

 chironomid larvae (insects), and the mollusc Viviparus 

 bengalensis (Gastropoda) 

 

 Species LC5 (mg/litre) LC50 (mg/litre) LC95 (mg/litre) 

 

 Daphnia magna 1.5 (0.8-2.5) 20 (19.2-21.0) 38.5 (37.5-39.5) 

 Chironomid 5.0 346.0 (238-455) 865.0 (750-1018) 

 larvae 

 Viviparus 2.0 254.0 (185-320) 637.0 (575-700) 

 bengalensis 

 

 From Das & Konar (1988) 

 (b) Molluscs 

 The feeding rate and growth of mussels ( Mytilus edilus L.) was 

 markedly reduced when they were exposed to 30 or 130 μg/litre diesel 

 fuel for eight months (Widdows et al., 1985). Recovery of 

 physiological responses (clearance rate, respiration, food absorption 

 efficiency, and ammonia excretion) after transfer to unpolluted water 

 was concomitant with the depuration of hydrocarbons from the tissues. 

 Mussels exposed to either dose recovered completely within about 55 

 days. 

 The effects on the nutrient storage system and reproductive 

 cell systems of the mussel M. edilus of exposure to a diesel 

 hydrocarbon-sea water emulsion and subsequent depuration were studied 

 in order to assess the capacity of these systems to recover after 

 discontinuation of exposure to the oil. After 144 days of exposure to 

 hydrocarbon concentrations of 27 and 128 units, the volume of storage 

 cell types was significantly reduced and there was a reduction in the 

 volume of ripe gametes. After 53 days of depuration, the volume of the 

 storage cells and of developing gametes increased. Exposure to either 

 concentration also increased the volume of atretic (degenerating) 

 gametes, but depuration allowed a return to normal (Lowe & Pipe, 

 1986). The authors suggested that exposure to the hydrocarbons reduced 

 the storage reserves and increased gamete atresia and resorption, so 

 that the storage pool was partially replenished, enabling the organism 

 to tolerate better the hydrocarbon insult. 

 The sensitivity of M. edulis to pollution with diesel fuel 

 depends on the salinity of the water (Tedengren & Kautsky, 1987). Low 

 salinity and diesel fuel acted synergistically to a greater degree in 

 Baltic than in North Sea mussels. 

 Adults and larvae of M. edulis were exposed to microencapsulated 

 diesel fuel at concentrations of 200, 600, 1000, 1300, or 

 5000 μg/litre and the effects on mortality, larval growth, and 

 spawning frequency were recorded (Stromgren & Nielsen, 1991). The EC50

 for spawning in mussels exposed for 30 days was about 800 μg/litre, 

 and the LC50 (30days) for maturing mussels was about 5000 μg/litre. 

 The longitudinal growth of larvae was significantly reduced at 

 10 μg/litre; the EC50 for growth (10 days) corresponded to about 

 25-30 μg/litre (Stromgren & Nielsen, 1991), which is lower than the 

 EC50 of about 1000 μg/litre for growth of juvenile mussels reported 

 by Stromgren & Reiersen (1988). 

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 Diesel fuel is therefore more toxic to mussel larvae than to 

 juveniles. 

 The EC50 values (10 days) for growth of larvae of the Quahog 

 clam, Mercenaria spp., exposed to water-soluble fractions of various 

 crude and refined fuels were 220-4200 μg/litre, indicating that the 

 insoluble fractions of hydrocarbons, ingested as microcapsules, are 

 far more toxic than the water-soluble fractions alone (Byrne & Calder, 

 1977). Stromgren et al. (1986) drew the same conclusion from their 

 results for the growth of juvenile mussels. Larval mortality during 

 exposure to diesel fuel increased steeply up to 50 μg/litre, at which 

 dose only 20-30% survived 10 days of exposure. At 500 μg/litre, there 

 was 100% mortality. Byrne & Calder (1977) reported LC50 values (10 

 days) of 50-2100 μg/litre for larvae of Mercenaria spp.

 (c) Crustaceans 

 Freshwater crabs (Barytelphusa cunicularis) were exposed to 

 sublethal concentrations of diesel fuel (4.5, 3.7, 3.2, and 2.6 ppm) 

 for 24, 48, 72, and 96 h, respectively (Sarojini et al., 1989). The 

 oxygen consumption of the crabs was measured as an index of stress 

 caused by the fuel and compared with that of normal controls. The 

 crabs responded in general by lowering their oxygen consumption up to 

 8 h (down to 50% at 4 h), particularly at the lower doses; with longer 

 exposures, the oxygen consumption was higher than (approx. 120% at 

 24 h) or equal to (at 96 h) that of the controls. 

 Gammarus spp. (Crustacea, Amphipoda) were obtained from marine 

 and brackish water in the North and Baltic Seas and tested in two 

 laboratories for their sensitivity to diesel-fuel pollution (Tedengren 

 et al., 1988). G. oceanicus was obtained from the Fucus belt at a 

 depth of 1-3 m and G. duebeni from rock pools of various salinities. 

 The respiration, excretion, and atomic O:N and O:P ratios of the two 

 species were compared after a 6-h exposure to 10 mg/litre diesel fuel 

 emulsified in a syringe and injected into experimental aquaria; the 

 resulting hydrocarbons were not measured. Exposure to diesel fuel 

 generally resulted in decreased oxygen consumption and a rise in 

 nutrient excretion, leading to lowered O:N and O:P ratios. 

 G. oceanicus was the most sensitive, and the response was aggravated 

 by simultaneous lowering or raising of the salinity. No signs of 

 impaired swimming or other physical or mechanical effects were 

 detected in either species. The investigators concluded that 

 G. duebenihas a greater tolerance to pollutants and changes in 

 salinity, probably because it has broad physiological niches and has 

 evolved in and become adapted to more variable environments. 

 In a comparison of the effects of an oil-water dispersion of 

 diesel fuel, kerosene, gasoline, and benzene on the tidepool copepod 

 Tigriopus californicus, diesel fuel was the most detrimental: a 

 concentration of 0.10 ml/litre sea water caused 100% mortality within 

 five days (Barnett & Kontogiannis, 1975). 

 (d) Fish 

 Freshwater 

 Table 19 shows the results of a series of 96-h static tests for 

 acute toxicity with diesel fuel in freshwater on several species of 

 juvenile salmonids, Oncorhynchus kisutch (coho), O. gorbuscha

 (pink), and O. mykiss (rainbow trout), exposed at 14°C in 16 h of 

 light and 8 h of darkness (Wan et al., 1990). The average loading 

 density was 250 mg/litre (range, 100-420 mg/litre) of Canadian diesel 

 fuel with a pour-point of -17.8°C. Three types of water were used for 

 dilution: soft acid city tapwater, hard alkaline lakewater, and 

 intermediate reconstituted deionized city tapwater. The LC50 values 

 varied between the species from 32 to 33216 mg/litre. Diesel fuel was 

 more toxic to pink salmon than to coho salmon or rainbow trout, 

 irrespective of the water type. 

 The LC values for diesel fuel in golden orfe (Leuciscus idus

 melanotus) in a static test were: LC0 = 40-120 mg/litre; LC50 = 

 120-160 mg/litre; LC100 = 160-205 mg/litre (Juhnke & Lüdemann, 

 1978). 

 Various freshwater fish (Fundulus diaphanus, Roccus saxatilis,

 Lepomis gibbosus, Roccus americanus, Anguilla rostrata, and Cyrinus

 carpio) were exposed to No. 2 or No. 4 fuel oil (both dispersed) in 

 a static test at 19°C, pH 7.1, and 60 mg/litre hardness (Rehwoldt et 

 al., 1974). The 96-h LC50 values for No. 2 fuel oil ranged from 

 22.2 mg/litre for striped bass (Roccus saxatilis) to 49.1 mg/litre 

 for carp (Cyrinus carpio); those for No.4 fuel oil ranged from 

 21 mg/litre for banded killifish (Fundulus diaphanus) to 48.1 mg/litre 

 for carp. These concentrations represent total oil added and not the 

 oil dissolved in the water column. 

 Table 19. Acute toxicity of diesel fuel to juvenile Pacific salmonids in different 

 types of freshwater 

 

 Water type Salmonid LC50 (mg/litre 

 

 24-h 48-h 72-h 96-h 

 Soft Coho 28 972 28 972 12 345 10 299 

 Pink 1 972 276 84 74 

 Rainbow > 32 000 5 525 4 600 3 017 

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 Intermediate Coho > 55 560 > 55 560 33 216 33 216 

 (reconstituted) Pink 1 829 376 133 123 

 Rainbow 168 363 168 363 28 787 2 186 

 Hard (lake) Coho > 26 743 26 743 4 845 3 333 

 Pink 1 404 302 48 32 

 Rainbow > 23 108 23 108 5 102 2 447 

 

 From Wan et al. (1990). Coho, Oncorhynchus kisutch; pink, O. gorbuscha; rainbow 

 trout, O. mykiss 

 The LC50 values of water-soluble fractions and emulsions and 

 the floating layer of No. 2 fuel oil for four freshwater species under 

 static and flow-through conditions are shown in Table 20 (Hedtke & 

 Puglisi, 1982). 

 Marine 

 In an investigation of the threshold doses at which cod (Gadus

 morhua L.) detected samples of Ekofisk diesel fuel, sea water was 

 allowed to gravitate through the diesel fuel. The total content of 

 dissolved materials, estimated by gas chromatography, were 15% 

 benzenes, 2% toluenes, 6% xylenes, 15% naphthalenes, 3% phenols, 42% 

 n-alkanes (C10-C25), and 17% unidentified compounds. There were 

 no visible surface films or microdroplets in the samples, although the 

 authors suspected the presence of undissolved microdroplets. Behaviour 

 was observed with a sea-water olfactometer, and reaction patterns 

 after injection of samples (snapping, increased activity, coughing, 

 darting, backing) were noted. The most frequent reaction was snapping 

 of jaws followed by a short period of activity. None of the doses 

 produced alarm reactions. The mean activity scores increased with 

 increasing doses of oil compounds. In a set of four experiments, the 

 threshold for detection of diesel oil compounds was 100-400 ng/litre, 

 showing that cod detect fuel compounds at doses lower than those 

 hitherto observed (Hellstrom & Doving, 1983). 

 The effect of acute exposure to the water-soluble fraction of 

 Arctic diesel fuel (1:9 with sea water) on survival and metabolic rate 

 was studied in an Antarctic fish (Pagothenia borchgrevinki). The 

 fish proved to be extremely tolerant and withstood an undiluted 

 water-soluble fraction for at least 72 h. None died as a direct 

 consequence of contact with the water-soluble fraction, but they 

 showed signs of stress. In unpolluted water, little spontaneous 

 swimming activity was seen, but on transfer into water containing 

 diesel fuel they became agitated and increased their swimming activity 

 for a short time. Their ventilation rates increased but later 

 decreased; the depth of each ventilation increased considerably. 

 Coughing became apparent shortly after transfer and persisted for up 

 to 72 h. The haematocrit increased and remained elevated throughout 

 the experiment. Oxygen consumption was increased to about twice that 

 of the controls (Davison et al., 1992). 

 In further studies on P. borchgrevinki (Davison et al., 1993), 

 a water-soluble fraction was prepared (1:2 with sea water) and then 

 diluted to 33%; the fish were kept for seven days. On initial 

 placement, behaviour similar to that with the higher concentration in 

 the previous experiment was noted. After seven days, the only 

 noticeable differences between exposed and control fish of similar 

 weight and length were large amounts of mucus streaming from opercula, 

 increased coughing, and slightly deeper ventilation. Plasma chloride 

 and osmolarity were similar in the two groups. Haematocrit and 

 haemoglobin concentration were significantly higher in the treated 

 fish; spleen weights and oxygen consumption were similar. This 

 Antarctic fish can thus survive prolonged periods of exposure to low 

 levels of water-soluble hydrocarbons. 

 Table 20. 96-h LC50 values for No. 2 fuel oil on freshwater organisms under various conditions 

 

 Species Life stage Test conditions Effect Concentration

 (μl/litre water) 

 

 Jordanella floridae (flagfish) Adult Water-soluble fraction of 10% No mortality No dilution 

 oil-water mixture; static 

 Emulsion; flow-through LC50 60.5 

 Pimephales promelas (fathead minnow) Adult Emulsion; flow-through LC50 38.6 

 Water-soluble fraction of 10% No mortality No dilution 

 oil-water mixture; static 

 Floating layer; static LC50 > 160 000 

 48 300 (2nd 

 sample) 

 Rana sylvatica (frog) Larvae Water-soluble fraction of LC50 413 000 

 10% oil-water mixture; static 

 Emulsion; static LC50 26.4 

 Emulsion; flow-through LC50 4.9 

 Floating layer; static LC50 < 5000 

 Ambystoma maculatum (salamander) Larvae Emulsion; flow-through LC50 86.4 

 

 From Hedtke & Puglisi (1982) 

 (e) Amphibians 

 Larvae of the frog Rana sylvatica were tested in 96-h static and 

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 flow-through tests with No. 2 fuel oil as a water-soluble fraction, an 

 emulsion, or a floating layer (Hedtke & Puglisi, 1982) (Table 20). 

 Flow-through exposure to the emulsion was the most toxic (LC50 = 

 4.9 μl/litre), and static exposure to the water-soluble fraction was 

 the least toxic (LC50 = 413 000 μl/litre). The LC50 of No. 2 fuel 

 oil emulsion in larvae of the salamander Ambystoma maculatum in a 

 flow-through test was 86.4 μl/litre). 

 A9.1.3 Terrestrial organisms 

 A9.1.3.1 Plants 

 Seed germination and growth of soya beans and ryegrass were 

 inhibited by a diesel fuel spill of 2.3 ml/m2 (Wang & Bartha, 1990; 

 see sections A3.2.4 and A9.1.1.2). Four weeks after the spill, 

 biodegradation had at least partially restored the ability of the soil 

 to support seed germination and plant growth. Morphological effects, 

 such as reverse geotropism, were noted on some partially emerged 

 seedlings. In untreated diesel-contaminated soil, there was no 

 evidence of seed germination or plant growth. Parallel experiments 

 showed that heating oil was less toxic. 

 A9.1.3.2 Invertebrates 

 No data were available. 

 A9.1.3.3 Vertebrates 

 Birds are affected externally and internally by oil 

 contamination. The fuel rapidly destroys the waterproofing of the 

 birds' plumage, and as the birds attempt to preen the contaminant off 

 their feathers they ingest fuel. When No. 1 fuel oil was administered 

 by gavage at doses of 1-4 ml/kg body weight to ducks, a dose of 

 2 ml/kg caused lipid pneumonia, extreme inflammation of the lungs, and 

 fatty infiltration and degeneration of the liver after 24 h (Croxall, 

 1977). Administration of 1 ml of diesel or No. 1 fuel oil/kg produced 

 severe irritation of the digestive tract (enteritis), with diarrhoea 

 and bile pigments in faeces. Signs of toxic nephrosis were also noted. 

 Adrenal enlargement (mainly hyperplasia of cortical tissue), 

 depression of plasma cholinesterase levels, and incoordination, 

 ataxia, and tremors were reported at higher doses. The treatment was 

 not fatal to healthy birds, even at doses up to 20 ml/kg body weight; 

 however, when No. 1 fuel and diesel fuel were administered to birds 

 under stress, the LD50 was 3-4 ml/kg body weight (Hartung & Hunt, 

 1966). 

 A9.2 Field observations 

 The following information is derived mostly from observations 

 made after diesel spills (see Table 10). 

 A9.2.1 Microorganisms 

 A9.2.1.1 Water 

 No data were available. 

 A9.2.1.2 Soil 

 Six weeks after the ship Bahia Paraiso spilled Arctic diesel 

 fuel into the Antarctic Sea, the impact of the spill on microbial 

 ecology was investigated (Karl, 1992). The acute effects on the 

 metabolic activities of sedimentary microorganisms appeared to be 

 negligible, even in saturated sea water. 

 A9.2.2 Aquatic organisms 

 In field studies conducted after fuel spills to investigate the 

 effects on populations and ecosystems, zooplankton appeared to be 

 highly vulnerable to dispersed and dissolved petroleum constituents 

 but less so to floating oils. Field observations on oil spills in 

 general showed that individual organisms were affected in many ways, 

 including direct mortality (fish eggs, copepods, mixed plankton), 

 external contamination by fuel (chorion of fish eggs, cuticles, and 

 feeding appendages of crustacea), tissue contamination by aromatic 

 constituents, abnormal development of fish embryos, and altered 

 metabolic rates (US National Research Council, 1985). A spill of 

 No. 2 diesel fuel was extremely toxic: faunal repopulation of the 

 affected areas did not occur during the subsequent eight months 

 (Blumer et al., 1970). A spill of 750000 litres of No. 2 diesel fuel 

 caused substantial mortality in some taxa of the intertidal 

 population, whereas others showed little or no effect. There was 

 substantial recovery within six months, and there was no observable 

 mortality among the subtidal fauna or flora (Woodin et al., 1972). 

 After a spill of marine diesel fuel (2000-3000 t) off Hong Kong, much 

 of the oil was carried to land by onshore winds. Wormald (1976) 

 described the effects of the oil spill on intertidal meiofauna. Within 

 four days of the spill, there was almost total mortality: nematodes 

 and harpacticoid copepods were observed in an advanced state of decay, 

 and other meiofauna were not detected. The aromatic fractions probably 

 evaporated within four to six weeks but persisted longer in deeper 

 sediment. Harpacticoids and nematodes did not recolonize the beach 

 until nearly eight months after the spill. The density of meiofauna at 

 all stations observed reached a maximum 10 months after the spill and 

 subsequently showed large fluctuations, which were probably the result 

 of ecological successions during recovery of the beach fauna. One year 

 later, an increase in the number of macrofauna, especially polychaete 

 worms, was noted, which may have been responsible for the decrease in 

 meiofaunal populations. High rainfall 11 months after the spill may 

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 have brought the soluble aromatic compounds nearer to the surface and 

 decreased the harpacticoids and nematode populations. After 15 months, 

 the meiofauna were again well established. Recovery at high shore 

 stations began only when the oil content of the sediment had decreased 

 by at least 50%, primarily through physical dispersion. Recolonization 

 of the lower shore had occurred earlier. Stirling (1977) studied the 

 effects of this spill on rocky shore fauna (see also Table 10), 

 concentrating on large, common species of gastropods (Monodonta labio,

 Thais clavigera, Nerita albicilla, N. polita, Lunella coronata,

 Clypeomorus humilis, and Planaxis sulcatus), bivalve molluscs (Donax

 semignosus, Atactodea striata, Tapes philippinarum, and Circe

 stutzeri), and crustaceans (shore and hermit crabs). Acute mortality 

 of gastropods was greatest at moderately contaminated sites where 

 oil-dispersing chemicals had been applied to floating oil slicks. 

 Long-term disturbances were most significant at the heavily polluted 

 sites where dispersants had not been used. Recovery of animals taken 

 from the oiled beaches was studied in clean salt water in the 

 laboratory. Bivalve molluscs and the gastropods Monodonta labioand

 Thais clavigera were the most sensitive and Clypeomorus humilisand

 Planaxis sulcatus the least sensitive. Field observations of acute 

 mortality were consistent with this order of sensitivity. Population 

 studies showed the greatest reductions in Monodonta labio and Nerita

 albicilla, which were eliminated for at least 13 months from the 

 site of greatest oil pollution. 

 The release of 600 000 litres of Arctic diesel fuel from the 

 Bahia Paraiso in 1989 coated intertidal macroalgae, limpets, and 

 birds as well as sediments and shores (Kennicutt et al., 1991b). 

 Macroalgae (Leptosomia simplex and Monostroma spp.) were only 

 moderately affected. Intertidal limpet (Nacella concinna) populations 

 were reduced by 50% within the first few weeks after the spill 

 (Kennicutt et al., 1990), and a year later had still not fully 

 recovered (Kennicutt & Sweet, 1992). Bottom-feeding organisms, such as 

 clams (Laternula elliptica) and fish (Harpagifer anarcticus and 

 Notothenia coriiceps neglecta) were found to have PAHs in their gut 

 contents and muscle tissues (Kennicutt et al., 1991b). After the 

 spill, all of the chicks of the local population of South Polar skuas 

 (Catharacta maccormicki) died, although few of the adults or the 

 chicks died from direct contact with oil (Eppley, 1992). Within less 

 than two years, and at many locations within a few weeks, the PAH 

 content of sediment and intertidal organisms returned to background 

 levels (Kennicutt & Sweet, 1992), owing partly to the high volatility 

 of the spilled fluid and the high energy environment. Sampling of 

 intertidal limpets showed that the tissue contaminants were primarily 

 naphthalenes, but fluorenes and phenanthrenes were often the most 

 abundant aromatic contaminants in tissues with higher concentrations 

 of PAHs (Kennicutt & Sweet, 1992; Kennicutt et al., 1992b) After a 

 spill of 8000 litres of diesel fuel into an unspoiled freshwater 

 stream in California, United States, most animals were affected within 

 one to four days. Thousands of aquatic insects perished; some 

 crayfish, aquatic leeches, and freshwater planarians were killed; and 

 over 2500 fish, tadpoles (but no frogs), snakes, a turtle, and common 

 merganser (Mergus merganser) were found dead (Bury, 1972). 

 A9.2.3 Terrestrial organisms 

 A9.2.3.1 Plants 

 Diesel fuel was applied at 10 litres/m2 to the soil of five 

 common plant communities in north-east Greenland, comprising wet 

 marsh, grassland, and three types of dwarf-shrub heath. The plant 

 species were observed for up to three years after the application. 

 Within a few days, most species had lost chlorophyll or had abscissing 

 leaves. Species with xeromorphic leaf characteristics reacted more 

 slowly than species with orthophyllous leaves. During three successive 

 growing seasons, shrubs and forbs showed no signs of recovery. 

 Graminoids showed slight resistance and recovered in all mesic and wet 

 plots but were killed in dry plots. Three species of sedge (Carex

 bigelowii, C. saxatilis, and C. stans) and mosses recovered to some 

 extent in all plots. Recovery of mosses was excellent in the wet 

 plots, good in the mesic plots, and poor in the dry plots. In general, 

 the phytotoxic effects of diesel fuel were much more pronounced than 

 those of crude oil in similar plots (Holt, 1987). 

 A9.2.3.2 Invertebrates 

 No data were available. 

 A9.2.3.3 Vertebrates 

 No data were available. 

 A10. EVALUATION OF HUMAN HEALTH RISKS AND EFFECTS ON THE ENVIRONMENT

 A10.1 Evaluation of human health risks 

 Diesel fuel is produced commercially in various qualities with 

 regard to volatility, aromaticity, cetane number, and sulfur content. 

 The composition of diesel fuel, which influences the type and amount 

 of compounds emitted in the exhaust, has not changed greatly during 

 the last few decades, although the cetane number has been slightly 

 increased, resulting in better ignition, and the sulfur content, which 

 influences the release of particulate matter, has been reduced in some 

 countries. Owing to the lack of data on diesel fuel, some data on 

 heating oils and kerosenes (jet fuels) with compositions similar to 

 that of diesel fuel are included in the evaluations of toxicological 

 and environmental effects. 

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 A10.1.1 Exposure of the general population 

 The general population can be exposed to diesel fuel and other 

 middle distillates at filling stations, as a result of accidental 

 spills, when handling such fuels, or when using kerosene for domestic 

 cooking or heating. No data on exposure were available. 

 A10.1.2 Occupational exposure 

 Workers can be exposed to diesel fuel and other middle 

 distillates during manual handling and discharge of the fuel, i.e. 

 during retailing at filling stations; manufacture, repair, 

 maintenance, and testing of diesel engines and other equipment; in 

 jobs where diesel fuel is used as a cleaning agent or solvent; and in 

 the handling and routine sampling of diesel fuel in the laboratory. At 

 room temperature, very low concentrations of vapours are likely to be 

 generated from diesel fuel because of its low volatility; significant 

 levels of vapour are likely to occur only in confined spaces and at 

 high temperatures. 

 A10.1.3 Non-neoplastic effects 

 Diesel fuels are toxic when ingested, usually accidentally. 

 Ingestion may result in regurgitation and aspiration, which can cause 

 chemically induced pneumonia. The latter effect is, however, not 

 specific for diesel fuel and can occur with all hydrocarbons of a 

 particular viscosity range. 

 Exposure to vapours is minimal during normal handling of diesel 

 fuel. The most likely effect on human health is dermatitis as a result 

 of skin contact. Dermal absorption takes place and can result in acute 

 toxic effects on the kidney. The health effects of long-term 

 absorption of low levels are unknown, but the available data on acute 

 human toxicity indicate that practices such as washing hands in diesel 

 fuel should be avoided. Although groundwater contamination and entry 

 into drinking-water are potential sources of adverse health effects, 

 such contamination would be noticeable and affect palatability so that 

 inadvertent ingestion of contaminated drinking-water is unlikely. 

 In experimental animals, diesel fuel has little acute toxicity after 

 exposure orally, dermally, or by inhalation. The oral LD50 values in 

 rats were > 5000 mg/kg body weight and those in mice, rabbits, and 

 guinea-pigs even higher. After short-term dermal exposure of mice for 

 14 consecutive days, the NOAEL for two middle distillates (marine 

 diesel and JP-5 navy fuel) was 5000-8000 mg/kg body weight per day. 

 Inhalation of up to 0.2 mg/litre had a neurodepressive effect in mice 

 but not in rats. Subchronic exposure to various distillate fuels 

 induced mainly alpha2-microglobulin nephropathy in male rats, which is 

 not considered relevant for humans. 

 Female mice that received dermal applications of 250 or 500 mg/kg 

 body weight per day of marine diesel fuel or JP-5 navy fuel on five 

 days per week for 103 weeks showed decreased survival due to severe 

 ulceration. Rats and mice exposed by inhalation to 1 or 5 mg/litre had 

 significant alterations in organ weight. 

 Diesel fuel irritates the skin but not the eye. 

 Exposure to diesel or jet fuels orally or by inhalation was 

 neither embryotoxic nor teratogenic in rats; although doses toxic to 

 the dams reduced fetal weight, no effects on viability were seen. 

 No clear evidence of mutagenic activity was seen in a series of tests 

 in Salmonella typhimurium. A positive response achieved only under 

 special conditions appeared to be equivocal. Other tests for 

 genotoxicity in vitro or in vivo did not show clearly positive 

 responses. 

 Owing to lack of data, a quantitative risk assessment is not 

 possible. 

 A10.1.4 Neoplastic effects 

 A case-control study of cancers at several sites in relation to 

 exposure to diesel fuel suggested an increased risk for lung cancer 

 other than adenocarcinoma and for prostatic cancer. In neither case 

 was there an exposure-response relationship. As few studies were 

 available, the number of cases was small, and the confidence intervals 

 were correspondingly wide, no conclusion can be drawn at present about 

 the carcinogenicity to humans of diesel fuel. 

 Twelve studies of dermal carcinogenicity in animals demonstrated 

 that diesel fuels have weak carcinogenic potency in mice. As no clear 

 genotoxicity is seen, cancer may be induced by nongenotoxic 

 mechanisms, such as chronic dermal irritation characterized by 

 repeated cycles of skin lesions and epidermal hyperplasia. 

 A10.2 Evaluation of effects on the environment 

 Although there are numerous data on the environmental behaviour 

 of the individual components of diesel fuel, few data are available 

 on diesel fuel as a whole. The environment can be polluted by 

 accidental release of diesel fuel on a large scale, such as during 

 tanker disasters and pipeline leaks, or on a smaller scale, from 

 contamination of soil around factories and garages. 

 In water, diesel fuel spreads out almost immediately, polar and 

 low-relative-molecular-mass components dissolve and leach out of the 

 slick, volatile components evaporate from the water surface, and 

 microbial degradation begins. The extent to which such 'weathering' 

 takes place depends on the temperature and climatic conditions, and 

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 the chemical composition of spills changes with time. After spillage 

 on water, some fractions evaporate, and the evaporated diesel 

 components are degraded photochemically. In sediment, diesel fuel is 

 generally delivered to bottom sediments by settling particles. In 

 soil, the various components of diesel fuel migrate at different 

 rates, depending on the soil type. 

 The individual constituents of diesel fuel are inherently 

 biodegradable, but the rates depend greatly on the physical and 

 climatic conditions and microbial composition. PAHs are the most 

 recalcitrant molecules. 

 Aquatic organisms, in particular molluscs, bioaccumulate 

 hydrocarbons to various extents, but the hydrocarbons are depurated on 

 transfer to clean water. Bioaccumulation of diesel fuel may occur, but 

 there are few data to indicate biomagnification. 

 Although there have been a number of spills of diesel fuel, few 

 reports are available on their environmental effects. Generally, 

 diesel fuel is more toxic than crude oil to aquatic and plant species. 

 Spills of diesel fuel have an immediate detrimental effect on the 

 environment, causing substantial mortality of biota; recolonization 

 occurs after about one year, depending on the animal and plant species 

 involved and the chemical and physical content of the spill residues. 

 Aquatic organisms that survive diesel fuel spills can still be 

 affected by external contamination and tissue accumulation; abnormal 

 development and altered metabolic rates are signs of such stress. 

 There are few data on the effects of diesel fuel on aquatic and 

 terrestrial organisms in experimental situations. In studies of 

 water-soluble fractions and emulsions of diesel fuel, the actual 

 chemical composition has rarely been analysed, although this is 

 crucial to an understanding of the toxicity of diesel fuel. No data 

 are available about flow-through conditions or mesocosms, which better 

 reflect environmental conditions 

 A11. RECOMMENDATIONS

 A11.1 Recommendations for the protection of human health 

 Exposure to diesel fuel may cause irritation and dermatitis; 

 therefore, skin contact should be avoided, and diesel fuel should not 

 be used for cleaning purposes. 

 A11.2 Recommendation for the protection of the environment 

 As for all petroleum products, accidental releases to the 

 environment should be avoided and should be cleaned up as soon as 

 possible if they occur. 

 A11.3 Recommendations for further research 

 A basic data set on the aquatic toxicity of diesel fuels, 

 including complete analysis of test substances, should be generated. 

 The fate and environmental impact of diesel fuel spills and leakages 

 should be investigated in laboratory and controlled field studies. 

 The exposure of humans to diesel fuel in various situations should be 

 quantified. 

 The mechanism of the carcinogenic action of diesel fuel on the 

 skin of experimental animals should be clarified. 

 A12. PREVIOUS EVALUATIONS BY INTERNATIONAL BODIES

 The carcinogenic risks of diesel fuels for human beings were 

 evaluated by a working group convened by the International Agency for 

 Research on Cancer in 1988 (International Agency for Research on 

 Cancer, 1989a). It concluded that there was inadequate evidence for 

 the carcinogenicity of diesel fuels in humans, and there was limited 

 evidence for the carcinogenicity of marine diesel fuel in experimental 

 animals. 

 PART B

 B1. SUMMARY

 B1.1 Identity, physical and chemical properties, and analytical 

 methods 

 Diesel engine exhaust emissions contain hundreds of chemical 

 compounds, which are emitted partly in the gaseous phase and partly in 

 the particulate phase of the exhaust. The major gaseous products of 

 combustion are carbon dioxide, oxygen, nitrogen, and water vapour; 

 carbon monoxide, sulfur dioxide, nitrogen oxides, and hydrocarbons and 

 their derivatives are also present. Benzene and toluene are present in 

 the lower weight percent range in the gaseous part of the hydrocarbon 

 fraction. Other gaseous exhaust components are low-relative-molecular- 

 mass polycyclic aromatic hydrocarbons (PAHs). 

 A main characteristic of diesel exhaust is the release of 

 particles at a rate about 20 times greater than that from 

 gasoline-fuelled vehicles. The particles are composed of elemental 

 carbon, organic compounds adsorbed from fuel and lubricating oil, 

 sulfates from fuel sulfur, and traces of metallic components. Most of 

 the total particulate matter appears to occur in the submicrometre 

 range, between 0.02 and 0.5 μm. Agglomeration may occur during aging, 

 up to a maximal diameter of 30 μm. The emitted particles have a large 

 surface area. Organic compounds generally contribute 10-30% of the 

 total particulate matter, but poorly designed and maintained engines 

 may result in as much as 90%. Higher-relative-molecular-mass, 

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 oxygenated and nitro-PAHs occur at concentrations of parts per million 

 in this fraction. 

 Specific transient or steady-state driving cycles are used in 

 measuring vehicle emissions. The exhaust can be sampled from undiluted 

 or diluted exhaust gas. It is difficult to obtain artefact-free 

 samples, as exhaust constituents can undergo chemical reactions, 

 adsorption and desorption processes, and condensation and diffusion. 

 The toxicologically relevant PAHs in diesel particulate matter are 

 usually determined by Soxhlet extraction, clean-up, and fractionation, 

 with subsequent analysis by high-performance liquid chromatography or 

 gas chromatography coupled with mass spectrometry. 

 B1.2 Sources of human and environmental exposure 

 Diesel engine exhausts are emitted mainly from motor vehicles; 

 other sources are stationary, railway locomotive, and ship diesel 

 engines. The emissions from diesel motor vehicles have been well 

 described, but the individual results are often not comparable owing 

 to differences in parameters such as driving cycle, engine type, and 

 fuel composition. The individual components are emitted in the 

 following quantities: carbon dioxide, about 1 kg/km; carbon monoxide, 

 nitrogen oxides, total gaseous hydrocarbons, and particulate matter, 

 0.1-20 g/km; and aliphatic compounds, alcohols, aldehydes, light 

 aromatics, and PAHs, micrograms per kilometer. The emissions of carbon 

 monoxide, nitrogen oxides, total gaseous hydrocarbons, and particulate 

 matter are regulated by law in a number of countries. 

 In principle, there is no difference between the quality and 

 quantity of exhaust emissions from light- and heavy-duty engines, 

 although heavy-duty vehicles release larger relative amounts of 

 particulate matter. Exhaust emissions depend on driving cycle 

 (transient or steady state), engine conditions (injection and 

 aspiration techniques, maintenance, total mileage), and fuel 

 composition (sulfur content, aromaticity, volatility); adjustment of 

 the engine plays a major role. 

 The release of particulate matter increases with decreasing 

 air:fuel ratio, increasing load, and increasing temperature. More 

 particulate is released from older, intensively used engines than from 

 new, low-mileage engines, probably because of a greater consumption of 

 lubricating oil. The emission of particles from light-duty diesel 

 vehicles is also correlated with the sulfur content of the fuel, as 

 the formation of metal sulfates increases the particle mass; particle 

 emissions from heavy-duty vehicles have not yet been established. 

 Increasing fuel aromaticity also increases particle emissions. 

 PAHs and oxygenated PAHs from diesel and spark-ignition engines 

 are qualitatively similar. Oxygenated and nitrated PAHs are emitted in 

 the low microgram per kilometer range, but the actual concentrations 

 of these compounds are uncertain, as decomposition and formation can 

 occur during sampling. PAH emissions increase with increasing load and 

 temperature and with the age of the engine, probably owing to 

 increased consumption of lubricating oil. PAH emissions also depend on 

 the injection technique of the engine: they increase with increasing 

 air:fuel ratio in engines with direct injection, whereas they decrease 

 in engines with indirect injection. The aromaticity and volatility of 

 the fuel are directly correlated with the emission of PAHs. 

 Malfunction of engine devices, especially the fuel injection system, 

 increases the emission of the main exhaust components. There are few 

 data on the contribution of diesel motor emissions to the total 

 man-made release of combustion products. 

 Diesel exhaust emissions can be reduced by improving engine 

 design and by use of particle traps (trap oxidizers) and catalytic 

 converters. While particle traps remove both the soot and soluble 

 organic compounds adsorbed onto the particles, catalytic converters 

 reduce the levels mainly of carbon monoxide and gaseous hydrocarbons. 

 In practice, it is dificult to regenerate particulate traps. Catalytic 

 converters require fuels with a low sulfur content, as sulfur poisons 

 the active centres of the catalyst. 

 B1.3 Environmental transport, distribution, and transformation 

 The compartment first affected by diesel exhaust emissions is the 

 atmosphere. The hydrosphere and geosphere are contaminated indirectly 

 by dry and wet deposition. The environmental fate of the individual 

 constituents of diesel exhaust is generally well known: Particles 

 behave like (non-reacting) gas molecules with regard to their 

 mechanical transport in the atmosphere; they may be transported over 

 long distances and even penetrate the stratosphere. The overall 

 removal rate of diesel particles is estimated to be low, resulting in 

 an atmospheric lifetime of several days. During aging, particles may 

 coagulate, with higher fall-out rates, thus reducing the total 

 airborne level. The elemental carbon of diesel particulates may act as 

 a catalyst in the formation of sulfuric acid by oxidation of sulfuric 

 dioxide. The organic components adsorbed on elemental carbon may 

 undergo a number of physical and chemical reactions with other 

 atmospheric compounds and during exposure to sunlight. 

 B1.4 Environmental levels and human exposure 

 As diesel exhaust is a complex mixture of a great variety of 

 compounds, general 'environmental levels' cannot be given. The 

 individual components of diesel exhaust should be detectable in all 

 compartments of the environment, although their source cannot usually 

 be verified. The environmental levels of most of the individual 

 constituents are known. 

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 The general population is most likely to be exposed to diesel 

 exhaust in busy streets or parking areas, particularly underground. 

 The identification of sources is difficult, and the contribution of 

 diesel exhaust to total pollution by traffic combustion products is 

 generally calculated on the basis of emission factors and the 

 percentage of diesel-fuelled vehicles. The levels of exposure of the 

 general population and workers to diesel particulate matter are 

 toxicologically relevant. The daily average ambient concentrations of 

 diesel particulates near roads are 8-42 μg/m3. The estimated annual 

 average concentrations were 5-10 μg/m3 in urban areas and 

 < 1.5 μg/m3 in rural areas in Germany and 1-2 μg/m3 in urban 

 areas and 0.6-1 μg/m3 in rural areas in the United States of America. 

 The concentrations are directly correlated with traffic density and 

 decrease with increasing distance from roads. Identification of 

 sources may also be difficult in work-places, especially in mines, 

 where the total dust burden is high. Carbon core analysis has been 

 used to determine specific exposure to diesel exhaust in the 

 work-place, and the levels of particulate matter to which workers are 

 exposed have been reported to be 0.04-0.134 mg/m3 for truck drivers 

 and 0.004-0.192 mg/m3 for railroad workers. Total respirable 

 particles and total suspended particles have also been used as 

 measures of occupational exposure. 

 B1.5 Kinetics and metabolism in laboratory animals and humans 

 B1.5.1 Deposition 

 Diesel exhaust particles, with a mass median aerodynamic diameter 

 of about 0.2 μm, undergo some filtration in the nose, and the 

 deposition efficiency in the lung is only slightly greater than the 

 minimal value found for particles with a mass median aerodynamic 

 diameter of about 0.5 μm. Thus, 10-15% of inhaled diesel soot 

 particles are deposited in the alveolar region of the lung of rats and 

 guinea-pigs; in humans, about 10% is deposited in the alveolar region. 

 B1.5.2 Retention and clearance of particles 

 Mucociliary clearance of particles from ciliated airways is 

 almost complete within 24 h. The long-term clearance of diesel 

 particles from the alveolar region was measured in several studies in 

 rats exposed by inhalation to labelled diesel or test particles. 

 Half-times of 60-100 days were reported for controls with low lung 

 burdens (< 1 mg/lung), whereas the half-times increased to 100-600 

 days in rats with lung burdens increasing from 1 to 60 mg/lung. In 

 several studies, effects were seen to be caused by particle overload, 

 which has been described in a variety of species and with a number of 

 particulate materials. The phenomenon is generally observed when the 

 deposition rate of particles of low solubility and low acute toxicity 

 exceeds their clearance rate for a considerable time. The half-time of 

 unimpaired alveolar clearance in humans is several hundred days, which 

 is longer than that in rats. 

 A dosimetric lung model was developed on the basis of data on the 

 deposition and retention of diesel particles in rats after long-term 

 inhalation and of data on particle deposition and retention in humans. 

 The model can be used to predict retention of diesel particles and 

 adsorbed organic material in the lungs of people of different ages. No 

 data are available on changes in the retention of individual compounds 

 after prolonged exposure to diesel exhaust. 

 B1.5.2 Retention and clearance of polycyclic aromatic hydrocarbons 

 adsorbed onto diesel soot 

 PAHs in diesel soot adhere strongly to the surface of particles. 

 About 50% of the PAHs adsorbed onto diesel particles is cleared from 

 the lung within one day, but the retention half-times for the 

 remaining PAHs were 18-36 days. Studies with 3 H-benzo[ a]pyrene and 

 14C-nitropyrene show that when PAHs are associated with particulate 

 matter, their clearance from the lungs is significantly delayed in 

 comparison with the clearance of inhaled PAHs not associated with 

 particulate matter. 

 B1.5.4 Metabolism 

 Benzo[ a]pyrene coated on diesel exhaust particles was metabolized 

 by oxidation to benzo[ a]pyrene phenols, diols, and quinones in the 

 lung and in cell cultures of pulmonary macrophages. Nitropyrene 

 adsorbed to diesel particles was metabolized to acetylaminopyrene- 

 phenol after inhalation. More DNA adducts were found in the lungs and 

 type II cells of rats exposed to diesel exhaust than in controls. The 

 oxidative metabolism of some organic compounds to epoxides may be 

 responsible for the formation of these adducts, but adducts were found 

 only after exposure to particles. Certain organic substances in diesel 

 exhaust have been shown to be responsible for the formation of DNA 

 adducts; however, the carbonaceous core itself (without extractable 

 organic material) can also induce adducts, by chronic damage of 

 epithelial cells. 

 B1.6 Effects on laboratory mammals and in vitro test systems 

 The few data available suggest that diesel exhaust has little 

 acute toxicity. Mice treated intratracheally with diesel exhaust 

 particles died due to lung oedema; the LD50 was about 20 mg/kg body 

 weight. Methanol-extracted diesel exhaust particles were not lethal a 

 concentrations up to about 33 mg/kg body weight. In hamsters, the LD50

 after intraperitoneal administration was 1280 mg/kg body weight. No 

 data are available for exposure by inhalation. 

 Exposure of rats, guinea-pigs, and cats to diesel exhaust with a 

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 particle content of 6 mg/m3 for about four weeks altered lung 

 function, including a 35% increase in pulmonary flow resistance in 

 guinea-pigs and a 10% decrease in vital capacity (expiratory flow) in 

 cats. Histopathologically, focal thickening of alveolar walls, a 

 significantly increased type-II cell labelling index, and 

 accumulations of particleladen macrophages were found. The 

 accumulations were located near the terminal bronchioles and became 

 larger, due to macrophage attachment (sequestration), during a 

 subsequent recovery period. 

 Mice, rats, hamsters, cats, and monkeys did not have drastic 

 decreases in body weight or reduced survival times after long-term 

 inhalation of up to 4 mg/m3 . Dose-related toxic effects seen in all 

 species after long-term inhalation of diesel exhaust were: increases 

 up to 400% in lung weight; pulmonary inflammation measurable by 

 biochemical (cytoplasmic marker enzymes, collagen) and cytological 

 (increase in polymorphonuclear neutrophils) parameters; impairment of 

 lung mechanics; increasing numbers of particle-laden macrophages with 

 focal accumulations (sequestration) under overload conditions; and 

 subsequent proliferative alterations of epithelial cells and onset of 

 fibrosis. 

 Limited information on reproductive and developmental toxicity 

 suggests that inhalation of diesel exhaust is not critical. In most 

 experiments, no effects were seen in mice, rats, hamsters, rabbits, or 

 monkeys; however, after intraperitoneal injection, sperm abnormalities 

 were seen in mice given diesel exhaust particles and embryotoxicity 

 occurred in hamsters given diesel exhaust extract. 

 Most tests for genotoxicity in vitro have been performed with 

 diesel exhaust extracts rather than with total exhaust; positive 

 responses were found in the absence of metabolic activation, i.e. the 

 genotoxic effects appeared to be PAH-independent. About one-half of 

 investigations in vivo gave negative responses; the only positive 

 responses were sister chromatid exchange induction with total diesel 

 exhaust and with organic extracts and micronucleus induction with 

 organic extracts. 

 Immunotoxic effects were generally not seen after inhalation of 

 diesel exhaust; however, an enhanced anti-ovalbumin immunoglobulin E 

 antibody titre was seen in one study and an increased susceptibility 

 to infections in mice in two experiments. Studies in rats suggested 

 that inhalation of diesel exhaust affects behavioural and 

 neurophysiological status. 

 In studies of the carcinogenicity of diesel exhaust administered 

 by inhalation to rats, the gaseous phase (without the particulate 

 fraction) was not carcinogenic. In all valid studies in rats, diesel 

 exhaust was found to be carcinogenic at particle concentrations of > 

 2 mg/m3, corresponding to an equivalent continuous exposure of about 

 1mg/m3. No effect was seen in hamsters or mice. In studies by 

 intratracheal instillation, both diesel exhaust particles and carbon 

 black induced tumours, and the surface area of the carbonaceous 

 particles appeared to be correlated with the tumorigenic potency. 

 Long-term inhalation of carbon black virtually devoid of PAHs at 

 similar concentrations also resulted in lung tumours in rats. 

 It is not clear whether the carcinogenicity of diesel exhaust 

 involves DNA-reactive or non-DNA-reactive mechanisms (or a 

 combination). Various models have been used to elucidate the 

 carcinogenicity of diesel exhaust. 

 B1.7 Effects on humans 

 Diesel exhaust contributes to air pollution in general. Although 

 the role of diesel particles cannot be singled out in acute or chronic 

 studies, they may be partly responsible for the range of health 

 effects found to be associated with air pollution. 

 Typical diesel exhaust has a characteristic odour, which some 

 people find offensive, particularly at high concentrations. The 

 symptoms seen after acute and chronic exposure to diesel exhaust have 

 been described in studies and anecdotal reports of occupationally 

 exposed subjects. Acute exposure to diesel exhaust has been associated 

 with irritation of the ocular and nasal mucous membranes, and an 

 increased frequency of respiratory symptoms has been observed in 

 occupational cohorts; however, the contribution of diesel particulates 

 is not known. No consistent short-term effect on pulmonary functions 

 has been found, but asthma attacks have been reported. 

 In a controlled study in which eight healthy non-smoking 

 volunteers were exposed to diluted diesel exhaust in a chamber for 

 60 min, the phagocytosis rate of alveolar macrophages in broncho- 

 alveolar lavage fluid was reduced. 

 Some cross-sectional and longitudinal studies on workers with 

 long-term occupational exposure to diesel exhaust show decrements in 

 lung function and an increased prevalence of respiratory symptoms, but 

 these studies are limited by short exposure. Cohort studies in which 

 deaths from cardiovascular and/or cerebrovascular disease due to 

 diesel emissions were investigated did not show a significant excess. 

 The relationships between cancers of the lung and of the urinary 

 bladder and occupational exposure to diesel exhaust have been 

 evaluated in a number of epidemiological studies. Only those studies 

 that were considered relevant for evaluating the carcinogenic effects 

 of diesel exhaust are included in this monograph. The most relevant 

 studies with regard to lung cancer are those of railroad workers, bus 

 garage workers, and stevedores, who have definite exposure to diesel 

 exhaust. The four most informative studies all reported an increased 

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 risk for lung cancer, with relative risks ranging from 1.4 for 

 railroad workers and 1.3-2.4 for bus garage workers (depending on 

 exposure category), to a three- to sixfold increase in risk for 

 stevedores (depending on the exposure assessment used, but with wide 

 confidence intervals). Adjustment for smoking was possible in one 

 case-control study of railroad workers and in the study of stevedores, 

 and in both cases, the effect of diesel exposure was not materially 

 influenced. In the three studies in which smoking could not be 

 adjusted for, the analysis was based on comparisons of subgroups of 

 the cohorts, so that confounding by tobacco smoking was less likely 

 than when external comparison groups were used. 

 Several case-control studies have been conducted to examine the 

 relationship between urinary bladder cancer and presumed exposure to 

 diesel exhaust. An increased risk was found, especially for truck 

 drivers; however, all of these studies are limited by poor 

 characterization of exposure. Hence, a causative association between 

 exposure to diesel exhaust and an increased risk for urinary bladder 

 cancer cannot be established. 

 B1.8 Effects on other organisms in the laboratory and the field 

 The effect of diesel emissions as such have been addressed in 

 only one study, of green algae. 

 B1.9 Evaluation of human health risks 

 The risk assessment paradigm of the United States National 

 Academy of Sciences (US National Research Council, 1983) was used to 

 assess the risks for both cancer and non-cancer end-points. The four 

 steps in this process comprise: (1) hazard identification, (2) 

 dose-response assessment, (3) exposure assessment, and (4) risk 

 characterization. 

 Epidemiological studies of long duration with well-defined 

 exposure and follow-up (> 20 years) are considered to be the most 

 informative. Four studies of lung cancer in occupationally exposed 

 individuals met these criteria. The relative risks for lung cancer 

 associated with exposure to diesel exhaust were generally low and were 

 susceptible to chance, to the effects of unmeasured confounding 

 factours, and to the difficulty in accurately adjusting for known 

 confounding factors. Studies with less precise definitions of exposure 

 support the conclusions of these studies. Overall, it is considered 

 that diesel exhaust is probably carcinogenic to humans; however, no 

 quantitative data are available for estimating human risk. 

 B1.9.1 Non-neoplastic effects 

 Two general approaches were used for risk characterization: a 

 no-observed-adverse effect level (NOAEL) divided by an uncertainty 

 factor; and a benchmark concentration. In both approaches, a 

 sophisticated dosimetric model was used which decreases any 

 uncertainty in interspecies extrapolation of dose. 

 The no-effect level of diesel exhaust particles in humans was 

 calculated to be 0.139 mg/m3. The guidance value for the general 

 population calculated from the dosimetric model was 5.6 μg/m3, and 

 that calculated without the model was 2.3 μg/m3. 

 The benchmark concentration approach takes into account the 

 entire exposure-response relationship rather than relying on a single 

 data point from studies by inhalation, as in the NOAEL approach. Three 

 sensitive end-points were identified: chronic alveolar inflammation, 

 impaired lung clearance, and hyperplastic lung lesions. The benchmark 

 concentrations, calculated from the same dosimetric model used in the 

 NOAEL approach, were 0.9-2 μg/m3for inflammation, 1.2-3 μg/m3 for 

 impaired lung clearance, and 6.3-14 μg/m3 for hyperplastic lesions. 

 B1.9.2 Neoplastic effects 

 A linearized multistage model was used to estimate unit risks due 

 to exposure to diesel exhaust. Because the results of the available 

 epidemiological studies were considered inadequate for a quantitative 

 estimate of unit risk, data from several studies of long-term 

 inhalation in rats were used in which carcinogenesis occurred at 

 concentrations >2 mg/m3. A unit risk of 3.4 × 10-5 μg/m3 (geometric 

 mean of four risk estimates) diesel exhaust particles was calculated. 

 An alternative biologically based model yielded a similar unit risk, 

 under the assumption that diesel particles affect cell initiation 

 and/or proliferation at low concentrations. 

 B1.10 Evaluation of effects on the environment 

 Insufficient information was available to evaluate the specific 

 effects of diesel exhaust emissions. The effects of combusted diesel 

 fuel should be similar to those of other fossil fuels and are related 

 to the consumption of diesel fuel. 

 B2. IDENTITY AND ANALYTICAL METHODS

 B2.1 Identity 

 Diesel engine emissions contain hundreds of chemical compounds, 

 which are emitted partly in the gaseous phase and partly in the 

 particulate phase of the exhaust. These substances form particles or 

 contribute to the gaseous phase of the emissions, depending on vapour 

 pressure, temperature, and the concentration of individual species. 

 The amount and composition of diesel exhaust are related to engine 

 conditions and fuel specifications (see sections B3.1.2.1 and 

 B3.1.2.2). A total of 445 compounds has been identified or tentatively 

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 identified as constituents of diesel exhaust emissions (Westerholm, 

 1987). 

 Diesel exhaust has an offensive odour (odour threshold, 320 ppm). 

 Compounds with a relative molecular mass > 80 mainly determine the 

 odour (Scheepers & Bos, 1992b). Partridge et al. (1987) concluded that 

 benzaldehyde and a methylbenzaldehyde isomer are the major substances 

 responsible; unburnt aromatic hydrocarbons may also contribute. 

 Aldehyde levels and odour emissions are directly correlated with the 

 total hydrocarbon content of the exhaust; decreased hydrocarbon levels 

 lead to diesel exhaust with less odour (Organisation for Economic 

 Co-operation and Development, 1993). 

 B2.1.1 Chemical composition of diesel exhaust gases 

 The main gaseous products of diesel exhaust are carbon dioxide, 

 oxygen, nitrogen, and water vapour; carbon monoxide, sulfur dioxide, 

 nitrogen oxides, and hydrocarbons and their derivatives are also 

 present. A representative composition of diesel exhaust gas 

 (light-duty engine) is shown in Table 21. 

 The levels of carbon monoxide, nitrogen oxides, total 

 hydrocarbons, and particulates emitted by diesel engines are regulated 

 by law in a number of countries (see section B3.2). The composition of 

 diesel exhaust gases is similar to that of gasoline engine gases, but 

 because of the relatively higher fuel:air ratio, carbon monoxide and 

 hydrocarbons occur in lower concentrations in diesel exhaust, and the 

 emission of nitrogen oxides, particulate matter, and sulfur compounds 

 is higher (the latter being due mainly to the higher sulfur content of 

 diesel fuels). The relative concentrations in the aldehyde fraction 

 are as follows: about 45% by weight formaldehyde, 17% by weight 

 acetaldehyde, 14% by weight acetone and acrolein, < 10% by weight 

 crotonaldehyde, propionaldehyde, isobutyraldehyde, benzaldehyde, and 

 hexanaldehyde; methylethylketone is also present (Volkswagen AG, 

 1989). 

 Table 21. Composition of light-duty diesel engine exhaust 

 

 Component Concentration 

 (% by weight) 

 Carbon dioxide 7.1 

 Water vapour 2.6 

 Oxygen 15.0 

 Nitrogen 75.2 

 Carbon monoxide 0.03 

 Hydrocarbons 0.0007 

 Nitrogen oxides 0.03 

 Hydrogen 0.002 

 Sulfur dioxide 0.01 

 Sulfates 0.00016 

 Aldehydes 0.0014 

 Ammonia 0.00005 

 Particulates 0.006 

 

 Adapted from Volkswagen AG (1989) 

 Diesel exhaust contains toxicologically relevant compounds such 

 as benzene, toluene, ethylbenzene, xylene, and PAHs. In the 

 hydrocarbon fraction, benzene and toluene are present in relative 

 concentrations of 11 and 4% by weight, respectively (Volkswagen AG, 

 1989). 

 Possible sources of PAHs in diesel exhaust are unburnt PAHs from 

 the fuel, pyrosynthesis of PAHs during combustion, crankcase oils, and 

 engine and/or exhaust system deposits (Scheepers & Bos, 1992a). These 

 constituents occur partly in the gaseous fraction of total 

 hydrocarbons (benzene, toluene, ethylbenzene, and xylene components, 

 PAHs of lower relative molecular mass) and partly in the particulate 

 fraction due to adsorption (PAHs of higher relative molecular mass). 

 The partitioning of constituents between the particulate and gas 

 phases has been measured by several investigators (Hampton et al., 

 1983; Schuetzle, 1983; Schuetzle & Frazier, 1986). Most PAHs with five 

 or more rings and aliphatic hydrocarbons with more than 18 carbon 

 atoms are expected to be primarily adsorbed onto particles (Schuetzle, 

 1983). There is a direct relationship between adsorption behaviour and 

 vapour pressure (Hampton et al., 1983); compounds with vapour 

 pressures < 10-5 mbar (7.5 × 10-6 mm Hg; 2.09 kPa) at room 

 temperature occur predominantly in the particulate phase. An empirical 

 relationship between boiling-point and particle- to gas-phase 

 partition coefficients has been derived for PAHs and aliphatic 

 hydrocarbons in order to estimate gas-phase emission rates (Schuetzle 

 & Frazier, 1986). According to this equation, the concentration of 

 e.g. anthracene in the gaseous phase is about 20 times higher than 

 that in the particle phase, whereas the levels of e.g. pyrene and 

 fluoranthene are nearly equal in the two phases. Oxygenated PAHs are 

 found in diesel engine exhaust at concentrations as high (Volkswagen 

 AG, 1989) or twice as high (Jensen & Hites, 1983) as those of their 

 parent PAHs, perhaps because these engines have a larger air:fuel 

 ratio than gasoline motors (Scheepers & Bos, 1992a). 9-Fluorenone and 

 9,10-anthracenequinone are especially abundant in diesel exhaust 

 (Schuetzle & Frazier, 1986). In tests of diesel passenger cars by 

 Volkswagen AG (1989), phenalene-1-one, naphthalene dicarboxylic acid 

 anhydride, cyclopenta[ def]phenanthrene-4-one, monoaldehydes of 

 phenanthrene and anthracene, mono- and diketones of benzanthracenes 

 and benzo[cd]pyrene, and benzofluorenones were also found (for 

 artefact formation during sampling, see section B2.2.1; for emission 

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 factors, see section B3.1.1.1). 

 Nitrogen-substituted PAHs are formed during combustion as a 

 result of either nitration of PAHs by nitric acid or addition of 

 nitrogen monoxide or dioxide to PAH free radicals generated during 

 combustion (Schuetzle, 1983). In the exhaust of a four-cylinder diesel 

 engine, nitrofluorene, dinitrofluorenone, nitroanthracene, 

 nitrofluoranthene, mono- and dinitropyrenes, and nitrobenzo[ a]pyrene 

 were detected at concentrations about one order of magnitude lower 

 than those of oxygenated PAHs (Volkswagen AG, 1989). 

 A number of investigators have found nitrated PAHs in extracts of 

 diesel engine exhaust particles (Handa et al., 1983; Hartung et al. 

 1984). Many three-, four-, and five-ring structures are involved 

 (Schuetzle et al., 1982). The concentration of 1-nitropyrene, one of 

 the prevalent species, has been reported to be 15-25 mg/kg particulate 

 matter, whereas benzo[ a]pyrene has been found at concentrations up 

 to 50 mg/kg. The nitrated PAHs are important in determining the health 

 effects of exposure to diesel exhaust, since they are effective 

 mutagens in microbial and human cell systems (Pederson & Siak, 1981; 

 Pitts et al., 1982; Patton et al., 1986). Some nitrated PAHs are 

 carcinogenic to animals (Ohgaki et al., 1985; Imaida et al., 1991). 

 Combustion products originating from fuel and lubricating oil 

 additives or from corrosion may also occur. For example, nitrate-based 

 cetane improvers (see also section A2.1.2) are assumed to form nitro- 

 PAHs (Organisation for Economic Co-operation and Development, 1993). 

 B2.1.2 Type and composition of emitted particulate matter 

 Diesel exhaust is characterized by a higher content (10-20-fold) 

 of particulate matter than that of gasoline-fuelled passenger cars 

 (Egebäck & Bertilsson, 1983; Volkswagen AG, 1989; Williams et al., 

 1989; CONCAWE, 1990b; Hammerle et al., 1994a). How soot particles are 

 formed is still under discussion, but the precursor is probably 

 acetylene generated during combustion. As a result of the numerous 

 cracking, dehydration, and polymerization processes, quite large 

 amounts of carbon, hydrogen, hydroxyl, and oxygen radicals are 

 available in the combustion chamber, which can produce cyclic and 

 polycyclic aromatic hydrocarbons from acetylene by polymerization and 

 ring closure. With increasing polymerization, the carbon content of 

 the macromolecule increases, finally generating graphite-like soot 

 particles (Klingenberg et al., 1991). 

 Investigations of two four-cylinder engines with direct and 

 indirect injection (see also section B3.1.2.1) showed that the emitted 

 particles range in shape and size from spherical particles of 

 < 0.01 μm to cluster and chain agglomerates with maximal dimensions 

 of 30 μm (Dolan et al., 1980; Amann & Siegla, 1982; Klingenberg et 

 al., 1991). The formation of agglomerates (coagulation, 'aging') is 

 dependent not only on engine and exhaust conditions but also on 

 environmental factors, such as photochemical processes and humidity. 

 Between 50 and 80% of the total particulate emission occurs in the 

 range of 0.02-0.5 μm (Israel et al., 1982). According to Amann & 

 Siegla (1982), the emitted particles have a concentric, lamellar 

 structure arranged around the centre, similar to the structure of 

 carbon black. 

 Emitted soot particles are composed of elemental carbon, adsorbed 

 organic compounds (soluble organic fraction) from fuel and lubricating 

 oil, traces of metallic compounds (iron, calcium, and zinc at < 0.6% 

 by weight; Volkswagen AG, 1989), and sulfates. The organic components 

 of emitted particles are distributed over the surface. Numerous data 

 on the relative proportions of organic compounds are available 

 (Horvath et al., 1987; Williams et al., 1987; Volkswagen AG, 1989; 

 Williams et al., 1989; CONCAWE, 1992). Depending on the engine 

 conditions and testing cycle, the organic compounds comprise 10-90% of 

 the total particulate mass. The ranges of various constituents of 

 particulate matter in nine light-duty and four heavy-duty vehicles 

 (see also section B3.1.2.1) are shown in Table 22. The driving cycles 

 used were combined European Union tests (ECE-15 and 'high speed' 

 extra-urban driving cycle [EUDC]) for the light-duty vehicles and 

 modified ECE-R49 tests for the heavy-duty engines (see also section 

 B2.2.1); four fuels with different sulfur contents and an aromatic 

 content of about 25% by volume were used (CONCAWE, 1992). (For a 

 description of the influence of fuel composition on exhaust emissions, 

 see section B3.1.2.2.) 

 This study showed considerable variation, and no obvious 

 influence of fuel composition or engine conditions was discernible, 

 although a difference was seen between fuel and lubricating oil 

 hydrocarbons derived from light- and heavy-duty vehicles, 

 respectively. This is probably due to the different driving cycles: 

 transient in the case of light vehicles, steady state in the case of 

 heavy-duty engines. In the individual data, adjustment of the engine 

 appeared to play a major role. In the same study, PAHs were determined 

 in the soluble organic fraction of the exhausts of three light-duty 

 vehicles representing different engine conditions and of the four 

 heavy-duty engines. The data are shown in Table 23. The constituents 

 of the particulate matter of the exhaust are clearly dependent on the 

 driving cycle used. Under steady-state conditions (heavy-duty 

 engines), the PAH content is about one order of magnitude lower than 

 that under transient conditions (light-duty vehicles). In addition, 

 transient conditions lead to considerable variations in levels. In the 

 study of Volkswagen AG (1989) on a four-cylinder diesel engine in the 

 US-72-test, a hot start was used, and higher levels of fluoranthene, 

 pyrene, benzo[ ghi]fluoranthene and benzo[ c]phenanthrene were 

 found, perhaps due to either engine condition or driving cycle. 

 According to Volkswagen AG (1989), some of the PAHs, and especially 

 pyrene, benz[ a]anthracene and benzo[ a]pyrene, seemed to decompose 

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 during sampling (see section B2.2.1). 

 Table 22. Particulate matter content of exhausts from light- and heavy-duty vehicles 

 

 Constitutent Particulate matter (% by weight) Reference 

 

 Light-duty vehiclesa Heavy-duty vehiclesa

 

 Carbon 32.6-85.1 39.7-81.7 CONCAWE (1992) 

 82-88 (passenger 68-89 Williams et al. 

 cars) (1989)b

 76-83 (light vans) 

 60-75 Hammerle et al. 

 (1994a)c

 Fuel-derived 1.1-55.0 9.8-32.5 CONCAWE (1992) 

 hydrocarbons 6.0-18 Hammerle et al. 

 (1994a)c

 Lubricating 4.2-54.4 4.0-25.9 CONCAWE (1992) 

 oil-derived 5.7-15 Hammerle et al. 

 hydrocarbons (1994a)c

 Soluble organic 10.2-64.7 14.0-58.4 CONCAWE (1992) 

 fraction 14-26 (passenger 22-90 Williams et al. 

 cars) (1989)b

 36-48 (light vans) 

 Sulfate (excluding 0.6-12.2 1.4-7.5 CONCAWE (1992) 

 bound water) 3.3 (passenger 0.3-6.9 Williams et al. 

 cars) (1989)b

 2.5 (light vans) 1.5-2.0 Hammerle et al. 

 (1994a)c

 

 a According to the Organisation for Economic Co-operation and Development (1993), 

 light-duty vehicles are generally classified as vehicles with a weight < 3.5 t, 

 occasionally < 5 t; heavy-duty vehicles are those weighing > 5 t. 

 b Measurements for four passenger cars and 15 light vans in different Australian 

 driving cycles corresponding roughly to US-FTP-72 and -75 tests for heavy-duty 

 vehicles, and 10 trucks and two buses in one Australian urban traffic driving cycle 

 c Five passenger cars and light vans in European Motor Vehicle Emissions group cycle 

 and US-FTP-75 test 

 Table 23. Polycyclic aromatic hydrocarbon content of the soluble organic fraction of 

 particulate matter in diesel exhaust 

 

 Constituent Soluble organic fraction Referenceb

 (mg/kg particulate matter 

 

 Light-duty Heavy-duty 

 vehiclesa vehicles 

 

 Fluoranthene 8-238 4-52 CONCAWE (1992) 

 553-560 Volkswagen AG (1989) 

 Pyrene 11-287 7-90 CONCAWE (1992) 

 579-668 Volkswagen AG (1989) 

 Benzo[ghi]fluoranthene 36-61 3-6 CONCAWE (1992) 

 + benzo[c]phenanthrene 163-179 Volkswagen AG (1989) 

 Benz[a]anthracene 9-285 1-16 CONCAWE (1992) 

 61-82 Volkswagen AG (1989) 

 Triphenylene and 14-138 4-13 CONCAWE (1992) 

 chrysene 117-138 Volkswagen AG (1989) 

 Benzo[b,j]fluoranthene 4-87 1-10 CONCAWE (1992) 

 180-193c Volkswagen AG (1989) 

 Benzo[a]fluoranthen 6-69 CONCAWE (1992) 

 Benzo[e]pyrene 8-40 1-2 CONCAWE (1992) 

 85-90 Volkswagen AG (1989) 

 Benzo[a]pyrene 2-48 1-3 CONCAWE (1992) 

 38-54 Volkswagen AG (1989) 

 Perylene 5-32 2 CONCAWE (1992) 

 4-8 Volkswagen AG (1989) 

 Dibenz[a,j]anthracene 10-78 CONCAWE (1992) 

 Indeno[123-cd]pyrene 6-54 CONCAWE (1992) 

 55-73 Volkswagen AG (1989) 

 Dinbenz[a,h]- or 3-40 CONCAWE (1992) 

 -[a,c]anthracene 

 Benzo[ghi]perylene 25-65 1-5 CONCAWE (1992) 

 75-82 Volkswagen AG (1989) 

 Anthracene 3-7 CONCAWE (1992) 

 Dibenz[a,i]pyrene 8-31 CONCAWE (1992) 

 Coronene and 9-52 CONCAWE (1992) 

 dibenzo[a,e]pyrene 33-48d Volkswagen AG (1989) 

 

 a According to the Organisation for Economic Co-operation and Development (1993), 

 light-duty vehicles are generally classified as vehicles with a weight < 3.5 t, 

 occasionally < 5 t; heavy-duty vehicles are those weighing > 5 t. 

 b From Volkswagen AG (1989): US-72 tests with one four-cylinder engine 

 c Including benzo[k]fluoranthene 

 d Excluding dibenz[a,e]pyrene 

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 B2.2 Analytical methods 

 B2.2.1 Sampling 

 Driving cycles are specified to simulate on-road conditions for 

 measuring vehicle emissions (Grimmer et al., 1988). The test 

 procedures can be divided in two basic types: steady-state and 

 transient cycle tests. In the European Union and Japan, mainly 

 steady-state tests are used, in which emissions from engines are 

 measured at specified combinations of speed and load. The most widely 

 used official tests for light- and heavy-duty vehicles are as follows: 

 Light-duty vehicles:

 * US FTP-75: transient cycle; cold start; driving distance, 17.8 

 km; 10-min break after 28.7 min (United States) (Volkswagen AG, 

 1989) 

 * US SET: transient cycle; 'sulfate emission test'; hot start; 

 simulating rush-hour freeway driving; driving distance, 21.7 km 

 (United States) (Volkswagen AG, 1989) 

 * ECE 15: transient cycle; cold start; simulating city-centre 

 driving; driving distance, 4.052 km (European Union) (CONCAWE, 

 1990a) 

 * US HDC: steady-state cycle; 'highway driving cycle'; hot start; 

 driving distance, 16.5 km; maximal speed, 96.4 km/h (United 

 States) (Volkswagen AG, 1989) 

 * EUDC: steady-state cycle; 'extra-urban driving cycle'; hot start 

 (after ECE 15); driving distance, 6.755 km; maximal speed, 

 120km/h (European Union) (CONCAWE, 1990a) 

 Heavy-duty vehicles:

 * HD-FTP: transient cycle; 'heavy-duty federal test procedure'; 

 simulating metropolitan driving (United States) (Organisation for 

 Economic Co-operation and Development, 1993); 

 * ECE 13: steady-state cycle at 13 different modes; identical to 

 ECE R49 (European Union) (Organisation for Economic Co-operation 

 and Development, 1993). Various bus cycles are also used to test 

 heavy-duty vehicles that are characterized by frequent 

 stop-and-go driving (Westerholm & Egebäck, 1991; Prakash et al., 

 1992). 

 It is difficult to avoid artefacts in sampling. Exhaust gas 

 constituents can undergo chemical reactions, adsorption and desorption 

 processes, and condensation or diffusion. For example, oxygenated and 

 nitrated PAHs are chemically unstable, and artefacts may form on the 

 sampling device, especially if large sampling volumes are needed (Lee 

 & Schuetzle, 1983). Both decreases and increases in the concentrations 

 of PAHs and oxy-PAHs were observed during sampling in a study by 

 Volkswagen AG (1989); in particular, degradation of pyrene and 

 nitropyrene and formation of naphthalene dicarboxylic acid anhydride 

 on the filter occurred. PAHs can be converted into nitroarenes (Pitts 

 et al., 1978; Lee et al., 1980; Gibson et al., 1981; Lee & Schuetzle, 

 1983; Schuetzle & Perez, 1983; Gaddo et al., 1984; Levsen et al., 

 1988). 

 The sampling techniques used for the collection of the gaseous 

 and particulate phases of diesel exhaust comprise dilution tube 

 sampling and raw gas sampling. 

 B2.2.1.1 Sampling from undiluted exhaust gas (raw gas sampling) 

 The device for sampling motor vehicle exhaust (total flow method; 

 Kraft & Lies, 1981; Grimmer et al., 1973) consists of a glass cooler, 

 a condensate separator, and a special micron filter of 

 paraffin-impregnated glass-fibre material providing separation of 

 > 99.9% of particles of 0.3-0.5 μm. The cooler is fed with cold tap 

 water, and the filter is placed on top of the cooler to remove any 

 uncondensed liquid or solid exhaust gas constituents that may pass 

 through the cooler coil. The particulate filter retains undissolved 

 particles of the exhaust gas, while the condensate consists of the 

 dissolved components (Volkswagen AG, 1989). 

 The US Environmental Protection Agency (Lies et al., 1986) 

 defines the 'particulate phase' as all materials (with the exception 

 of condensed water) which, at a temperature of < 51.7°C, are retained 

 on a special filter after dilution with air. Large volumes are 

 collected with this type of sampling, making analysis of trace 

 components difficult. The sample volumes are reduced by diverting the 

 exhaust emission flow and sampling only a part. It is difficult to 

 ensure a representative partial flow, as the amount of exhaust gas 

 produced varies considerably over time (Volkswagen AG, 1989). 

 B2.2.1.2 Sampling from diluted exhaust (dilution tube sampling) 

 The exhaust is mixed with ambient air in a dilution tunnel in a 

 constant volume sampler method (Behn et al., 1985). The total flow of 

 air and exhaust is kept constant with a suitable fan in a constant 

 volume sampler unit. This sampling technique more realistically 

 reflects the immediate dilution of exhaust leaving the tailpipe of 

 vehicles on the road. The concentrations of exhaust components are, 

 however, reduced in accordance with the degree of dilution (magnitude, 

 1:10), and components that are present only at low concentrations 

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 cannot be determined. 

 There are various techniques for sampling gaseous constituents. 

 Substances present at sufficiently high concentrations are commonly 

 sampled in a plastic bag; adsorption onto solid materials, consisting 

 of extremely porous, tiny plastic pellets (e.g. Tenax; diameter, 

 0.1-0.2 mm; specific surface area, 20-50 m2/g), or absorption in 

 liquids are also used. Particulate constituents are sampled by 

 filtration (Lee & Schuetzle, 1983; Volkswagen AG, 1989). 

 B2.2.2 Extraction from particles 

 PAHs adsorbed onto diesel exhaust particles are of toxicological 

 relevance, and there are numerous methods for extracting these 

 constituents. The most frequently used method is Soxhlet extraction, 

 which permits extraction of 99% of the soluble organic fraction within 

 8 h; an additional 16 h are necessary to extract the remaining 1%. 

 Extraction is frequently carried out by sequentially changing the 

 solvents, from polar to nonpolar, e.g. toluene, toluene or n-propanol, 

 dichloromethane, and acetonitrile. PAHs may be further extracted by 

 refluxing the exhaust particulates in solvent for 1 h. Sublimation and 

 extraction by ultrasonic agitation are also used (Lee & Schuetzle, 

 1983; Levsen, 1988), and supercritical fluids such as carbon dioxide 

 are effective (Hawthorne & Miller, 1986). The extraction efficiency of 

 various solvents is still under discussion (Köhler & Eichhoff, 1967; 

 Swarin & Williams, 1980; Schuetzle & Perez, 1981; Grimmer et al., 

 1982; Lee & Schuetzle, 1983; Schuetzle et al., 1985; Levsen, 1988). 

 Aromatic solvents and their combinations seem to be best suited for 

 extracting PAHs from diesel particulates (Levsen, 1988). 

 B2.2.3 Clean-up and fractionation 

 Complex fractionation schemes for separating the exhaust extract 

 into aliphatic compounds, aromatic compounds, and moderately and 

 highly polar fractions after the removal of acidic and basic fractions 

 have been described by Petersen & Chuang (1982) and Levsen (1992). 

 During fractionation, further artefacts may be produced by the 

 components of a complex sampling mixture like diesel exhaust, 

 especially with acidic and basic extraction and aggressive column 

 separation procedures. 

 B2.2.4 Chemical analysis 

 Chemical analysis of separated, cleaned compounds of diesel 

 exhaust involves numerous techniques, including thin-layer 

 chromatography, gas chromatography, gas chromatography with mass 

 spectrometric detection, and high-performance liquid chromatography 

 (US National Institute for Occupational Safety and Health, 1991). 

 Jinno et al. (1986) determined PAHs by supercritical fluid 

 chromatography with a photodiode array detector. 

 The detection methods vary widely and include ultra-violet, 

 visible, and fluorescence spectrophotometry, mass spectrometry, and 

 more or less specific devices, such as flame ionization, nitrogen 

 flame ionization, and sulfur-specific and electron-capture detectors 

 (US National Institute for Occupational Safety and Health, 1991). A 

 thermal optical method for determining elemental carbon is currently 

 being used as a surrogate for measurement of worker exposure in almost 

 all internal investigations at the US National Institute for 

 Occupational Safety and Health (Niemeier, personal communication, 

 1994). 

 Analytical methods are available for determining the organic 

 constituents of diesel particulate matter, with special emphasis on 

 the determination of PAHs and their nitrated and oxygenated 

 derivatives (Levsen, 1988). 

 B2.3 Conversion factors 

 Because diesel exhaust emissions are complex mixtures of 

 different gases and particles, it is impossible to give a conversion 

 factor for converting parts per million to SI units. 

 B3. SOURCES OF HUMAN AND ENVIRONMENTAL EXPOSURE

 B3.1 Anthropogenic sources 

 Diesel exhaust emissions are exclusively man-made and are 

 distributed primarily in the atmosphere. The hydrosphere and geosphere 

 may also be affected owing to dry and wet deposition of the exhaust 

 constituents; however, determination of the source of deposited 

 compounds is difficult. No data are available on the individual 

 components of diesel exhaust and their deposition. 

 B3.1.1 Diesel exhaust emissions 

 Diesel fuels are widely used as transport fuels, and exhaust 

 emissions are released mainly by road traffic. Although many 

 investigations of these emissions have been reported, the individual 

 results are frequently not comparable because the experimental 

 parameters, e.g. driving cycles, are different, or different 

 dimensions were chosen. For example, the results of tests on emissions 

 from light-duty vehicles refer mainly to kilometres driven, whereas 

 those for heavy-duty vehicles are related to the engine power in 

 kilowatt-hours. Furthermore, the statistical power of studies of 

 emission factors is often limited by the small number of vehicles or 

 engines examined. Some investigators change more than one parameter 

 (e.g. sulfur content or aromaticity of the fuel) during their studies, 

 so that the specific cause of changes in exhaust composition is 

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 difficult to assess. Adjustment of individual engine and fuel 

 parameters plays a major role in determining the quality and quantity 

 of exhaust emissions (see sections B3.1.2.1 and B3.1.2.2). 

 Further sources of diesel exhaust emissions include off-road and 

 stationary engines (reciprocating or gas turbine), electricity 

 generating plants, pipeline pumping, gas compression, commercial and 

 industrial furnace installations, and space and water heaters in 

 plants and factories (see section A3.2.1.2). Diesel exhaust is also 

 emitted from marine and inland ships' engines; residual fuels and 

 other heavy grades (for example Bunker C) are used in ocean shipping 

 (von Meyerinck, personal communication, 1994). 

 B3.1.1.1 Emission of chemical constituents with the gaseous portion 

 of diesel exhaust 

 The exhaust emissions from diesel-fuelled vehicles are generally 

 given as milligrams of component emitted per kilometre of driving 

 distance (Egebäck & Bertilsson, 1983; Westerholm et al., 1986; 

 Westerholm, 1987; Volkswagen AG, 1989; CONCAWE, 1990b; Westerholm & 

 Egebäck, 1991; Prakash et al., 1992; Scheepers & Bos, 1992a). Data for 

 verifying tests are issued by national regulatory bodies, e.g. the 

 German Federal Office for Motor Vehicles (1993, 1994). Depending on 

 the testing cycle, diesel engine, and fuel (see sections B3.1.1.1 and 

 B3.1.1.2), the data show considerable differences even though the 

 values are of the same order of magnitude. Emission factors used in 

 different regions to estimate the effects of regulated chemical 

 constituents (carbon monoxide, nitrogen oxides, and hydrocarbons) in 

 air are shown in Table 24. 

 Like all hydrocarbon fuel-burning engines, diesel engines release 

 significant amounts of carbon dioxide. Westerholm & Egebäck (1991) 

 measured emission factors of about 1 kg/km from a bus and a truck in 

 the US transient cycle and the bus cycle. In measurements of emissions 

 from six buses in four driving cycles (US transient cycle and three 

 bus cycles), Prakash et al. (1992) found emission factors up to about 

 4 kg/km, especially in the bus cycles. For five European diesel 

 passenger cars and one light van, Hammerle et al. (1994a) determined 

 emission factors of 162-252 g/km carbon dioxide in the European Motor 

 Vehicle Emissions cycle and the US FTP-75 test. Diesel engines are the 

 most efficient of all common types of combustion engines, with peak 

 thermal efficiencies typically > 40%, owing to the relatively large 

 air:fuel ratio during combustion (see section B3.1.2.1) (Organisation 

 for Economic Co-operation and Development, 1993). 

 Table 24. Emission factors for diesel vehicles in 1985 used as standards for estimating total impact 

 

 Region Passenger cars Commercial vehicles 

 g/km g/kg Average < 5 t > 5 t 

 

 g/km g/kg g/km g/kg g/km g/kg 

 Carbon monoxide 

 Denmark 1.0 2.0 

 Germanya 1.5 20 16 

 Netherlands 2.7 35 3.9 14 2.0 20 4.6 14 

 European Union 19 19 16 

 Austria 22.8 22.8 20 

 Sweden 10.5 

 Switzerland 4.0 

 United Statesb 3.1-6.2 

 Nitrogen oxides 

 Germanya 1.0 14 58 

 Netherlands 0.8 10 18.3 66 0.6 6 22.8 69 

 European Union 14 18 62 

 Sweden 39 

 Switzerland 14.0 

 United Statesb 3.1 

 Hydrocarbons 

 Germanya 0.5 7 12 

 Netherlands 0.6 10 4.6 17 0.9 9 6.3 19 

 

 Table 24 (contd) 

 Region Passenger cars Commercial vehicles 

 g/km g/kg Average < 5 t > 5 t 

 

 g/km g/kg g/km g/kg g/km g/kg 

 Hydrocarbons (contd) 

 European Union 10 13 9 

 Sweden 3.9 

 Switzerland 3.0 

 United Statesb 1.2 

 

 Adapted from Organisation for Economic Co-operation and Development (1993) 

 a Excluding former German Democratic Republic 

 b 1975-83, trucks tested in the US transient cycle 

 Cyanides, ammonia, and sulfur dioxide are detectable in the 

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 gaseous portion of diesel exhaust. The average emission factors given 

 by Volkswagen AG (1989) for seven passenger diesel cars with four- and 

 five-cylinder engines in three driving cycles (US 75 test with cold 

 start, US sulfate emission test, US highway driving test) were 

 0.6 mg/km cyanides, 1.1 mg/km ammonia, and 233.0 mg/km sulfur dioxide. 

 The emission of individual organic components and classes of 

 compounds, summarized as total hydrocarbons, are shown in Table 25, 

 which provides an overview of the quantities of individual substances 

 emitted in diesel exhausts. Heavy-duty vehicles release more 

 low-boiling hydrocarbons than passenger cars; however, the difference 

 could be due to the driving cycle used, which involves frequent 

 changes of speed and load (see section B2.2.1). The emissions of 

 adsorbed organic components, such as PAHs (see section B3.1.1.2), are 

 correlated with the release of particulate matter. 

 B3.1.1.2 Emission of particulate matter and adsorbed components in 

 diesel exhaust gases 

 The emission of total particulate matter from diesel exhaust is 

 shown in Table 26. Analysis of the particulate matter released from 

 heavy-duty vehicles gave the following emission factors (Westerholm & 

 Egebäck, 1991): 170-370 mg/km carbon, 8-71 mg/km soluble organic 

 compounds derived from fuel, 56-167 mg/km soluble organic compounds 

 derived from lubricating oil, 1.4-37 mg/km soluble sulfates, and 

 0.6-3.7 mg/km nitrate. Comparable values were not available for 

 light-duty vehicles. 

 As PAHs and oxygenated PAHs from diesel and spark-ignition 

 engines are qualitatively similar, their differentiation in the 

 environment is difficult (Behymer & Hites, 1984); however, 

 benzo[ b]naphtho-[2,1-d]thiophene is specific for diesel exhaust and 

 can therefore be used as a marker (Grimmer et al., 1979). Emissions of 

 PAH components are shown in Table 27. 

 In experiments with one bus and one truck, Westerholm & Egebäck 

 (1991) detected 30-220 μg/km of particulate-associated PAHs. The 

 compounds measured included dibenzothiophene and its 4- and 3-methyl 

 derivatives, 2-methylfluorene, phenanthrene and its methylated 

 derivatives, anthracene and its 2-methyl derivative, fluoranthene, 

 pyrene and its 1- and 2-methyl derivatives, retene, benzo[ a]fluorene, 

 benzo[ ghi]fluoranthene, cyclopenta[ cd]pyrene, benzo[ a]anthracene, 

 chrysene or triphenylene, benzo[ b,k]fluoranthene, benzo[ e]pyrene, 

 benzo[ a]pyrene, perylene, indeno[1,2,3-cd]fluoranthene, 

 indeno[1,2,3-cd]pyrene, picene, benzo[ ghi]perylene, and coronene. 

 The emission factors for 1-nitropyrene were 0.13-7.3 μg/km. 

 Table 25. Emission factors for individual organic constituents and 

 classes of compounds in the gaseous portion of diesel 

 exhaust 

 

 Class of compound Emission factor (mg/km) 

 or constituent 

 Light-duty vehiclesa Heavy-duty vehiclesa

 

 Straight-chain aliphatic hydrocarbons

 Sum of C1-C4 5.3-6.6 (C1 + C2)b

 < 1 - < 143c

 Sum of > C4 < 1-5c

 Olefins 

 Ethylene 25.6-90.7d 32-135e

 13.5-16.9b 19.0-82.9f

 < 1-31c

 Propylene 7.3-22e

 8.1-44.0f

 1,3-Butadiene 0.2g

 Acetylene 5.7-7.4b 27.9-106.9 (+ ethane)f

 Alcohols Methanol 1.6d

 Ethanol < 1.2-22.2d

 Aldehydes 

 Formaldehyde 8.1b 60-255e

 7.9-20.7d 140-150h

 4.2-9.1g 19.0-207.4 f*

 Acetaldehyde 3.1b 18-137e

 < 22-36d 40-50h

 2.0-4.4g

 Crotonaldehyde 1.2b

 Acrolein < 1-1.8d 8.5-36e

 4h

 Benzaldehyde 0.6b 10-14h

 Light aromatic compounds

 Benzene 2.6-4.3b 4.5-13.1e

 ND-6c 6.9-30.5f

 9.5-18.1d

 0.15-3.47g

 

 Table 25. (cont'd) 

 Class of compound Emission factor (mg/km) 

 or constituent 

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 Light-duty vehiclesa Heavy-duty vehiclesa

 

 Toluene 1.1-1.9b 2-13.7e

 ND-2c 7.4-32.5f

 < 1.0d

 Ethylbenzene NDc

 Xylenes NDc 7.8-41.7f

 Phenols 0.7-1.5b

 

 ND, not determined 

 a According to the Organisation for Economic Co-operation and 

 Development (1993), light-duty vehicles are generally classified as 

 vehicles with a weight < 3.5 t, occasionally < 5 t; heavy-duty 

 vehicles are those weighing > 5 t. 

 b From Volkswagen AG (1989): various numbers of diesel passenger cars 

 in three driving cycles (US-75 test with cold start, US sulfate 

 emission test, US highway driving test); determination of aldehydes 

 only in the US-75 test 

 c From Scheepers & Bos (1992a): two diesel passenger cars (< 50 000 and 

 > 100 000 km on odometer) in ECE test, 15 min at 90 km/h and 15 min 

 at 120 km/h 

 d From Egebäck & Bertilsson (1983): two passenger cars in US-78 test 

 e From Westerholm & Egebäck (1991): a bus and a truck in bus cycle with 

 different diesel fuels 

 f From Prakash et al. (1992): one bus in four driving cycles (US 

 transient cycle, three bus cycles) with the exception (*) of eight 

 buses in the same driving cycles 

 g From Hammerle et al. (1994a): five passenger cars and one light van 

 in European Motor Vehicle Emissions Group cycle 

 h From Westerholm et al. (1986): one heavy-duty vehicle on a chassis 

 dynamometer with two diesel fuels 

 i Mainly phenols, cresols and xylenols 

 Table 26. Emission factors for total particulate matter from diesel exhaust 

 

 Measurement conditions Emission factor (mg/km) Reference 

 

 Light-duty vehiclesa

 Seven passenger cars in three driving cycles 166.4-238.7 Volkswagen AG (1989) 

 (US-FTP-75 test with cold start; US sulfate emission 

 test; US highway driving test) 

 Four passenger cars, 15 light vans in three 180-250 (passenger cars) Williams et al. (1989) 

 Australian driving cycles (corresponding roughly to 360-440 (light vans) 

 US-72 and US-75 tests) 

 Seven passenger cars, two light vans in combined 70-365 (passenger cars) CONCAWE (1990b) 

 ECE 15/EUDC test with four diesel fuels 233-609 (light vans) 

 Various Germanyb, 300 Organisation for Economic 

 Netherlands, 600 Co-operation and Development 

 Sweden, 400 (1993) 

 61 passenger cars and 30 light vans without catalyst 39-188 (mean, 104) Federal Office for Motor Vehicles

 (optimally tuned) incombined ECE 15/EUDC test (1993) 

 73 passenger cars and 45 light vans with catalyst 48-127 (mean, 90) Federal Office for Motor Vehicles

 (optimally tuned) in combined ECE 15/EUDC test (1993) 

 

 Table 26 (contd) 

 

 Measurement conditions Emission factor (mg/km) Reference 

 

 44 passenger cars and 8 light vans without catalyst 52-117 (mean, 95) Federal Office for Motor Vehicles

 (optimally tuned) inUS FTP-75 test (1993) 

 118 passenger cars and 34 light vans with catalyst 50-118 (mean, 71) Federal Office for Motor Vehicles

 (optimally tuned) inUS FTP-75 test (1993) 

 Five passenger cars and 1 light van in European Motor 52-117 Hammerle et al. (1994a) 

 Vehicle Emissions Group cycle and US FTP-75 test 

 Heavy-duty vehiclesa 

 One vehicle on chassis dynamometer (bus cycle); 680-1000 Westerholm et al. (1986) 

 two diesel fuels with different contents of sulfur and 

 aromatic compounds 

 10 trucks, 2 buses in one Australian driving cycle 800-7150 Williams et al. (1989) 

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 simulating urban traffic 

 One bus, one truck in two driving cycles (bus cycle; 230-600 Westerholm & Egebäck (1991) 

 US transient cycle) with two diesel fuels 

 106 trucks and buses in ECE-R49 driving cycle 0.056-0.606 g/kWh Federal Office for Motor Vehicles

 (1994) 

 

 Table 26 (contd) 

 

 Measurement conditions Emission factor (mg/km) Reference 

 

 Various Netherlands, 800 (< 5 t) Organisation for Economic 

 3300 (> 5 t) Co-operation and Development 

 Sweden, 400 (< 5 t) (1993) 

 1700 (> 5 t) 

 13 trucks and buses (three with particulate trap, 584-804 (without trap) Lowenthal et al. (1994) 

 10 without) in bus cycle with two diesel fuels 67-206 (with trap) 

 

 a According to the Organisation for Economic Co-operation and Development (1993), light-duty vehicles are generally classified as 

 vehicles with a weight < 3.5 t, occasionally < 5 t; heavy-duty vehicles are those weighing > 5 t. 

 b Without the former German Democratic Republic 

 Table 27. Emission factors for polycyclic aromatic hydrocarbons in 

 diesel exhaust 

 

 Constituent Emission factor (μg/km) 

 Light-duty vehiclesa Heavy-duty vehiclesa

 

 Anthracene 17-63b 0.9-3.2c; 9-26d; 

 3-14d+; 1.6e

 Phenanthrene 140f 4.2-25c

 295-524b 163-308d; 79-186d+; 

 12.2e

 Fluoranthene 172f 10-39c

 58-200g 27-34d; 14-17d+

 60.4-79.7g 13.0e

 Pyrene 186 15-102c

 < 0.9-22 28-31d; 9-21d+

 66.6-87.1 22.6e

 Chrysene 40 9.5-26c

 14-67 8-32d; 4-12d+

 10.7-22.3 Not measurede

 Benzo[b,k]fluoranthene 40 1.6-8.4c

 2.6-47 9-12d,h; 2-8d,h+

 10.3-15.2 5.6e

 Benzo[ghi]fluoranthene 40f 1.4-13c; 6.9e

 Cyclopenta[cd]pyrene 2f 2.5-11c

 0.81ag* 1.4e

 Benzo[e]pyrene 3-38b 1.6-23c

 13.8-16.9 5-9d; 1-7d+; 2.6e

 Benzo[a]pyrene 10 0.8-12c

 < 1-19 2-3d; 0.4-2d+

 4.0-5.3 1.3e

 Benzo[a]anthracene 25 3.0-12c

 8-43 5-12d; 1-4d+

 2.7-3.9 3.6e

 Indeno[123-cd]pyrene 15f 0.7-15c

 3.5-4.4g

 Benzo[ghi]perylene 20 0.6-30c

 < 1-18 2-4d; 0.5-1d+

 8.7-11.7 Not detected 

 (detection limit 

 not given)e 

 

 Table 27 (contd) 

 Constituent Emission factor (μg/km) 

 Light-duty vehiclesa Heavy-duty vehiclesa

 

 Perylene < 1-2b Not measuredc

 0.5-0.6g 1.0e

 Coronene 10f < 0.1-12c

 5.43g* Not detected 

 (detection limit 

 not given)e

 

 a According to the Organisation for Economic Co-operation and 

 Development (1993), light-duty vehicles are generally classified as 

 vehicles with a weight < 3.5 t, occasionally < 5 t; heavy-duty 

 vehicles are those weighing > 5 t. 

 b From Scheepers & Bos (1992a): two diesel passenger cars (< 50 000 

 and > 100 000 km on odometer) in ECE test 

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 c From Westerholm et al. (1986): one heavy-duty vehicle on a chassis 

 dynamometer (bus cycle) 

 d From Lowenthal et al. (1994): 13 trucks and buses (three with 

 particulate trap [d+], 10 without) in bus cycle 

 e From Rogge et al. (1993): two heavy-duty vehicles in special 

 driving cycle 

 f From Egebäck & Bertilsson (1983): average of two passenger cars in 

 US-78 test 

 g From Volkswagen AG (1989): seven passenger cars in three driving 

 cycles (US-75 test with cold start, US sulfate emission test, US 

 highway driving test) with the exception (*) of one four-cylinder 

 engine, US-72 test with hot start 

 h Isomers not specified 

 The emission of oxygenated PAHs by two diesel passenger cars (one 

 four-cylinder and one five-cylinder engine, US 72 test with hot start) 

 was 4-40 μg/km. In a comparable test (one four-cylinder engine, same 

 driving cycle), the emission of nitro-PAHs was 0.1-3.5 μg/km. As a 

 result of possible artefact formation during sampling (see section 

 B2.2.1), these measurements are uncertain (Volkswagen AG, 1989). It is 

 suspected that nitrate-based cetane improvers (see section A2.1.2) 

 could increase nitro-PAH emissions in exhaust (Organisation for 

 Economic Co-operation and Development, 1993). 

 There are no significant differences in the emissions of adsorbed 

 single substances between light- and heavy-duty vehicles, although 

 heavy-duty vehicles release larger relative amounts of particulate 

 matter (Salmeen et al., 1985). 

 The chlorine content of diesel fuel is typically < 1 ppm 

 (Oehme et al., 1991). Thus, no dioxins were found in the exhaust of 

 heavy vehicles, at a detection limit of 100 pg/litre of fuel (Marklund 

 et al., 1990). The dioxin emissions from one light-duty (indirect 

 injection) and one heavy-duty (direct injection) diesel engine under 

 different load conditions on a chassis dynamometer were 0.009-0.141 ng 

 of toxicity equivalents per litre of fuel consumed. The highest value 

 was reported in emissions from the light-duty engine at full load. 

 Overall, the emissions were of the same order of magnitude as the 

 dioxin emissions from a petrol-fuelled engine with a catalytic 

 converter (Schwind et al., 1991). 

 B3.1.2 Parameters that influence diesel exhaust emissions 

 B3.1.2.1 Engine conditions 

 In general, diesel engines are operated with excess air; the 

 air:fuel ratio is about 1.5, and at lower air:fuel ratios, much more 

 smoke is emitted (Organisation for Economic Co-operation and 

 Development, 1993). Wide local variations in the equivalence ratio and 

 the temperature of the mixture are caused by the heterogeneous nature 

 of the combustion process. To avoid over-rich mixtures and to improve 

 the air:fuel mixing processes, wall wetting and delay of fuel 

 injection are used (CONCAWE, 1986). In naturally aspirated engines, 

 the amount of air in the cylinder is independent of the power output. 

 For these engines, the maximal power output is limited by the amount 

 of fuel that can be injected without smoke formation. In turbocharged 

 engines, however, increasing the amount of fuel injected increases the 

 energy in the exhaust gas, and the turbocharger pumps more air into 

 the combustion chamber. For this reason, the power output of 

 turbocharged engines is not, in general, limited by smoke. Low 

 air:fuel ratios can occur only during transient acceleration. Most 

 turbocharged engines are further equipped with a cooling system 

 (intercooler) in which compressed air reduces adverse thermal effects. 

 In both types of engines, fuel is injected either directly into the 

 combustion chamber or indirectly into a separate pre-chamber where it 

 is mixed and partly burnt before reaching the main combustion chamber 

 (Organisation for Economic Co-operation and Development, 1993). 

 Scheepers & Bos (1992a) reported that most heavy-duty vehicles have 

 direct injection motors, and indirect injection is used for light-duty 

 vehicles. 

 The most important influences of engine conditions on diesel 

 exhaust emissions are summarized in Table 28. Contrasting results are 

 sometimes obtained with regard to the effect of engine conditions on 

 diesel exhaust emissions. Adjustment of the engine plays a major role 

 (CONCAWE, 1990b), which was slightly less in the US FTP-75 test cycle 

 than in the European cycle. 

 Table 28. Influence of engine conditions on diesel exhaust emissions 

 

 Condition Change Influence on exhaust emissions Reference 

 

 Air:fuel ratio Increase Increased emissions of hydrocarbons and particulate soluble Organisation for Economic 

 fraction; decreased particulate and nitrogen oxide emissions Co-operation and 

 from turbocharged and intercooled engines Development (1993) 

 Increased PAH emissions, decreased particulate emissions from Barbella et al. (1988) 

 direct injection engines; decreased PAH and particulate emissions 

 from indirect injection engines 

 Increased nitrogen oxide emissions, decreased particulate Iida et al. (1986) 

 emissions from direct injection engines 

 Injection timing Advance Increased particulate emissions from indirect injection engines Du et al. (1984); Williams et 

 al. (1989) 

 Decreased particulate and hydrocarbon emissions; increased Organisation for Economic 

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 nitrogen oxide emissions Co-operation and Development (1993)

 No influence on concentrations of PAHs and oxy-PAHs adsorbed Jensen & Hites (1983)

 on particulate matter 

 Delay Decreased nitrogen oxide emissions, increased volumetric fuel Organisation for Economic 

 consumption Co-operation and Development (1993)

 

 Table 28. Influence of engine conditions on diesel exhaust emissions 

 

 Condition Change Influence on exhaust emissions Reference 

 

 Injection timing Delay Decreased particulate emissions from indirect injection engines; Williams et al. (1989) 

 (contd) increased particulate emissions from direct injection engines 

 Small effect on PAH emissions from indirect injection engines Schuetzle & Frazier (1986) 

 Small effect on particulate emissions from direct injection engines Campbell et al. (1981a) 

 No influence on concentrations of PAHs and oxy-PAHs adsorbed Jensen & Hites (1983)

 on particulate matter 

 Load and Increase Increased particulate and PAH emissions at high loads; decreased Pipho et al. (1986) 

 temperature particulate emissions at very high load from indirect injection 

 engines 

 Decreased concentrations of PAHs and oxy-PAHs adsorbed on Jensen & Hites (1983)

 particulate matter 

 Decrease Decreased particulate and nitrogen oxide emissions; extremely Organisation for Economic 

 cold charge air may increase hydrocarbon emissions Co-operation and 

 Development (1993) 

 Lowest PAH emissions at medium load; enrichment of three- Pipho et al. (1986) 

 and four-ring PAHs during idling (indirect injection engines) 

 

 PAH, polycyclic aromatic hydrocarbons 

 (a) Engine aging 

 Increased emissions of hydrocarbons, particulates, and PAHs have 

 been reported from older, more intensively used light- and heavy-duty 

 vehicle engines in comparison with newer ones (Stenberg et al., 1983; 

 Braddock & Perry, 1986; Scheepers & Bos, 1992a). Stenberg et al. 

 (1983) proposed that the combustion of more lubricating oil in older 

 vehicles contributes to the enhanced emissions. Prakash et al. (1992) 

 measured the emission characteristics of several buses and reported 

 that a properly maintained engine would not emit significantly more 

 hydrocarbons and nitrogen oxides during its lifetime, whereas carbon 

 monoxide and particulate emissions could increase with age. These 

 findings are similar to those of Volkswagen AG (1989) on the influence 

 of distance travelled on exhaust emissions from one diesel passenger 

 car over a total distance of about 30 000 km in three driving cycles 

 (US FTP test, US sulfate emission test, US highway driving test). The 

 average deterioration factors, relative to the emissions at about 

 2500 km, were carbon monoxide, 0.97; nitrogen oxides, 0.96; 

 hydrocarbons, 0.91; particulates, 1.07; fluoranthene, 0.96; pyrene, 

 1.06; chrysene, 0.62; benzo[ b,k]fluoranthene, 1.11; benzo[ e]pyrene, 

 1.51; benzo[ a]pyrene, 0.68; perylene, 0.96; indeno[1,2,3-cd]pyrene, 

 2.91; and benzo[ ghi]perylene, 3.43. 

 (b) Lubricating oil 

 As a result of emission control techniques such as turbocharging, 

 intercooling, and injection timing, the relative importance of 

 emissions caused by lubricating oils has increased (Organisation for 

 Economic Co-operation and Development, 1993). Lubricating oils have 

 been hypothesized to be a sink for incomplete combustion products such 

 as PAHs and their derivatives, which are scrubbed from the exhaust 

 gas. When this 'enriched' lubricating oil leaks into the combustion 

 chamber, the constituents may be emitted in the exhaust (Scheepers & 

 Bos, 1992a; see section B2.1.1). McKee & Plutnick (1989) found, 

 however, that carcinogenic PAHs accumulate in gasoline- but not in 

 diesel-fuelled engine oils. 

 Oil consumption can be reduced by improving engine manufacturing 

 specifications and engine seals (Organisation for Economic 

 Co-operation and Development, 1993). The particle-bound hydrocarbons 

 derived from lubricating oil contribute up to about 50% by weight in 

 light-duty vehicles and to a maximum of about 26% by weight of the 

 total emitted particulate matter (see section B2.1.2, Table 22). 

 Experiments with 13C radiolabelled lubricating oil in three 

 light-duty vehicles showed that addition of up to 3% lubricating oil 

 increases the emitted particulate matter by about 50%, and the 

 particulates consist mainly of the soluble organic fraction adsorbed 

 onto the particles (Williams et al., 1989). 

 B3.1.2.2 Fuel specification 

 Fuel parameters influence the particulate emissions of diesel 

 engines but seem to be less important than other parameters like 

 engine adjustment, load, and maintenance (Weidmann et al., 1988). 

 The actual trend in legislation of the quality of diesel fuel, i.e. to 

 a lower sulfur and aromatic content, will improve emissions, 

 especially of particles. In addition, the more stringent emission 

 standards in many countries will decrease diesel-related emissions. 

 (a) Sulfur content 

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 There have been numerous investigations on the influence of 

 sulfur content in diesel fuel on the release of particulate matter 

 (CONCAWE, 1990b; Van Beckhoven, 1991; Westerholm & Egebäck, 1991; 

 Scheepers & Bos, 1992a). The sulfur content is presumed to be directly 

 correlated with the release of particulate matter. About 3-5% of the 

 fuel sulfur in light-duty vehicles and 2-3% of that in heavy-duty 

 vehicles reacts with metal sulfates which are adsorbed onto the 

 particulate matter, increasing its mass and its hygroscopic 

 properties, as metal sulfates tend to absorb significant amounts of 

 water from the atmosphere (Organisation for Economic Co-operation and 

 Development, 1993). 

 A reduced sulfur content leads to decreased levels of 

 particulates in the exhaust of light-duty vehicles. For example, 

 investigations on seven passenger cars and two light vans in a 

 combined ECE 15/EUDC testing cycle with four diesel fuels of different 

 sulfur contents (0.055, 0.12, 0.22, and 0.31% by weight) showed a 

 statistically significant reduction in the emission of particulates up 

 to a maximum of 7.4%. The investigators noted variations in 

 particulate levels between the different vehicles, however, that were 

 about two orders of magnitude higher than could be attributed directly 

 to the influence of the sulfur content (CONCAWE, 1990b). 

 Reduction of the emission rates of heavy-duty vehicles by 

 lowering the fuel sulfur content is still under discussion. In a study 

 of four heavy-duty engines in the ECE R49-13 mode driving cycle with 

 the same four fuels as described above, no statistically significant 

 reduction in emitted particulate matte was seen (CONCAWE, 1990b). In 

 experiments with one heavy-duty vehicle on a chassis dynamometer bus 

 cycle with two different fuels, however, a considerable reduction in 

 the release of particles was found (Westerholm et al., 1986). This 

 result was confirmed by Westerholm & Egebäck (1991) who investigated 

 one bus and one truck in three driving cycles (ECE 13 test, bus cycle, 

 US transient test) with eight diesel fuels of different sulfur and 

 aromatic contents. Comparable results were found by Gairing et al. 

 (1994) in tests with one heavy-duty engine (direct injection) in ECE 

 R49 with 12 different fuels. Adjustment of the engines again appeared 

 to be a decisive factor. 

 (b) Aromaticity (density) 

 Aromaticity can be directly associated with density, as a higher 

 density is frequently achieved by a larger content of aromatic 

 compounds. Obviously, increasing the aromaticity leads to increased 

 emissions of particulate matter, although volumetric fuel consumption 

 is decreased (CONCAWE, 1986). This finding was confirmed by Hare 

 (1986) for light- and heavy-duty vehicles on the basis of data from 

 the automobile industry. The presumed increase in the release of 

 particulates is 0.5-1.9% for a 1% by volume change in aromatic 

 content. In a study of four light-duty vehicles in three Australian 

 driving cycles (resembling roughly the US 72 and 75 tests), Williams 

 et al. (1989) found reductions in particulate emissions of 22-27% at a 

 10% difference in fuel aromaticity. Unfortunately, the two fuels also 

 differed in sulfur content and volatility. Van Beckhoven (1991) 

 achieved comparable results with passenger cars with indirect 

 injection but found no significant influence for heavy-duty direct 

 injection engines. Experiments by Westerholm & Egebäck (1991) on one 

 bus and one truck showed a reduction in the emission of particulates 

 when fuel with low levels of sulfur and aromatics was used. The 

 increased aromatic content is probably also the source of higher 

 levels of PAHs and nitro-PAHs in the exhaust (Schuetzle & Frazier, 

 1986; Westerholm, 1987; Westerholm & Egebäck, 1991; Organisation for 

 Economic Co-operation and Development, 1993). 

 (c) Volatility 

 The volatility of diesel fuels is described by the boiling range, 

 and especially by the 10% boiling-point (low boiling end fraction) and 

 the 90% boiling-point (high boiling end fraction) of the mixture. The 

 influence of the boiling range, particularly the 90% boiling-point, on 

 the release of particulate matter is still under discussion. While 

 some investigators (Hare, 1986; Williams et al., 1989) assume that 

 emissions of particulate matter increase with an increased 90% 

 boiling-point, others have not been able to confirm this effect, 

 suggesting that other parameters, such as sulfur content and 

 aromaticity, are responsible for the increase (Westerholm & Egebäck, 

 1991; Organisation for Economic Co-operation and Development, 1993). 

 (d) Cetane number 

 An increase in cetane number lowers the emission of diesel 

 particulate matter. A slight decrease in cetane number, combined with 

 a small increase in the density of diesel fuels (see section A2.1.3), 

 was predicted in 1987 to result in an increase in emissions from 3 to 

 12% for carbon monoxide, and to maxima of 2% for nitrogen oxides, 7% 

 for hydrocarbons, and 6% for particles (CONCAWE, 1987). 

 B3.1.2.3 Malfunction 

 Malfunctions or defective components of the engine or exhaust gas 

 system may result in considerably higher emissions than those from a 

 properly maintained engine. Up to twofold increases in emissions of 

 carbon monoxide, hydrocarbons, and particulate matter have been 

 measured even in the absence of a significant effect on power or fuel 

 consumption (Ullman et al., 1984). Malfunction of the fuel injection 

 system may contributed markedly to higher emissions (Organisation for 

 Economic Co-operation and Development, 1993). Volkswagen AG (1989) 

 tested a diesel passenger car with defective injection nozzles in 

 three driving cycles (US FTP test, US sulfate emission test, US 

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 highway driving cycle) and found statistically significant increases 

 in the emissions of carbon monoxide (up to about 25%), hydrocarbons 

 (up to about 45%), and particulate matter (up to about 15%), whereas 

 the release of nitrogen oxides was almost unaffected. The amounts of 

 benzene and PAHs emitted were slightly increased. Comparable results 

 were obtained by Williams et al. (1989) for the release of particles 

 by several light-duty vehicles equipped with defective injectors. 

 Malfunction of US medium- to heavy-duty vehicle diesel engines 

 increased the amount of nitrogen oxide emitted to about 4%, that of 

 hydrocarbons to about 75%, and that of particulates to about 140% 

 (Organisation for Economic Co-operation and Development, 1993). 

 B3.1.3 Total emissions by diesel engines 

 Few data are available on the emissions of different constituents 

 of diesel exhaust into the atmosphere and their contribution to the 

 total release by traffic and industry. The contribution of heavy-duty 

 vehicles seems to be much greater than that of passenger cars, despite 

 lower percent kilometres. For example, in westen Germany, only 8% of 

 the total annual urban mileage was attributable to heavy-duty vehicles 

 (Fromme, 1990). In contrast, in 1987, power plants contributed 15.3% 

 (85 000 t), industry 63.5% (360 000 t), domestic and minor consumers 

 8.1% (44 000 t), and total traffic 13% (72 000 t) to the particles 

 released (Metz, 1989). The contribution of diesel particulate matter 

 to the total particle burden of the atmosphere is highly dependent on 

 local conditions (Table 29). 

 Diesel vehicles, particularly in the light-duty category, 

 represent a smaller proportion of motor traffic in the United States 

 than in most European countries. Measurements from two heavy-duty 

 vehicles in 1982 indicated that light- and heavy-duty diesel vehicles 

 contributed about 6% to the total fine aerosol, organic carbon 

 emissions in the Los Angeles basin, about 1200 kg/day being emitted by 

 heavy-duty vehicles and 600-870 kg/day by light-duty vehicles 

 (Hildemann et al., 1991; Rogge et al., 1993). 

 B3.1.4 Control of emissions 

 The automotive industry has made efforts to reduce diesel exhaust 

 emissions (Obländer, 1991; Fortnagel, 1992; Hammerle et al., 1994b), 

 and technology is advancing. 

 B3.1.4.1 Particle traps 

 Particle traps are placed in the exhaust system to collect 

 particulate matter and to clean the filter by burning the trapped 

 particles (trap oxidizers). Most traps are based on cellular ceramic 

 monolith material or ceramic silica fibre coils. Many regeneration 

 techniques have been developed for trap oxidizers (Organisation for 

 Economic Co-operation and Development, 1993), including thermal 

 regeneration, which is the burning of collected particulate matter, 

 and catalytic regeneration, in which fuel catalysts, e.g. iron and 

 copper, containing organic compounds form finely dispersed metal 

 particles during combustion to reduce the burning temperature of the 

 diesel particles so that there is more efficient regeneration 

 (Volkswagen AG, 1989; Hammerle et al., 1994b). Traps remove the 

 soluble organic fraction adsorbed onto particles and the dry 

 carbonaceous soot, while catalysts can remove substances only from the 

 soluble organic fraction. In catalytic regeneration, over 95% of the 

 metal used as fuel catalyst is retained in the trap (Hammerle et al., 

 1994b). 

 Studies of the emissions of one light-duty diesel passenger car 

 by Volkswagen AG (1989) showed that the release of particulates was 

 reduced by a thermal trap by at least 80% during the collection phase 

 and by about 60% during the regeneration phase; the reduction was 80% 

 for the whole cycle. Sulfate emissions decreased to about 50%; 

 however, emission of carbon monoxide increased by about 10%, probably 

 due to additional burning and/or incomplete oxidation of particulate 

 matter on the trap. Comparable experiments with a catalytically 

 regenerated trap, with addition of a manganese compound, also showed a 

 trap efficiency of about 80% for particulate matter. Hydrocarbon and 

 carbon monoxide emissions were slightly increased, probably due to 

 incomplete oxidation on the trap. Sulfate emissions were reduced to 

 less than half, emissions of PAHs were reduced to about 25%, and those 

 of phenol and aldehydes to about 25-33%. About 10% of the manganese 

 catalyst was detected in the exhaust. 

 Measurements with a heavy-duty vehicle on a chassis dynamometer 

 to test two particle traps showed decreases of 79 and 86% in the 

 release of particles, depending on the trap and fuel characteristics. 

 The emissions of hydrocarbon, carbon monoxide, aldehydes, and PAHs 

 were slightly reduced (Westerholm et al., 1986). 

 Table 29. Diesel exhaust emissions and their contribution to total anthropogenic emissions 

 

 Region Year Annual emissions (kt/year) Reference 

 

 NOx CO HC PM SO2

 

 Light-duty vehicles

 Germanya 1986 52 (3.3)b 76 (1.2)b 23 (2.2)b 15 (26.3)b NR Fromme (1990) 

 1987 NR NR NR 12 (2.2)c NR Metz (1989) 

 United Kingdom 1991 (0.7)c (0.4)c (1.1)c (2)c,d (0.2)c Quality of Urban Air Review 

 Group (1993) 

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 Light- and heavy-duty vehicles

 Europe NR NR NR NR NR (1.6)c OECD (1993) 

 United States 1984 NR NR NR NR 620 (3)c OECD (1993) 

 1986 NR NR NR 54.8 (20)b NR Carey (1987) 

 (4)c

 Germanya 1989 640 240 150 55 NR Federal Environment 

 Agency(1991) 

 Heavy-duty vehicles

 OECD (Europe) 1980 1548 (13)c NR 393 (4)c NR 361 (2)c OECD (1993) 

 Germanya 1986 502 (32.2)b 130 (2.1)b 104 (10.0)b 37 (64.7)b 35 (2)c OECD (1993); Fromme (1990) 

 (17)c (2)c (4)c (7)c

 1987 NR NR NR 32.5 (5.9)c NR Metz (1989) 

 

 Table 29 (cont'd). 

 

 Region Year Annual emissions (kt/year) Reference 

 

 NOx CO HC PM SO2

 

 Heavy-duty vehicles (contd) 

 Germany 1988 614 351 1.31 NR 38 Federal Environment Agency 

 (1992) 

 United Kingdom 1991 (19.9)c (1.9)c (5.4)c (14)c,d (1.0)c Quality of Urban Air 

 Review Group (1993) 

 Canadae 1985 265 104 37 20 21 Environment Canada 

 (1990) 

 

 NOx, nitrogen oxides; CO, carbon monoxide; HC, hydrocarbons; PM, particulate matter; SO2, sulfur dioxide; NR, not reported; OECD, 

 Organsiation for Economic Co-operation and Development 

 a Excluding the former German Democratic Republic 

 b Percentage of total traffic emissions 

 c Percentage of total man-made emissions 

 d PM10

 e Sum of light- and heavy-duty trucks 

 The effect of a ceramic wall-flow monolith particulate trap was 

 studied on the emissions of a 1979 heavy-duty diesel engine with 

 direct injection in two steady-state modes. Reductions of 70% (50% at 

 full load) and 86% (75% at full load) in particle release were found. 

 There was also a decrease in the soluble organic fraction, whereas the 

 emitted portion of volatile organic carbons was only slightly reduced. 

 The trap had almost no effect on the release of nitrogen oxides (Dorie 

 et al., 1987). 

 The measurements of Lowenthal et al. (1994) on 13 trucks and 

 buses (three with particulate traps, 10 without) in a bus cycle showed 

 a similar reduction in the release of particles (Table 26). There was 

 a significant decrease in the emission of particle-bound PAHs. 

 B3.1.4.2 Catalytic converters 

 Diesel catalytic converters reduce gaseous and particle-bound 

 hydrocarbon constituents of the exhaust, e.g. aldehydes, PAHs, nitro- 

 PAHs, and carbon monoxide. Regeneration systems are not needed, as 

 particulate matter is not collected by common flow-through catalytic 

 converters. The efficiency in controlling particulates is, however, 

 much lower than that of traps. Disadvantages of catalytic converters 

 are further conversion of nitrogen monoxide to the more toxic nitrogen 

 dioxide and of sulfur dioxide to particulate sulfates (Organisation 

 for Economic Co-operation and Development, 1993). Catalysts that 

 selectively oxidize organic compounds and oxidize almost no sulfur 

 dioxide are currently in use. Removal of sulfur from diesel fuels 

 would allow the use of more active catalysts; use of catalysts in 

 diesel vehicles run on sulfur-containing fuel is limited because the 

 strong adsorbing tendency of sulfur partly inactivates the catalyst 

 (Hammerle et al., 1994b; see section A2.1.1). 

 B3.2 Regulatory approaches 

 The levels of carbon monoxide, nitrogen oxides, total 

 hydrocarbons, and particulates emitted by diesel engines are regulated 

 by law in a number of countries (Table 30). Most other industrialized 

 countries have adapted United States or European regulations (for 

 details, see CONCAWE, 1990a and Mercedes-Benz AG, 1994a). 

 B4. ENVIRONMENTAL TRANSPORT, DISTRIBUTION, AND TRANSFORMATION

 Few data are available on the fate of diesel exhaust in the 

 atmosphere, which is the first environmental compartment affected. In 

 general, the effects on the overall environment of diesel fuel 

 combustion are typical of those of fossil fuel burning. The 

 contribution of diesel fuel emissions is proportional to diesel fuel 

 consumption both locally and globally. 

 Table 30. Limit values for components of diesel exhaust 

 

 Region Carbon Nitrogen Hydrocarbons Particulates Comments 

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 monoxide oxides 

 

 Light-duty vehicles (g/km)

 Austria 2.1 0.62 0.25 0.124 < 3.5 t; since 1991; from 1995, 

 adoption of European Union

 standards planned 

 Canada 2.1 0.62 0.25 0.12 Since 1987 

 European Union 2.72 0.97 (with 0.14 Since 1992 

 hydrocarbons) 

 1.0 0.7 0.08 From 1996 

 Finland Since 1993 

 Japan 2.1 0.7 0.62 None Since 1986 

 2.1 0.5 0.4 0.2 Since 1994 

 Sweden, Norway 2.1 0.62 (city) 0.25 0.124 < 3.5 t; from motor year 1992 

 0.76 (highway) 

 Switzerland 2.1 0.62 (city) 0.25 0.124 < 3.5 t; since 1988; from 1995, 

 0.76 (highway) adoption of European Union

 standards planned 

 USA (California) 2.1-5.2 0.2-0.6 0.2-0.3 (except 0.05 (up to Depending on mileage 

 methane) 31 000 km) 

 US Environmental 2.1-2.6 0.6-0.8 0.2 0.05-0.12 Depending on mileage 

 Protection Agency 

 

 Table 30 (contd) 

 

 Region Carbon Nitrogen Hydrocarbons Particulates Comments 

 monoxide oxides 

 

 Heavy-duty vehicles (g/kWh)

 Austria 4.9 9.0 1.23 0.4 

 Canada 15.5 5.0 1.3 0.25 g/bhp-h 

 15.5 5.0 1.3 0.1 g/bhp-h; from 1995-97 

 European Union 4.5 8.0 1.1 0.36 Since 1992 

 4.0 7.0 1.1 0.15 From 1995-96 

 Japan 7.4 5.0 2.9 0.7 Indirect injection engines

 7.4 6.0 2.9 0.7 Direct injection engines 

 Sweden 4.9 9.0 1.23 0.4 

 USA 15.5 5.0 1.3 0.07 g/bhp-h; bus 

 15.5 4.0 1.3 0.1 g/bhp-h; truck 

 15.5 5.0 1.3 0.05 g/bhp-h; bus; from 1998 

 15.5 4.0 1.3 0.1 g/bhp-h; truck; from 1998 

 

 Adapted from Mercedes-Benz AG (1994b); reference year, 1994, unless otherwise stated; bhp-h, brake horsepower-hour 

 Thus, the major components of diesel exhaust contribute to acid 

 deposition (nitrogen and sulfur oxides), tropospheric ozone formation 

 (carbon monoxide, nitrogen oxides, and hydrocarbons), and global 

 warming (carbon dioxide and particulates; carbon monoxide, nitrogen 

 oxides and hydrocarbons by ozone formation). 

 The environmental fate of released particulate matter and of 

 organic compounds, particularly the PAHs, is important environmentally. 

 The mechanisms of the distribution and transformation of individual 

 hydrocarbons in diesel exhaust have been well described (IPCS, 1986, 

 1993). 

 B4.1 Transport and distribution between media 

 The major fraction (50-80%) of the particulate emissions of 

 diesel engines is in the submicron size, ranging from 0.02 to 0.5 μm 

 (see section B2.1.2). Once particles have been emitted, their 

 mechanical transport in the atmosphere is like that of gas molecules 

 (nonreactive). Together with carbon particles from other combustion 

 processes, they may be transported over long distances and even 

 penetrate the stratosphere (Muhlbaier Dasch & Cadle, 1989). 

 Only one study was available on the agglomeration behaviour of 

 the particles in the atmosphere. Albrechcinski et al. (1985) measured 

 the aging behaviour of particulate matter from a 1978 diesel passenger 

 car in a 600-m3 model chamber with a nominal exhaust gas dilution of 

 150:1 and found peak mean aerosol diameters, based on volume size 

 distributions, of 0.1-0.18 μm for 'fresh' aerosol. The concentrations 

 of total particulate decreased during aging of the aerosol due to 

 coagulation, fall-out, and perhaps losses to the walls of the chamber. 

 The average decrease was 20% after 8 h and 60% after 24 h. Excess 

 nitrogen dioxide seemed to inhibit particle growth. Particles with an 

 average diameter of 1-10 μm constituted approximately 10% of the fresh 

 aerosol, but this percentage decreased during aging as a result of 

 apparently rapid fall-out of larger particles. It is not clear whether 

 these results are also representative of the particle emission pattern 

 of modern diesel passenger cars. 

 Model experiments of the gas-phase chemistry of nitrogen oxides, 

 total hydrocarbons, and sulfur dioxide from diesel exhaust were 

 performed by varying parameters such as irradiation, nitrogen dioxide 

 concentration, and ozone concentration (Albrechcinski et al., 1985). 

 Irradiation alone had only a minimal effect, but excess nitrogen 

 dioxide led to higher rates of decay of nitrogen monoxide in the dark 

 than under irradiation, probably because of photodissociation of 

 nitrogen dioxide to nitrogen monoxide. As nitrogen monoxide is rapidly 

 converted to nitrogen dioxide in the presence of excess ozone, the 

 nitrogen oxide concentration decreased as the ozone concentration 

 reached a maximum, presumably partly because of the formation of 

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 nitric acid which was deposited onto the chamber walls. Since reactive 

 organic compounds were not added, the authors considered that the 

 experiments were not representative of urban atmospheres. 

 The hydrosphere and geosphere may be affected indirectly by 

 diesel exhaust emissions after dry or wet deposition of particulate 

 matter or individual constituents (see section B4.2). In experiments 

 with dysprosium-traced diesel fuel, Horvath et al. (1988) (see section 

 B5.1) found 0.012-0.07 g diesel particulate matter per gram of road 

 dust. 

 B4.2 Transformation and removal 

 Atmospheric removal of airborne carbon particles consists mainly 

 of dry deposition and scavenging by precipitation (wet deposition). 

 The rate of wet removal is directly correlated to the ratio of organic 

 to elemental carbon and is low for small ratios (Muhlbaier Dasch & 

 Cadle, 1989). As the overall removal rate of diesel particulates is 

 estimated to be low, the atmospheric life-time is several days 

 (Jaenicke, 1986). 

 The elemental carbon of diesel particulates may act as a catalyst 

 in the formation of sulfuric acid by oxidation of sulfur dioxide. The 

 oxidation reaction is assumed to occur on the surface of solid soot 

 particles or in liquid drops containing soot particles (Novakov, 1984; 

 Mészáros & Mészáros, 1989). Furthermore, diesel particles themselves 

 contain sulfate, adsorbed in the form of metal sulfates, at a 

 concentration of about 1-12% by weight, depending on the sulfur 

 content of the fuel (see section B2.1.2), which may be washed off if 

 the particles come into contact with precipitation. The organic 

 compounds adsorbed on the emitted particulate matter may undergo a 

 number of physical and chemical reactions (volatilization of 

 low-relative-molecular-mass compounds, formation of secondary 

 aerosols, oxidation, nitration) with other atmospheric compounds or 

 during exposure to sunlight (Pitts et al., 1985). The estimated 

 half-lives for unbound PAHs in the atmosphere range from one day 

 (naphthalene) to one week (e.g. pyrene, chrysene, benzofluoranthenes, 

 benzo[a]pyrene) (Mackay et al., 1992; see Table 11); however, PAHs 

 adsorbed onto particles may be more stable to nitrogen dioxide and 

 ozone than airborne PAHs (Gibson et al., 1981). 

 B5. ENVIRONMENTAL LEVELS AND HUMAN EXPOSURE

 Because diesel exhaust is a complex mixture of a great variety of 

 compounds (see also section B2.1), general 'environmental levels' 

 cannot be described. The individual constituents of diesel exhaust 

 should be detectable in all compartments of the environment. Since 

 diesel exhaust is only one of numerous other sources, the levels of 

 individual compounds cannot be correlated directly to diesel exhaust. 

 Particulate matter appears to be the most relevant fraction of 

 diesel exhaust for the general population and workers exposed to 

 diesel exhaust emissions from a toxicological point of view. The 

 concentration of particles is about 10- to 20-fold higher in diesel 

 exhaust than in the exhaust from gasoline-fuelled vehicles, and the 

 particle diameters are in the respirable range. 

 B5.1 Exposure of the general population 

 The general population is exposed to high levels of diesel 

 exhaust in certain microenvironments, such as busy streets and parking 

 areas. Exposure to the main gaseous components of diesel exhaust -- 

 carbon dioxide, carbon monoxide, nitrogen oxides, and total 

 hydrocarbons -- can be estimated from the emission factors given in 

 section B3, the kilometrage of diesel vehicles in relation to total 

 traffic, and atmospheric dispersion models (Cuddihy et al., 1984; 

 Volkswagen AG, 1989). In view of the fact that measured emission 

 factors vary widely (see section B3.1.1) and are mainly dependent on 

 adjustment of individual engines, the validity of these estimations is 

 limited. 

 On a global basis, there are wide variations in the contribution 

 of diesel emissions to total airborne particulate matter, which 

 depends on the following factors: percentage of diesel vehicles in the 

 total volume of traffic; type, age, and maintenance of individual 

 engines (see section B3.1.2.1); fuel quality (e.g. sulfur content and 

 aromaticity; see section B3.1.2.2); and emission control techniques. 

 Particle concentrations in environmental air samples are usually given 

 as total particle concentrations, with no differentiation by source. 

 The contribution of diesel particulate matter is then estimated on the 

 basis of the percentage of diesel vehicle emissions in the total 

 emissions from traffic or total man-made emissions. Emissions from 

 running stationary diesel engines have up to now not been taken into 

 account. Data on emissions from light- and heavy-duty vehicles in some 

 industrialized countries are shown in Table 30 (section B3.1.3). The 

 proportion of the concentrations to which people are exposed that is 

 attributable to diesel vehicles varies widely, depending on traffic 

 flow and composition in the vicinity and the magnitude of background 

 pollution from other sources. 

 In a study in the United Kingdom (Waller et al., 1965), 

 measurements were made at a sampling site at the centre of a busy 

 street canyon, where traffic flows were typically 1200 gasoline and 

 600 diesel vehicles per hour, in order to assess the maximal 

 concentrations of traffic pollutants in urban areas. The contributions 

 of airborne particulate matter, expressed as seasonal means for 

 daytime working hours, were 200-421 μg/m3, after allowance for the 

 urban background measured at nearby control sites. The additional 

 particulate matter was attributed primarily to the diesel vehicles, 

 while the corresponding contribution to carbon monoxide, averaging 

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 15 ppm (17 mg/m3), was associated mainly with the gasoline vehicles. 

 In France, Joumard & Perrin (1988) measured atmospheric 

 particulate matter (diameter, 0.01-25 μm) in a 30-40-m wide street 

 open to pedestrians, with two central lanes reserved for use by bus 

 services involving weekday traffic of more than 1000 vehicles per day 

 in each direction. The measurement point was in the immediate vicinity 

 of two bus stops, 3 m from the edge of the pavement and at a height of 

 2.5 m. The particle concentrations, determined by measuring ß 

 radiation, were 34 μg/m3 during the period 23.00-05.00 h and 

 67 μg/m3 during 07.00-19.30 h. 

 Airborne particle concentrations were calculated for an 

 eight-lane American freeway and for four- and six-lane European 

 autoroutes. The one-dimensional Gaussian model used neglects chemical 

 reactions during transport and possible deposition on the ground and 

 assumes turbulent mixing in the air. The calculated maximal 

 concentrations were 7-13 μg/m3 close to the road, and these 

 decreased with distance from the measuring point. About 100 m away, 

 the estimated particle concentration at a height of 1.5 m was three to 

 four times lower than that next to the motorway (Volkswagen AG, 1989). 

 Particle emissions, especially from diesel vehicles, were 

 estimated roughly for various locations by the lead surrogate method, 

 in which historical ambient lead concentrations in urban areas are 

 used as indices of mobile source pollutant levels. Particle emission 

 factors for light- and heavy-duty vehicles and the distribution 

 characteristics of lead and diesel particulate are also taken into 

 consideration (Rykowski & Brochu, 1986). The results are shown in 

 Table 31. 

 Concentrations of particles from diesel engines in the 

 environment were determined in Vienna, Austria, at several measuring 

 points during a four-week period. As there was only one distributor of 

 diesel fuel for the whole network of service stations in Vienna, the 

 rare earth element dysprosium was added as an indicator to the fuel at 

 this central point, which was distributed to diesel vehicles at 

 service stations and then emitted with the exhaust. Dust samples 

 collected from the air were subjected to neutron activation analysis 

 and the level of dysprosium was determined. The proportion of 

 dysprosium in diesel soot was calculated on the basis of emission 

 factors for diesel engines in the literature and from laboratory 

 experiments, assuming that the marker is totally transferred from fuel 

 to exhaust during combustion. At seven of the 11 measuring points for 

 different traffic densities, the concentrations were almost linearly 

 correlated to traffic density. Ambient particulate levels increased by 

 5.5 μg/m3 per 500 diesel vehicles per hour, from 10.3 in a residential 

 area to 23.6 μg/m3 near an urban freeway; the mean value was 

 14.4 μg/m3. The diesel particulate concentration in the centre of 

 Vienna was calculated to be 11 μg/m3 by correlating the measured 

 values and traffic density. At four measuring stations, significant 

 deviations from linearity were found which were due to local 

 conditions. The concentration of the marker was below the detection 

 limit before the testing period and one year later (Horvath et al., 

 1988). A deficiency of the study is that the dysprosium concentrations 

 of diesel fuel before the addition were not taken into account, so 

 that the emission factors used may not reflect the true situation 

 (Holländer, personal communication, 1994). Nevertheless, the measured 

 ambient particle concentrations fit well with estimated data for 

 diesel exhaust emissions by other investigators. 

 Table 31. Estimated particle concentrations emitted from diesel 

 engine exhaust 

 

 Location and year Concentration 

 (μg/m3) 

 

 United Statesa, cities with > 1 million 1.3-3 

 residents (1984) 

 United Statesa, cities with 100 000-250 000 residents 0.7-1.7 

 Naples, Italy, urban area (1982) 7.2-35.1 

 Birmingham, United Kingdom, urban area (1982) 3.2-20.3 

 Birmingham, United Kingdom, university area (1982) 0.8-5.5 

 Stockholm, Sweden, inner city (1982) 2.5-16.4 

 

 From Rykowski & Brochu (1986) 

 a According to Cuddihy et al. (1984), the proportion of 

 diesel-fuelled light-duty vehicles in the United States was 

 about 2%. 

 In a programme to measure airborne diesel soot levels in 

 Düsseldorf, Germany, the total carbon content of fine dust (particle 

 diameter, < 7μm) at a busy crossing was 8-42 μm3 as a daily 

 average, 18 μg/m3 as an annual average, 21 μg/m3 on workdays, and 

 14 μg/m3 on weekends. The carbon content after solvent extraction 

 (elemental carbon) was 6-32 μg/m3 as a daily average, 16 μg/m3 on 

 workdays, and 10 μg/m3 on weekends. In a residential area in 

 Duisburg, Germany, the concentration of elemental carbon was 3 μg/m3. 

 The method of determination was as follows: a defined volume of air 

 was sucked through a fibreglass filter, and the respirable particle 

 fraction was separated. This fine dust was further separated into an 

 incinerable portion (according to German standard method TRGS 900), 

 total carbon, and the carbon content after liquid extraction 

 (elemental carbon). Total and elemental carbon were determined by 

 coulometry. By correlation with diurnal changes in carbon and nitrogen 

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 monoxide concentrations, the main particle source was shown to be 

 automobile traffic at the sampling location. Correlation of a traffic 

 census with working day and weekend particle levels showed that the 

 airborne particulate matter was due primarily to diesel vehicles 

 (Elbers & Muratyan (1991). Further measurements at the same place in 

 1991 and 1992 confirmed the results (Elbers & Richter, 1994). 

 Validation of the analytical method gave detection limits of 0.39 for 

 elemental carbon (relative standard deviation, 14% or 4.4 μg/m3) and 

 0.65 μg/m3 for total carbon (relative standard deviation, 13% or 

 7.8 μg/m3). 

 The weekly average ambient concentrations of diesel particulate 

 in Germany were estimated to be 5-10 μg/m3 in urban areas, 15-25 μg/m3

 in urban areas close to busy streets, and < 1.5 μg/m3 in rural 

 areas; however, the method used for the estimations was not reported 

 (State Committee for Immission Protection, 1992). 

 Estimates of the US Environmental Protection Agency for 1986 gave 

 annual mean ambient concentrations of diesel particle in the United 

 States of 2.6 μg/m3 in urban areas and 2.4 μg/m3 in rural areas. A 

 prediction for 1995 gave values of 1.5 μg/m3 for urban and 1.2 μg/m3

 for rural areas (Mauderly, 1992). Higher concentrations were estimated 

 by the Motor Vehicles Manufacturing Association (Sienicki & Mago, 

 1992), which predicted a mean value of 2.7 μg/m3 for the city of Los 

 Angeles in 1995. Lower levels were estimated in a study by the US 

 Environmental Protection Agency (1993) in which national average 

 emission factors for diesel vehicles for 1988 were multiplied by urban 

 and rural mileage. For 1990 and 1995, the annual exposure levels were 

 estimated to be 2.0 and 1.2 μg/m3 in urban air and 1.1 and 0.6 μg/m3

 in rural air, respectively. These estimates were confirmed by ambient 

 monitoring. Using data from the early 1980s, when the proportion of 

 diesel vehicles, the number of kilometres travelled, and emission 

 standards differed from present characteristics, McClellan (1986) 

 derived ambient diesel particulate concentrations of 10-30 μg/m3 on 

 American urban freeways and in urban street canyons. 

 B5.2 Occupational exposure

 The levels of particulate matter to which workers are exposed 

 when their predominant exposure to exhaust is that from diesel engines 

 are described in this section. It is difficult to determine the 

 contribution of diesel exhaust to respirable particles, as they 

 include not only those from diesel engines but also others generated 

 in the worker's environment, such as sand, dirt, coal dust, and 

 cigarette smoke particles. Thus, the levels of total and respirable 

 particulates reported in jobs with potential exposure to diesel 

 exhaust may be significant overestimates of the actual exposure. Only 

 two occupational groups have been studied in this regard: railroad 

 workers (Woskie et al., 1988a,b) and mechanics and drivers in the 

 trucking industry (Zaebst et al., 1991). The specific exposures of 

 these groups to diesel particles range from 0.026 to 0.192 mg/m3. In 

 the railroad workers, cigarette smoke was found to account for a 

 substantial proportion of total respirable particulate matter, and the 

 geometric mean exposure to respirable particulates of workers not 

 exposed to diesel exhaust was reduced by over 80% when the 

 contribution of cigarette particulate was considered (Woskie et al., 

 1988a). 

 The principal marker chosen to measure exposure of workers in the 

 trucking industry (including road drivers, local drivers, stevedores, 

 and mechanics) to diesel exhaust was elemental carbon, which is 

 derived from the core of the diesel exhaust particle and represents 

 about 20% of respirable particulate; cigarette smoke does not 

 contribute appreciable amounts of elemental carbon. Mechanics and 

 stevedores had the highest exposure to diesel exhaust, and truck 

 drivers had lower levels (Zaebst et al., 1991). The degree to which a 

 marker of diesel exhaust exposure actually represents true exposure 

 depends on the nature of all sources of respirable particles in the 

 work-place. Occupational exposure to particulates is summarized in 

 Table 32. 

 Table 32. Reported occupational exposure to particulates among 

 workers exposed to diesel exhaust 

 

 Occupational group Particles (mg/m3) 

 Total Respirable Diesel 

 Railroad workers 0.01-1.99 0.06-0.41 0.051-0.192a

 Mine workers 0-23.0 0-16.1 

 Truck drivers 0.1-1.0 0.13-1.2 0.025b

 Bus garage and bus 0.15-1.2 0.01-0.61 

 workers 

 Stevedores 0.157b

 Truck mechanics 0.133b

 

 a Estimated using nicotine to account for exposure to cigarette smoke 

 b Based on carbon core analysis, with an estimated 20% of respirable 

 particulate due to carbon (Steenland et al., 1992) 

 Because 1-nitropyrene is associated with the particle fraction of 

 diesel exhaust, this compound was used as an indicator of the 

 particulate fraction of diesel exhaust derived from various sources 

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 (e.g. ships, railroad engines, heavy-duty road vehicles, fork-lift 

 trucks) (Scheepers et al., 1994a,b). The 1-nitropyrene content of 

 fresh and aged diesel exhaust was measured in small air samples 

 extracted with acetone by sonication and detected by gas 

 chromatography-mass spectrometry. The following concentrations of 

 respirable diesel exhaust were determined: 0.044-0.33 mg/m3 in 

 various work-places with fork-lift trucks, 0.10-0.37 mg/m3 in 

 railroad engine repair shops, 0.080mg/m3 in a river vessel, and 0.67 

 or 3.33 mg/m3 in the breathing zone of railroad workers. 

 B5.2.1 Truck drivers and mechanics 

 In a study of 15 truck drivers in Geneva, Switzerland, exposure 

 to particulate matter was measured during one working day with a 

 direct-reading instrument and by sampling beside the drivers in the 

 truck cabin (Guillemin et al., 1992). Local drivers had greater 

 exposure to particulate matter (0.3 mg/m3) than long-distance 

 drivers (0.1 mg/m3) and spent more time in polluted areas, such as 

 streets with heavy traffic and construction sites. Smoking did not 

 influence the exposure of professional truck drivers to particulate 

 matter, probably because the ventilation rate of the truck cabins was 

 relatively high, even on cold days. 

 Industrial hygiene surveys were conducted during warm and cold 

 weather at eight terminals and truck repair shops to determine 

 exposure to submicrometre particles of elemental carbon among American 

 workers in one of four jobs -- road drivers, local drivers, stevedores, 

 and mechanics -- all of whom were exposed mainly to diesel aerosol 

 (Zaebst et al., 1991). The overall arithmetic mean exposure was 

 5.1 μg/m3 for 72 long-distance road drivers, 5.4 μg/m3 for 66 

 local drivers, 26.6 μg/m3 for 80 mechanics, and 31.3 μg/m3 for 54 

 stevedores exposed to diesel fork-lift trucks. The background 

 concentrations in the same cities were 3.4 μg/m3 on 21 major 

 highways and 1.4 μg/m3 in 23 residential areas. The exposures of the 

 truck drivers were significantly higher than the background 

 concentrations in residential areas but could not be distinguished 

 from the background highway concentrations. 

 Area air sampling in an American truck repair shop in 1987 gave 

 the following results, depending on the sampling location: 0.225 and 

 0.32 μg/m3 submicrometre particles, 0.26 and 0.51 μg/m3 respirable 

 particles, and 0.63 and 0.66 μg/m3 total particulate matter. The 

 values for elemental carbon were 86-118 μg/m3 submicrometre 

 particles and 159-214 μg/m3 total carbon. In personal samples from 

 four mechanics, 79-193 μg/m3 submicrometre elemental carbon were 

 found (US National Institute for Occupational Safety and Health, 

 1990a). 

 The concentrations of particles collected on fibreglass filters 

 at 25 work-places in Germany where mainly fork-lift trucks and trucks 

 were used were 0.02-0.8 mg/m3 in area samples and 0.13-1.2 mg/m3

 in personal samples (Lehmann et al., 1990). Area measurements in two 

 German truck repair garages (five samples from each) showed 

 concentrations of incinerable fine dust (according to German standard 

 method TRGS 900) of 0.11-0.40 mg/m3 (Blome et al., 1990). 

 Personal samples from truck drivers who loaded diesel-engined 

 trucks onto car ferries in Sweden showed particle concentrations of 

 0.1-1.0 mg/m3 (Ulfvarson et al., 1987). The drivers may also have 

 been exposed to diesel exhaust from the ferries. 

 B5.2.2 Bus garage and other bus workers 

 In area samples taken in an American bus garage in 1989, the 

 concentrations of particles were 0-0.1 mg/m3 submicrometre 

 particles, 0-0.3 mg/m3 respirable particles, 0-0.22 mg/m3 total 

 particulate matter, and 0.014-0.326 mg/m3 elemental carbon (US 

 National Institute for Occupational Safety and Health, 1990b). 

 The concentrations of smoke were measured in two diesel bus 

 garages in London, United Kingdom, from high-volume samplers for 

 successive periods through the day and night, which were linked to bus 

 movements and the exposure of the maintenance staff. The contribution 

 from the buses was assessed by subtracting the background values at 

 control sites outside the garages. In the most polluted garage, 

 0.3-1.2mg/m3 of smoke were measured during working periods (Waller 

 et al., 1985). 

 In Sweden, a particle concentration of 0.46 mg/m3 was found 

 during personal sampling in periods of high activity (arrival and 

 departure of buses) (Ulfvarson et al., 1987). 

 Area air sampling of the concentrations of incinerable fine dust 

 (according to German standard method TRGS 900) in two bus depots (six 

 samples in each) and one bus garage (three samples) in Germany showed 

 concentrations of 0.22-0.37 mg/m3 (Blome et al., 1990). 

 The respirable dust levels in bus garages in Italy and the United 

 States ranged from <0.01 to 0.73 mg/m3 (Gamble et al., 1987a). The 

 total dust levels in bus garages in Denver, Colorado, United States, 

 were 0.01-0.81 mg/m3 (Apol, 1983; Pryor, 1983). 

 B5.2.3 Fork-lift truck operators 

 Area samples taken in one American trucking terminal where 

 diesel-powered fork-lift trucks were used in 1987 contained 

 48-62 μg/m3 submicrometre particles, 34-57 μg/m3 respirable 

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 particles, and 62-97 μg/m3 total particles (US National Institute 

 for Occupational Safety and Health, 1989a). The concentrations of 

 elemental carbon in area samples from another American trucking 

 terminal in 1988 were 40-44 μg/m3, and those in personal samples 

 from fork-lift operators were 33-77 μg/m3 (US National Institute for 

 Occupational Safety and Health, 1989b). Area samples taken in an 

 American freight dock contained concentrations of <12 and 294 μg/m3

 respirable dust. The levels were significantly higher in areas where 

 unfiltered rather than filtered diesel motors were used (US National 

 Institute for Occupational Safety and Health, 1990c). 

 A mean concentration of 31.3 μg/m3 of submicrometre elemental 

 carbon was found in personal samples from stevedores operating 

 diesel-powered fork-lift trucks. About 10 times less was found for 

 operators of gasoline- or propane-powered trucks (Zaebst et al., 

 1991). 

 The concentrations of particles in the breathing zone during use 

 of diesel-powered fork-lift trucks for loading, unloading, and 

 warehousing operations in American ammunition storage magazines were 

 < 0.01 to1.3 mg/m3 (Ungers, 1984) and 0.5-5.0 mg/m3 (Ungers, 1985). 

 B5.2.4 Railroad workers 

 The mean levels of total particulate matter were 0.38 mg/m3

 (range, 0.1-0.8) in Finnish locomotive cabs and 1.99 mg/m3 (range, 

 0.07-8.7) in roundhouses (Heino et al., 1978). In three German engine 

 sheds, the ambient concentrations of incinerable fine dust were 

 0.1-0.41mg/m3 (Blome et al., 1990). 

 A summary of American literature showed time-weighted average 

 levels of 0.05-0.07 mg/m3 (8-h) in tunnels, 0.16 mg/m3 (7.5-h) 

 during freighting, 0.01 mg/m3 (5-h) in switchyards, and 0.27 mg/m3

 (8-h) in cabooses (Hobbs et al., 1977). The arithmetic mean 

 concentrations of total respirable particles in personal samples from 

 shop workers, engineers, brakemen, conductors, and farmers in the 

 American railroad industry (after correction for the estimated 

 contribution of cigarette smoke particulates) were 51-192 μg/m3

 (Woskie et al., 1988a). 

 B5.2.5 Mine workers 

 Diesel vehicles and machines have been used in nearly all 

 American mines since the 1960s (Wichmann & Brüske-Hohlfeld, 1991). The 

 mean concentration of diesel particulate matter in personal and area 

 samples in mines where diesel equipment was used was 4.6 mg/m3

 (range, 0.2-14) (Holland, 1978). Total respirable dust levels of 

 0.6-1.7 mg/m3 were found by personal sampling (Wheeler et al., 

 1981); average concentrations of 0.9-2.7 mg/m3 were found in 

 full-shift personal samples, and the range for full-shift area samples 

 was 0-16.1 mg/m3 (Reger et al., 1982). The 8-h time-weighted average 

 level of respirable particulate matter in personal samples taken in an 

 American molybdenum mine was 0.2-1.9 mg/m3 (Cornwell, 1982). Total 

 respirable dust concentrations of 1.1-4.4 mg/m3 were reported in an 

 American gold mine (Daniel, 1984). The US Mine Safety and Health 

 Administration reported that the concentrations of diesel particulate 

 matter in American mines other than coal mines were 0.3-1.5 mg/m3

 (Mauderly, 1992). 

 Data from a salt mine in Canada showed a diesel particulate level 

 of about 0.5 mg/m3 (Johnson & Carlson, 1986). 

 In area samples from different work-places in eight German coal 

 mines, the levels of airborne diesel particulate matter (incinerable 

 fine dust) were 0.19-0.70 mg/m3 (Blome et al., 1990). In German 

 potash-salt mines, depending on the district, 0.2-0.4 mg/m3 of 

 diesel particles were measured (Bauer et al., 1990). 

 B5.2.6 Fire fighters 

 The average concentration of total particulate matter in personal 

 samples from fire-fighters in Boston, New York City, and Los Angeles, 

 United States, in 1985 was between < 0.1 and 0.48 mg/m3. On a typical 

 day in Boston or New York City, exposure to diesel exhaust particles 

 was estimated to be about 0.225 mg/m3 after correction for the 

 contributions of background and smoking. Simulation of 'worst-case' 

 exposures in Los Angeles fire stations gave a maximal concentration of 

 0.748 mg/m3 total particles (Froines et al., 1987). 

 B5.3 Biomonitoring 

 B5.3.1 Urinary mutagenicity 

 The occurrence of mutagens, measured by the Ames test, in the 

 urine and faeces of eight car mechanics occupationally exposed to 

 diesel exhaust was compared with that of a reference group of nine 

 office workers. The samples were collected over 48 h; information was 

 also gathered on dietary intake, smoking habits, and medication. No 

 enhancement of the incidence or degree of faecal or urinary 

 mutagenicity was seen (Willems et al., 1989). 

 Post-shift urinary mutagenicity was measured by the Ames test in 

 306 samples from 87 railroad workers with a range of exposures to 

 diesel exhaust (Schenker et al., 1992). Exposure was measured 

 throughout the work shift by constant-flow personal sampling pumps. In 

 separate analyses of smokers and nonsmokers, no independent 

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 association was seen with exposure to diesel exhaust. The workers with 

 the highest median exposure to respirable particles attributable to 

 diesel exhaust (113 μg/m3) were railroad engineering shop workers. 

 In studies of the effect of diesel exhaust on stevedores on 

 'roll-on-roll-off' ships (Ulfvarson et al., 1987), no difference in 

 mutagenicity to Salmonella typhimurium TA98 or Escherichia coli WP 

 2 uvr A was seen in urine collected during periods of exposure and 

 of no exposure. Similarly, no increase in urinary mutagenicity was 

 found in samples from six volunteers before and after exposure to 

 diesel exhaust collected from an experimental automobile run for 3.7 h 

 at 60 km/h and 2580 rpm. 

 B5.3.2 Other analyses 

 Samples of total suspended particulate matter were collected in a 

 repair shop for train engines, and the diesel exhaust concentrations 

 were determined using 1-nitropyrene as a biomarker (see section B5.2). 

 Urinary metabolites and the corresponding nitro-substituted 

 derivatives were detected by immunoassay in the urine of three 

 diesel-engine mechanics. They had a significantly increased excretion 

 of metabolites in comparison with two office clerks (Scheepers et al., 

 1994b). 

 B6. KINETICS AND METABOLISM IN LABORATORY ANIMALS AND HUMANS

 B6.1 Deposition 

 The mass median aerodynamic diameter of diesel exhaust particles 

 in long-term studies in animals exposed by inhalation was 0.17-0.25 μm 

 (Lewis et al., 1986; Lee et al., 1987; Wolff et al., 1987; 

 Creutzenberg et al., 1990). The deposition efficiency of particles of 

 this size range is lower than that of smaller particles, for which the 

 deposition by diffusion increases with decreasing diameter. The 

 deposition efficiency of particles with a diameter > 0.5 μm increases 

 with the aerodynamic diameter, owing to sedimentation and impaction. 

 The nose has hardly any filter effect for diesel particles because the 

 fraction of particles < 0.4 μm deposited in the nose is very low 

 (Heyder et al., 1986). 

 After short-term inhalation by rats of 0.29-μm fused 

 aluminosilicate particles, 8% was deposited in the bronchi and 13% in 

 the lungs (Raabe et al., 1988). A total of 10-20% diesel exhaust 

 particles was deposited in rats and guinea-pigs (Chan et al., 1981; 

 Lee et al., 1983; Dutcher et al., 1984). In humans, the alveolar 

 deposition efficiency of 0.2-μm particles was 10-20%, and no bronchial 

 deposition was detected (Heyder et al., 1986). 

 These experimental results agree well with those of a predictive 

 model for deposition of inhaled diesel exhaust particles in laboratory 

 animals and humans (Yu & Xu, 1987). In humans, the deposition 

 efficiency was about 7% in the alveolar region and 4% in the 

 tracheobronchial region. The model can also predict the fractions that 

 will be deposited in different airway generations; maximal deposition 

 occurs in the alveolar region (twentieth generation) of adults and of 

 children over two years of age. 

 The length and concentration of exposure had no significant 

 effect on deposition in rats exposed to 0, 0.4, 3.5, or 7.1 mg/m3

 diesel exhaust particles for 6, 12, 18, or 24 months, when deposition 

 of 0.1-μm gallium oxide particles was used as the indicator (Wolff et 

 al., 1987). 

 B6.2 Retention and clearance of particles 

 The kinetics of inhaled substances are conveniently described by 

 their pulmonary clearance and retention. These terms are often used 

 interchangeably, but it should be kept in mind that the fraction 

 cleared from the lung plus the fraction retained in the lung account 

 for the total deposited amount (retention = deposition - clearance). 

 Thus, in the following paragraphs, the term 'clearance' refers to a 

 clearance rate ( r, per unit of time) and the term 'retention' to a 

 biological half-time ( t  ́), provided there is a constant rate of 

 exponential clearance (ln2/ t  ́). 

 Clearance of diesel particles from the alveolar region is 

 important in the long-term effects of particles on cells, as it is 

 more than two orders of magnitude slower than mucociliary clearance, 

 measured in several studies in rats administered labelled diesel or 

 surrogate particles by inhalation. The pulmonary retention half-times 

 in studies in which the lung burden of diesel soot was also reported 

 are summarized in Table 33. The equivalent continuous exposure 

 concentration is calculated by multiplying the actual concentration by 

 the number of hours of weekly exposure divided by 168 h. This figure 

 allows a comparison of exposure levels in studies with different 

 exposure protocols. The assumption is that Habers' law ( c × t = 

 constant) is applicable. This is probably valid until a certain burden 

 of particulate is reached in the lung; however, when that level is 

 exceeded (particle overload), the calculation is increasingly invalid. 

 The retention half-time in these studies was 60-100 days in 

 control rats with low lung burdens and up to 600 days in animals with 

 high lung burdens. In a double logarithmic plot of retention 

 half-times and lung burden, a linear relationship can be seen for lung 

 burdens of diesel particles above 1mg per lung (Figure 1). 

 The gaseous phase of diesel exhaust appears to have no effect on 

 alveolar clearance in rats or hamsters (Heinrich et al., 1986a). 

 The retardation of lung clearance is not specific to diesel 

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 exhaust but is known as 'lung overloading by particles'. This effect 

 is characterized by (i) an overwhelming of normal alveolar 

 macrophage-mediated clearance processes under certain conditions of 

 exposure, (ii) resulting in lung burdens greater than predicted from 

 deposition kinetics at low concentrations, (iii) with associated 

 pathophysiological changes including altered macrophage function, 

 inflammation, and pulmonary fibrosis, and (iv) an uncertain 

 association with an increased incidence of lung tumours in rats 

 (McClellan, 1990). 

 The effect of overloading lung clearance mechanisms was 

 investigated in NMRI and C57Bl mice, Wistar and Fischer 344 rats, and 

 Syrian golden hamsters exposed to particulates, including test toner 

 (polymer pigmented with carbon black), polyvinyl chloride, carbon 

 black, diesel exhaust, and two crystalline forms of titanium dioxide 

 (anatase and rutile), at concentrations of 0.8-64 mg/m3 for up to 

 two years. In rats, lung overloading generally occurred after exposure 

 to 0.5-1.5 mg per lung or about 1 mg of material per gram of lung 

 tissue. A two- to 10-fold decrease in the clearance rate was seen 

 after heavy particulate loading in all of these rodent species (Muhle 

 et al., 1990). 

 In comparisons of the effects of particles of different 

 densities, the retained volume of particles appears to be a more 

 useful parameter than the retained mass, as alveolar macrophages have 

 an upper volumetric uptake limit. The particulate overload effect 

 appears to be initiated in rats when the average particle volume per 

 alveolar macrophage exceeds about 60m3, and alveolar 

 macrophage-mediated particle clearance virtually ceases when the 

 phagacytosed particulate volume exceeds an average of 600m3 (Morrow, 

 1988). 

 At a lung burden above threshold, signs of lung overloading in 

 Fischer 344 rats persisted for 15 months after cessation of exposure 

 (Bellmann et al., 1992). Retardation of alveolar clearance was also 

 observed in hamsters and mice at a lung burden above about 1 mg per 

 lung. For mice, no data were available with regard to lung burdens 

 below 1 mg per lung, but retardation of alveolar clearance is probably 

 already present at lower lung burdens. Lung overloading is thus seen 

 in a variety of species with various materials. It is generally 

 observed after the threshold lung burden of particles of low 

 solubility and low acute toxicity is exceeded for a considerable time 

 (Muhle et al., 1990). The effects of overloading should be considered 

 in extrapolating the health effects seen at high concentrations in 

 experiental animals to the low concentrations occurring in the 

 environment or the work-place. 

 The alveolar clearance rates of highly insoluble particles differ 

 among species, with retention half-times ranging from 50 to 100 days 

 in rodents to several hundred days in dogs and man (Figure 2). In 

 human lung, the retention half-time of insoluble, nontoxic particles 

 may be >500 days (Bailey et al., 1985a,b). 

 Table 33. Pulmonary retention of insoluble particles in rats after exposure to diesel exhaust, and lung burden of diesel soot 

 

 Strain and sex No./group Duration of Exposure Pulmonary retention Reference 

 exposure 

 (h/week) 

 Concentration (mg/m3) Duration Lung burden Material Half-time 

 (weeks) (mg/lung) studied (days) 

 Actual Equivalent 

 continuous 

 

 Fischer 344, 4 140 0 0 0 0 14C-Diesel 77 Chan et al.

 male 0.25 0.21 7 0.2 exhaust 90 (1984) 

 0.25 0.21 16 0.5 92 

 6.00 5.00 1 0.7 166 

 6.00 5.00 9 6.5 562 

 6.00 5.00 16 11.8 (> 1000) 

 Wistar, female 5-7 90 0 0 13 0 59Fe2O3 61 Creutzenberg

 0.84 0.45 0.63 (0.3 μm) 94 et al. (1990

 2.5 1.34 2.5 119 Heinrich et

 6.98 3.74 8.2 330 al. (1995) 

 0 0 52 0 72 

 0.84 0.45 2.8 121 

 2.5 1.34 10.7 254 

 6.98 3.74 35.7 541 

 0 0 78 0 96 

 0.84 0.45 5.5a 221 

 2.5 1.34 12.2 272 

 6.98 3.74 58.8 687 

 

 Table 33 (contd) 

 

 Strain and sex No./group Duration of Exposure Pulmonary retention Reference 

 exposure 

 (h/week) 

 Concentration (mg/m3) Duration Lung burden Material Half-time 

 (weeks) (mg/lung) studied (days) 

 Actual Equivalent 

 continuous 

 

 Fischer 344, 8 35 0.15 0.03 18 0.035 Diesel 87 Griffis et a

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 male and 0.94 0.20 0.22 exhaust 99 (1983) 

 female 4.10 0.85 1.89 165 

 Fischer 344, 4 140 6.00 5.00 1 1.7 14C-Diesel 61 Lee et al. 

 male 6.00 5.00 3 4.4 exhaust 124 (1987) 

 6.00 5.00 6 10.4 192 

 Fischer 344, 15-16 (lung 35 0 0 104 0 134Cs-Fused 79 Wolff et al.

 male and burden) 0.35 0.07 0.6 aluminosilicate 81 (1987) 

 female 10 3.50 0.73 11.5 particles 264 

 (retention) 7.00 1.46 20.5 (2 μm) 240 

 

 a Measured; value derived by interpolation from data at 52 and 104 weeks 

 

 

 Retention of diesel particles in the lungs and lymph nodes has 

 been reported in Fischer 344 and Wistar rats after long-term 

 inhalation (Brightwell et al., 1986; Ishinishi et al., 1986; Mauderly 

 et al., 1987; Strom et al., 1988; Creutzenberg et al., 1990; Strom et 

 al., 1990). Some results with regard to lung burden are included in 

 Table 33. Because clearance of lung burdens above about 1 mg per lung 

 was impaired after long-term, continuous inhalation of a concentration 

 equivalent to about 0.5mg/m3, no steady-state lung burden was found 

 at serial sacrifice at up to two years. About 20% of the lung burden 

 of diesel particles was found in lung-associated lymph nodes at that 

 time. 

 Mathematical models have been developed to calculate the 

 retention of diesel particles in rats. Yu & Yoon (1990) and Yu et al. 

 (1991) developed a dosimetry model to predict the retention of diesel 

 particles and associated organic compounds in rats and humans of 

 different ages. The model indicates that lung clearance would not be 

 impaired in humans exposed to a concentration < 0.05 mg/m3 for 

 24 h/day. The highest lung burden per unit of lung weight was 

 calculated for five-year-old children. This model was used to assess 

 the risk of inhaling diesel particles (Pepelko & Chen, 1993). 

 B6.3 Retention and clearance of polycyclic aromatic hydrocarbons 

 adsorbed onto diesel soot 

 The clearance of particles from ciliated airways by the 

 mucociliary escalator after bronchial deposition is virtually complete 

 within 24 h. For soluble organic material like PAHs on the surface of 

 carbon particles, diffusion-limited clearance through the airway 

 epithelium to capillary blood was found to be slower in the bronchial 

 region than in the alveoli (Gerde et al., 1991a, 1993a,b). 

 PAHs in diesel soot adhere strongly to the surface of the 

 particles. Several studies have shown that the association of PAHs 

 with particles significantly slows the clearance of the PAHs from 

 lungs in comparison with the clearance of inhaled PAHs unassociated 

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 with particulate matter. 

 After inhalation by Fischer 344 rats of 3H-benzo[ a]pyrene 

 adsorbed onto diesel soot (0.1% by mass) for 30 min, biphasic lung 

 clearance was noted. In a first, fast phase, about 50% of the inhaled 

 compound was cleared with a half-time of about 1 h, predominantly by 

 mucociliary clearance. At the end of exposure, about 15% of the 3H 

 label was found in blood, liver, and kidney, indicating rapid, direct 

 absorption of this fraction of 3H-benzo[ a]pyrene and its metabolites 

 into blood. The remaining 50% was retained in the lung, with a 

 half-time of 18 days; this is one-third of the retention half-time of 

 diesel particles. Thus, removal of benzo[ a]pyrene and its metabolites 

 from the particle carrier may be the rate-limiting step of this 

 clearance process (Sun et al., 1984). In contrast, more than 95% of 

 pure 3H-benzo[a]pyrene was cleared from the lung within 12 h after 

 inhalation (Sun et al., 1982). 

 These results were confirmed and extended to another PAH, 

 1-nitropyrene (Bond et al., 1986a,b), when the clearance of 

 14C-labelled compound adsorbed to diesel soot was determined by the 

 same method in Fischer 344 rats. After exposure to 490 ng/litre of 

 pure labelled compound, about 90% was cleared in the first, fast 

 clearance phase, with a retention half-time of 1 h; after exposure to 

 650 ng/litre of 14C-1-nitropyrene adsorbed onto diesel particles, 

 45% of the labelled compound was cleared from the lungs in the first 

 phase, with a half-time of about 2 h. The remaining 55% was retained 

 with a half-time of 36 days, which was twice the corresponding value 

 for 3H-benzo[ a]pyrene in the study of Sun et al. (1984). 

 On the basis of their data on the clearance of 3H-benzo[ a]pyrene 

 and 14C-1-nitropyrene, Bond et al. (1986b) predicted equilibrium 

 lung burdens in humans after long-term inhalation. Assuming inhalation 

 of 3.5 g/m3 of particles containing 0.1% benzo[ a]pyrene and 

 1-nitropyrene over an 8-h working day, they predicted equilibria of 

 160 ng benzo[ a]pyrene and 31 ng 1-nitropyrene per lung. No data are 

 available on changes in the retention of individual compounds after 

 prolonged exposure to diesel exhaust. 

 The clearance of a very low concentration (2.6 g/g particles) of 

 3H-benzo[ a]pyrene adsorbed onto diesel particles was measured in 

 Sprague-Dawley rats after intratracheal instillation (Bevan & Ruggio, 

 1991). Only 25% was cleared in the early, fast phase; a long-term 

 retention half-time of eight days was calculated for the remainder 

 during a three-day follow-up, which was similar to the clearance in 

 that period in the study of Sun et al. (1984). 

 B6.4 Metabolism 

 In the studies of Sun et al. (1984) and Bond et al. (1986a,b), 

 the levels of 3H-benzo[ a]pyrene and 14C-1-nitropyrene and their 

 metabolites in extracts of lung homogenates after inhalation of diesel 

 exhaust particles were measured by high-performance liquid 

 chromatography. Sun et al. detected oxidized metabolites 30 min after 

 inhalation: 35% of the 3H-benzo[ a]pyrene had been metabolized in 

 equal amounts to phenols (3-hydroxy- and 9-hydroxybenzo[ a]pyrene) 

 and quinones (1,6 and 3,6 isomers). Twenty days later, only 13% 

 phenols and 5% quinones were detected. In the study of Bond et al. 

 (1986b), about 30% of the 3H-1-nitro-pyrene had been metabolized to 

 acetylaminopyrenephenol (6 and 8 isomers) and about 40% remained 

 unmetabolized 1 h after inhalation. Oxidative metabolism of 

 14C-benzo[ a]pyrene, in solution or adsorbed onto diesel particles 

 at a concentration of 500 pmol/106 cells, was also detected in cell 

 cultures of pulmonary macrophages obtained from beagle dogs. The 

 quantity of metabolites increased with incubation time up to 45 and 

 125 pmol/106 cells in extracts and in the media, respectively, after 

 48 h of incubation. After incubation for 6 h, the major metabolites 

 found in extracts of cells were benzo[ a]pyrene-7,8-diol (0.5pmol/106

 cells) and benzo[a]pyrene-4,5-diol (0.2 pmol/106 cells); those in 

 extracts of culture medium were benzo[ a]pyrene-7,8-diol (1.7 pmol/106

 cells) and benzo[ a]pyrene-9,10-diol (1.4 pmol/106 cells), in 

 comparison with a total concentration of metabolites of 2.5 pmol/106

 cells in the extracts and 6 pmol/10 6 cells in the medium. Minor 

 metabolites were benzo[ a]pyrene phenols (3-hydroxy- and 

 9-hydroxy-benzo[ a]pyrene) and benzo[ a]pyrene quinones (6,12, 1,5, 

 and 3,5 isomers). The quantities of metabolite were similar when 

 macrophages were incubated with benzo[ a]pyrene in solution or 

 adsorbed onto diesel particles (Bond et al., 1984). 

 Using the 32P-postlabelling technique, Wong et al. (1986) found 

 increased DNA adduct formation in the lungs of Fischer 344 rats after 

 exposure for 31 months to diesel exhaust containing 7.1 mg/m3

 particles. After exposure of Fischer 344 rats and Syrian golden 

 hamsters to dilutions of diesel engine exhaust for six months to two 

 years, the level of haemoglobin adducts (2-hydroxyethylvaline and 

 2-hydroxypropylvaline), corresponding to the metabolic conversion of 

 5-10% of inhaled ethylene and propylene to its oxides, increased 

 dose-dependently (Törnqvist et al., 1988). An adduct of 

 benzo[ a]pyrenediol epoxide with deoxyguanosine was identified after 

 inhalation of benzo[a]pyrene adsorbed onto carbon black (20 mg/g) 

 (Wolff et al., 1989), demonstrating the production of epoxides of PAHs 

 by oxidative metabolism. 

 Methods for extracting diesel soot before testing for 

 genotoxicity in vitro have been discussed. As dichloromethane and 

 dimethyl sulfoxide do not correspond to leaching conditions in the 

 lung, it can be assumed that the bioavailability of genotoxic 

 materials is lower in lungs than in vitro. An investigation of 

 dipalmitoyl phosphatidylcholine, the primary component of 

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 physiological surfactant, demonstrated that the genotoxicity 

 associated with diesel particles inhaled into the lung can be 

 activated by the solubilization and dispersion properties of pulmonary 

 surfactants. This finding was confirmed in mammalian cells for sister 

 chromatid induction (Keane et al., 1991) and for chromosomal 

 aberrations and micronucleus formation (Gu et al., 1991, 1992). 

 B7. EFFECTS ON LABORATORY MAMMALS AND IN VITRO SYSTEMS

 B7.1 Single exposure 

 Data on the acute toxicity of diesel exhaust are very limited; 

 the two available studies suggest that diesel exhaust particles and 

 their extracts have little acute toxicity. 

 Male ICR mice were administered diesel exhaust particles by 

 intratracheal instillation, and mortality due to lung oedema was 

 assessed for up to 24 h. At a dose of 0.9 mg per animal, all animals 

 died within 24 h. The LD50 value was 0.6 mg per animal, equivalent 

 to about 20 mg/kg body weight. Diesel exhaust particles washed three 

 times with methanol did not cause death at a dose of 1 mg per mouse, 

 suggesting that the primary source of toxicity is the extractable 

 organic compounds rather than the particles themselves. These 

 compounds may produce superoxide radicals that damage endothelial 

 cells (Sagai et al., 1993). 

 The LD50 value for diesel exhaust extract in adult Syrian 

 golden hamsters after intraperitoneal injection was 1280 mg/kg body 

 weight (Pereira et al., 1982). 

 B7.2 Short-term exposure 

 Tracer-monitored DNA synthesis, indicating a proliferative 

 response, was observed in whole lung tissue of groups of 3-10 Fischer 

 344 rats exposed to diesel exhaust by inhalation at 6 mg/m3 for 

 20h/day on seven days per week for periods of 1-14 days. The response 

 was maximal after two days of exposure, showing a fourfold increase. 

 The type II cell labelling index was significantly higher (fourfold) 

 than that in controls after two and three days of exposure to diesel 

 exhaust. Both values returned to control levels after a one-week 

 recovery period. Experiments involving incorporation of 14C-palmitic 

 acid revealed transient changes in lipid metabolism after one day of 

 exposure, with a threefold increase in the amount of phosphatidyl- 

 choline in lung tissue (Wright, 1986). 

 Exposure of various species by inhalation to 6 mg/m3 resulted 

 in slight alterations in lung function and histopathological changes. 

 Groups of 10 male Chinese hamsters were exposed for 8 h/day on 

 seven days per week for six months to particle concentrations of 

 either 6 or 12 mg/m3 diesel exhaust. 

 Measurements of pulmonary function indicated dose-related 

 increases in lung weight and dose-related decreases in vital and 

 diffusion capacity. Pathological evaluation revealed oedema, 

 thickening of the alveolar lining, a possible increase in collagen, 

 and the presence of numerous particle-laden macrophages, which almost 

 filled the alveolar spaces (Vinegar et al., 1981). 

 Groups of 41-51 male and female Hartley guinea-pigs were exposed 

 for 20 h/day on seven days per week to exhaust from a light-duty 

 diesel engine diluted to attain a concentration of 6 mg/m3

 particulate matter. Separate groups were exposed to raw exhaust and 

 exhaust that had been irradiated with ultra-violet light for an 

 average of about 1 h. Pulmonary function was measured, and 

 electrocardiography was conducted on animals exposed for four weeks; 

 those examined for histological changes were exposed for eight weeks. 

 The only changes noted after four weeks were a 35% increase in 

 pulmonary flow resistance and a small, but significant decrease in 

 heart rate in animals exposed to irradiated exhaust. No changes in the 

 electrocardiogram were noted. The pathological changes were limited to 

 hyperplasia of alveolar lining cells and slight focal thickening of 

 the interstitium in occasional alveoli with accumulation of 

 particle-laden macrophages. Growth rates were unaffected (Wiester et 

 al., 1980). 

 As part of the same study, cats (Pepelko et al., 1981) and male 

 rats (15 per group) (Pepelko, 1982) were exposed for four weeks to 

 unirradiated exhaust under identical conditions. The pulmonary 

 function of rats was unchanged; the only changes were significant 

 increases in vital and total lung capacity, but these differences were 

 quite small and of questionable significance. The only functional 

 change noted in the cats was a decrease in maximal expiratory flow 

 rate at 10% of vital capacity. The pathological changes were again 

 limited to focal thickening of the alveolar walls near accumulations 

 of particle-laden macrophages. In general, the functional and 

 pathological changes were limited under these experimental conditions. 

 Kaplan et al. (1982) exposed male Fischer 344 rats (168 per 

 group), A/J mice (672 per group), and male Syrian golden hamsters (236 

 per group) to 1.5 mg/m3 of diesel exhaust particles for 20 h/day on 

 seven days per week for three months or to clean air. Animals were 

 killed at the end of exposure and after an additional six-month 

 recovery period. Mortality was not increased during the observation 

 period, and body weight was not significantly altered in any species. 

 At the end of exposure, the relative weight of the lung was 

 significantly increased in rats. In mice, the pulmonary adenoma 

 response was increased but not significantly. In all three species, 

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 grey to black discolouration of the lungs and lung-associated lymph 

 nodes were observed. Microscopically, most of the particulate was 

 found in macrophages, but some was free. After six months' exposure to 

 clean air, the lungs of all species had considerably less pigment 

 accumulated in foci. 

 Sixteen male Fischer 344 rats were exposed to 6 mg/m3 diesel 

 exhaust for periods ranging from 6 h to 63 days, with subsequent 

 histological examination of the lungs. The numbers of diesel 

 particulate-containing alveolar macrophages, type II alveolar cells, 

 and inflammatory cells were found to be increased over those in eight 

 controls. After a nine-week exposure, accumulation of macrophages was 

 observed near the terminal bronchioles (White & Garg, 1981). In rats 

 that inhaled 6 mg/m3 diesel exhaust for two weeks and were either 

 killed immediately or allowed to recover for six weeks before 

 sacrifice, there was no statistical difference in the number of 

 macrophage aggregates (240 000 and 220 000 per lung); however, the 

 aggregates in the recovery group had significantly higher average 

 diameter and volume, demonstrating macrophage attachment after the end 

 of exposure (Garg, 1983). 

 The observations of Wiester et al. (1980) and Garg (1983) 

 demonstrate the importance of alveolar macrophages in the clearance of 

 particles of low solubility. These are engulfed by alveolar 

 macrophages and eliminated via the mucociliary escalator and 

 gastrointestinal tract, or, in the case of lung particle overloading, 

 increasing fractions are sequestered in focal areas of the lung tissue 

 and transferred to the lymph nodes (Muhle et al., 1990). 

 B7.3 Long-term exposure and studies of carcinogenicity 

 B7.3.1 Non-neoplastic effects 

 No obvious signs of toxicity were observed in groups of 183 male 

 and 183 female Fischer 344 rats exposed by inhalation to diesel 

 exhaust at 0.35, 3.5, or 7.1 mg/m3 for 7 h/day on five days per week 

 for up to 30 months (Mauderly et al., 1987). The body weights did not 

 differ significantly from those of controls, and the exposures did not 

 affect the life span of animals of either sex. Focal fibrotic and 

 proliferative lung disease was observed in parallel with progressive 

 accumulation of diesel soot in the lung. Henderson et al. (1988) 

 reported the results of biochemical and cytological analyses of lung 

 lavage fluid and lung tissue from rats and mice exposed in the same 

 study, including determinations of lactic dehydrogenase, glutathione 

 reductase, ß-glucuronidase, glutathione, and hydroxyproline, and the 

 numbers of macrophages and neutrophils. No changes were seen in rats 

 or mice exposed to 0.35 mg/m3 , but at higher concentrations dose- 

 and duration-dependent increases in biochemical parameters and cell 

 numbers in lavage fluid were observed, indicating a chronic 

 inflammatory response. Lung weights were also increased in male and 

 female mice exposed to the two higher levels for any length of time, 

 in rats exposed to 7.0 mg/m3 for 12 months or longer, in female rats 

 exposed to 3.5 mg/m3 for 18 months, and in males exposed to 

 3.5 mg/m3 for 24 months. Tissue enzyme levels, measured in lung 

 lavage fluid as an indicator of damage, were consistently raised in 

 rats and mice at the two higher exposure levels and in lung tissue of 

 rats and mice at various times (most pronounced at 7 mg/m3). These 

 changes probably indicate an increase in lung tissue due to increased 

 inflammatory cells and epithelial cell proliferation. 

 In the same study, Mauderly et al. (1988) described focal 

 proliferative, fibrotic, and emphysematous changes in the lungs of 

 animals at the higher doses. Measurements in vivo revealed a 

 reduction in lung volume and compliance. 

 In a follow-up study, Mauderly et al. (1990) exposed male Fischer 

 344 rats that were either normal or had pre-existing pulmonary 

 emphysema (elastase-treated) to diesel soot at 3.5 mg/m3 for 7 h/day 

 on five days per week for 24 months, to determine whether 

 emphysematous rats were more susceptible to diesel exhaust. No 

 increase in susceptibility was seen. The emphysematous lungs had a 

 lower accumulation of particles than the normal lungs, which prevented 

 an overproportional response of the compromised animals. 

 Male and female Fischer 344 rats exposed to diesel exhaust 

 particles at 0.7, 2.2, or 6.6 mg/m3 for 16 h/day on five days per 

 week for two years or to filtered diesel exhaust showed an 

 exposure-related reduction in the rate of weight gain throughout the 

 study at the highest dose and an increase in absolute lung weight at 

 the two higher doses (Brightwell et al., 1986, 1989). 

 Groups of 72 male and 72 female Fischer 344 rats exposed to 

 diesel exhaust particles at 2 mg/m3 for 7 h/day on five days per 

 week for 24 months showed alveolar type II cell hyperplasia, 

 inhibition of long-term clearance of particles and pulmonary 

 lipidosis. No immunological abnormalities, no induction of pulmonary 

 or hepatic xenobiotic metabolizing enzymes, and no effects on 

 mortality, body weight gain, organ:body weight ratios or clinical 

 chemical parameters were seen (Lewis et al., 1986, 1989). In the same 

 study, a dose-related depression in phagocytic activity was seen in 

 alveolar macrophages (Castranova et al., 1985), and a trend to 

 increased pulmonary arterial wall thickness was observed in comparison 

 with controls (Vallyathan et al., 1986). 

 In groups of 15 male monkeys, exposure to diesel exhaust (as 

 described above) resulted in mild obstructive airway disease, but 

 there was no evidence of restrictive lung disease. The effects were 

 observed throughout the exposure period, after 6, 12, 18, and 24 

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 months (Lewis et al., 1989). 

 Reduced body weight, significantly increased lung:body weight 

 ratios, and type II cell proliferation were seen in female Fischer 344 

 rats exposed to whole-fraction diesel exhaust at 5 mg/m3 for 8 h/day 

 on seven days per week for 24 months (Iwai et al., 1986). 

 Groups of 96 male and 96 female Syrian golden hamsters, female 

 NMRI mice, and female Wistar rats were exposed to diesel engine 

 emissions at 4.4 mg/m3 for 19 h/day on five days per week for 

 120-140 weeks (Heinrich et al., 1986a; Stöber, 1986). The body weights 

 of mice were significantly reduced, by about 12%. Lung weights were 

 increased after two years of exposure, by two- to threefold in rats 

 and mice and by 50-70% in hamsters. Different levels of histological 

 response were seen in the three species. Hamsters had thickened 

 alveolar septa and bronchioalveolar hyperplasia. Of the mice, 64% had 

 bronchioalveolar hyperplasia (controls, 5%), 71% had multifocal 

 alveolar lipoproteinosis, and 43% had multifocal interstitial fibrosis 

 (controls, 4%). The nose, larynx, and trachea were not affected. 

 Treated rats showed severe inflammatory changes in the lungs, 

 thickened septa, foci of macrophages, and hyperplastic and metaplastic 

 lesions, but no significant changes in respiratory rate, minute 

 volume, compliance, or resistance were seen in 14 exposed rats. 

 Significantly increased airway resistance and a significant decrease 

 in dynamic lung compliance were observed in rats after two years of 

 exposure. The hamsters had a significant increase in airway resistance 

 and a nonsignificant reduction in lung compliance at termination of a 

 one-year exposure; these changes persisted during the second year of 

 exposure. In the same experiments, filtered diesel exhaust did not 

 have the same effects as total exhaust in any of the three species 

 (Heinrich et al., 1986a). 

 Groups of 27 female Fischer 344 rats and about 50 male and 50 

 female C57Bl/6N and ICR mice were exposed to particle concentrations 

 of 2-4 mg/m3 for 4 h/day on four days per week for up to 24 months. 

 After 12 months, the incidence of alveolar hyperplasia was increased 

 in all animals. Exposed rats had more severe inflammation than 

 controls, with inflammatory exudate into the nose, and bronchitis and 

 pneumonia, but this effect was ascribed to the housing, which was not 

 specific pathogen-free (Takemoto et al., 1986). 

 Groups of nine male Hartley guinea-pigs were exposed at 

 concentrations of 0.25, 0.75, or 1.5 mg/m3 for 20 h/day on 5.5 days 

 per week for up to two years. An analysis of the alveolar capillary 

 membrane by quantitative morphometry showed that it was thickened as a 

 result of an increase in the absolute tissue volume of interstitium 

 and type II cells. Exposure to 0.75 mg/m3 for six months caused 

 fibrosis in regions of macrophage clusters and focal type II cell 

 proliferation, as observed under the light microscope. No appreciable 

 change in morphometric parameters was seen after exposure to the 

 lowest dose, but the higher doses increased the thickness of alveolar 

 septa and the numbers of various types of alveolar cells (Barnhart et 

 al., 1981, 1982). 

 As part of this investigation, Fischer 344 rats were exposed by 

 inhalation to 0.25 or 1.5 mg/m3 diesel exhaust particles, and 

 various biochemical and cytological studies were conducted up to 36 

 weeks (Misiorowski et al., 1980). At the high dose, normalized lung 

 weight, the rate of collagen synthesis, and the cellular and lipid 

 content of lung tissue were significantly increased after six months. 

 It was concluded that the reactivity of fibrogenic cells had been 

 enhanced. In a long-term study of respiratory end-points in male 

 guinea-pigs, including light and electron microscopy, lavage cytology, 

 and lung tissue biochemistry, the lowest-observable-adverse-effect 

 level (LOAEL) was 0.796 and the no-observable-adverse-effect level 

 (NOAEL) was 0.258 mg/m3 (US Environmental Protection Agency, 1992b). 

 Groups of 120 male Fischer 344 rats, 450 male A/J mice, and 120 

 male Syrian hamsters were exposed to 0.25, 0.75, or 1.5 mg/m3 diesel 

 exhaust particles for 20 h/day on seven days per week for 15 months. 

 Mortality was not increased in any species. A dose-related deposition 

 of pigment was observed histopathologically in alveolar macrophages 

 and regional lymph nodes. Accumulation of alveolar macrophages was 

 associated with an increase in connective tissue in alveolar walls, 

 with mild fibrosis and proliferation of type II pneumocytes; these 

 effects were termed pneumoconiosis. No treatment-related responses 

 were found in organs other than the respiratory tract. The LOAEL was 

 0.735 and the NOAEL, 0.242 mg/m3 (Kaplan et al., 1983). 

 Groups of 120 male and 95 female Fischer 344/Jcl rats were 

 exposed to light-duty diesel engine exhaust particulates at 0, 0.1, 

 0.4, 1.1, or 2.3 mg/m3 or heavy-duty diesel engine exhaust 

 particulates at 0, 0.5, 1.0, 1.8, or 3.7 mg/m3 for 16 h/day on six 

 days per week for up to 30 months (Ishinishi et al., 1986, 1988; 

 Suzuki et al., 1990). The body weights of females exposed to the 

 highest dose of heavy-duty engine exhaust were decreased throughout 

 the study by 15-20% in comparison with controls. No changes were 

 observed histopathologically in the lungs at any concentration. 

 Accumulation of particle-laden macrophages was observed at levels 

 > 0.4 mg/m3. In areas of macrophage accumulation, bronchiolar 

 epithelium replaced alveolar epithelium in the ducts. Proliferation of 

 bronchiolar epithelium and type II cells and oedematous thickening and 

 fibrosis of the alveolar septum were observed, which developed into 

 small fibrotic lesions classified as hyperplastic. The incidences of 

 hyperplastic lesions were 4, 4, 6, 12, and 87 per 124 rats exposed to 

 light-duty engine exhaust and 1, 3, 7, 14, and 25 per 124 rats in 

 those exposed to heavy-duty engine exhaust. The LOAELs were 

 1.2 mg/m3 for light-duty and 1.0 mg/m3 for heavy-duty exhaust, and 

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 the NOAELs were 0.4 and 0.5 mg/m3, respectively (US Environmental 

 Protection Agency, 1992b). 

 In the same experimental series, Kato et al. (1992) studied 

 non-neoplastic lesions in the respiratory organs of the rats every six 

 months. The marked changes consisted of intake of diesel particles by 

 type I epithelium, hypertrophy, and glandular proliferation of type II 

 epithelium, with many extended microvilli and increased numbers and 

 size of lamellar inclusion bodies, focal increase of collagen fibres 

 in the interstitium, and infiltration of particle-laden macrophages, 

 neutrophils, mast cells, and plasma cells into the interstitium of 

 alveolar septa. The most marked changes in the airway were focal 

 shortening of cilia and protrusions of nonciliated cells. These 

 morphological changes appeared in all groups exposed to particle 

 concentrations > 1 mg/m3 after six months of exposure and were more 

 marked with increasing particle concentration and with time. 

 Exposure of Syrian golden hamsters to 4 or 11 mg/m3 diesel 

 exhaust for 7 h/day on five days per week for five months resulted in 

 enlargement of liver sinusoids and loss of cristae in mitochondria 

 (Meiss et al., 1981). 

 The induction of pulmonary adenomas and carcinomas in rats after 

 long-term inhalation of carbon black is proposed to be due partly to 

 inflammatory cells and their mediators (Driscoll et al., 1995; 

 Oberdörster et al., 1995; Driscoll et al., in press). After exposure 

 of rats to carbon black at 1, 7, or 50 mg/m3 for 6 h/day on five 

 days per week for 13 weeks, 353, 1923, and 7112 μg of carbon, 

 respectively, were deposited per lung. After exposure to air or to 

 1 mg/m3 of carbon black, no macrophage inflammatory protein-2 

 (MIP-2) mRNA expression and no increase in inflammatory cells was 

 observed; with 7 or 50mg/m3, both MIP-2 mRNA and the number of 

 neutrophils in bronchoalveolar lavage fluid were increased, and the 

 hprt frequencies were 3.2 and 4.2 times greater than in controls. 

 Groups of 25 cats were exposed to either clean air or diesel 

 exhaust for 8 h/day on seven days per week for two years at a 

 concentration of 6 mg/m3 through week 62 and to 12 mg/m3 for weeks 

 62-124. Some of the cats were then held in clean air for an additional 

 six months. No response was seen after 61 weeks, but after 123 weeks 

 signs of restrictive lung disease were observed. Total lung capacity, 

 forced vital capacity, functional residual capacity, peak expiratory 

 flow rates, and diffusion capacity were significantly decreased 

 (Moorman et al., 1985). Morphological evaluation revealed 

 exposure-related lesions in the centriacinar region of the lungs, 

 bronchiolar epithelial metaplasia associated with the presence of 

 ciliated and basal cells, and alveolar macrophages containing diesel 

 particle-like inclusions. After six months' recovery in clean air, the 

 metaplasia had disappeared but the fibrosis had progressed (Hyde et 

 al., 1985). In exposed cats, the epithelium of the terminal and 

 respiratory bronchioles consisted of ciliated, basal, and Clara cells, 

 whereas controls had only Clara cells (Plopper et al., 1983). These 

 observations indicate that the foci of the lesions were the 

 epithelium, the interstitial compartments, and the centriacinar region 

 of the lung. The metaplastic changes suggest that cancer may be 

 induced by continuous exposure, while the other major effect is 

 pulmonary fibrosis resulting in restrictive disease which is not 

 ameliorated and in fact progresses after removal from exposure. 

 Progression of effects is probably due to continued lung overloading 

 with particulate matter, despite cessation of exposure. 

 The dose-dependent effects on lung morphology, histopathology, 

 biochemistry, and cytology after long-term exposure to diesel exhaust 

 described above are reflected in the following findings seen in rats 

 at a lung burden of about 0.5 mg/lung (Henderson et al., 1988; Muhle 

 et al., 1990): 

 -- The wet and dry weights of lungs increase by up to fourfold in 

 comparison with those of concurrent controls. This is due to 

 severe functional overloading in the lung, resulting in enhanced 

 leukocyte influx and tissue proliferation. 

 -- Pulmonary inflammation is manifested by cytological (increased 

 numbers of polymorphonuclear neutrophils) and biochemical (lactic 

 dehydrogenase, collagen in lung lavage fluid) parameters. 

 -- The retention of material is characterized by an increasing 

 number of particle-laden macrophages and by black discolouration 

 of lungs due to sequestration of accumulated particles. 

 Additionally, increased transfer of material to the 

 lung-associated lymph nodes is observed. 

 -- Later findings during inhalation are proliferative alterations of 

 the epithelial cells and onset of fibrosis. 

 B7.3.2 Carcinogenicity 

 B7.3.2.1 Inhalation 

 Rats were exposed in several studies to diesel emissions 

 containing > 2 mg/m3 of particles for more than two years, 

 resulting in the induction of pulmonary tumours (Table 34). Many 

 organic and inorganic gaseous components were also present in the test 

 atmospheres, and the relatively high concentration of some pulmonary 

 irritants like nitrogen dioxide, aldehydes, and sulfur dioxide may 

 have contributed to the inflammatory response and to epithelial cell 

 damage and subsequent cell proliferation. Exposure to gaseous PAHs, 

 like naphthalene which is toxic to Clara cells, may influence the 

 metabolic state of pulmonary cells. It is not clear however, whether 

 the combined exposure to particles and gases in these experiments 

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 favoured tumour induction. It should be noted that Brightwell et al. 

 (1986), Heinrich et al. (1986a), Iwai et al. (1986), Ishinishi et al. 

 (1986), and Takaki et al. (1989) have reported that the gaseous phase, 

 i.e. the proportion of exhaust without particles, does not induce 

 pulmonary tumours. 

 Table 34. Carcinogenicity of diesel engine exhaust in rats 

 

 Strain No. and Exposure concentration Duration Lung Pulmonary tumours Probability Reference 

 sex (mg/m3)a (observation burden of error (%)b

 period) (mg/lung) No. % Mean 

 Actual Continuous (f+m) (%) 

 

 Wistar 40 m 8.3 1.5 6 h/d, 5 d/week, up NR 1 17c NR Karagianes

 40 m Clean air to 20 months 0 et al. 

 (20 months) (1981) 

 Fischer 72 f 6.6 3.1 16 h/d, 5 d/week, 24 NR 39 54 38.5 < 0.1 Brightwell

 344 71 m months (30 months) 16 23 et al. 

 72 f 2.2 1.1 11 15 9.7 < 0.1 (1986, 1989

 72 m 3 4 

 71 f 0.7 0.4 0 0.7 

 72 m 1 1 

 Filtered exhaust 0 

 0 

 142 f Clean air 1 1 1.4 

 140 m 3 2 

 Wistar 95 f 4.4 2.5 19 h/d, 5 d/week, 32 NR 17 18 < 0.1 Heinrich et

 92 f Filtered exhaust months (up to death) 0 al. (1986a)

 96 f Clean air 0 

 

 Table 34 (contd) 

 

 Strain No. and Exposure concentration Duration Lung Pulmonary tumours Probability Reference 

 sex (mg/m3)a (observation burden of error (%)b

 period) (mg/lung) No. % Mean 

 Actual Continuous (f+m) (%) 

 

 Fischer 

 344/Jcl 

 Light-duty 60 f 2 1.1 16 h/d, 6 d/week, 30 NR 1 2 2.4 NR Ishinishi 

 engine 64 m months (30 months) 2 3 et al. 

 59 f 1 0.6 2 3 4.1 (1986,1988;

 64 m 3 5 Takaki et a

 61 f 0.4 0.2 0 0.8 (1989) 

 64 m 1 2 

 59 f 0.1 0.06 2 3 1.6 

 64 m 0 

 59 f Clean air 2 3 3.3 

 64 m 2 3 

 Heavy-duty 60 f 4 2.3 3 5 6.5 1.8 

 engine 64 m 5 8 

 59 f 2 1.1 1 2 3.3 

 64 m 3 5 

 61 f 1 0.6 0 0 

 64 m 0 

 59 f 0.4 0.2 1 2 0.8 

 64 m 0 

 59 f Clean air 1 2 0.8 

 64 m 0 

 16 m Filtered exhaust 0 

 

 Table 34 (contd) 

 

 Strain No. and Exposure concentration Duration Lung Pulmonary tumours Probability Reference 

 sex (mg/m3)a (observation burden of error (%)b

 period) (mg/lung) No. % Mean 

 Actual Continuous (f+m) (%) 

 

 Fischer 19 f 4.9 1.6 8 h/d, 7 d/week, 24 NR 8 42 < 1d Iwai et al.

 344 16 f Filtered exhaust months (24 or 30 0 (1986) 

 22 f Clean air months) 1 5 

 Fischer 15 f 2.0-4.0 0.2-0.4 4 h/d, 4 d/week, 24 NR 0 NR Takemoto 

 344 15 f Clean air months (24 months) 0 et al. 

 (1986) 

 Fischer 69 f 7 1.5 7 h/d, 5 d/week, 30 NR 13 19 16.1 < 0.1 (f) Mauderly et

 344/Crl 74 m months (up to death) 10 14 1.7 (m) al. (1986)

 68 f 3.5 0.7 2 3 4.6 

 63 m 4 6 

 68 f 0.35 0.07 0 0.7 

 70 m 1 1 

 68 f Clean air 0 1.4 

 73 m 2 3 

 Fischer 227 f+m 7 1.5 7 h/d, 5 d/week, 30 20.8 12.8 < 0.1 Mauderly et

 344/N Crl 221 f+m 3.5 0.7 months (up to death) 11.5 3.6 4.8 al. (1987)

 223 f+m 0.35 0.07 0.6 1.3 

 230 f+m Clean air (24 months) 0.9 

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 Table 34 (contd) 

 

 Strain No. and Exposure concentration Duration Lung Pulmonary tumours Probability Reference 

 sex (mg/m3)a (observation burden of error (%)b

 period) (mg/lung) No. % Mean 

 Actual Continuous (f+m) (%) 

 

 Wistar 100 f 7.0 3.8 18 h/d, 5 d/week, 24 63.9 22 22.0 < 0.1 Heinrich et

 200 f 2.5 1.3 months (30 months) 23.7 11 5.5 < 1 al. (1992,

 198 f 0.8 0.5 6.3 0 1995); 

 217 f Clean air (24 months) NR 1 0.5 Heinrich 

 (1994) 

 Fischer 212 f+m 6.3 3.0 16 h/d, 5 d/week, 24 85.4 38 17.9 17.9 NR Nikula et a

 344/N 210 f+m 2.4 1.1 months (24 months) 40.7 13 6.2 6.2 (1994) 

 214 f+m Clean air (23 months) 3 1.4 1.4 

 Fischer 49 f 4.7 1.3 15 h/d, 3 d/week, 24, NR 6 12.2 NR Kawabata 

 344/N 42 f 4.7 1.3 12, or 6 months 8 19.0 et al. 

 45 f 4.7 1.3 1 2.2 (1993) 

 48 f Clean air 5 10.4 

 Fischer 183 f+m 2.0 0.4 7 h/d, 5 d/week, 24 NR 8 4.4 4.4 NR Lewis et al

 344/N 180 f+m Clean air months 6 3.3 3.3 (1989) 

 

 From Pott & Heinrich (1987) and supplemented; NR, not reported 

 a Mass median aerodynamic diameter, 0.17-0.25 μm; 'Continuous', equivalent continuous value 

 b Unilateral Fisher's exact test 

 c Only six animals investigated 

 d With Yates' correction 

 No difference in lung tumour incidence was seen in groups of male 

 and female rats exposed for 7 h/day on five days per week for 24 

 months either to diesel exhaust particulates at 2 mg/m3 or to 

 filtered air (Lewis et al., 1989). 

 Exposure of six male Wistar rats to diesel exhaust soot at 

 8.3 mg/m3 and coal dust for up to 20 months gave inconclusive 

 results (Karagianes et al., 1981). The study had little statistical 

 power owing to the small group size, and the insufficient duration of 

 exposure may have prevented detection of tumours, although one mammary 

 fibroadenoma and one lung bronchiolar adenoma were detected. One 

 subcutal fibrosarcoma and one renal lymphoma were seen in controls. 

 Eight bronchioalveolar adenomas and nine squamous-cell tumours 

 were seen in 95 rats (18%) that had inhaled 4.4 mg/m3 diesel exhaust 

 for 19 h/day on five days per week for 32 months. No tumours were 

 observed in controls (Heinrich et al., 1986a). The dose-dependent 

 carcinogenic potency of diesel exhaust was confirmed in a study in 

 which rats were exposed to diesel exhaust at concentrations of 0.8, 

 2.5, or 7.0 mg/m3 for 18 h/day on five days per week for 24 months 

 (Heinrich et al., 1992; Heinrich, 1994; Heinrich et al., 1995). 

 In male and female rats exposed to diesel exhaust at 6.6 mg/m3, 

 a high incidence of lung tumours was observed in animals dying or 

 sacrificed after 24 months (24/25 females, 12/27 males). The incidence 

 of lung tumours (Table 34) was derived by pooling pulmonary adenomas; 

 squamous-cell carcinomas; adenocarcinomas; mixed ademomas, 

 adenocarcinomas, and squamous-cell carcinomas; and mesotheliomas. 

 Non-neoplastic pulmonary lesions were not described (Brightwell et 

 al., 1986, 1989). 

 Groups of 24 female Fischer 344 rats were exposed to clean air, 

 to whole-fraction (4.9 mg/m3 particulates) fuel, or to filtered 

 diesel exhaust for 8 h/day on seven days per week for 24 months. After 

 six months of exposure, the rats exposed to whole exhaust had lower 

 body weights than those in the other two groups; after 18 months, both 

 exposed groups showed body weight reduction. The relative lung weight 

 was increased after 12 months' exposure to whole exhaust, and 

 epithelial proliferation and significantly elevated numbers of lung 

 tumours were seen in animals exposed to the whole fraction after six 

 months. Increased incidences of leukaemia and mammary gland tumours 

 were also reported in animals exposed to whole or filtered exhaust; 

 however, because of the small numbers of animals, the significance of 

 the results cannot be determined (Iwai et al., 1986). 

 A total of 140 female and 140 male Fischer 344/N rats (in groups 

 of three males and three females, five males and five females, or 

 eight males and eight females, depending on the end-point) were 

 exposed for 16 h/day on five days per week for up to 24 months, 

 beginning at eight weeks of age, to particles of diesel exhaust or 

 carbon black at 2.5 or 6.5 mg/m3 of air, or to clean air (Mauderly 

 et al., 1994). Rats were killed after 3, 6, 12, 18, or 23 months of 

 exposure for histopathological assessment and measurement of lung and 

 lung-associated lymph node burdens of particles, lung weight, 

 bronchoalveolar lavage indicators of inflammation, DNA adducts in 

 whole lung and alveolar type II cells, and chromosomal anomalies in 

 circulating lymphocytes. Diesel exhaust and carbon black had nearly 

 identical effects, with a similar relation to exposure. There was a 

 dose-related slowing of particle clearance after three months, with 

 progressive accumulation of particles in lungs and lymph nodes. 

 Inflammation, epithelial proliferation, and fibrosis were progressive 

 and related to dose. Diesel exhaust slightly increased the number of 

 lung DNA adducts, and the numbers of DNA adducts in type II cells were 

 increased by both diesel exhaust and carbon black. No exposure-related 

 chromosomal damage was found in circulating lymphocytes. The incidence 

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 of primary lung neoplasms was increased significantly and was related 

 to the doses of both diesel exhaust and carbon black. The types of 

 neoplasms were identical and included benign adenomas, malignant 

 adenocarcinomas, squamous-cell carcinomas, and adenosquamous 

 carcinomas; squamous cysts were also seen. The neoplasms had similar 

 growth characteristics when transplanted; 50-67% of the transplanted 

 squamous-cell carcinomas and 25-40% of the transplanted 

 adenocarcinomas grew after injection into athymic mice (Table 35), 

 whereas the squamous cysts did not. 

 Fischer 344/Jcl rats were exposed to a range of concentrations of 

 exhaust emission particulates from light-duty (up to 2 mg/m3) or 

 heavy-duty diesel engines (up to 4 mg/m3) for 16 h/day on six days 

 per week for up to 30 months. After 18 months, marked hyperplasia of 

 type II cells was noted in the groups at higher exposures. After 30 

 months, treatment-related pulmonary hyperplastic lesions were 

 detected, and a dose-response relationship was seen for tumours in the 

 groups exposed to heavy-duty but not light-duty diesel exhaust. The 

 lung tumours were diagnosed as adenocarcinomas, squamous-cell 

 carcinomas, or adenosquamous carcinomas. A significant correlation was 

 observed between the incidence of anthracosis and areas with 

 hyperplastic lesions; furthermore, anthracosis and hyperplastic 

 lesions did not appear in lungs exposed to particle-free exhaust. The 

 authors concluded that the occurrence of hyperplastic lesions was 

 dependent on the presence of carbon particles (Ishinishi et al., 1986, 

 1988; Takaki et al., 1989). 

 Table 35. Growth in athymic mice of lung tumours from rats exposed to 

 diesel exhaust and carbon black 

 

 Type of tumour Carbon black Diesel exhaust 

 Number Growing Number Growing 

 implanted No. % implanted No. % 

 Adenocarcinom 8 2 25 10 4 40 

 Squamous-cell 2 1 50 3 2 67 

 carcinoma 

 Squamous cyst 19 0 0 7 0 0 

 

 From Mauderly et al. (1994) 

 In a large-scale study of unfiltered diesel exhaust, 1097 Fischer 

 344 rats were exposed for up to 30 months to 0.35, 3.5, or 7.0 mg/m3

 of diesel soot. A group of 365 rats exposed to clean air served as 

 controls. Exposure to exhaust did not cause overt signs of toxicity, 

 and no significant, exposure-related alterations in body weight were 

 observed. Rats were killed at six-month intervals, examined for their 

 lung burdens of diesel soot, and subjected to complete necropsy. 

 Diesel soot accumulated at all doses but minimally in the low-dose 

 group. An increased incidence of tumours was observed in the groups at 

 the medium and high doses; most (81%) of the tumours were observed 

 after two years of exposure. The inhaled soot concentration and the 

 lung burden of diesel soot were highly significantly related to tumour 

 incidence ( P < 0.001) (Mauderly et al., 1987). In a follow-up study 

 with longer daily exposure (16 h/day), the dose-dependency of the 

 tumour incidence was reproduced (Nikula et al., 1994). In this study, 

 the carcinogenicity of diesel exhaust soot (8% extractable organic 

 material; 2.5 mg/m3) was compared with that of carbon black (0.12% 

 extractable organic material; 6.5 mg/m3 ) in 1152 male and female 

 Fischer 344 rats exposed for 16 h/day on five days per week for up to 

 24 months and examined histopathologically. The lung burden of 

 particles was greater after exposure to diesel exhaust than to carbon 

 black, but the neoplastic response in the lung was similar and usually 

 occurred late in the study. When the lung burden of particles was used 

 as the dose parameter, the carcinogenicity of carbon black was 

 greater than that of diesel exhaust soot. 

 Groups of 50 four-week-old female Fischer 344 rats were exposed 

 to diesel soot at a mean concentration of 4.73 mg/m3 for 15 h/day 

 three times per week for 6, 12, or 24 months, and animals that died 

 after 18-30 months were evaluated for tumours. After 30 months, all 

 animals, including controls, were sacrificed and examined for lung 

 tumours. The incidences of lung tumours were 10.4% in controls and 

 2.2% after six months' exposure to diesel exhaust, 19.0% after 12 

 months, and 12.2% after 24 months. No statistical analysis was 

 presented, but it seems unlikely that there was a significant effect 

 (Kawabata et al., 1993). 

 Concurrent administration of known carcinogens with diesel 

 exhaust has also been studied. Exposure of rats to diesel exhaust 

 given an intraperitoneal injection of N-nitrosodiisopropylamine or 

 N-nitrosodiethylamine did not influence the rates of tumours induced 

 by the nitrosamines (Takemoto et al., 1986). The effects of treatment 

 of hamsters with N-nitrosodiethylamine or benzo[ a]pyrene were not 

 influenced by subsequent administration of diesel exhaust, whereas 

 pretreatment of mice with benzo[ a]pyrene or dibenzanthracene followed 

 by diesel exhaust gave inconsistent results. Exposure to diesel 

 exhaust did not affect the total tumour rates in rats pretreated with 

 6.25 or 12.5 g/kg body weight of N-nitrosodipentylamine; however, 

 the incidence of squamous-cell tumours was increased in both 

 pretreated groups (Heinrich et al., 1986a). 

 Hamsters were exposed for two years to unfiltered diesel exhaust 

 at 0, 0.7, 2.2, or 6.6 mg/m3 or to filtered diesel exhaust, and 

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 groups of control and treated hamsters were administered 

 N-nitrosodiethylamine subcutaneously before the beginning of 

 exposure. The rate of pulmonary tumours was not increased by diesel 

 exhaust, with or without pretreatment with the nitrosamine. Several 

 hamsters that developed 'wet tail' infection after six months on test, 

 resulting in significant mortality (46%), were treated with 

 oxytetracycline, chloramphenicol, and dimetridazole (Brightwell et 

 al., 1986, 1989). 

 Overall, the only clear effect in these studies of 

 co-carcinogenicity in rats was an increase in the percentage of 

 malignant tumours in animals treated with diesel exhaust plus 

 carcinogens in comparison with the carcinogen alone (Heinrich et al., 

 1986a). 

 The results of studies in other species (mice, hamsters, and 

 monkeys) treated by inhalation are given in Table 36. Heinrich et al. 

 (1982) found significant increases in lung tumour incidence in mice, 

 but this result could not be repeated in later studies (Heinrich et 

 al., 1986a, 1992, 1995). Small but statistically significant increases 

 in lung tumour incidence were reported in ICR and C57Bl mice (Takemoto 

 et al., 1986) and in female Sencar mice (Pepelko & Peirano, 1983); 

 however, because only small increases in non-malignant tumours were 

 seen only in females in the study of Pepelko & Peirano (1983), the 

 results must be considered to be weakly positive or equivocal. 

 Hamsters showed no response to diesel exhaust. 

 Table 36. Long-term studies of diesel exhaust by inhalation in species other than rats 

 

 Strain, species No. and sex Exposure Results Reference 

 

 Material Particles Duration 

 (mg/m3) 

 

 NMRI mouse 2 × 96 f (a) Exhaust 4 19 h/d, 5 d/week, Lung tumours (adenomas and Heinrich et 

 (b) Filtered 27-28 months adenocarcinomas) (a) 24/76 (32%), (1986a) 

 (c) Clean air including 13 (17%) adenocarcinomas; 

 (b) 29/93 (31%), including 18 (19%) 

 adenocarcinomas; (c) 11/84 (13%), 

 including 2 (2.4%) adenocarcinomas 

 Incidence in historical controls, 

 < 32% 

 ICR and 315 ICR, Exhaust or 2.0-4.0 4 h/d, 4 d/week, Lung tumours (adenomas and Takemoto et 

 C57Bl/6N 297 C57Bl/6N clean air 13-28 months adenocarcinomas). ICR: 14/56; (1986) 

 mice, newborn (sex 7/60 in controls; C57Bl/6N: 

 unspecified) 17/150; 1/51 in controls 

 Sencar mouse 2 × 130 f (a) Exhaust 12 8 h/d, 7 d/week, Adenomas and carcinomas Pepelko & 

 2 × 130 m (b) Clean air to 15 months of (a) m: 5.9%; f: 16.3% Peirano (198

 age (from (b) m: 3.8%; f: 7.2% 

 conception to 

 sacrifice) 

 NMRI mouse 2 × 80 f (a) Exhaust 7.5 18 h/d, 5 d/week, Lung tumours Heinrich et 

 (b) Clean air 13.5 months, 9.5 (a) 32.1% (1992, 1995)

 months' recovery (b) 30% 

 

 Table 36 (contd) 

 

 Strain, species No. and sex Exposure Results Reference 

 

 Material Particles Duration 

 (mg/m3) 

 

 NMRI and 3 × 120 f (a) Exhaust 4.5 18 h/d, 5 d/week; Lung tumours Heinrich et 

 C57Bl/6N mice 3 × 120 f (b) Filtered NMRI, 23 months; NMRI: (a) 23.3% (1992, 1995)

 (c) Clean air C57Bl, 24 months (b) 46.7% 

 + 6 months' (c) 30% 

 recovery C57Bl: (a) 8.5% 

 (b) 3.6% 

 (c) 5.1% 

 Syrian golden 3 × 48 f (a) Exhaust 3.9 ± 0.5 7-8 h/d, 5 d/week, No effect on survival, no lung Heinrich et 

 hamster (b) Filtered up to 30 months tumours (1982) 

 (c) Clean air 

 Syrian golden 3 × 48 f (a) Exhaust 4 19 h/d, 5 d/week, Normal life span, no lung tumours Heinrich et 

 hamster 3 × 48 m (b) Filtered 27-28 months (1986a) 

 (c) Clean air 

 Syrian golden 52 f + 52 m (a) Exhaust 0.7, 2.2, 16 h/d, 5 d/week, No significant increase in Brightwell 

 hamster 104 f + 104 m (b) Filtered 6.6 24 months frequency of tumours in et al. 

 (controls) (c) Clean air respiratory tract (1986, 1989)

 Cat 2 × 25 m (a) Exhaust 6 (1st 8 h/d, 7 d/week, Lung function: decrease in closing Pepelko & 

 yr), 12 24 months volume after 1 year; reduction Peraino (198

 (2nd yr) in inspiratory, vital, and total 

 (b) Clean air lung capacity after 2 years; 

 diagnosis: pulmonary fibrosis of 

 the interstitial or 

 intra-alveolar type 

 

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 Table 36 (contd) 

 

 Strain, species No. and sex Exposure Results Reference 

 

 Material Particles Duration 

 (mg/m3) 

 

 Cynomolgus 4 × 15 m (a) Coal dust 2.0 7 h/d, 5 d/week, No difference in tumour incidence Lewis et al.

 monkey (b) Exhaust 2.0 24 months among groups (1986) 

 (c) Coal dust 1.0 

 + exhaust 1.0 

 (d) Clean air 

 

 It is clear that repeated inhalation of diesel exhaust at 

 concentrations of more than about 2 mg/m3 (actual value), 

 corresponding to a calculated equivalent continuous concentration of 

 about 1 mg/m3, increases the incidence of pulmonary tumours. These 

 tumours occur late in life after exposures of 24 months. 

 B7.3.2.2 Other routes of exposure 

 Studies have also been conducted by intratracheal instillation in 

 rats and hamsters and by painting on mouse skin (Table 37). While the 

 former are especially useful for hazard identification and for 

 evaluating specific mechanistic aspects, they are less useful for the 

 purposes of risk characterization and no attempt was made to identify 

 critical studies. The results of the studies by intratracheal 

 instillation, however, confirm that both diesel exhaust particles and 

 carbon black induce lung tumours and demonstrate that the specific 

 surface area of carbonaceous particles is correlated with the 

 tumorigenic potency. Both of these findings support the suggestion 

 that a nonspecific particle effect is of crucial importance for the 

 induction of lung tumours by diesel exhaust. The dermal experiments, 

 conducted by Nesnow et al. (1982a,b, 1983), have been used to estimate 

 risk quantitatively, by the comparative potency method. 

 B7.4 Dermal and ocular irritation; dermal sensitization 

 No data were available. 

 B7.5 Reproductive toxicity, embryotoxicity, and teratogenicity 

 B7.5.1 Reproductive toxicity 

 In a two-generation study of reproduction, 100 male and 100 

 female CD-1 mice were exposed by inhalation to exhaust from a 

 light-duty diesel engine for 8 h/day on seven days per week, at a 

 concentration of 12 mg/m3. Most treatment-related effects were 

 minimal. Overall fertility and survival rates were not significantly 

 altered (Pepelko & Peirano, 1983). 

 (C57Bl/6 × C3H)F mice (number not given) showed sperm 

 abnormalities (reduced sperm count and weight of testis; 

 teratospermia) after daily intraperitoneal injections of 50, 100, or 

 200 mg/kg body weight of diesel exhaust particles for five days. The 

 highest dose caused an eightfold increase in abnormalities over that 

 in controls and a significant decrease in sperm number (Quinto & De 

 Marinis, 1984). 

 Table 37. Carcinogenicity of diesel exhaust after exposure other than by inhalation 

 

 Strain, No. and Exposure Schedule, Results Refere

 species sex duration 

 Route Material Dose 

 (mg) 

 

 Fischer 344 (a) 31 f Intratracheal (a) Activated carbon 1/animal 10/week, Survival rate, 71-83% Kawaba

 rat (b) 59 f instillation (b) Diesel particles 1/animal 30 months' (lowest ingroup b). Malignant et al.

 (c) 53 f (c) None observation lung tumours: (a) 7/23; (1986)

 (d) 27 f (d) Vehicle (b) 20/42; (c) 0/44; (d) 1/23; 

 P < 0.01. Benign and 

 malignant tumours combined: 

 (a) 11/23; (b) 31/42 

 Osborne- Groups Lung Organic material from Observation (a) 1 bronchioalveolar adenoma; Grimme

 Mendel rat of 35 f implant diesel exhaust: until (b) 5 squamous-cell carcinomas; et al.

 (a) Hydrophilic fraction 6.7 spontaneous (c) 1 bronchioalveolar adenoma; (1987)

 (b) Hydrophobic fraction 20.0 death (d) 6 carcinomas; 

 (c) Nonaromatic compounds 19.2 (e) No tumours 

 + PAHs (2 or (f) 1 carcinoma 

 3 rings) (g) 7 carcinomas, 1 adenoma 

 (d) PAHs ( > 4 rings) 0.2 (h) No tumours 

 (e) Polar PAHs 0.3 (i) 1 adenoma 

 (f) Nitro-PAHs 0.2 

 (g) Reconstituted 

 hydrophobic fraction 19.9 

 (h) None 

 (i) Vehicle 

 

 Table 37 (contd) 

 

 Strain, No. and Exposure Schedule, Results Refere

 species sex duration 

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 Route Material Dose 

 (mg) 

 

 Wistar rat (a) 40 f Intratracheal (a) Diesel soot (34 m2/g) (a) 3 × 15 Primary lung tumours (%) Pott &

 (b) 58 f instillation (b) Diesel soot (70 m2/g) (b) 3 × 10 (a) 65 Roller

 (c) 38 f (c) Diesel soot (70 m2/g) (c) 3 × 20 (b) 60 (1994)

 (d) 37 f (d) Carbon black (270 (d) 3 × 15 (c) 66 Pott e

 m2/g) (d) 65 al.(19

 (e) 37 f (e) Activated charcoal (e) 3 × 10 

 (f) 39 f (860 m2/g) 3 × 20 (e) 27 

 (g) 40 f (f) NaCl solution (f) 3 × 10 (f) 0 

 (g) NaCl solution (g) 0.4 × 20 until (g) 0 

 ml spontaneous 

 death or 131 

 weeks 

 Wistar rat Groups Intratracheal (a) Diesel soot (native) (a) 1 × 15 Primary lung tumours (%): Heinri

 of 48 f instillation (b) Diesel soot (toluene (b) 2 × 15 (a) 17 (1994)

 extract; 130 m2/g) 1 × 15 

 (c) Carbon black (c) 1 × 15 (b) 23 

 (toluene extract; (d) 1 × 15 4 

 270 m2/g; primary (e) Vehicle control (c) 21 

 particle, 15 nm) 

 (d) Carbon black (toluene (d) 8 

 extract; 270 m2/g; (e) 0 

 primary particle, 

 15 nm) 

 (e) NaCl solution 

 

 Table 37 (contd) 

 

 Strain, No. and Exposure Schedule, Results Refere

 species sex duration 

 Route Material Dose 

 (mg) 

 

 Syrian Groups Intratracheal (a) Diesel particles 1.25, 1/week, 15 1 lung adenoma at high dose Shefne

 golden of 50 m; instillation (b) Diesel particles + 2.5, in groups (a) and (c) after 61 et al.

 hamster various same amounts of weeks weeks; no lung tumours in (1982

 controls ferric oxide controls 

 (c) Diesel particle 

 extract 

 + ferric oxide 

 Syrian (a) 3 × Intratracheal (a) Exhaust extract 0.1, 0.5, 1/week, 15 Survival rates: (a) 95, 92, Kunita

 golden 62 m instillation (b) Vehicle 1 weeks 71%; (b) 98%. No difference in et al.

 hamster (b) 59 m (c) 0.5 mg tumour incidence between (a) (1986)

 (c) 62 m benzo[a]pyrene and (b); 88% respiratory 

 tumours in positive controls 

 C57Bl 12 m, Dermal Acetone extract of 0.5 ml 3 times/week 16 mice dead by 10 weeks, 33 Kotin

 mouse 40 f, particles for life or skin tumours by 13 months, 2 et al.

 69 22-23 months skin papillomas, no tumours in (1955)

 controls controls 

 A mouse 50 m, Dermal Acetone extract of 0.5 ml 3 times/week Males: 8 skin tumours by 16 

 25 f, particles for life or 1 papilloma, 3 squamous-cell 

 34 22-23 months carcinomas. Females: 20 skin 

 controls tumours by 13 months,17 tumours 

 at 13-17 months, no tumours in 

 controls 

 

 Table 37 (contd) 

 

 Strain, No. and Exposure Schedule, Results Refere

 species sex duration 

 Route Material Dose 

 (mg) 

 

 Sencar Groups Dermal Dichloromethane 0.1, 0.5, 1/week, 50-52 Skin carcinomas: Nesnow

 mouse of 40 m extracts of particles 1.0, 2.0, weeks Engine A: 3% (m), 5% (f) at et al.

 + 40 f from engines (A, B, E) or 4.0 4 mg Engine B: 3% (m) at 0.5 mg (1982a

 Benzo[a]pyrene 12.6- Engine E: 3% (f) at 0.1 mg 1983)

 202 μg Positive control: 10-90% 

 C57Bl/6N Groups Subcutaneous Particles in olive oil 10, 25, 1/week, 5 First tumours palpated in: Kunita

 mouse of injection containing 5% dimethyl 50, 100, weeks; 18 week 47 at 25 mg/kg bw et al.

 15-30 f sulfoxide 200, or months' week 30 at 50 mg/kg bw (1986)

 500 mg/kg observvation week 27 at 100 mg/kg bw 

 bw week 39 at 200 or 500 mg/kg bw 

 Malignant fibrous histiocytomas 

 in 5/22 mice at 500 mg/kg bw; 

 0/38 in controls 

 

 PAH, polycyclic aromatic hydrocarbon; TPA, 12-O-tetradecanoylphorbol 13-acetate 

 Groups of 15 male cynomolgus monkeys were exposed by inhalation 

 to 2 mg/m3 diesel particulates for 7 h/day on five days per week for 

 two years. Sperm motility and velocity were similar to those of 

 controls (Lewis et al., 1989). 

 In a test for dominant lethal mutation, male Fischer 344 rats 

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 inhaled 2 mg/m3 diesel exhaust for 7 h/day on five days per week for 

 six months and were subsequently mated with untreated females. Live 

 and dead implants and preimplantation losses were analysed on days 

 19-20 of gestation: no significant effects were observed (Lewis et 

 al., 1989). In a similar test, 100 male and 54 female T stock mice 

 were exposed to 6 mg/m3 diesel exhaust for 8 h/day on seven days per 

 week for seven weeks. There were no significant dominant lethal 

 effects in males or females. A reduced number of corpora lutea 

 (reproductive function) was the only significant result (Pepelko & 

 Peirano, 1983). 

 B7.5.2 Embryotoxicity 

 No increase in the frequency of sister chromatid exchange was 

 seen in the livers of fetuses of Syrian golden hamsters that inhaled 

 diesel exhaust particles at 12 mg/m3 for 8 h/day on days 5-13 of 

 gestation. An intraperitoneal injection of 300 mg/kg body weight of 

 diesel particulates on day 12 of gestation also had no significant 

 effect on this end-point; however, intraperitoneal injection of 23% 

 particulate mass extracted with methylene chloride on day 12 resulted 

 in a dose-dependent increase in sister chromatid exchange frequency in 

 fetal liver on day 13, and a doubling was seen at 320 mg/kg body 

 weight. It was concluded that chemicals must be eluted from diesel 

 particles in order for the genotoxic material to cross the placenta 

 (Pereira et al., 1982). 

 B7.5.3 Teratogenicity 

 Sprague-Dawley rats and New Zealand white rabbits were exposed by 

 inhalation to exhaust from a light-duty diesel engine, at a 

 particulate matter concentration of 6 mg/m3, for 8 h/day on seven 

 days per week. 

 Twenty rats were exposed on days 5-16 of gestation and 20 rabbits 

 on days 6-18. The numbers of viable fetuses per litter, dead fetuses 

 per litter, resorptions per litter, implantation sites per litter, 

 corpora lutea per litter, and average fetal weight did not differ 

 significantly from those of controls (Pepelko & Peirano, 1983). 

 Reproductive and developmental toxicity are considered unlikely 

 to be critical end-points for diesel exhaust. 

 B7.6 Mutagenicity and related end-points 

 B7.6.1 In vitro 

 The genetic effects of particles and particle extracts have been 

 described (Lewtas & Williams, 1986; Morimoto et al., 1986; Henschler, 

 1987). Diesel exhaust extracts rather than particles were used in most 

 of these studies. Point mutations were observed in vitro in bacteria 

 and mammalian cells. Extracts caused chromosomal aberrations, DNA 

 damage, sister chromatid exchange, and cell transformation (Table 38). 

 The mutagenic potency of diesel engine exhaust depended in several 

 studies on the characteristics of the diesel fuel and the type, age, 

 and operating conditions of the engine (Henschler, 1987). As a rule, 

 organic extracts of particles were mutagenic in the absence of an 

 exogenous metabolic activating system (S9) (Ball et al., 1990); 

 addition of S9 decreased (Lewtas, 1983) or suppressed (Morimoto et 

 al., 1986) the mutagenic activity, perhaps by increasing protein 

 binding of mutagenic material or by metabolic detoxification of 

 directly acting mutagens, such as the nitroarenes, in the Ames test. 

 It can therefore be concluded that PAHs and thioarenes, which must be 

 metabolically activated, do not account for the mutagenic potency of 

 diesel particles. Salmeen et al. (1985) and Beland et al. (1985) 

 showed that nitroarenes are the main genotoxic agents in Salmonella

 typhimurium T98 in the absence of S9. A number of other 

 investigators have reported the presence of nitrated PAHs in extracts 

 of diesel engine exhaust particles (Handa et al., 1983), including 

 many three-, four-, and five-ring structures (Schuetzle et al., 1982). 

 The concentration of 1-nitropyrene, one of the prevalent species, has 

 been reported to be 15-25 mg/kg particulate matter, whereas 

 benzo[ a]pyrene has been found at concentrations up to 50 mg/kg. The 

 nitrated PAHs are important in the health effects of diesel exhaust 

 since they are effective mutagens in microbial and human cell systems 

 (Patton et al., 1986). Some nitrated PAHs are also carcinogenic in 

 animals (Imaida et al., 1991). Ball & Young (1992) found that strain 

 T102, which does not respond to the mutagenic action of nitroarenes, 

 responds to a class of oxidizing compounds that can interact with DNA; 

 these compounds are not nitroarenes or typical PAHs. 

 The effects of diesel soot particles with and without adsorbed 

 organic substances, diesel soot extract without particles, an isolated 

 fraction of PAHs, and titanium dioxide and carbon black (Printex 90) 

 as reference particles were investigated in vitro on hamster lung 

 epithelial cells (Mohr & Riebe-Imre, 1992). The substances were added 

 to the cells at concentrations of 100-300 mg/litre. Diesel soot 

 extract, but not the PAH moiety isolated from the extract, stimulated 

 mixed-function oxygenases. The diesel soot extract was more cytotoxic 

 than the PAH fraction for the epithelium of the hamster respiratory 

 tract, but both mixtures induced the development of micronuclei. Under 

 the study conditions, only the PAH fraction led to transformation of 

 cells. The respiratory epithelium of hamsters was more sensitive than 

 human lung epithelial cells investigated in parallel, perhaps because 

 hamster cells are generally more easily transformed than human cells. 

 Diesel soot particles, titanium dioxide, and Printex 90 had hardly any 

 cytotoxic effect but triggered transformation. The authors concluded 

 that a combination of effects of particles and PAHs are responsible 

 for the degeneration of cells. 

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 Schiffmann & Henschler (1992) studied the effects of diesel soot 

 extract and isolated fractions of PAHs, oxy-PAHs, and nitro-PAHs on 

 hamster embryo fibroblasts in vitro. The end-points investigated 

 were induction of micronuclei, unscheduled DNA synthesis, and cell 

 transformation. Diesel soot extract induced micronuclei at 

 concentrations of 80-400 mg/litre, whereas the fractions of various 

 PAHs were strongly cytotoxic. Diesel soot extract and the PAH fraction 

 transformed the fibroblasts; the nitro- and oxy-PAH fractions had a 

 weaker transforming effect, but their cytotoxic potency was clearly 

 stronger. Kinetochore analysis showed a high percentage (37%) of 

 chromosomes in micronuclei. No unscheduled DNA synthesis was induced. 

 Micronuclei were also induced in human embryonic lung fibroblasts 

 treated with diesel soot extract under comparable experimental 

 conditions. 

 B7.6.2 In vivo 

 The genotoxicity of total diesel exhaust, diesel particles, and 

 diesel soot extracts in vivo has been investigated in somatic cells 

 (Table 38). All of the substances induced genotoxic responses. Total 

 exhaust induced only sister chromatid exchange in Syrian golden 

 hamsters. The frequency of micronuclei was not increased significantly 

 in mice, even at high doses (up to 640 mg/kg body weight). Organic 

 extracts had clear genotoxic effects in various assays (Henschler, 

 1987). 

 No mutagenic activity was found in urine taken from rats exposed 

 to diesel exhaust emission by inhalation at 2 mg/m3 for 7 h/day on 

 five days per week for up to two years. A slight but nonsignificant 

 increase in micronuclei was observed in the bone marrow of mice that 

 had been exposed for six months; no increase in micronuclei was 

 detected in rats over a 24-month period (Ong et al., 1985). 

 In studies of heritable mutations in T stock mice, males were 

 examined for point mutations, induction of dominant lethal mutations, 

 translocations, and spermatogonial survival; females were examined for 

 oocyte death and dominant lethal mutations. No significant effect was 

 seen on germ cells. A reduced number of corpora lutea (reproductive 

 function) was the only significant result (Pepelko & Peirano, 1983). 

 B7.6.3 DNA adduct formation 

 Extensive research has been done to determine whether the DNA 

 adducts induced in lungs by diesel exhaust are related to later 

 tumorigenesis. 

 In rats that inhaled benzo[ a]pyrene absorbed to carbon black 

 (20 mg/g), an adduct of the diol epoxide with deoxyguanosine was 

 identified (Wolff et al., 1989), demonstrating that epoxides of PAHs 

 are produced by oxidative metabolism. Haemoglobin and albumin adducts 

 were also investigated. 

 Methods have been developed to detect DNA adducts of 

 1-nitropyrene or 1,6-dinitropyrene, which are markers of diesel engine 

 exhaust. The adducts are analysed in rat tissue or peripheral blood 

 lymphocytes by the 32P-postlabelling method and may be useful for 

 the dosimetry of 1-nitropyrene or diesel exhaust particulates in 

 occupational settings (El-Bayoumy et al., 1994). Studies on adduct 

 formation in lung DNA induced by inhaled diesel exhaust have been 

 conducted by Wong et al. (1986), Wolff et al. (1990), Bond et al. 

 (1988, 1989, 1990a,b), and Gallagher et al. (1993, 1994), all 

 involving the 32P-postlabelling technique. In general, these studies 

 suggest that DNA adducts are good measures of the 'effective dose' of 

 carcinogenic compounds. 

 Wong et al. (1986) found increased DNA adduct formation in the 

 lungs of Fischer 344 rats exposed to diesel exhaust particles at 

 7.1 mg/m3 for 31 months. After Fischer 344 rats and Syrian golden 

 hamsters were exposed to dilutions of diesel engine exhaust for six 

 months to two years, the level of haemoglobin adducts (2-hydroxy- 

 ethylvaline and 2-hydroxypropylvaline) increased dose-dependently, 

 corresponding to metabolic conversion of 5-10% of inhaled ethylene and 

 propylene to their oxides (Törnqvist et al., 1988). 

 Bond et al. (1988) designed experiments to determine the location 

 of DNA adducts in the respiratory tract of rats exposed to exhaust. 

 Fischer 344 rats were exposed for 12 weeks to diesel exhaust soot at 

 10 mg/m3; they were then sacrificed, and various regions of the 

 respiratory tract were removed and analysed for DNA adducts. Adducts 

 were found only in peripheral lung tissue and nasal tissue; the total 

 levels were highest in the peripheral tissue (about 18 adducts per 109

 bases). Thus, the levels of total DNA adducts and exhaust-induced 

 adducts are highest in the region of the rat respiratory tract where 

 tumours are formed after exposure to a carcinogenic concentration of 

 diesel exhaust (Mauderly et al., 1987). 

 Bond et al. (1990c) exposed groups of Fischer 344 rats to soot at 

 0.35, 3.5, 7.0, or 10 mg/m3 for 12 weeks and found that the levels 

 of DNA adducts were similar, at about 14 adducts per 109 bases. This 

 level is nearly twice as high as that found in sham-exposed rats. 

 Thus, DNA adduct formation in lungs is independent of the 

 concentration of exhaust at the levels tested. One explanation for 

 these results (Bond et al., 1990a) is that the lung enzymes 

 responsible for the metabolism of soot-associated chemicals to 

 metabolites that bind to DNA were saturated at the concentrations 

 tested. These data also suggest that other factors are important in 

 the carcinogenicity of diesel exhaust, since the number of adducts was 

 elevated at an exposure level (0.35 mg/m3) that did not increase 

 lung tumour incidence. The induction of DNA adducts at low 

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 concentrations is likely to result in tumour initiation by the organic 

 compounds present; at higher concentrations, the particles will induce 

 cell death, and subsequent proliferation may well act as a promotional 

 event. The combination may then result in detectable increases in 

 tumour incidence. 

 Bond et al. (1990a) also investigated the time course for DNA 

 adduct formation and persistence. Fischer 344 rats were exposed to 

 soot at 7 mg/m3 for up to 12 weeks and were sacrificed at 2, 4, 8, 

 12, 14, and 16 weeks after the start of exposure. DNA adducts 

 accumulated slowly in the lung, and the number was highest at the end 

 of exposure, representing about 160% of the level seen in controls 

 exposed to air only. The levels declined rapidly after termination of 

 exposure and were not significantly different from those of controls 

 four weeks later. Thus, steady-state levels of DNA adducts would be 

 reached during long-term exposure to diesel exhaust. 

 Bond et al. (1989, 1990c) and Wolff et al. (1990) investigated 

 whether exposure to carbon particles without associated mutagenic 

 organic chemicals also increases DNA adduct levels. Rats were exposed 

 either to diesel exhaust or carbon black at 0, 3.5, or 10 mg/m3 for 

 12 weeks. Solvent-extractable organic compounds made up about 30% of 

 the diesel soot but only about 0.04% of the carbon black particles. 

 Exposure to the highest levels of both carbon black and diesel exhaust 

 increased the DNA adduct levels in lungs, although the levels in rats 

 exposed to diesel exhaust were about 30% higher than those in rats 

 exposed to carbon black. Heavy exposure to carbon particles can 

 therefore increase DNA adduct formation, although the concentrations 

 are lower than those of exhaust-related adducts. 

 Bond et al. (1990b) investigated whether DNA adducts could be 

 formed in specific cells of the rat lung, i.e. alveolar type II cells. 

 After exposure of rats to 6.2 mg/m3 diesel exhaust or carbon black 

 particles for 12 weeks (16 h/day on five days per week), type II cells 

 were isolated and their DNA analysed for adducts. Both diesel exhaust 

 and carbon black resulted in about a fourfold increase in total DNA 

 adducts in type II cells. DNA adduct levels in peripheral lung tissue 

 were increased by 60-80% in male and female Fischer 344 rats and 

 female cynomolgus monkeys but not in female B6C3F1 mice or female 

 Syrian hamsters after inhalation of diesel soot at 8.1 mg/m3 for 12 

 weeks (Bond et al., 1989, 1990c). 

 Gallagher et al. (1993, 1994) exposed female Wistar rats to 

 diesel soot at 7.5 mg/m3 and to carbon black at 11.3 mg/m3 for 24 

 months and measured DNA adducts in lungs. The mean adduct levels were 

 similar in the two groups but were not significantly greater than 

 those in controls. Time-course studies indicated that the levels in 

 the lungs of rats exposed to diesel exhaust were lower at 24 months 

 than after two or six months of exposure, presumably as a result of 

 dilution due to increased cell proliferation. The level of a single 

 DNA adduct, thought to be derived from a nitro-PAH in diesel exhaust 

 and not observed in rats exposed to carbon black or titanium oxide, 

 was elevated over that in controls after two, six, and 24 months. The 

 DNA adduct levels in control rats increased over the duration of the 

 24-month study as an effect of age. 

 Gallagher et al. (1993) compared DNA adduct formation after 

 exposure to diesel emissions in vitro and in vivo. After exposure 

 of human lymphocytes to diesel extract, five major DNA adducts were 

 detected, one of which was characterized as an adduct with 

 benzo[a]pyrene. One was also detectable in reaction products of calf 

 thymus DNA and diesel particle extract in vitro and in skin and lung 

 DNA from mice treated dermally with 50 mg diesel extract in vivo. The 

 differences in DNA patterns in vitro and in vivo (skin and lung) 

 may reflect differences in metabolic pathways. 

 Taken together, the studies of DNA adducts suggest that some 

 organic chemicals in diesel exhaust can form DNA adducts in lung 

 tissue and may play a role in the carcinogenic effects. As pointed out 

 by Bond et al. (1989), however, DNA adducts alone cannot explain the 

 carcinogenicity of diesel exhaust, and other factors, such as chronic 

 inflammation and cell proliferation, are also important. 

 B7.7 Special studies 

 B7.7.1 Immunotoxicity 

 During the clearance process, one possible pathway is 

 translocation of diesel particulates into the lymphatic channels. 

 After male guinea-pigs were exposed to diesel exhaust at a particle 

 concentration of 1.5mg/m3 for four or eight weeks, the B- and T-cell 

 counts in lymph nodes were not altered, and there were no significant 

 changes in blood or spleen (Dziedzic, 1981). 

 Fischer 344 rats were exposed to 2 mg/m3 diesel exhaust for 

 7h/day on five days per week for 12 or 24 months and the immunological 

 function of splenic B and T cells was measured by enumerating 

 antibody-producing cells in the spleen or monitoring the proliferative 

 response. No changes were observed (Mentnech et al., 1984). 

 Table 38. Genotoxicity of diesel exhaust, particles, and extracts 

 

 Test organism End-point Exhaust Particles Extract Reference 

 

 Mutagenicity

 Bacteria

 S. typhimurium Point mutation (his) + + Huisingh et al. (1978) 

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 S. typhimurium Point mutation (his) + + Loprieno et al. (1980) 

 S. typhimurium Point mutation (his) + Clark & Vigil (1980) 

 S. typhimurium Point mutation (his) + + Li & Royer (1982) 

 S. typhimurium Point mutation (his) + Salmeen et al. (1984) 

 S. typhimurium Point mutation (his) + Ong et al. (1985) 

 S. typhimurium Point mutation (his) + Bechtold et al. (1986) 

 S. typhimurium Point mutation (his; + Whong et al (1986) 

 SOS umu test) 

 S. typhimurium Point mutation (his) + Wallace et al. (1987) 

 S. typhimurium Point mutation (his) +a Wallace et al. (1990) 

 S. typhimurium Point mutation (his) + Lewis et al. (1989) 

 S. typhimurium Point mutation (his) + Rasmussen (1990) 

 S. typhimurium Point mutation (his) + + Keane et al. (1991) 

 S. typhimurium, E. coli Point mutation (trp) + Crebelli et al. (1991) 

 E. coli Point mutation (trp) + Lewtas (1983) 

 Mammalian cells 

 L5178Y mouse Point mutation (tk) + Lewtas (1983) 

 lymphoma cells 

 L5178Y mouse Point mutation (tk) + Mitchell et al. (1981) 

 lymphoma cells 

 

 Table 38 (contd) 

 

 Test organism End-point Exhaust Particles Extract Reference 

 

 Mutagenicity (contd) 

 Chinese hamster Point mutation (hprt) + Chescheir et al. (1981) 

 ovary cells 

 Chinese hamster Point mutation (hprt) (+) Chescheir et al. (1981) 

 ovary cells 

 Chinese hamster Point mutation (hprt) (+) Casto et al. (1981) 

 ovary cells 

 Chinese hamster Point mutation (hprt, + Morimoto et al. (1986) 

 lung V79 cells ATPase) 

 Human xeroderma Point mutation (hprt) + + McCormick et al. (1980) 

 pigmentosum fibroblasts 

 Human lymphoblast Point mutation (tk) + Barfknecht et al. (1981) 

 TK6 cells 

 Balb/c3T3 mouse Point mutation (ATPase) + (+) Curren et al. (1981) 

 fibroblasts 

 DNA damage

 Syrian hamster DNA chain breaks - Casto et al. (1981) 

 embryo cells (alkaline elution) 

 Human xeroderma DNA damage + + McCormick et al. (1980) 

 pigmentosum fibroblasts 

 Rat primary Unscheduled DNA + Lewtas (1983) 

 hepatocytes synthesis 

 Chinese hamster lung Unscheduled DNA +a + Gu et al. (1994) 

 V79 cells synthesis 

 

 Table 38 (contd) 

 

 Test organism End-point Exhaust Particles Extract Reference 

 

 Chromosomal effects

 Chinese hamster Sister chromatid exchange + Lewtas (1983) 

 ovary cells 

 Chinese hamster Chromosomal aberrations + Lewtas (1983) 

 ovary cells 

 Chinese hamster Chromosomal aberrations +b Hasegawa et al. (1988) 

 lung V79 cells -c

 Chinese hamster Sister chromatid exchange + Hasegawa et al. (1988) 

 lung V79 cells 

 Chinese hamster Sister chromatid exchange + + Keane et al. (1991) 

 lung V79 cells 

 Human lymphocytes Chromosomal aberrations + Lewtas (1983) 

 Chinese hamster Sister chromatid exchange + Morimoto et al. (1986) 

 lung V79 cells 

 Human lymphocytes Sister chromatid exchange (+) Tucker et al. (1986) 

 Human lymhoblastoid Sister chromatid exchange + Morimoto et al. (1986) 

 cells 

 Hamster embryo Micronuclei + Schiffmann & Henschler 

 fibroblasts (1992) 

 Chinese hamster lung Micronuclei +a + Gu et al. (1992) 

 V79 and ovary cells 

 

 Table 38 (contd) 

 

 Test organism End-point Exhaust Particles Extract Reference 

 

 Cell transformation

 Balb/c3T3 mouse fibroblasts Cell transformation (+) Curren et al. (1981) 

 Balb/c3T3 mouse fibroblasts Cell transformation +b Hasegawa et al. (1988) 

 (+)c

 Hamster lung epithelial cells Cell transformation + + Mohr & Riebre-Imre (1992) 

 Hamster embryo fibroblasts Cell transformation + Schiffmann & Henschler (1992) 

 In vivoa

 Mouse Micronuclei, bone marrow - - + Pereira (1982) 

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 Mouse Micronuclei, bone marrow - Lewis et al. (1989) 

 Mouse Micronuclei, bone marrow - Morimoto et al. (1986) 

 Mouse Micronuclei, bone marrow - - - Pepelko & Peraino (1983) 

 Mouse Micronuclei, bone marrow (+) Ong et al. (1985) 

 Rat Micronuclei, bone marrow - Ishinishi et al. (1988)

 Rat Micronuclei, bone marrow - Ong et al. (1985) 

 Chinese hamster Micronuclei, bone marrow (+) - - Pepelko & Peraino (1983) 

 Mouse Sister chromatid exchange, - + + Pereira (1982) 

 bone marrow 

 Rat Sister chromatid exchange, - Ishinishi et al. (1988)

 bone marrow 

 Rat Sister chromatid exchange, - Morimoto et al. (1986) 

 bone marrow 

 Rat Sister chromatid exchange, - Ong et al. (1985) 

 peripheral blood leukocytes 

 

 Table 38 (contd) 

 

 Test organism End-point Exhaust Particles Extract Reference 

 

 Rat Sister chromatid exchange, - Lewis et al. (1989) 

 lymphocytes 

 Syrian golden Sister chromatid exchange, + Pereira (1982) 

 hamster lung cells (inhalation) 

 Syrian golden Sister chromatid exchange, + Guerrero et al. (1981) 

 hamster lung cells (instillation) 

 Syrian golden Sister cromatid exchange, + + Pereira (1982) 

 hamster lung cells (instillation) 

 Syrian golden Sister chromatid exchange + Morimoto et al. (1986) 

 hamster liver cells (transplacental) 

 Syrian golden hprt mutation + Morimoto et al. (1986) 

 hamster (transplacental) 

 Mouse Mutation, S. typhimurium - Morimoto et al. (1986) 

 (host-mediated assay) 

 Mouse Heritable effects on germ - Pepelko & Peirano (1983)

 cells (various assays; m/f) 

 Drosophila Heritable effects (sex-linked Schuler & Niemeier (1981) 

 melanogaster recessive lethal mutation) - 

 

 his, histidine independence; trp, tryptophane independence; hprt, hypoxanthine-guanine-phosphoryltransferase (8-aza- or 

 6-thioguanine resistance); tk, thymidine kinase (bromodeoxyuridine or trifluorothymidine resistance); ATPase, Na+/K+-ATPase 

 (ouabain resistance); +, positive; (+), weakly positive 

 a Dispersed in artificial surfactant 

 b Light-duty engine 

 c Heavy-duty engine 

 d Modified from Henschler (1987) and supplemented 

 Fischer 344 rats and CD-1 mice were exposed to diesel exhaust 

 particles at 0.35, 3.5, or 7 mg/m3 for 6, 12, 18, or 24 months to 

 investigate whether the accumulation of diesel particulates in lymph 

 nodes (indicated by black discolouration) influences the subsequent 

 response to immunization by sheep red blood cells, evaluated by the 

 presence of immunoglobulin (Ig) M antibody-forming cells. In rats, the 

 total number of lymphoid and antibody-forming cells was significantly 

 increased at the medium and high aerosol concentrations. In mice, the 

 number of lymphoid cells was increased only at the high concentration. 

 The authors concluded that diesel exhaust particles have only a 

 minimal effect on the immune and antigen filtration functions in 

 lung-associated lymph nodes because the relative numbers of 

 antibody-forming cells and specific IgM, IgG, and IgA antibodies in 

 rat sera were not significantly changed (Bice et al., 1985). 

 Five intranasal inoculations of various doses of a suspension of 

 diesel engine exhaust particles in ovalbumin were administered to BDF1 

 mice at intervals of three weeks. Ovalbumin IgE antibody titres, 

 assayed by passive cutaneous anaphylaxis, were enhanced by doses as 

 low as 1 μg (Takafuji et al., 1987, 1989). Similarly, primary IgE 

 responses were increased after intraperitoneal administration to mice 

 of ovalbumin or cedar pollen allergen mixed with diesel exhaust 

 particulates (Muranaka et al., 1986). 

 Female CR/CD-1 mice were exposed by inhalation to 6-7 mg/m3

 diesel exhaust for 2-6 h (acute), 8 h/day for 2-16 days (subacute), 

 or 8h/day for about 300 days (chronic). Immediately after the end 

 of exposure, animals were exposed to the infectious aerosols 

 S. typhimurium, Streptococcus pyogenes, or A/PR8-34 influenza virus. 

 Increased susceptibility to post-infection mortality was seen with the 

 bacterial but not the viral pathogens. Nitrogen dioxide and acrolein 

 vapour had specific effects (Campbell et al., 1981b). 

 CD-1 mice were exposed to 2 mg/m3 diesel exhaust for one to six 

 months. After three months of exposure and subsequent infection with 

 influenza virus, an enhanced severity of response was seen, involving 

 significant lung consolidation and focal macular collections of 

 particle-laden macrophages (Hahon et al., 1985). 

 B7.7.2 Behavioural effects 

 Sprague-Dawley rats were exposed for 8 h/day on seven days per 

 week for 16 weeks to diesel exhaust diluted to a particulate matter 

 concentration of 6 mg/m3. Spontaneous locomotor activity, measured 

 weekly on Wahman LC-34 running wheels, was significantly decreased 

 during 8, 9, 11, and 12 weeks of exposure. In rats exposed for 

 20 h/day on seven days per week for six weeks, forced activity on a 

 motorized treadmill was measured during the last week. Exhaustion 

 occurred in less than half the time that it occurred in control 

 animals. Groups of 10 rats were exposed to diesel exhaust at 6 mg/m3

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 for 20 h/day on days 1-7 post partum and were then held in clean air 

 until 15 months of age. In bar pressing acquisition training carried 

 out at five-day intervals for the next 42 days, the rate of learning 

 was much slower than in control rats. The difference was highly 

 statistically significant (Pepelko & Peirano, 1983). 

 As these three studies were conducted at a high concentration, 

 6 mg/m3, the practical consequences of the effects observed are not 

 known. The results, while limited in scope, indicate, however, that 

 behavioural and neurophysiological effects may be important toxic 

 end-points which should be investigated further. 

 B7.8 Factors that modify toxicity; toxicity of metabolites 

 Little information is available, but chemicals and other factors 

 may modify the toxicity of diesel emissions. For instance, 

 chlorophyllin, a derivative of the green pigment chlorophyll, has been 

 reported to inhibit or reduce the mutagenic activity of diesel 

 particulate extracts in the Ames test (Ong et al., 1986). 

 B7.9 Mechanisms of toxicity; mode of action 

 It is not clear whether DNA-reactive or non-DNA-reactive 

 mechanisms, or a combination of the two, are responsible for the 

 carcinogenic action of inhaled diesel exhaust in laboratory animals. 

 The results of several studies indicated that many PAHs (e.g. 

 benzo[ a]pyrene) cause a carcinogenic response in rodents, but it is 

 not known whether the same PAHs when associated with diesel exhaust 

 also induce a carcinogenic response. One hypothesis for the mechanism 

 of the tumorigenic response is that organic chemicals (e.g. PAHs, 

 nitro-PAHs) desorb from soot particles, are metabolized to reactive 

 metabolites, and interact with lung DNA to initiate carcinogenesis. 

 This would be a predominantly DNA-reactive mechanism. The observation 

 that organic chemicals associated with diesel soot can be metabolized 

 by lung cells to metabolites that can form DNA adducts after long-term 

 exposure to diesel exhaust supports this hypothesis. Studies with 

 carbon black essentially devoid of PAHs but which also form DNA 

 adducts do not, however, corroborate the PAH-DNA-reactive concept. 

 Another hypothesis is that the lung tumours that arise in rats 

 exposed to high levels of diesel exhaust are due to overloading of the 

 normal lung particle clearance mechanisms, accumulation of soot 

 particles, and cell damage followed by regenerative cell 

 proliferation. Enhanced cell proliferation may increase the mutation 

 frequency of key target genes. In this hypothesis, genotoxic chemicals 

 may not be causative factors in tumorigenicity. This view is supported 

 by the observations that lung cancer can be induced in rodents by 

 inhalation of highly insoluble particles of low toxicity that are 

 virtually devoid of organic chemicals (e.g. talc, carbon black, coal 

 dust, titanium dioxide), although high concentrations of these 

 particles (overload) are typically necessary. 

 A third hypothesis, which draws upon the above two mechanisms, is 

 that carcinogenesis is initiated by exposure to organic compounds 

 associated with diesel soot and promoted by the chronic inflammation, 

 cytotoxicity, and cell proliferation arising from the high 

 concentrations of particles deposited and retained in the lungs. 

 Again, however, the tumorigenic response observed with particles alone 

 (carbon black, titanium dioxide) does not support this hypothesis. 

 A key consideration is the relative contribution of different 

 mechanisms at different levels of exposure. As discussed later in this 

 section, high concentrations of particles, including diesel exhaust, 

 leading to high lung burdens, compromise normal clearance mechanisms. 

 Therefore, certain mechanisms may be invoked at high lung burdens that 

 may not occur at lower lung burdens. Genotoxic aromatic compounds may 

 take on increasing importance at lower concentrations. 

 Figure 3 is a diagram outlining the possible mechanism of action 

 of diesel exhaust, including the effects of overload conditions. 

 B7.9.1 Carcinogenic effects 

 B7.9.1.1 DNA-reactive mechanisms 

 Diesel exhaust contains hundreds of chemicals, including PAHs, 

 nitro-PAHs, alkyl-PAHs, oxy-PAHs, oxy-nitro-PAHs, and aldehydes 

 (Scheepers & Bos, 1992b), many of which are known mutagens and 

 carcinogens in laboratory animals. For example, inhaled 

 benzo[ a]pyrene (in tar and pitch) is carcinogenic in rat lung 

 (Heinrich et al., 1994). Nitro-PAHs are potent mutagens and, in some 

 instances, carcinogenic. In pharmacokinetic studies cited in this 

 monograph, clearance of PAHs and nitro-PAHs associated with the diesel 

 particulate fraction is retarded or delayed. Other studies have shown 

 clearly that the organic compounds associated with diesel soot are 

 bioavailable to lung cells. Mechanisms for the delayed clearance of 

 the PAHs have been discussed (Bond et al., 1986b; Gerde et al., 

 1991b). PAHs require metabolic activation to metabolites (e.g. 

 epoxides) that can potentially bind to DNA. In the case of the PAHs 

 associated with diesel soot, it is likely that alveolar lung cells 

 (e.g. type II cells) are responsible for their metabolic activation, 

 so that they can bind to lung cell DNA (Bond et al., 1983). 

 Additional evidence for a DNA-reactive mechanism in the 

 carcinogenicity of diesel exhaust is that exposure of laboratory 

 animals, including rats and monkeys, to diesel exhaust results in the 

 formation of DNA adducts in lung cells (see section B7.6). DNA adducts 

 and subsequent DNA replication can result in mutations that play a key 

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 role in initiating the carcinogenic response. These mutations could 

 involve activation of oncogenes or inactivation of tumour suppressor 

 genes. There may be some as yet unidentified chemicals in diesel 

 exhaust with high mutagenic potential; furthermore, chemical 

 interactions (additive or inhibitory) may occur among the components 

 of diesel exhaust (Ball & Young, 1992). 

 B7.9.1.2 Cytotoxicity with regenerative cell proliferation 

 Another mechanism by which diesel exhaust may induce 

 carcinogenesis involves cell killing, or cytotoxicity, by the 

 particles or the reactive gases in exhaust, followed by regenerative 

 proliferation of lung cells. Enhanced cell replication may result in 

 an increased frequency of spontaneous mutations. Mutations could also 

 arise from PAH-DNA adducts or from oxidative DNA damage caused by the 

 reactive oxygen and nitrogen species in diesel soot, resulting in the 

 inflammatory response. Driscoll et al. (1994) showed that the hprt 

 gene mutation frequency in rat lung epithelial cells was significantly 

 increased when the cells were incubated in vitro with inflammatory 

 cells obtained by bronchoalveolar lavage from rats exposed to quartz 

 particles. This appears to be an important mechanism in lung tumour 

 induction by particles that elicit a chronic inflammatory response in 

 the lung. Sagai et al. (1993) showed that diesel exhaust particles 

 could produce superoxide anions and hydroxyl radicals in the absence 

 of biological activation (detection by cytochrome c and electron spin 

 resonance). Reactive oxygen species may induce specific DNA adducts, 

 such as 8-hydroxydeoxyguanosine. As mentioned above, mutations could 

 involve activation of oncogenes or inactivation of tumour suppressor 

 genes. 

 Several data sets cited in this monograph support this 

 hypothesis. For example, carbon black particles, which are virtually 

 devoid of PAHs but are morphologically similar to diesel soot 

 particles, induce lung cancer in rats. High particle burdens in rodent 

 lungs result in an inflammatory response (Henderson et al., 1988). 

 Release of cytokines and reactive oxygen and nitrogen species during 

 the inflammatory response to particles may result in cell death. Some 

 evidence exists (Wright, 1986) that diesel exhaust enhances lung cell 

 replication. 

 B7.9.1.3 Effects of particles 

 The importance of pulmonary particle burden on lung tumour 

 induction has been demonstrated clearly in long-term studies by 

 inhalation in rats. As reviewed above, rats have similarly increased 

 lung tumour incidences when exposed to diesel exhaust or carbon black 

 particles by inhalation for 24 months. Similarly, carbon black 

 particles practically devoid of PAHs induce pulmonary tumours after 

 intratracheal instillation. The very large surface area of carbon 

 black and of diesel exhaust particles after desorption of adsorbed 

 organic compounds in vivo may be involved mechanistically in a 

 tumorigenic effect. Heinrich (1994) showed that the tumour response to 

 different types of carbon black particles instilled intratracheally 

 correlated well with their respective surface areas. Pott (1991) and 

 Pott et al. (1993) suggested that particles with a large surface area 

 have greater effects in humans than in rats because insoluble 

 particles with no specific toxicity remain significantly longer in the 

 terminal airways of humans than of rats (retention half-time, about 70 

 days in rats and about 500 days in humans). 

 The correlation between particle surface area and lung tumour 

 incidence was examined (Oberdörster & Yu, 1990) by evaluating 

 published studies of inhalation of diesel and other particles. Tumour 

 induction in rats was best correlated with the surface area of the 

 particles retained in the lung rather than with the particle mass, 

 particle volume, or number of particles, regardless of the PAH 

 content. It was suggested that particle surface area and surface 

 properties play a decisive role ('critical surface area') and that 

 absorbed PAHs are not responsible for the tumour response in rats 

 exposed to diesel exhaust. In the human situation, however, it could 

 not be excluded that organic compounds and gas-phase components are 

 also involved, since the human particulate lung burden is much lower 

 than those achieved in rats after long-term inhalation. 

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 Inhalation of diesel engine exhaust can result not only in 

 pulmonary tumours but also in inflammation and fibrosis and in a delay 

 in alveolar (not bronchial) pulmonary clearance. The mechanism by 

 which tumours develop due to particle overload and its associated 

 pathological and anatomical changes may be restricted to rats and may 

 not occur under environmental conditions in humans, since the lung 

 burdens of humans do not reach the levels that induce lung tumours in 

 rats. This is of importance for quantitative risk assessment. Only 

 occupational exposure to diesel exhaust may result in lung burdens 

 near or at overload conditions, particularly if the lung is already 

 compromised by exposure to other dusts. Bohning et al. (1982) reported 

 retarded particle clearance in smokers; in these people, additional 

 exposure to diesel exhaust may induce overload and associated toxic 

 effects. It is not known, however, whether the mechanisms of 

 particle-induced lung tumours are the same in rats and humans, and 

 this information is necessary for extrapolating data from rats to 

 humans. 

 Not only diesel soot (0.8, 2.5, or 7.0 mg/m3) but also carbon 

 black nearly completely devoid of organic compounds (Printex 90, 

 7.5-12 mg/m3; particle size, 10 nm) and ultrafine titanium dioxide 

 particles (7.5-15 mg/m3; particle size, 20 nm) caused lung tumours 

 in female Wistar rats exposed by inhalation for 18 h/day on five days 

 per week for 24 months. The tumour rate increased with increasing 

 particle concentrations, independently of the type of particles 

 inhaled. No lung tumours were observed in the rats exposed to the 

 lowest concentration of diesel particles. The authors concluded that 

 the carcinogenic component of diesel exhaust is in the inner part of 

 the diesel soot particle, the carbon core, and is not the relatively 

 small amount of carcinogenic PAHs (3.9 g benzo[ a]pyrene per gram of 

 diesel soot) (Heinrich et al., 1992; Heinrich, 1994; Heinrich et al., 

 1995). These results were confirmed in another two-year study, in 

 which male and female rats were exposed by inhalation to various 

 concentrations of carbon black and diesel exhaust. Lung tumours were 

 observed with both particle types (Nikula et al., 1994). 

 Diesel soot does not appear to have a specific carcinogenic 

 effect in rats; rather, there is a nonspecific effect of particles. 

 B7.9.1.4 Effects of polycyclic aromatic hydrocarbons 

 Exposure of rats by inhalation to 2.6 mg/m3 of an aerosol of 

 tar-pitch condensate with no carbon core but containing 50 μg/m3

 benzo[ a]pyrene and other PAHs for 10 months caused lung tumours at a 

 rate of 39%. The same amount of tar-pitch vapour condensed onto the 

 surface of carbon black particles at 2 and 6 mg/m3 resulted in 

 tumour rates that were roughly two times higher (89 and 72%). Since 

 exposure to 6 mg/m3 carbon black almost devoid of extractable 

 organic material caused a lung tumour rate of 18%, the tumour rate of 

 72% seen after combined exposure to tar-pitch vapour and carbon black 

 particles indicates a syncarcinogenic effect of PAHs and carbon black. 

 A possible mechanism is an effect of deposition of PAHs (Heinrich et 

 al., 1994). As the level of benzo[ a]pyrene in the coal-tar pitch was 

 about three orders of magnitude greater than those in diesel soot, 

 PAHs may play a negligible role in the tumorigenicity of diesel soot 

 in rats. The PAH profile in diesel soot is, however, quite different 

 from that in coal-tar pitch, as diesel soot contains highly mutagenic, 

 carcinogenic nitro-PAHs and other poorly characterized mutagens that 

 are not present in coal-tar pitch or on some of the carbon black 

 particles used in experimental studies (Heinrich et al., 1994; Nikula 

 et al., 1994). 

 In a study of various extracts of diesel exhaust particles, 

 30-40% of the total mutagenicity could be attributed to a group of six 

 nitroarenes (Salmeen et al., 1984). 

 A diesel exhaust particle extract was separated into a water- and 

 a lipid-soluble fraction, and the latter was further separated into a 

 PAH-free, a PAH-containing, and a polar fraction by column 

 chromatography. These fractions were then tested in Osborne-Mendel 

 rats by pulmonary implantation at doses corresponding to the 

 composition of the original diesel exhaust. The water-soluble fraction 

 did not induce tumours; the incidences induced by the lipid-soluble 

 fractions were 0% with the PAH-free fraction, 25% with the 

 PAH-containing fraction, and 0% with the polar fraction. The 

 PAH-containing fraction, comprising only 1% by weight of the total 

 extract, was shown to be responsible for the carcinogenic activity 

 (Grimmer et al., 1991). 

 Various dichloromethane extracts, each representing a complex 

 mixture, were obtained from particulate emissions of four 

 diesel-fuelled and one gasoline-fuelled automobiles (combustion), a 

 coke oven battery (pyrolysis), and a roofing tar pot (evaporation), 

 and their tumorigenic potency was compared in Sencar mice. It was 

 concluded that the benzo[ a]pyrene content alone could not explain 

 the tumorigenic activity of the mixtures (Nesnow et al., 1982a, 1983). 

 The lung tumour rates in rats exposed to atmospheres containing 

 PAHs depend not only on the PAH concentrations of the exhaust gas but 

 also on parameters such as the composition of the carrier particle 

 (mass ratio of carbon core to adsorbed layer of organics), the 

 dissolution rate of particle-attached organic compounds, the retention 

 half-time, and the cytotoxic effect of the carrier particle in the 

 lung (Heinrich et al., 1991). 

 Extracted diesel soot given intratracheally to rats induced lung 

 tumours, but native, unchanged diesel soot resulted in higher tumour 

 rates than extracted soot. Carbon black also caused tumours after 

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 intratracheal administration, and the rate increased with decreasing 

 size of the primary particles (Heinrich, 1994). 

 Carbon black particles almost completely devoid of organic 

 compounds (< 0.046% extractable organic compounds and 0.6 ng/g 

 benzo[ a]pyrene) caused tumours in the lungs of 17% of rats after 

 exposure to a concentration of 6 mg/m3 for 18 h/day on five days per 

 week for 10 months. No lung tumours occurred in controls exposed to 

 clean air. Thus, the particle effect may be responsible for induction 

 of lung tumours in rats exposed to diesel engine exhaust, and the 

 effect may be related to the surface area of the carbon particle. A 

 PAH depot effect could lead, however, to retarded dissolution of PAHs 

 from the carrier, resulting in very efficient use of the extremely 

 small amount of carcinogenic PAHs retained in the lung after exposure 

 to diluted diesel engine exhaust, which contained benzo[ a]pyrene at 

 about 10 ng/m3 (Heinrich et al., 1991). Since diesel particles 

 induce DNA adducts at lower concentrations than carbon black (Bond et 

 al., 1989, 1990c; Wolff et al., 1990), PAHs may have tumour initiating 

 properties that are too weak to be detected at low doses; at higher 

 doses, promotional effects of the particles, perhaps with additional 

 initiation, may synergize to produce detectable carcinogenic effects. 

 B7.9.2 Non-carcinogenic effects 

 Diesel exhaust contains various respiratory irritants in the gas 

 phase and in particulate matter. Both can induce inflammatory 

 responses in the airways and alveolar regions of the lung. Airway 

 inflammation involves damage to epithelial cells, including lipid 

 peroxidation of cell membranes by oxidizing gaseous pollutants such as 

 nitrogen dioxide. Indirect effects of particles, resulting from 

 phagocytosis, can include the formation and release of various 

 mediators, including oxidants, such as superoxide anions and hydroxyl 

 radicals, and cytokines. These mediators may play a role in focal loss 

 or shortening of cilia, type II cell hypertrophy, and hyperplasia. The 

 latter changes can lead to the hyperplastic lesions seen in animals 

 exposed to diesel exahaust (Ishinishi et al., 1986, 1988; Suzuki et 

 al., 1990; Kato et al., 1992). Phagocytosis and subsequent clearance 

 of particles by alveolar macrophages can be compromised by high 

 particle burdens (Wolff et al., 1989; Creutzenberg et al., 1990), 

 which may also increase the access of particles to the interstitium, 

 leading to focal fibrosis (Henderson et al., 1988). 

 Inflammation, altered lung clearance, and hyperplastic lesions 

 can be considered early markers of exposure to diesel exhaust and are 

 the basis of the non-neoplastic effects used to determine both the 

 NOAEL and the 'benchmark concentration' described in section B10.1.3. 

 B8. EFFECTS ON HUMANS

 B8.1 General population 

 B8.1.1 Acute exposure: olfactory, nasal, and ocular irritation 

 Acute exposure to diesel exhaust has been associated with 

 irritation of the eyes and nose. Signs and symptoms reported after 

 acute exposure to diesel exhaust are described in section B8.2.1. 

 The exhaust from e.g. poorly maintained engines or engines under 

 load may be visible as a black, smoky cloud. WHO (1987) considered 

 that sensory effects were parameters that could be used in setting 

 occupational exposure limits. The characteristic odour of diesel 

 exhaust provides a warning of its presence. At higher concentrations 

 and under certain operating conditions, the odour can be offensive. 

 The odour-causing agents are not known; however, compounds with a 

 relative molecular mass > 80 are probably those mainly responsible, 

 and aliphatic olefins (C1-C6, including acetylene), hydrocarbons 

 with more than six carbons, and aliphatic aldehydes are probably not 

 involved. Substances with low odour thresholds, such as nitrogen 

 dioxide (0.3 ppm) and acrolein (0.5 ppm), appear to contribute to the 

 odour of diesel exhaust to minor extents (5.3 and 0.25%, respectively) 

 (Oelert & Florian, 1972). 

 The ability to detect the odour and the irritating effects of 

 diesel exhaust vary. For example, when six subjects smelled diesel 

 exhaust diluted with air, the dilution factors needed to achieve the 

 odour detection threshold varied from 140 to 475. The concentrations 

 of different constituents of the exhaust at the odour threshold also 

 varied: formaldehyde, 0.012-0.088 ppm; acrolein, 0.011-0.046 ppm; and 

 nitrogen dioxide, 0.11-2.28 ppm (Linnell & Scott, 1962). When six 

 subjects were exposed to three concentrations of diesel exhaust for 

 10 min, the mean concentrations at the odour threshold were 1.3-4.2 ppm 

 nitrogen dioxide, 0.2-1 ppm sulfur dioxide, < 0.1 ppm formaldehyde, 

 and < 0.05 ppm acrolein. Three of the subjects exposed to the highest 

 level discontinued exposure before 10 min, while none at the lowest 

 level discontinued exposure although some experienced eye irritation 

 (Battigelli, 1965). 

 The health effects of inorganic gases present in diesel exhaust 

 are not specific and are therefore not discussed in detail; however, 

 it must be noted that these gases contribute to the environmental 

 burden. 

 B8.1.2 Air pollution 

 The concentrations of some air pollutants, such as particulates 

 and sulfur dioxide from the burning of coal for domestic heating and 

 industrial purposes, are in many parts of the world much lower than 

 they were several decades ago, and the associated adverse health 

 effects have diminished accordingly. A number of epidemiological 

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 studies have demonstrated, however, that the relatively low remaining 

 levels of air pollutants are associated with a range of health 

 indices, including day-to-day changes in mortality (Schwartz, 1993), 

 visits to hospital emergency departments (Schwartz et al., 1993), and 

 changes in measures of lung function (Pope & Dockery, 1992). In most 

 studies, the associations have been strongest with the fine 

 particulate component of pollution, some of which may be derived from 

 diesel exhausts. 

 Vehicle traffic, both gasoline and diesel, also contributes to 

 the nitrogen dioxide content of urban air, and there is evidence, 

 primarily from experimental studies (Bauer et al., 1986; Koenig et 

 al., 1988; Grant et al., 1993) that it can induce short-term 

 decrements in lung function in asthmatic and non-asthmatic patients. 

 Nitrogen dioxide and volatile hydrocarbons are involved in the 

 formation of ozone and associated photochemical pollutants. 

 Associations have also been demonstrated between long-term 

 exposure to urban air pollutants and death rates from certain chronic 

 conditions. Confounding factors often make interpretation difficult, 

 but in an investigation conducted in the United States (Dockery et 

 al., 1993), air pollution attributable to fine particles was 

 positively associated with lung cancer and cardiopulmonary disease, 

 after adjustment for smoking and other relevant risk factors, but not 

 with other causes considered collectively. 

 In neither short- nor long-term studies can the possible role of 

 diesel particulates be specified, but diesel emissions contribute to 

 urban particulates, especially in Europe and developing countries. The 

 acidic and sulfate components of particulates, which are derived 

 primarily from stationary fuel-burning sources, appeared to be 

 implicated in a number of studies. 

 B8.2 Occupational exposure 

 B8.2.1 Effects on the respiratory system 

 B8.2.1.1 Symptoms 

 Most of the information about symptoms after acute exposure to 

 diesel exhaust comes from anecdotal reports of occupationally exposed 

 individuals. It was noted in a bus garage in London, United Kingdom, 

 that the buses produce a 'lachrymatory mist' when they were started up 

 from cold (Commins et al., 1956). In a review of 13 cases of acute 

 overexposure to diesel exhaust in five underground coal mines in Utah 

 and Colorado, United States, between 1974 and 1985, interviews in 1986 

 with the miners revealed that 12 had experienced symptoms of mucous 

 membrane irritation, headache, and light-headedness; eight had 

 reported nausea, and four reported a sensation of unreality and 

 'heartburn' (Kahn et al., 1988). 

 In a study designed to investigate the acute effects of diesel 

 exhaust on respiratory symptoms, a questionnaire was administered to 

 232 male workers in four diesel bus garages, and personal samples of 

 nitrogen dioxide and respirable particulate were obtained. After 

 adjustment for age and smoking (current, ex-, never), workers with the 

 highest exposure to respirable particulate (0.31 mg/m3) reported 

 significantly more cough, itchy or burning eyes, headache, difficult 

 or laboured breathing, a feeling of chest constriction, and wheeze 

 than workers with lower exposures. Those exposed to nitrogen dioxide 

 at >0.4 mg/m3 (> 0.3 ppm) also more frequently reported itchy or 

 burning eyes, difficult or laboured breathing, a feeling of chest 

 constriction, and wheezing. In comparison with a group of lead acid 

 battery workers, the reporting of the following symptoms as 

 'sometimes' or 'often' was significantly more prevalent among the 

 workers in the diesel bus garage: eyes itch, burn, or water (49.5 

 versus 23.5%), headache (24.2 versus 12.1%), difficult or laboured 

 breathing (13.5 versus 3.6%), nausea (13.5 versus 4.5%), and wheeze 

 (13.7 versus 4.5%) (Gamble et al., 1987a). 

 In comparison with 11 office workers, 17 ferry stevedores had a 

 greater prevalance of wheezing (24 versus 9%), chest tightness (29 

 versus 9%), nasal complaints (47 versus 0%), chest pain (24 versus 

 0%), and eye irritation (59 versus 27%); however, more of the 

 stevedores smoked. The concentrations of nitrogen dioxide (0.3 mg/m3) 

 and sulfur dioxide (0.7mg/m3) were both < 0.25 ppm; respirable 

 particulate was not measured (Purdham et al., 1987). In a study in an 

 iron ore mine where diesel engines were used underground, more workers 

 who were smokers reported pressure over the chest or difficulty in 

 getting air than the nonsmokers. No such difference was observed among 

 smoking and nonsmoking surface workers. The underground workers who 

 were smokers also had more episodes of a productive cough lasting 

 three weeks during several winters (Jorgensen & Svensson, 1970). 

 B8.2.1.2 Acute changes in pulmonary function 

 The pulmonary function of 60 coal miners who worked in mines 

 equipped with diesel engines was compared with that of 90 coal miners 

 not exposed to diesel exhaust. There were similar proportions of 

 current smokers (45% in the exposed group and 43% in the unexposed 

 group). Measurements made with personal dust samplers and passive 

 nitrogen dioxide dosimeters showed average concentrations of 

 0.04 mg/m3 (0.2 ppm) nitrogen dioxide, 0.4mg/m3 (0.3 ppm) 

 formaldehyde, and 2.0 mg/m3 respirable dust in the exposed group; 

 the unexposed group was exposed to 1.4 mg/m3 respirable dust. Forced 

 vital capacity (FVC) and forced expiratory volume in 1 sec (FEV) were 

 reduced during the work shift for both the diesel-exposed and 

 unexposed groups. The reduction was slightly but not significantly 

 greater in smokers than in ex- and nonsmokers. An additional analysis 

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 with adjustment for age, exposure to respirable dust, and years of 

 underground mining still revealed no difference in shift-related 

 pulmonary function between miners exposed and unexposed to diesel 

 exhaust (Ames et al., 1982). 

 No significant shift-related change in FVC or FEV was seen among 

 workers on ferries transporting diesel trucks and other vehicles in 

 comparison with controls (Purdham et al., 1987), and no significant 

 change in spirometry measured over a shift was seen in 232 workers in 

 four diesel bus garages (Gamble et al., 1987a). Ulfvarson et al. 

 (1987), however, found significant decrements in FVC and FEV1 across 

 a shift in 23 ferry workers who had had no exposure to diesel for 10 

 days, with no difference between smokers and nonsmokers. The 

 concentration range of total particles was 0.13-1 mg/m3, that of 

 formaldehyde 0.04-0.6mg/m3 (< 0.03-0.5 ppm), and that of nitrogen 

 dioxide 0.12-4.6mg/m3 (0.06-2.3 ppm). In a repetition of the study, 

 a significant shift-related decrement was noted in FVC but not in 

 FEV1. In a later study in which filters were put on the diesel 

 trucks, a shift-related decrement in FVC was seen, but no subsequent 

 shift-related changes in FEV were noted, with or without filters 

 (Ulfvarson & Alexandersson, 19901). 

 Three male railroad workers developed asthma after heavy exposure 

 to locomotive emissions (Wade & Newman, 1993). The workers, none of 

 whom were current smokers, had no previous history of asthma or of any 

 respiratory disease, except one who had seasonal rhinitis. They were 

 riding immediately behind the lead engines of the trains, where diesel 

 exhaust was blown almost continually into the cab. In two, the acute 

 onset of asthma occurred within the first hours of exposure. 

 B8.2.1.3 Pulmonary effects 

 In a study to investigate the effects of diesel exhaust on the 

 cells found in bronchoalveolar lavage (BAL) fluid (Rudell et al., 

 1990), eight healthy, nonsmoking volunteers were exposed to diesel 

 exhaust (for 60 min according to Rudell et al., 1989) at least three 

 weeks after an initial BAL. The median steady-state concentrations 

 measured in the exhaust were 4.6mg/m3 (3.7 ppm) nitric oxide, 

 3.1 mg/m3 (1.6 ppm) nitrogen dioxide, 22.5mg/m3 (27 ppm) carbon 

 monoxide, 0.5 mg/m3 formaldehyde, and 4.3 × 105 particles/cm3; 

 according to Rudell et al. (1989), this particle concentration 

 corresponds to a mass concentration of approximately 100 μg/m3. BAL 

 was performed again 18 h after exposure. A significant reduction 

 (P < 0.02) in the total number of mast cells was observed; the number 

 of neutrophils was slightly but significantly (P < 0.05) increased in 

 comparison with the values before exposure. The ratio of 

 T-helper:suppressor cytotoxic cells was elevated ( P < 0.02), and the 

 rate of phagocytosis of opsonized yeast cells by alveolar macrophages 

 in vitro was reduced (P < 0.02). The number of lymphocytes remained 

 unchanged. 

 B8.2.2 Epidemiological studies (noncarcinogenic effects) 

 Some but not all of the results from cross-sectional and 

 longitudinal studies on workers with occupational exposure to low 

 levels of diesel engine exhaust show decrements in lung function and 

 an increased prevalence of respiratory symptoms. 

 B8.2.2.1 Effects on the respiratory system 

 A group of 550 underground workers and 273 surface workers in six 

 coal mines where diesel-powered equipment was used were matched for 

 smoking status, age, height, and years of underground mining to 

 workers at other underground coal mines where diesel units were not 

 used. The workers at the mines with diesel engines reported 

 significantly more persistent cough (23.6%) than controls (16.5%) and 

 more frequently had exacerbations of cough and phlegm (21.7 and 16.2%, 

 respectively). Pulmonary function (FVC and FEV ) was decreased in both 

 surface and underground workers in mines where diesel engines were 

 used in comparison with surface and underground miners in other mines. 

 There was no consistent relationship between years of underground 

 mining and respiratory symptoms and pulmonary function; however, the 

 mean time spent in underground mining was only 4.7 years. Full-shift 

 area samples showed concentrations of respirable dust ranging from 0.4 

 to 16.1 mg/m3 for various jobs; the mean values from personal 

 samples were 0.93-2.73 mg/m3, and the nitrogen dioxide levels in 

 personal samples were 0.16-0.26 mg/m3 (0.13-0.22 ppm) (Reger et al., 

 1982). 

 Pulmonary function and respiratory symptoms were studied in 1976 

 in 630 miners in six potash mines where diesel-powered vehicles had 

 been introduced between 1950 and 1964. There was no consistent 

 relationship with exposure to diesel exhaust, considered in several 

 ways, including years of exposure, cumulative exposure to dust, 

 nitrogen dioxide concentration, and prevalence of diesel use in the 

 mine. The mean length of exposure to diesel engines was, however, 

 relatively short: 5-14 years across mines. In addition, cumulative 

 exposure was measured only to total dust rather than respirable dust. 

 The mean values for total dust in the mines ranged from 9 to 

 23 mg/m3 (personal sampling); the ratio of total dust to respirable 

 dust ranged from 2 to 11 (area sampling), and the nitrogen dioxide 

 concentration was 0.2-6.3mg/m3 (0.1-3.3 ppm) (personal sampling) 

 (Attfield et al., 1982). 

 A total of 259 miners in five salt mines where diesel equipment 

 was used in some of the mines were studied with regard to the number 

 of years worked underground and cumulative exposure to respirable 

 particulate and nitrogen dioxide. These parameters were associated 

 with phlegm after adjustment for age and smoking but not cough. The 

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 average exposure to respirable particulate in the five mines was 

 0.2-0.7 mg/m3, and the average exposure to nitrogen dioxide was 

 0.6-4.8mg/m3 (0.3-2.5 ppm). Pulmonary function (FEV 1, FVC, peak 

 flow) was not related to the three parameters but was slightly reduced 

 in comparison with that of other blue-collar workers. In another 

 analysis in the same population, phlegm but not pulmonary function was 

 associated with years of work underground in mines where diesel 

 engines were used, after adjustment for age and smoking. There was a 

 nonsignificant trend for an association between cough and shortness of 

 breath with years of exposure (Gamble & Jones, 1983). 

 Longitudinal changes in pulmonary function and chronic 

 respiratory symptoms were studied between 1977 and 1982 in 280 miners 

 exposed to diesel exhaust and 838 miners not exposed to diesel exhaust 

 in American underground coal mines. The mean number of years of 

 underground work ranged from 6.6 to 17.4 years across mines. Area 

 samples taken in 1977 revealed 'low' levels of dust and diesel exhaust 

 constituents, which were reported not to exceed 25% of current 

 standards, but the actual values were not given. The exposed workers 

 had smaller average decrements in FVC and FEV1 than workers not 

 exposed to diesel exhaust after adjustment for age, smoking, and years 

 of underground work. Additional analysis revealed no relationship with 

 cumulative years of underground work, but the level of pulmonary 

 function was not considered as a predictor of longitudinal change. The 

 exposed miners also had a lower five-year incidence of cough, phlegm, 

 and breathlessness than the miners not exposed to exhaust (Ames et 

 al., 1984). 

 Pulmonary function and respiratory symptoms were studied in 283 

 male diesel bus workers in four garages in two cities. The number of 

 years worked was a significant predictor of lower FVC and FEV1

 adjustment for age, height, race, and smoking status. In comparison 

 after with another blue-collar population, the bus garage workers had 

 a higher prevalence of cough and phlegm after adjustment for age and 

 smoking. The prevalence of these symptoms was not related to the 

 number of years worked (Gamble et al., 1987b). 

 B8.2.2.2 Effects on the circulatory system 

 No consistent excess of deaths due to cardiovascular disease has 

 been identified in cohort studies of workers with potential exposure 

 to diesel emissions. Motor vehicle examiners (Stern et al., 1981), who 

 are probably exposed to exhaust from a variety of vehicles, had a 

 slight, nonsignificant increase in deaths due to cardiovascular 

 disease (standardized mortality ratio [SMR] = 105). No difference in 

 mortality was seen among men working in potash mines with 

 diesel-powered equipment in comparison with men in potash mines with 

 no diesel engines (Waxweiler et al., 1973). In a pilot study of 129 

 men employed in a bus company in 1951-59 for whom mortality was 

 ascertained until 1978 (Edling & Axelson, 1984), a fourfold increase 

 in cardiovascular deaths was seen in garage workers. The increase was 

 calculated on the basis of at least 15 years since first exposure and 

 10 or more years of exposure, but was based on only four deaths. This 

 finding was not confirmed in a follow-up of 694 men through 1983 

 (Edling et al., 1987). In a study of 8490 garage maintenance workers 

 with at least one continuous year of service between 1967 and 1975, a 

 deficit of deaths due to cardiovascular disease was seen (Rushton et 

 al., 1983). 

 B8.2.3 Epidemiological studies (carcinogenic effects) 

 The relationship between cancers of the lung and bladder and 

 occupational exposure to diesel exhaust has been evaluated in a number 

 of epidemiological studies. The occupations examined included diesel 

 truck drivers, bus garage workers, railroad workers, heavy equipment 

 operators, and stevedores. The risk for lung cancer in relation to 

 exposure to diesel exhaust, either self-reported or assumed from 

 occupational categories, has also been evaluated in case-control 

 studies. Only those studies that were considered relevant for an 

 evaluation of the carcinogenic effects of diesel exposure are included 

 in this assessment. 

 B8.2.3.1 Lung cancer 

 The epidemiological studies are summarized in Tables 39-41. Table 

 39 is a summary of nine case-control and cohort studies of workers 

 exposed to diesel exhaust, Table 40 summarizes nine population- and 

 hospital-based studies, and Table 41 presents two studies based on 

 information on exposure derived from registries (surveillance 

 studies). 

 Until recently, the epidemiological study of lung cancer and 

 exposure to diesel exhaust was limited by failure to consider the 

 latency and duration of exposure necessary for the development of lung 

 cancer, both generally considered to be about 20 years (Schenker & 

 Speizer, 1979). Studies of exposed workers have also been limited by a 

 lack of worker- and industry-specific data on exposure. Such data were 

 available only for the American railroad and trucking industries. For 

 other occupational groups, such as bus garage workers and stevedores, 

 indices of exposure were derived from vehicle use, fuel consumption, 

 or years of exposure, or simply job title unsubstantiated by exposure 

 assessment. In studies based in hospitals, the general population, or 

 registries, information on usual work in a job with exposure to 

 vehicle exhaust was derived from self- or surrogate reporting; 

 self-reporting of exposure to diesel fumes has also been used. Studies 

 with short durations of exposure and follow-up are not useful for 

 determining whether diesel exhaust is a human carcinogen. Studies in 

 which there is an imprecise definition of exposure to diesel exhaust 

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 (such as self-reported job title) do not allow detection of an effect, 

 since the extent of exposure is unknown. In studies in which an 

 elevated risk for lung cancer is noted, such imprecision can result in 

 wide confidence intervals. 

 The major potential confounding factor in occupational studies of 

 lung cancer is tobacco smoking. Such a factor must be related not only 

 to the outcome but also to the exposure. In order to assess whether 

 tobacco use is a true confounder in a study of occupation, the smoking 

 rates among individuals exposed and unexposed to diesel exhaust must 

 be known; however, owing to the retrospective nature of many 

 occupational studies, smoking histories are often not available. It is 

 unlikely that the smoking habits of workers exposed and unexposed to 

 diesel exhaust within the same occupational cohort are differentially 

 related to the exposure, but when the effect of exposure is small, in 

 the order of a relative risk of 1.5 (such has been found for diesel 

 exhaust and lung cancer in most studies), differences in smoking that 

 are unaccounted for could reduce the relative risk attributable to 

 exposure to diesel exhaust. Interpretation of the results of studies 

 lacking specific information about smoking is more uncertain when 

 small relative risks are seen. Despite imprecise exposure histories, 

 one strength of hospital- and registry-based studies of lung cancer is 

 that smoking histories are often available. 

 (a) Occupationally based cohort and case-control studies 

 Three studies have been conducted of railroad workers exposed to 

 diesel exhaust. The transition from steam- to diesel-powered 

 locomotives occurred in the United States during the 1950s. By 1959, 

 95% of the locomotives in service were diesel powered. In a 

 retrospective cohort study of American railroad workers, the mortality 

 of 55 407 white male workers aged 40-64 in 1959 who had worked on the 

 railroads for 10-20 years was ascertained through 1980, providing a 

 22-year period of follow-up (Garshick et al., 1988). A yearly 

 three-digit job code up to the time of death or retirement was 

 available from the Railroad Retirement Board. The workers had held 

 jobs in 39 selected categories, and an industrial hygiene survey was 

 conducted to categorize the job codes into those associated with 

 regular exposure to diesel exhaust (engineers, conductors, firemen, 

 brakemen, and diesel locomotive repair shop workers) and those not 

 exposed to diesel exhaust (clerks and signal maintainers). The 

 concentration of respirable particulate, adjusted for cigarette smoke, 

 was used as an indicator of exposure to diesel exhaust (Woskie et al., 

 1988a,b). A potentially confounding exposure in the railroad industry 

 is asbestos, which was used to insulate the steam locomotives run 

 previously. Thus, workers in steam locomotive repair shops would have 

 been exposed to asbestos. Workers who had the longest potential 

 duration of exposure, i.e. those aged 40-44 in jobs with exposure to 

 diesel exhaust in 1959, had a relative risk of dying of lung cancer of 

 1.45 (95% confidence interval [CI] = 1.11-1.89). Workers aged 45-49 in 

 1959, who would have had slightly less exposure, had a relative risk 

 of 1.33 (95% CI = 1.03-1.73). Exclusion of the workers with potential 

 past exposure to asbestos did not appreciably change these relative 

 risks. 

 The US Environmental Protection Agency has supported an effort to 

 obtain more detailed information on exposure in this study in order to 

 estimate unit risk (Pepelko & Chen, 1993). Adequate exposure-response 

 curves could not be drawn for years of exposure or for measurements of 

 current exposure. Possible reasons include an imprecise assessment of 

 past exposure, since only current measurements of exposure were 

 available; changes in exposure over time, since improved ventilation 

 and new diesel locomotives have been introduced, resulting in reduced 

 exposure; and the lack of exposure histories for the workers who would 

 have been exposed to diesel exhaust before 1959. In addition, the 

 industrial hygiene survey was performed in four smaller railroads, 

 where exposure may not reflect that throughout the industry; the 

 presence of non-diesel particulate in the respirable samples collected 

 could have led to exposure misclassification. Nevertheless, the 

 industrial hygiene survey validated the classification of jobs into 

 those associated and not associated with exposure. 

 In a case-control study of American railroad workers by the same 

 investigators (Garshick et al., 1987), deaths occurring between 1 

 March 1981 and 28 February 1982 were recorded, and 1256 from lung 

 cancer were matched by age to deaths from causes other than cancer or 

 accidents. Smoking histories were obtained from next-of-kin. After 

 adjustment for smoking and past exposure to asbestos, workers aged 64 

 at the time of death and with 20 years of work in a job with exposure 

 to diesel exhaust had an odds ratio of 1.41 (95% CI = 1.06-1.88). 

 A cohort study addressed mortality between 1965 and 1977 among 

 all 43 826 male railroad workers who had retired from the Canadian 

 National Railway Company before 1965 but who were still alive and 

 those who retired between 1965 and 1977. Occupation at the time of 

 retirement was used to classify workers as unexposed, possibly 

 exposed, or probably exposed to diesel fume. The relative risk of 

 dying of lung cancer was 1.20 for workers with possible exposure 

 (P = 0.013) and 1.35 for those probably exposed (P < 0.001). Similar 

 relative risks were obtained after exclusion of workers involved in 

 locomotive repair, who were most likely to have had past exposure to 

 asbestos. These results are consistent with those of the studies of 

 American railroad workers, although the degree to which the workers 

 were actually exposed to diesel fumes is not known. Only retired 

 workers were studied, excluding younger, active workers who would have 

 had the most exposure. No information was given about the duration of 

 exposure of the retired workers to diesel exhaust since many would 

 have worked primarily before the transition to diesel locomotives 

 (Howe et al., 1983). 

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 Table 39. Occupation-based case-control and cohort studies of lung cancer in groups exposed to diesel engine exhaust 

 

 Population Exposure assessment Results Limitations Reference 

 

 43 826 male pensioners of the Exposure classified by RR = 1.20 (P = 0.013) Incomplete exposure Howe et al. 

 Canadian National Railway experts on occupation at and 1.35 (P = 0.001) for assessment owing to (1983) 

 time of retirement: possible and probable lack of lifetime occupational 

 unexposed, possibly exposure, respectively. history. Difficult to 

 exposed, probably Significant trend in RR separate combustion products 

 exposed with increasing likelihood from diesel exhaust, 

 of exposure since the cohort would 

 have worked in both the 

 steam and diesel eras; 

 many would have had 

 relatively short exposure 

 to diesel. No data on 

 smoking; method of 

 categorizing exposure 

 not validated or described 

 in detail 

 Incident deaths between Personal exposure Adjusted for smoking and Possible misclassification Garshick et a

 1 March 1981 and 28 assessed by industrial to asbestos, OR = 1.41 of exposure to diesel (1987) 

 February 1982 in US railroad hygiene sampling in 39 (1.06-1.88) (< 64 years of exhaust since job title might 

 workers. 1256 cases of job categories; yearly age) for 20 years of work not reflect exposure in each 

 lung cancer and 2385 matched job title used to in a diesel-exposed job. case; however, this should 

 controls (up to two each, on dichotomize exposure For > 20 years of work in a reduce the OR. 

 age and date of death). Cases into exposed and diesel-exposed job relative 

 and controls had worked for unexposed between 1959 to 0-4 years, OR = 1.64 

 the railroad for > 10 years. and retirement (1.18-2.29) 

 

 Table 39 (contd) 

 

 Population Exposure assessment Results Limitations Reference 

 

 55 407 white male railroad Industrial hygiene data RR = 1.45 (1.11-1.89) in No data on smoking Garshick et a

 workers, aged 40-64 and used to categorize jobs workers aged 40-44 in (1988) 

 with 10-20 years of work in as exposed or unexposed 1959; RR = 1.33 (1.03- 

 1959. Mortality due to lung to diesel exhaust; jobs 1.73) in workers aged 45- 

 cancer (1694 deaths) well categorized for 49. Unexplained by exposure 

 determined retrospectively most of the cohort to asbestos. Workers with 

 through 1980 highest potential 

 cumulative exposure to 

 diesel exhaust had highest 

 risk for cancer 

 About 20 000 male London Five job categories used SMRs for all five job Duration of work not Waller (1981)

 Transport workers aged 45-64. to define exposure, categories < 100 for lung considered; impossible to 

 667 cases of lung cancer validated by cancer (healthy worker follow individuals after 

 ascertained among active environmental effect), but highest SMR in retirement; no adjustment for 

 workers > 25 years (1950-74) concentrations of highest exposure group, not smoking 

 benzo[a]pyrene and significantly greater than 

 particles measured least exposed (underground 

 in 1957 and 1979 train crew) 

 8490 male London Transport 100 job titles grouped SMR = 101 overall, but job No validation of exposure Rushton et al

 maintenance workers (cohort into 20 broad categories category 'general hand' by air sampling; short (1983) 

 mortality study). Mortality of showed increased SMR for (average, 6 years) follow-up; 

 workers employed for > 1 year lung cancer with no no adjustment for smoking 

 between 1 January 1967 apparent link to diesel 

 and 12 March 1975 exhaust 

 

 Table 39 (contd) 

 

 Population Exposure assessment Results Limitations Reference 

 

 695 workers in bus garages Intensity of exposure to SMR = 122 (71-196); for No adjustment for smoking Gustavsson et

 who had worked for > 6 months exhaust and asbestos increasing exposure index, al. (1990) 

 in 1945-70. 20 deaths from according to industrial RR = 1.34 (1.09-1.64), 1.81 

 lung cancer identified (nested hygiene estimate; (1.20-2.71), 2.43 

 case-control study) duration of exposure (1.32-4.47) 

 based on company records 

 Cohort study of 107 563 US Usual occupation (truck SMR = 153 (23 cases) No cases among non-smokers, Walrath et al

 veterans alive in 1954 and driver) among people who had but SMR calculated from (1985) 

 followed-up to 1 January 1970 ever smoked; no statistics smoking-specific rates 

 given 

 994 male lung cancer deaths Longest job held: diesel OR = 1.55 (0.97-2.47) for Extent of actual exposure Steenland et

 in 1982-83 and 1085 controls truck driver, gasoline long-haul drivers with > 18 to diesel exhaust unknown al. (1990, 19

 (excluding lung cancer, truck driver, both years of employment; OR = 

 bladder cancer, accidents). types, truck mechanic, 1.89 (1.04-3.42) for diesel 

 Cases and controls from stevedore. Exposure truck drivers with > 35 

 Teamsters Union who had filed validated by industrial years of employment 

 claims (requires 20-year hygiene survey (adjusted for smoking) 

 tenure) 

 Retrospective cohort study of Cohort assumed to be Lung cancer: SMR = 168 No adjustment for smoking; Gustafsson et

 stevedores in Sweden first exposed on basis of job (136-207) for incidence; exposure assumptions not al. (1986) 

 employed before 1974 for a duties, but no formal SMR = 132 (105-166) for fully justified; no 

 continuous period of 6 months. assessment made mortality calculations done to explore 

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 6071 workers employed in 1961 employment time as a surrogate 

 with mortality determined for exposure 

 through 1980. 89 cases of 

 lung cancer noted in Swedish 

 Cancer Registry (71 deaths) 

 

 Table 39 (contd) 

 

 Population Exposure assessment Results Limitations Reference 

 

 Stevedores in Swedish Estimated from use of Adjusted for smoking Crude adjustment for Emmelin et al

 population defined by fuel in each port and (yes/no) depending on smoking; no industrial (1993) 

 Gustafsson et al. but limited years of work since use index of exposure used; hygiene data to validate 

 to workers in ports for which of diesel equipment exposure-response estimates of exposure to 

 data data on diesel fuel relationship noted, diesel exhaust 

 consumption were available. relative odds for medium 

 Case-control study with 50 exposure ranging from 1.5 

 cases of lung cancer detected to 2.7 and that for high 

 in 1960-82 matched to 154 exposure ranging from 2.9 

 controls on port and date of to 6.8. Lower limit of 90% 

 birth confidence interval < 1, 

 except for one 

 high-exposure category 

 

 RR, relative risk; OR, crude odds ratio; SMR, standardized mortality ratio; in parentheses, 95% confidence interval (CI), unless 

 otherwise stated 

 Three studies reported findings among bus garage workers. Waller 

 (1981) studied lung cancer occurrence among London Transport staff on 

 the basis of job category. Diesel buses were introduced in the 1930s, 

 gradually replacing gasoline-powered vehicles and, in the 1950s, 

 electric trolley-buses. Mortality from lung cancer was ascertained for 

 active workers aged 45-64 between 1950 and 1974. A lower risk was seen 

 for people in all job categories in comparison with the general 

 population of the London area, indicating a 'healthy worker effect'. 

 The highest SMR was seen for workers who had the most exposure to 

 diesel exhaust (bus garage engineers), although the SMR was not 

 significantly different in workers with no exposure. Although this 

 study showed no relationship between job category and mortality from 

 lung cancer, the study had significant limitations. No retired workers 

 were followed up, so that workers who would have had significant 

 exposure were excluded. Since the results were not presented on the 

 basis of years of work (years of exposure to diesel fumes), workers 

 with little exposure were grouped with those with long exposure, 

 making it more difficult to detect an effect of diesel exhaust. 

 Rushton et al. (1983) ascertained the mortality of 8490 London 

 Transport bus garage workers who had been employed for at least one 

 year between 1967 and 1975. One hundred job titles were grouped into 

 20 broad categories. The overall SMR for lung cancer was not elevated, 

 and there was no relationship with any job with exposure to diesel 

 exhaust; however, the SMRs were not presented on the basis of years of 

 work in a job with exposure, and the duration of follow-up was short, 

 with a mean of 5.9 years. 

 Using a nested case-control design, Gustavsson et al. (1990) 

 studied a cohort of 695 men who had worked in five bus garages in 

 Stockholm, Sweden, in 1945-70. Diesel-powered buses were first 

 introduced in Stockholm in the 1930s, and after 1945 all of the 

 internal combustion engines in buses were diesel-powered. No 

 measurements of exposure were available, so exposure to diesel exhaust 

 was estimated by industrial hygienists on the basis of garage 

 ventilation, work practices, and the number of buses in the garages 

 and was graded on a five-point scale, each increase corresponding to a 

 50% increase in intensity. An index of cumulative exposure to diesel 

 exhaust was calculated for each worker by multiplying the exposure 

 level for each work period by the duration in years. Past exposure to 

 asbestos was estimated on the basis of historical measurements of 

 asbestos fibres obtained during brake-repair operations. Twenty cases 

 of lung cancer were identified and matched by age to six controls. The 

 relative risk for lung cancer increased with increasing index of 

 exposure to diesel exhaust: That at the lowest exposure level was 1.34 

 (95% CI = 1.09-1.74), that at an intermediate level was 1.81 

 (95% CI = 1.20-2.71), and that at the highest level was 2.43 (95% 

 CI = 1.32-4.47). No such increase was observed with a similar index of 

 exposure to asbestos. No information was available on smoking. 

 Diesel-powered trucks were introduced in the United States in the 

 1950s and 1960s. Trucking companies had completed the transition to 

 diesel trucks by 1960, while independent drivers and non-trucking 

 companies would have completed the transition later. Steenland et al. 

 (1990, 1992) studied 994 deaths from lung cancer occurring in 1982 and 

 1983 among male members of the Teamsters Union who had filed claims 

 for pension benefits (requiring at least 20 years of membership). Work 

 histories and smoking histories were obtained from next-of-kin; job 

 categories were also available from the Union records. The odds ratio 

 for lung cancer among long-haul drivers, who drove mostly diesel 

 trucks, with 18 or more years of employment after 1959 was 1.55 (95% 

 CI = 0.97-2.47) after adjustment for age, smoking, and exposure to 

 asbestos. Teamsters with 35 years or more of employment whose main job 

 was a diesel truck driver had a relative risk for lung cancer of 1.89 

 (95% CI = 1.04-3.42). For drivers of gasoline trucks, the relative 

 risk was only 1.34 and did not achieve conventional levels of 

 significance (95% CI = 0.81-2.22). 

 In an industrial hygiene survey (Zaebst et al., 1991; Steenland 

 et al., 1992) that accompanied this study, measurements of elemental 

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 carbon were used to estimate exposure to diesel exhaust. The truck 

 drivers appeared to have received much of their current exposure to 

 diesel exhaust from background levels on the road rather than directly 

 from their engines. No historical measurements of exposure were 

 available. 

 Gustafsson et al. (1986) studied the mortality of 6071 stevedores 

 in Sweden who had been employed for at least six months between 1961 

 and 1974 through 1980. The stevedores had been exposed to both 

 gasoline and diesel exhausts; diesel-powered trucks were first used in 

 Swedish ports in the late 1950s, with a rapid increase in use in the 

 1960s. The SMR for lung cancer was 132 (95% CI = 105-166). The 

 year-specific lung cancer rates in the stevedores between 1961 and 

 1980 were greater than those in the Swedish male population. 

 In order to refine the assessment of exposure among the 

 stevedores and to adjust for smoking, a case-control study was 

 conducted in this cohort (Emmelin et al., 1993). Cases and controls 

 were selected from among male stevedores who had been employed for at 

 least six months in 1950-74; the cases were those occurring in 

 1960-82. On the basis of 50 cases and 154 controls, with adjustment 

 for smoking (yes/no), the odds ratio for lung cancer was seen to 

 increase with increases in three indices of exposure: years since 

 diesel equipment was used in the port, estimates of cumulative fuel 

 consumption, and years that fuel use was above a minimal level in the 

 port. The increases were consistent with an exposure-response 

 relationship. Only one of the point estimates of the odds ratios for 

 lung cancer reached statistical significance. 

 Table 40. Population- and hospital-based studies of lung cancer in groups exposed to diesel engine exhaust 

 

 Population Exposure assessment Results Limitations Referenc

 

 7518 (3539 men, 3979 Occupation determined OR = 1.52 for truck drivers Exposure estimate based on Williams

 women) incident invasive at interview (P > 0.05) self-reporting; not validated et al. 

 cancers from the Third 47% non-response; controls (1977) 

 National Cancer Survey. Lung consisted of other cancers, 

 cancer cases: 432 in men, probably diluting risk 

 128 in women. Combined other estimate; few cause-specific

 cancer sites used as cancers and individual 

 controls occupations 

 Cohort study of 107 563 US Usual occupation (truck SMR = 153 (23 cases) No cases in nonsmokers, Walrath

 veterans alive in 1954 and driver) among people who had but SMR calculated using et al. 

 followed-up to 1 January 1970 ever smoked; no statistics smoking-specific rates (1985) 

 589 cases of lung cancer Job title from next-of-kin Adjustment for smoking; No validation of exposure Damber &

 reported to the Swedish for occupations held for (0.6-2.2) for professional groupings, so actual exposure Larsson

 Cancer registry 1972-77 with > 1 year drivers (> 20 years of to diesel exhaust uncertain (1987) 

 death before 1979; 562 employment) with dead 

 matched dead controls (sex, controls; OR = 1.1 (0.6-2.2) 

 age, year of death, with living controls 

 municipality) drawn from 

 National Registry of Causes 

 of Death; matched living 

 controls (sex, year of birth, 

 municipality) drawn from 

 National Population Registry 

 

 Table 40 (contd) 

 

 Population Exposure assessment Results Limitations Referenc

 

 Montreal, Canada, Interview with subject; Adjustment for smoking; Job title used to indicate Siemiaty

 hospital-based cases and job title translated into OR = 1.2 for squamous-cell exposure to diesel exhaust; et al. 

 controls; 857 cases of lung likely exposure to lung carcinoma (90% CI, not validated; exposure (1988) 

 cancer and 1523 controls (other combustion products by 1.0-1.5) for any exposure ill-defined 

 cancers than lung) industrial hygienist but not elevated for other 

 cell types. No relationship 

 with years of exposure or 

 intensity 

 461 981 male volunteers Self-reported occupation Adjustment for smoking; Exposure information Boffetta

 enrolled in the American and exposure to diesel > 16 years' exposure to based on self-reporting; et al. 

 Cancer Society prospective exhaust diesel exhaust, OR = 1.21 not validated (1988) 

 mortality study in 1982; aged (0.94-1.56); for 1-15 years, 

 40-79 at enrolment; 2-year OR = 1.05 (0.80-1.39). 

 follow-up; 378 622 men with Lung cancer mortality also 

 known exposure to diesel elevated in miners and heavy 

 exhaust equipment operators 

 1260 cases of lung cancer Job title obtained from For motor vehicle drivers Crude classification of Benhamou

 and 2084 controls matched occupational history (adjusted for smoking), exposure et al. 

 for age, sex, hospital obtained at interview; OR = 1.42 (1.07-1.89); for (1988) 

 admission in France in 1976-80 exposure based on any all transport equipment 

 work in a job operators, OR = 1.35 

 (1.05-1.75). Increase in risk 

 with duration of employment 

 

 Table 40 (contd) 

 

 Population Exposure assessment Results Limitations Referenc

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 Pooled data from three Job title from interviews Smoking-adjusted OR = No validation of exposure Hayes 

 case-control studies with with subjects or 1.5 (1.1-1.9) for truck classification; unclear if et al. 

 2291 male lung cancer cases next-of-kin; years of work drivers with > 10 years of most exposure was to (1989) 

 and 2570 controls. Analysis in motor exhaust-related work and job history obtained diesel exhaust or if job 

 limited to 1444 cases and occupation calculated by direct interview. For all titles selected as 'exposed'

 1893 controls who provided motor exhaust-related were actually exposed to 

 information at interview occupations and > 10 years diesel exhaust 

 of work, OR = 1.5 (1.2-1.9) 

 Hospital-based study of 2584 Occupational titles and Smoking-adjusted OR for Exposure histories not Boffetta

 cases in 18 hospitals in six self-reporting of exposure occupations with probable validated et al. 

 US cities; 5099 controls exposure to diesel exhaust (1990) 

 = 0.95 (0.78-1.16). For 

 self-reported exposure, 

 OR = 1.21 (0.78-2.02) 

 Detroit, USA, area; 3792 Interview to obtain full For drivers of heavy trucks Exposure histories not Swanson

 cases and 1966 controls occupational history; with > 20 years of work, validated et al. 

 identified through cancer analysis by job title OR = 2.5 (1.4-4.4), with (1993) 

 surveillance system adjustment for smoking; 

 exposure-response 

 relationship with years of 

 work. For drivers of light 

 trucks with > 20 years of 

 work, OR = 2.1 (0.9-4.6) 

 

 OR, odds ratio; SMR, standardized mortality ratio; in parentheses, 95% confidence interval (CI), unless otherwise stated 

 (b) Population- and hospital-based studies 

 In a study of 107 563 American veterans who were alive in 1954 

 and were followed to the end of 1969, the SMR among smokers who 

 reported their occupation as truck or tractor driver was 153, based on 

 23 cases. Most of these individuals would have had little exposure to 

 diesel exhaust, however, since diesel trucks were introduced in the 

 United States only in the 1950s and 1960s (Walrath et al., 1985). 

 In the Third National Cancer Survey in the United States, 

 self-reporting of work as a truck driver and adjustment for smoking 

 resulted in an odds ratio of 1.52, which was not statistically 

 significant (Williams et al., 1977). In a study of 589 cases of lung 

 cancer reported to the Swedish Cancer Registry between 1972 and 1977 

 among people who had died before 1979, the odds ratio for > 20 years 

 of work as a professional driver was 1.2 (95% CI = 0.6-2.2) after 

 adjustment for smoking (Damber & Larsson, 1987). In a hospital-based 

 study of 857 cases of lung cancer and controls, occupational histories 

 obtained by interview were interpreted by an industrial hygienist. 

 After adjustment for smoking, the odds ratio for squamous-cell 

 carcinoma of the lung was 1.2 (90% CI = 1.0-1.5) in association with 

 any exposure to diesel exhaust (Siemiatycki et al., 1988). The 

 mortality of 378 622 men between 1982 and 1984 was analysed in the 

 American Cancer Society prospective study of cancer on the basis of 

 self-reporting of exposure to diesel exhaust. After adjustment for 

 age, smoking, and other occupational exposures, including asbestos, 

 coal-tar and pitch, and gasoline exhaust, the relative risk for lung 

 cancer for men with 16 years of exposure was 1.21 (95% CI = 

 0.94-1.56). For truck drivers who reported exposure to diesel exhaust, 

 the relative risk was 1.22 (95% CI = 0.77-1.95) (Boffetta et al., 

 1988). 

 In a study in France, 1260 male cases of lung cancer and 2084 

 controls matched on age and hospital were collected between 1976 and 

 1980; job titles and smoking histories were obtained by interview, and 

 odds ratios were calculated on the basis of any work in a particular 

 occupation. After adjustment for smoking, the odds ratios were 1.35 

 (95% CI = 1.05-1.75) for transport equipment operators and 1.42 (95% 

 CI = 1.07-1.89) for motor vehicle drivers. There was no increase in 

 risk with increasing years of work in a job, but details of the 

 analysis were not presented (Benhamou et al., 1988). 

 The data from three case-control studies carried out by the 

 American National Cancer Institute between 1976 and 1983 were pooled 

 in order to study lung cancer in people with occupations associated 

 with motor vehicles. The analysis was limited to 1444 male patients 

 with lung cancer and 1893 controls who provided information on smoking 

 and occupation at an interview. The odds ratio for lung cancer for 10 

 or more years of employment in any occupation related to exhaust from 

 either diesel or non-diesel engines was 1.5 (95% CI = 1.2-1.9), after 

 adjustment for age and smoking. In truck drivers, the odds ratio was 

 1.5 (95% CI = 1.1-1.9) (Hayes et al., 1989). 

 In a case-control study of patients with lung cancer in 18 

 hospitals in six American cities, 2584 cases seen between 1969 and the 

 late 1980s were matched to at least one control on the basis of age, 

 sex, hospital, and year of interview. A smoking history and usual 

 occupation were obtained by interview. After 1985, reports of 

 self-reported exposure to diesel exhaust were obtained for 477 lung 

 cancer patients and 946 controls. Exposure was graded as 'probable' if 

 the individual had usually worked on railroads (the specific job was 

 not used) or in a variety of jobs related to motor vehicles. For these 

 individuals, the odds ratio for lung cancer was 1.31 (95% CI = 

 1.09-1.57); for those reporting usual occupation as a truck driver, 

 the odds ratio was 1.31 (95% CI = 1.03-1.67). After adjustment for 

 cigarette use, age, race, and date of interview, however, the odds 

 ratios for lung cancer were reduced to 0.95 (95% CI = 0.78-1.16) for 

 individuals with probable exposure and 0.88 (95% CI = 0.67-1.15) for 

 truck drivers. For self-reported exposure to diesel exhaust, the odds 

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 ratio was 1.21, after adjustment for smoking, age, and other potential 

 confounding variables including exposure to asbestos, education, and 

 race, but did not achieve statistical significance (95% CI = 

 0.73-2.02) (Boffetta et al., 1990). 

 In a study of 3792 cases of lung cancer in men in Detroit, United 

 States, newly diagnosed in 1984-87, an occupational history and 

 information on smoking were collected by interview with the subject or 

 a surrogate. Controls were men with colon or rectal cancer. After 

 adjustment for smoking, the odds ratio for lung cancer was 2.5 (95% CI 

 = 1.4-4.4) among white men who had driven heavy trucks for 20 years 

 and 2.1 (95% CI = 0.9-4.6) for drivers of light trucks for 20 years. 

 There was a significant increase in the odds ratio for lung cancer 

 with increasing years of work for drivers of both types of truck 

 (Swanson et al., 1993). 

 (c) Registry-based, surveillance studies 

 Table 41 summarizes two studies in which information on exposure 

 was based on occupational titles obtained from censuses. No 

 information was available on smoking or on length of employment. Both 

 studies reported an elevated risk for lung cancer. Ahlberg et al. 

 (1981) found a relative risk of 1.33 (95% CI = 1.13-1.56) for 

 professional drivers, and Hansen (1993) found an SMR for all 

 respiratory cancer in truck drivers of 160 (95% CI = 128-198). 

 Table 41. Surveillance studies of lung cancer in groups exposed to diesel engine exhaust 

 

 Population Exposure assessment Results Limitations Reference 

 

 Swedish census-based cancer Listing of occupation in RR = 1.33 (1.13-1.56) No validation of exposure; Ahlberg et al.

 incidence registry; 154 cases census no adjustment for smoking (1981) 

 among professional drivers 

 Retrospective cohort study of Job title in census 84 cancers in truck drivers; No adjustment for smoking; Hansen (1993) 

 14 225 truck drivers in 1970; SMR =160 (128-198); information on specific 

 mortality determined until expected number based exposure or length of 

 1980. Referent group of persons on rates in referent employment 

 with no exposure to combustion population 

 products on basis of census 

 job title 

 

 RR, relative risk; SMR, standardized mortality ratio; in parentheses, 95% confidence interval 

 Table 42. Case-control studies of urinary bladder cancer in individuals with possible exposure to diesel exhaust 

 

 Population Exposure assessment Results Reference 

 

 Incident cases in 480 men Any exposure to diesel and Based on 15 cases and controls with discordant Howe et al. 

 and 152 women in three traffic fumes obtained at exposure histories, OR for exposure to diesel and (1980) 

 Canadian provinces, April interview traffic fumes = 2.8 (0.8-11.8); not adjusted for 

 1974-June 1976; each case smoking 

 matched by age and sex to 

 a neighbourhood control 

 Incident cases in 303 white Occupation and industry For any employment in trucking, RR = 2.2 (1.1-4.4) Silverman et a

 men in metropolitan Detroit, obtained at interview based on 28 cases and 13 controls. For any work in (1983) 

 USA, December 1977-November railroad and railway express services, RR = 1.9 

 1978; 2986 controls (0.9-3.8) based on 22 cases and 12 controls, not 

 selected by random-digit adjusted for smoking. For any employment as a truck 

 dialling but of same age driver (42 cases and 18 controls), adjusted for 

 distribution as cases smoking, RR = 2.1 (1.4-4.4). For > 10 years as truck 

 driver, smoking-adjusted RR = 5.5 (1.8-17.3), and for 

 truck drivers who ever drove vehicles with diesel 

 engines, smoking-adjusted RR = 11.9 (2.3-61.1). 

 Elevated risk for truck drivers with employment after 

 rather than before 1950, when diesel truck use became 

 more prevalent 

 

 Table 42 (contd) 

 

 Population Exposure assessment Results Reference 

 

 White residents of New Occupation and exposure For any employment as a truck driver (35 cases, 53 Hoar & Hoove

 Hampshire and Vermont, to diesel fuel or engines controls), OR = 1.5 (0.9-2.6), not adjusted for smoking. (1985) 

 USA, who died of bladder by next-of-kin Those employed 1930-49 had the highest OR (2.6; 

 cancer 1975-79 (on death 1.3-5.1) after adjustment for coffee drinking and 

 certificate) matched to one smoking. For 26 cases and 39 controls who reported 

 control with cause of death exposure to diesel fuel or engines, OR = 1.5 (0.8-2.8), 

 other than suicide, matched not adjusted for smoking. Significant trend for 

 on state, sex, race, and age, increased relative odds up to 39 years of exposure 

 and a second control with to diesel exhaust 

 same criteria but also matched 

 on county. Information obtained 

 for 325 cases and 673 controls 

 Cases in 512 men in Turin, Occupation obtained at In truck drivers, based on 16 cases and 16 controls, Vineis & 

 Italy, matched by age to 596 interview OR = 1.2 (0.6-2.5), not adjusted for smoking Magnani (198

 hospital controls without cancer 

 Cases in 194 men in 18 hospitals Usual occupation obtained; Only 16 cases in occupations with potential exposure Wynder et al

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 in six US cities, January likelihood of exposure to to diesel exhaust. ORs all < 1 for warehousemen, bus (1985) 

 1981-May 1983. Controls diesel exhaust determined and truck drivers, and heavy equipment operators. In 

 were persons hospitalized at on basis of estimates of railroad workers, based on two cases and one control, 

 the same time as the case but percentage of workers with OR = 2. For any exposure, with adjustment for smoking, 

 for diseases not related to potential exposure in that OR = 0.87 (0.47-1.58). For high exposure, OR = 1.68 

 cigarette smoking. Each case occupation: high exposure, (0.49-5.73), not adjusted for smoking 

 matched to three controls > 20% of workers; moderate 

 (total, 582) by age, race, year exposure, 10-19% of workers 

 of interview, and hospital of 

 admission 

 

 Table 42 (contd) 

 

 Population Exposure assessment Results Reference 

 

 1909 new cases in white men Occupation obtained at After adjustment for smoking, RR for men usually Silverman 

 from 10 metropolitan areas in interview working as a truck driver = 1.5 (1.1-2.0), based on 99 et al. (1986

 the USA, 1977-78. Up to two cases and 123 controls. For those ever employed as 

 controls (total, 3569) selected truck driver, increased risk with increasing years of 

 by random-digit dialling and employment; however, truck drivers first employed 

 matched for age and < 40 years since diagnosis had no increased risk. OR 

 geographic area with case for bus driver as usual occupation = 1.5 (0.6-3.9), 

 based on 9 cases and 13 controls, adjusted for smoking 

 Cases in 99 men in La Plata, Occupational history Based on 20 cases ever employed as a truck or railway Iscovich et 

 Argentina, matched on age to obtained at interview driver, RR = 4.31 (P < 0.05); reduced whenr (1987) 

 99 hospital controls without adjusted for smoking, but no details provided 

 cancer and 99 neighbourhood 

 controls 

 Cases in 371 men and women Occupational history After adjustment for age and sex, RR = 1.55 (1.06-2.28) Jensen et al

 in the Danish Cancer Registry. at interview any employment as a land transport worker; based (1987) 

 Controls (771) selected randomly on 51 cases and 73 controls. After adjustment for 

 from general population smoking, age, and sex, years of work as a land transport 

 worker, and years of work as a bus, taxi, or truck 

 driver significantly associated with increased risk 

 Deaths in 731 men in Ohio, Yearly listing of Work as a truck driver > 20 years, OR = 12 (P < 0.01), Steenland 

 USA, 1960-82, identified on occupation obtained from six cases and one control; for > 20 years as a railroad et al. (1987

 death certificates and city commercial directories worker, OR = 2.21 (P < 0.01), based on 22 cases, not 

 matched to six controls without adjusted for smoking 

 tumours of the urinary tract or 

 pneumonia on age, year of 

 death, and race 

 

 Table 42 (contd) 

 

 Population Exposure assessment Results Reference 

 

 Cases in 826 men and women Occupational history and For any exposure of men to exhausts, OR adjusted for Risch et al.

 diagnosed 1979-82 in exposure to 'exhausts' cigarette smoking = 1.16 (0.91-1.48). For men ever (1988) 

 Edmonton, Calgary, Toronto, obtained at interview exposed 8-28 years before diagnosis, OR = 1.21 

 and Kingston, Canada, (0.93-1.58). For men in jobs with any contact with 

 matched by age, sex, and diesel or traffic fumes 8-28 years before diagnosis, 

 area of residence to 792 adjusted for smoking, OR = 1.69 (1.24-2.31); 

 randomly selected population significant trend with increasing years of exposure 

 controls 

 Cases in 486 men and women Interview with subject; After adjustment for smoking, OR = 1.0 (90% CI, Siemiatycki

 in Montreal, Canada, hospitals job title translated into 0.8-1.2) for any exposure to diesel exhaust, based et al. (1988

 and 2196 controls with likely exposure to on 82 cases with exposure 

 diseases other than lung combustion products by 

 or kidney cancer industrial hygienists 

 Cases in 136 men in 18 Usual occupation and For any exposure, OR = 1.24 (0.77-2.00), based on Iyer et al.

 hospitals in six US cities. self-reporting of exposure 41 cases, with adjustment for smoking (1990) 

 Two controls without to diesel exhaust obtained 

 tobacco-related diseases matched at interview; grouped into 

 to each case on age (< 2 years), probable and possible 

 race, hospital, and year of exposure 

 interview 

 

 Table 42 (contd) 

 

 Population Exposure assessment Results Reference 

 

 256 cases and 287 controls in Job titles for all jobs held For any exposure to diesel exhaust, RR = 1.7 Steineck et al

 population-based study of all obtained by postal (0.9-3.3), based on 25 cases and 19 controls, adjusted (1990) 

 urothelial cancer in Stockholm, questionnaire; industrial for year of birth and smoking. For subjects considered 

 Sweden, 1985-87, among hygeienists reviewed titles to have moderate or high exposure, RR = 1.1 (0.3-4.3), 

 men born 1911-45 and categorized subjects as but based on only four cases and five controls 

 exposed to various 

 substances 

 Cases in 658 men in seven Interview with subject; job After adjustment for smoking, OR for work in road Cordier et al.

 French hospitals, 1984-87, title and duties translated transport = 1.02 (0.62-1.69), based on 36 cases and (1993) 

 matched for age, race, and into likely exposure to 35 controls. For stevedores, OR = 1.31 (0.87-1.98); 

 place of residence to 658 diesel exhaust by industrial for material-handling equipment operator, OR = 7.67 

 controls selected randomly hygienists (0.96-61.4); and for transport equipment operators, 

 among patients admitted OR = 0.88 (0.62-1.26). For diesel fumes, OR = 0.99 

 for diagnoses other than (0.32-3.03), based on seven cases and two controls 

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 cancer 

 Cases in 153 men in one Occupational history For any work as a road transport worker, Notani et al.

 hospital in Bombay, India, obtained at interview smoking-adjusted OR = 1.36 (0.5-3.7), based on eight (1993) 

 1986-90, matched by age to cases and nine controls 

 212 controls with oral or 

 pharyngeal cancer or benign 

 oral disease 

 

 OR, odds ratio; RR, relative risk; in parentheses, 95% confidence interval (CI), unless otherwise stated 

 B8.2.3.2 Urinary bladder cancer 

 Fifteen case-control studies of urinary bladder cancer in 

 relation to presumed exposure to diesel exhaust are summarized in 

 Table 42. The limitation of all of these studies is that exposure to 

 diesel exhaust was not clearly characterized. Howe et al. (1980) used 

 any self-reported exposure to fumes that included diesel fumes, while 

 Hoar & Hoover (1985) used reports by next-of-kin of work with any 

 diesel fuel or engines or work as a truck driver. Risch et al. (1988) 

 obtained a history of exposure to exhaust by interview. Wynder et al. 

 (1985) estimated the likelihood of exposure to diesel exhaust during a 

 worker's lifetime on the basis of usual occupation, obtained at 

 interview, and attempted to divide exposure into high and moderate. In 

 a later study, self-reported exposure to diesel exhaust was recorded 

 (Iyer et al., 1990). Silverman et al. (1983), Vineis & Magnani (1985), 

 Silverman et al. (1986), Jensen et al. (1987), Iscovich et al. (1987), 

 and Notani et al. (1993) based their analyses of the risk for bladder 

 cancer on employment in an occupational category with a high 

 likelihood of exposure to diesel exhaust, such as truck driver, 

 railroad worker, transport worker, bus driver, and other related 

 occupations. In the studies of Siemiatycki et al. (1988) and Steineck 

 et al. (1990), occupational histories were reviewed by industrial 

 hygienists to link occupational titles to possible exposure. Cordier 

 et al. (1993) also used expert review of occupational histories to 

 estimate exposure to diesel exhaust on the basis of job title, but 

 additionally examined specific job titles. Furthermore, exposure was 

 usually assumed to have occurred if the person had ever been employed 

 in an occupation or had ever been exposed to diesel exhaust or other 

 fumes. Silverman et al. (1983, 1986) and Jensen et al. (1987) used 

 self-reported years of work as a truck driver. Self-reporting of 

 exposure poses a potential problem of differential recall among cases 

 and controls, as cases may recall exposure to diesel fumes or work in 

 a diesel-exposed job more readily than controls. Steenland et al. 

 (1987) used city directories listing occupation to obtain independent 

 occupational histories. 

 As the available occupational histories were crude, it was also 

 difficult to assess latency or duration of exposure. Silverman et al. 

 (1983) found that the relative risk (adjusted for smoking) was 5.5 

 (95% CI = 1.8-17.3) for truck drivers with 10 or more years of work 

 experience and 11.9 (95% CI = 2.3-61.1) for those with a history of 

 driving vehicles with diesel engines. Truck drivers employed after 

 1950, when diesel truck use became prevalent, had the highest risk. In 

 a later, larger study (Silverman et al., 1986), men who usually worked 

 as a truck driver or deliveryman had a relative risk of 1.5 (95% CI = 

 1.1-2.0), adjusted for smoking. The risk increased with increasing 

 years of work; however, truck drivers who had started work fewer than 

 40 years before diagnosis, who would have driven primarily diesel 

 engines, did not have an increased risk for bladder cancer. Hoar & 

 Hoover (1985) also noted increased relative odds with increasing years 

 of employment in jobs with reported exposure to diesel exhaust. 

 An additional limitation of the 15 case-control studies is that 

 results indicating an effect of presumed exposure to diesel exhaust or 

 a specific occupation are based on relatively few cases and controls, 

 even when conventional levels of statistical significance were 

 achieved. The study of Silverman et al. (1986), in which exposure was 

 defined as working as a truck driver or deliveryman, had the largest 

 number of exposed individuals (99 cases and 123 controls). Four 

 additional cohort studies not listed in the table (Howe et al., 1983; 

 Rushton et al., 1983; Schenker et al., 1984; Boffetta et al., 1988), 

 which were designed mainly to examine lung cancer and exposure to 

 diesel exhaust, also had too few cases of bladder cancer on which to 

 base meaningful conclusions. One cohort study of Danish bus drivers 

 (Netterstrom, 1988) showed an elevated SMR of 153, which was of 

 borderline statistical significance (95% CI = 91-217), but this result 

 was based on 13 cases. 

 Misclassification of exposure to diesel exhaust would hide any 

 increase in risk for bladder cancer, since many unexposed individuals 

 would be included with those classified as exposed. Diesel exhaust is 

 responsible for most of the respirable particles in mixed vehicle 

 exhausts, and exposure to respirable particles with adsorbed PAHs is 

 presumed to result ultimately in an increased risk for bladder cancer 

 due to metabolic transformation and urinary excretion of carcinogens. 

 The risk for bladder cancer is also increased in cigarette smokers and 

 in workers exposed to dyes containing aromatic amines (Ruder et al., 

 1990). Coffee has been suggested to be a risk factor for bladder 

 cancer but has not been clearly implicated (Howe et al., 1980). The 

 classification of exposure to diesel exhaust is sufficiently crude in 

 the papers summarized in Table 42, however, that even when smoking was 

 considered, the effect of other, unmeasured confounding exposures 

 cannot be excluded. The actual contribution of diesel exhaust to an 

 increased risk of bladder cancer is uncertain, even when an effect of 

 presumed exposure was noted (Silverman et al., 1983; Hoar & Hoover, 

 1985; Silverman et al., 1986; Iscovich et al., 1987; Steenland et al., 

 1987). Although the literature suggests that truck drivers have an 

 increased risk for bladder cancer, the specific exposure responsible 

 has not been determined. 

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 B9. EFFECTS ON OTHER ORGANISMS IN THE LABORATORY AND THE FIELD

 Virtually no data are available relating specifically to the 

 effects of diesel fuel exhaust emissions. 

 The growth and photosynthesis of liquid cultures of the green 

 alga Chlamydomonas reinhardtii were examined after incubation with 

 iso-octane extracts of diesel particulate exhaust containing 51 

 compounds (mainly polynuclear aromatic ketones and pure PAHs) 

 identified by gas chromatographic-mass spectrometric analysis. At 

 concentrations up to 0.125% by volume, dose-dependent growth 

 retardation of the algae was observed. Higher concentrations (no 

 details given) caused death. The algae adapted to sublethal 

 concentrations of the extract over a period of several days; 

 thereafter, toxic extracts at concentrations up to 2.5% by volume 

 affected neither growth nor photosynthesis. It was noted that the 

 amounts of certain components decreased during incubation, suggesting 

 uptake into the cells (Liebe & Fock, 1992). 

 B10. EVALUATION OF HUMAN HEALTH RISKS AND EFFECTS ON THE ENVIRONMENT

 Hundreds of chemical compounds are released during the combustion 

 of diesel fuel. The characteristics and amount of exhaust depend on 

 the type of diesel engine, its operating conditions and adjustment, 

 and the composition of the fuel. The following evaluation focuses 

 mainly on the risks to human health associated with exposure to diesel 

 particulate matter, since the large amount of soot particles emitted 

 is the main characteristic of diesel exhaust. 

 In general, the risk assessment paradigm proposed by the National 

 Academy of Sciences of the United States (US National Reserach 

 Council, 1983) will be followed. The four steps in this process are: 

 hazard identification, dose-response assessment, exposure assessment, 

 and risk characterization. The outcome of these individual steps is 

 critical for taking risk management decisions, including setting 

 exposure standards that have consequences for public health, and for 

 social, economic, and political issues. 

 The epidemiological studies in humans and the studies in 

 experimental animals considered useful for human health risk 

 assessment are discussed in this section. Both carcinogenic and other 

 effects are considered, but a threshold is assumed to exist only for 

 non-cancer effects. An IPCS method for deriving health-based guidance 

 exposure limits provides further details (IPCS, 1993). 

 B10.1 Exposure of the general population 

 The exposure of the general population to diesel exhaust varies 

 with proximity to diesel-powered vehicles. For example, higher levels 

 of diesel exhaust constituents are present in busy streets and parking 

 areas than in rural areas. The concentrations of the main gaseous 

 components resulting from diesel exhaust can be estimated from 

 specific emission factors, the contribution of diesel vehicles to 

 total traffic, and atmospheric dispersion models. As assumptions are 

 necessary to attribute the emissions of the gaseous components to 

 diesel sources, the validity of such estimates is considered to be 

 limited. 

 On a global basis, the contribution of diesel exhaust to the 

 total emissions of particulate matter varies widely, depending on the 

 percentage of diesel vehicles in the total volume of traffic, 

 maintenance of individual engines, fuel quality, and emission control 

 techniques. Such factors also lead to wide local variations in the 

 concentrations to which humans are exposed. 

 Measurements and calculations of ambient concentrations of diesel 

 particulates near roads provide a daily average range of 8-42 μg/m3. 

 The estimated annual average concentrations in Germany are 5-10 μg/m3

 in urban areas and 1.5 μg/m3 in rural areas, and those in the United 

 States are 1-2 μg/m3 in urban areas and 0.6-1 μg/m3 in rural 

 areas. As the proportion of diesel vehicles is smaller in the United 

 States than in Europe, the concentrations in 1990, estimated from 

 national averages, were 2.0 μg/m3 in an urban area and 1.1 μg/m3

 in a rural area, with predictions of 1.2 g/m3 for urban areas and 

 0.6 μg/m3 for rural areas in 1995. 

 Diesel particulates form part of the fine particle range 

 (< 2.5 μm diameter). The average concentration of this fraction of 

 suspended particulate matter as a whole, measured in six cities in the 

 United States during 1979-85, was 11-30 μg/m3 or, in terms of 

 inhalable particles (<10-15 μm diameter; equivalent to particulate 

 matter with a diameter < 10 μm [PM10]), 18-46 μg/m3 (Dockery et 

 al., 1993). In these locations, diesel particulates probably 

 represented less than 10% of the suspended particulates measured as 

 PM10; considerably higher proportions were found in London and other 

 large cities in the United Kingdom on the basis of data on emissions 

 (Quality of Urban Air Review Group, 1993), but few data are available 

 that are related directly to ambient concentrations of the diesel 

 component. The one experimental study that has been reported (Horvath 

 et al., 1985), carried out in Vienna, Austria, using chemically 

 labelled fuel, yielded a value for the background concentration of 

 diesel particulates within the city of 11 μg/m3. 

 B10.2 Occupational exposure 

 Occupational exposure to airborne diesel particulate matter has 

 been well determined for only two occupational groups, railroad 

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 workers (Howe et al., 1983; Garshick et al., 1987, 1988) and workers 

 in the trucking industry (stevedores, local and road truck drivers, 

 and mechanics) (Emmelin et al., 1993). The levels of exposure during 

 work shifts are about 51-192 μg/m3 for railroad workers exposed to 

 diesel locomotive exhaust, roughly 25 μg/m3 for truck drivers, and 

 156 μg/m3 for stevedores (assuming that elemental carbon represented 

 20% of respirable particulate). These levels would be expected to vary 

 with the amount of ventilation available. Exposure to diesel exhaust 

 can also vary over a worker's lifetime, even within the same job. In 

 the railroad industry, exposure to diesel exhaust was greater in the 

 years after the introduction of diesel equipment. Reports of working 

 conditions in the 1950s and 1960s in diesel repair shops cited 'smoky' 

 atmospheres that were probably related to use of diesel equipment and 

 poor ventilation (Woskie et al., 1988b). No direct information is 

 available that allows reconstruction of accurate levels of past 

 exposure. 

 Reports of concentrations of diesel exhaust in other industries 

 are not accurate because of the presence of other dusts, although 

 attempts have been made to measure the contribution of diesel exhaust 

 (Daniel, 1984; Lehmann et al., 1990). Even for American railroad 

 workers (Woskie et al., 1988a), the contribution of other dusts could 

 not be determined, although cigarette smoke particulate was taken into 

 consideration. Consequently, the concentrations of diesel exhaust 

 reported in some jobs on railroads where other dusts (such as sand) 

 were present might have been lower. 

 B10.3 Non-neoplastic effects 

 B10.3.1 Hazard identification 

 B10.3.1.1 Humans 

 Diesel exhaust contains gases that irritate the nose, throat, and 

 eyes. It also contains particles which, together with the gases, can 

 cause airway irritation. Diesel exhaust may be recognized by its 

 characteristic odour. After acute exposure, it may induce mucous 

 membrane irritation, headache, and light-headedness. When volunteers 

 were exposed to diesel exhaust with an estimated particle 

 concentration of 100 μg/m3 for 1 h, several indicators of an 

 inflammatory response were observed in bronchioalveolar lavage fluid 

 (see section B8.2.1). In a well-conducted study on diesel-bus garage 

 workers, those with the highest exposures to respirable particulate 

 (> 0.31 mg/m3) reported significantly more cough, itchy or burning 

 eyes, headache, and wheeze, after adjustment for age and smoking, than 

 people with lower exposure. The contribution of diesel exhaust to the 

 respirable particulate is not known. Exposure to nitrogen dioxide at 

 > 0.3 ppm also resulted in more eye irritation and wheeze. Studies of 

 exposure indicate, however, variability in the ability of individuals 

 to detect the odour and the irritating effects of diesel exhaust. 

 Several cases of persistent asthma and asthma attacks have been 

 reported after acute exposure. 

 No consistent change in pulmonary function has been reported over 

 a work shift, although in one study of ferry workers, a decline in FVC 

 and FEV1 was noted. Specific measurements of diesel exhaust are 

 lacking in these studies, although total dust and respirable dust were 

 sometimes measured. Cases of persistent asthma have been reported in 

 railroad workers acutely exposed to apparently high levels of whole 

 exhaust, but the mechanism is unknown. 

 Studies of the possible chronic effects of exposure on 

 respiratory parameters are limited to occupational cohorts who are 

 still at work and thus have relatively short durations of exposure. 

 Such cohorts are likely to be healthier than older cohorts, which 

 include retirees who had longer exposure. Although excess respiratory 

 symptoms and reduced pulmonary function have been reported in some 

 studies, it is not clear whether these are long-term effects of 

 exposure. 

 B10.3.1.2 Experimental animals 

 Long-term studies in laboratory animals are described in section 

 B7.3. Many end-points were measured in the respiratory system of 

 several species of rodent after two or more years of exposure and at 

 several intermediate times. Adverse effects were seen after a 

 sufficient particle load had accumulated in the lung; and the 

 appearance of the effects is determined by both the concentration and 

 the duration of exposure. The results of these studies illustrate the 

 response of the respiratory tract in terms of biochemistry, 

 histopathology, cytology, pulmonary function, inflammation, and 

 clearance of particles. Early events in the pathogenesis of this 

 response include phagocytosis of inhaled particles. As the lung burden 

 increases, particle-filled macrophages are observed in the alveoli. At 

 lung burdens associated with particle overload, migration of these 

 macrophages out of the lung appears to be inhibited, and an early 

 event in the development of lung damage is the accumulation and 

 aggregation of clusters of particle-filled macrophages. Degeneration 

 of macrophages is observed, and the numbers of macrophages and 

 neutrophils in the alveolar and interstitial spaces increase. 

 Damage to the alveolar epithelium in areas surrounding these 

 macrophage clusters includes cell damage and proliferation. 

 Biochemical changes are seen in lavage fluid and lung tissue. The 

 alterations to particle-filled macrophages result in decreased 

 function and impaired particle clearance, the latter leading to a more 

 rapid increase in the lung burden of particles. Late effects include 

 inflammatory and proliferative responses, leading to fibrotic 

 responses. The sequence of these events has not been distinguished 

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 clearly in experimental work; they are likely to be interrelated and 

 to occur, to some extent, concurrently. 

 The possible mechanism of action of diesel exhaust (discussed in 

 section B7.9) includes a role of the gas phase, as opposed to the 

 particle phase, in causing lung damage. The non-carcinogenic toxicity 

 of diesel exhaust is considered to be due to the particle content, 

 since no effects are seen in rodents exposed to diesel exhaust that 

 has been filtered to remove particulate matter. Another issue in the 

 dosimetry of diesel exhaust is the role of the insoluble carbon core 

 in relation to that of the adsorbed organic material. As discussed in 

 section B7.9, studies that show similarities in non-carcinogenic 

 responses to exposure to diesel exhaust and to carbon particles 

 without an organic component indicate a role of long-term retention of 

 the insoluble carbon core. 

 B10.3.2 Dose-response assessment 

 B10.3.2.1 Epidemiological studies 

 Variability in the reporting of odour and irritation indicates 

 that a subsegment of the population is sensitive to diesel exhaust; 

 however, the proportion of the population with this characteristic 

 cannot be estimated. Chronic effects have not been seen in 

 occupationally exposed people, but excess respiratory symptoms have 

 been reported after acute exposure. It is not possible to determine 

 the dose of diesel exhaust (on the basis of exposure to gas or 

 particles) that produces these symptoms. 

 B10.3.2.2 Studies in experimental animals 

 In order to select the pivotal study for establishing the NOAEL 

 or uncertainty factor, the most sensitive, relevant studies must be 

 identified. All of the long-term studies focus on effects on the 

 respiratory tract, which are clearly those most relevant. Studies of 

 relatively low concentrations are listed in Table 43, which gives the 

 target and actual exposure concentrations, the equivalent continuous 

 exposure of the animal, the equivalent continuous human exposure, and 

 the effect level. The equivalent continuous exposure of animals is 

 calculated by multiplying the actual exposure concentration by the 

 (number of hours of daily exposure/24) and by the (number of days per 

 week of exposure/7). This value is necessary for comparing exposure 

 concentrations among studies with different protocols, i.e. different 

 numbers of hours of exposure per day and/or days per week. 

 The equivalent continuous human exposure is calculated from the 

 particle deposition-clearance model of Yu & Yoon (1990), discussed in 

 section B6.2. This model is based on studies of rats since only those 

 studies provide data on the exposure-response relationship for 

 inhibition of particle clearance. 

 The model of Yu & Yoon (1990) is a sophisticated approach to 

 defining the relationship between the inhaled concentration and the 

 dose in lung tissue. It combines detailed models of rat and human lung 

 structure, aerodynamic models of the air flow in the airways, particle 

 deposition dynamics, and information on clearance of particles from 

 rat and human lung. The model is specific to diesel particles because 

 the characteristics of the particles used in the model are derived 

 from studies of diesel particles and because the information on lung 

 clearance is based on studies of diesel exhaust in rats. The model has 

 been adapted for diesel exhaust particles by allowing evaluation of 

 the insoluble carbon core and of the tightly and loosely bound organic 

 compounds separately. Values for deposition and clearance are combined 

 with input from experimental studies to calculate the burden of 

 particles in the lungs of the animals at the end of the study. The 

 continuous concentration that would result in the same lung burden in 

 humans is then calculated, as the mass of particles per unit of 

 alveolar surface area or unit of lung weight. This lung burden is 

 assumed to result in a similar effect in humans and in rats. With 

 these considerations, the equivalent human concentrations are 

 predicted on the basis of the assumption that the retained particle 

 mass per unit alveolar surface area is the appropriate dose measure 

 for extrapolation between species. The effect level used in the risk 

 assessment is based on an evaluation of the adversity of the effect. 

 For the purposes of risk characterization, the NOAEL or, if that 

 is not available, the LOAEL for the critical effect is related to 

 exposure. The critical effect is the first adverse effect that appears 

 when the critical concentration is reached at the target site. A 

 decision about whether an effect is critical is a matter of expert 

 judgement. An adverse effect is defined as a change in morphology, 

 physiology, growth, development, or the life span of an organism which 

 results in impairment of functional capacity or of capacity to 

 compensate for additional stress or an increase in susceptibility to 

 the harmful effects of other environmental influences (International 

 Union for Pure and Applied Chemistry, 1993). 

 The NOAEL is defined as the greatest concentration or amount of a 

 substance, found by experiment or observation, that causes no 

 alteration in morphology, functional capacity, growth, development, or 

 the life span of target organisms that are distinguishable from those 

 observed in normal (control) organisms of the same species and strain 

 under the same defined conditions of exposure (International Union for 

 Pure and Applied Chemistry, 1993). 

 The LOAEL is defined as the lowest concentration or amount of a 

 substance, found by experiment or observation, that causes an adverse 

 alteration in morphology, functional capacity, growth, development, or 

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 the life span of a target organism distinguishable from those of 

 normal (control) organisms of the same species and strain under 

 defined conditions of exposure (International Union for Pure and 

 Applied Chemistry, 1993). 

 Table 43. Exposure of experimental animals, equivalent continuous human exposure, and effect levels of long-term inhalation in studi

 of rats described in section B7.3 

 

 Length of End-points Target Actual Equivalent Equivalent Effect Study 

 exposure evaluateda exposure exposure continuous continuous levelb

 (mg/m3) (mg/m3) animal exposure human exposure 

 (mg/m3) (mg/m3) 

 

 7 h/d, HP, LL, 0.35 0.353 0.0735 0.042 N Mauderly 

 5 d/week, LTB, TC, 3.5 3.47 0.723 0.360 A et al. (1987) 

 30 months LB 7 7.08 1.47 0.582 A 

 Light-duty, HP 0.1 0.11 0.063 0.038 N Ishinishi 

 16 h/d, 0.4 0.41 0.23 0.139 N et al. (1986, 

 6 d/week, 1 1.18c 0.67 0.359 A 1988) 

 30 months 2 2.32 1.3 0.571 A 

 Heavy-duty, HP 0.4 0.46 0.26 0.155 N Ishinishi 

 16 h/d, 1 0.96 0.55 0.303 A et al. (1986, 

 6 d/week, 2 1.84 1.05 0.493 A 1988) 

 30 months 4 3.72 2.13 0.911 A 

 110 h/week, HP 0.25 0.258 0.17 NA N Barnhart 

 6 months 0.75 0.796 0.52 NA A et al. (1981) 

 1.5 1.53 1.0 NA A 

 7 h/d, HP, SB 2 1.95 0.57 0.336 A Lewis et al. 

 5 d/week, (1989) 

 24 months 

 

 Table 43 (contd) 

 

 Length of End-points Target Actual Equivalent Equivalent Effect Study 

 exposure evaluateda exposure exposure continuous continuous levelb

 (mg/m3) (mg/m3) animal exposure human exposure 

 (mg/m3) (mg/m3) 

 

 19 h/d, HP, LL, 4 4.24 2.40 1.02 A Heinrich et 

 5 d/week, TC, LB al. (1986a) 

 32 months 

 18 h/d, HP, LL, 0.8 0.84 0.45 0.23 A Heinrich et 

 5 d/week, TC, LB 2.5 2.50 1.34 0.59 A al. (1995) 

 30 months 7.5 6.98 3.74 1.56 A 

 

 NA, not available (guinea-pigs were used) 

 a HP, histopathological examination; LL, lung lavage fluid; LTB, lung tissue biochemistry; TC, tracer clearance; SB, serum biochemistry;

 LB, lung burden 

 b N, no effect; A, adverse effect 

 c According to Suzuki et al. (1990), 1.08 mg/m3

 The selected NOAEL is divided by uncertainty factors to account 

 for data gaps. For these data, uncertainty exists in two areas: 

 extrapolation from animals to humans and accounting for sensitive 

 subpopulations. The factor for accounting for sensitive subpopulations 

 is a default value of 10, as it is considered that there are no data 

 suggesting a different factor. An additional default value of 10 is 

 usually applied for interspecies extrapolation, which is nominally 

 considered to consist of 100.4 (2.5) for toxicodynamics and 100.6 

 (4.0) for toxicokinetics (IPCS, 1994). 

 The LOAELs and NOAELs are selected on the basis of the following 

 reasoning. The LOAEL is the lowest level at which adverse effects are 

 seen in studies of adequate quality. The NOAEL, the highest level at 

 which no effect is seen in the available studies, must be lower than 

 the selected LOAEL. The LOAELs and NOAELs are identified by a 

 comparison with the equivalent continuous human exposure level. The 

 LOAELs in these studies are strikingly similar, with values of 0.360, 

 0.359, 0.303, 0.336, and 0.23 mg/m3 in studies from the Inhalation 

 Toxicology Research Institute (United States; Mauderly et al., 1987), 

 the Health Effects Research Program on light- and heavy-duty diesel 

 engine exhausts (Japan; Ishinishi et al., 1986, 1988), the National 

 Institute for Occupational Safety and Health (United States; Lewis et 

 al., 1989), and the Fraunhofer Institute for Toxicology and Aerosol 

 Research (Germany; Heinrich et al., 1986a, 1995), respectively (see 

 Table 43). The consistency of these levels of effect, in view of the 

 diversity of end-points represented, gives a high level of confidence 

 in the end-points. 

 The study at the Inhalation Toxicology Research Institute was 

 selected as the most representative because it covers the greatest 

 variety of end-points, including histopathology, bronchiolar lavage 

 biochemistry and cytology, lung tissue biochemistry, and particle 

 clearance; LOAELs were observed for all of these end-points. The 

 studies of the Health Effects Research Program showed a similar LOAEL 

 but only for histological changes in the lung. The value for 

 equivalent continuous human exposure is not available from the study 

 carried out by the General Motors Corporation (Barnhart et al., 1981) 

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 because the main results were for guinea-pigs; although rats were 

 included in the study, detailed results were not presented. The 

 appropriate NOAEL in these studies is not selected on the basis of the 

 LOAEL. As close dosing intervals were used in the studies of of the 

 Health Effects Research Program, the NOAEL was selected on the basis 

 of studies of light-duty diesel engines, as 0.139 mg/m3. 

 B10.3.3 Exposure assessment 

 Exposure to diesel exhaust is discussed in sections B10.1 and 

 B10.2. 

 B10.3.4 Risk characterization 

 B10.3.4.1 Humans 

 A quantitative assessment of the risk for humans of 

 non-carcinogenic effects of exposure to diesel exhaust cannot be made 

 on the basis of studies in humans. A substantial volume of literature 

 shows an association between acute exposure to fine particulates and 

 morbidity and mortality in the general population. It is somewhat 

 uncertain whether there is a direct causal link and, if so, whether it 

 is related to a specific component of the suspended particulates. 

 Attention has been focused on fractions of suspended particulate 

 matter, currently measured as PM10 (diameter < 10 μm) or PM2.5

 (diameter < 2.5 μm), comprised mainly of diesel particulates in the 

 submicrometre range, which represent an increasing proportion in some 

 countries. There is also evidence that exposure to particulates is 

 involved in respiratory symptoms and in mortality from certain chronic 

 respiratory conditions. 

 B10.3.4.2 Experimental animals 

 Three approaches were used in assessing the risk for 

 non-carcinogenic effects of exposure to diesel exhaust, on the basis of 

 exposure (dose)-response assessment in experimental studies (see 

 section B10.3.2.2), and for deriving guidance values for exposure. 

 Approaches 1 and 2 are based on the NOAEL from studies in rats. The 

 difference between the two is that approach 1 involves a dosimetric 

 extrapolation model (Yu & Yoon, 1990) for converting the actual 

 concentration to which animals were exposed to an equivalent 

 continuous human exposure, thereby reducing the uncertainty in 

 interspecies extrapolation. 

 In approach 2, no dosimetric conversion is performed but the 

 usual uncertainty factors for interspecies and intraspecies 

 extrapolation are applied. In contrast to these NOAEL-defined 

 approaches, approach 3 is based on the principle of the 'benchmark 

 dose', in which a concentration of exposure to diesel exhaust is 

 derived from dose-response relationships observed in rats. 

 The model of Yu & Yoon (1990) takes into consideration the 

 specific characteristics of particle deposition and retention in rat 

 and human lung. Application of the model to studies of inhalation in 

 experimental animals is shown schematically in Figure 4. The deposited 

 and retained doses in the lung are calculated from the concentrations 

 in rats and expressed per unit lung weight or per unit alveolar 

 surface area. Under the assumption that the retained dose per lung 

 will lead to the same effect in rodent and human lung, a human 

 equivalent concentration can be calculated (as shown in Table 43), to 

 obtain an equivalent continuous human exposure. The equivalent 

 continuous exposure of animals shown in Table 43 was derived either by 

 calculating the continuous exposure at which the lung burden attained 

 in a study by inhalation (if measured) would have been reached, or by 

 calculating the lung burden in rats at the end of exposure on the 

 basis of the actual exposure parameters (also shown in Table 43) and 

 then calculating as above. The correlation between continuous exposure 

 in animals and humans in the model of Yu & Yoon (1990), assuming that 

 overload induces prolonged lung clearance, is shown in Figure 5. Use 

 of this approach, rather than simple adjustment of discontinuous to 

 continuous exposure by the c x t constant used in other assessments, 

 should reduce the uncertainty associated with the transformation. 

 Approach 1. The NOAEL of 0.41 mg/m3 from the study in rats 

 exposed by inhalation to light-duty engine exhaust (Ishinishi et al., 

 1986, 1988; Table 43) is converted to an equivalent continuous 

 exposure of 0.23 mg/m3 in rats and then to an equivalent continuous 

 exposure of 0.139 mg/m3 , assumed to be the NOAEL in humans. 

 Application of a sophisticated dosimetric model decreases the 

 uncertainty in interspecies extrapolation from 10 to 100.4 (IPCS, 

 1994). Application of the usual uncertainty factor of 10 for 

 intraspecies differences results in a total uncertainty factor of 

 10 × 100.4 = 25. 

 The guidance value derived from this approach is 

 0.139 mg/m3 = 5.6 μg/m3. 

 --------------- 

 25 

 No additional correction factor is required, resulting in a guidance 

 value (for the general population) of 5.6 μg/m3. 

 The inherent uncertainties in the dosimetric model are due to the 

 assumptions that must be made. A principal assumption is necessary to 

 estimate inhibition of clearance in humans, since data on this aspect 

 do not exist. It is assumed that clearance in humans is inhibited at 

 the same lung burden (mass per alveolar surface area) as in rats. The 

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 other principal assumption is that the correct dose measure for lung 

 damage is mass of particle core per alveolar surface area. Since the 

 damage is localized to specific areas, another measure may be more 

 appropriate. 

 

 Approach 2. In this approach, the equivalent continuous animal 

 exposure based on the NOAEL of 0.41 in rats (light-duty diesel 

 exhaust; Ishinishi et al., 1986, 1988; Table 47) is used to derive the 

 guideline value. Because the dosimetric model is not used, the default 

 value of 10 is applied for interspecies uncertainty and an uncertainty 

 factor of 10 is added for intraspecies differences. The guidance value 

 obtained with this approach is 

 0.23 mg/m3

 ------------- = 2.3 μg/m3

 100 

 Approach 3. An alternative to using the NOAEL is to derive a 

 'benchmark dose', as described by Crump (1984). In studies by 

 inhalation, the concentration rather than the dose is considered to be 

 more precise, and the 'benchmark concentration' is used. Like the 

 benchmark dose, this term covers the entire exposure-response 

 relationship in a given study rather than relying on only one data 

 point representing the NOAEL or LOAEL. This approach reduces the 

 uncertainty inherent in defining an NOAEL or LOAEL by considering the 

 upper 95% confidence interval of the full exposure-response curve from 

 a study in experimental animals, in which the lower 95% confidence 

 limit of a concentration corresponds to a 1, 5, or 10% increase in 

 response, defined as the percentage of animals responding in a 

 specific group. This exposure concentration is then the benchmark 

 concentration of the study. It is converted to the human benchmark 

 concentration on the basis of differences in pulmonary dosimetry 

 between the two species, which additionally reduces the use of 

 uncertainty factors. Because the full range of experimental results 

 from a specific study is used, the benchmark concentration approach 

 reduces statistical uncertainty. 

 In principle, this approach involves three steps. The first is 

 selection of the appropriate experimental study and end-point for 

 establishing an exposure-response curve. The second is calculation of 

 the benchmark concentration for the animals from a mathematical 

 description of the exposure-response curve and determination of the 

 95% confidence interval. Thirdly, the human benchmark concentration is 

 calculated; for exposure by inhalation, the exposure of the animals is 

 extrapolated dosimetrically to the human situation, with application 

 of uncertainty factors the size of which is determined as discussed 

 above. These factors generally consist of one for interspecies 

 extrapolation and one for sensitive subpopulations. The first two 

 steps of the benchmark concentration approach are shown schematically 

 in Figure 6. 

 

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 Two sets of data were used to derive the benchmark concentration 

 for diesel exhaust. The first was that of Ishinishi et al. (1988) from 

 a study in which rats were exposed to exhaust from a light-duty diesel 

 engine for two years at four concentrations. Hyperplastic lesions, 

 shown histopathologically to be a sensitive indicator of lung damage, 

 were used to establish a well-described exposure-response 

 relationship. The second data set was that of Creutzenberg et al. 

 (1990) for female Wistar rats exposed for 96 h per week for a total of 

 78 weeks to three concentrations of diesel exhaust. The most sensitive 

 end-points for exposure-related non-neoplastic changes were lung 

 clearance of particles and the occurrence of polymorphonuclear 

 neutrophils (PMN) in lung lavage fluid as indicators of inflammation. 

 Since these measurements are laborious, however, they were performed 

 only in a subset of the exposed animals, so that only six to eight 

 rats were studied per group. 

 The responses in the study of Ishinishi et al. (1988) were 

 expressed in terms of individual animals affected per total number of 

 exposed animals in each group, whereas the data of Creutzenberg et al. 

 (1990) were reported as group mean values plus or minus the standard 

 deviation, which is less useful for the benchmark concentration 

 approach. Individual responses in the latter study were, however, 

 provided by Bellmann (personal communication), so that the data from 

 this study could also be expressed in terms of percentage of animals 

 with impaired lung clearance. Impairment of lung function was 

 considered to be significant when the calculated pulmonary retention 

 half-time of the administered particles was at least 3.5 times greater 

 than their normal average half-time in the lungs of control animals. 

 Evaluation of the end-point chronic inflammation (PMN in lung 

 lavage fluid) proved to be more difficult, since all of the rats at 

 the lowest exposure level (0.8 mg/m3) in the study of Creutzenberg 

 et al. (1990) had increased PMN levels (100% response). Lung lavage 

 was performed at 22 and 24 months of exposure, and since the responses 

 at these two times were similar, the data were combined to increase 

 the numbers of animals per group to 11-14. The individual responses 

 (percentage of PMN among the total number of cells in the lavage 

 fluid) were used to derive the curve and the 95% confidence interval. 

 An excess of PMN of up to 3% of the total number of cells over the 

 background level was used to define the benchmark concentration. The 

 highest value observed in the control group was 2.75% PMN after 

 22 months of exposure. 

 The three data sets and the results of the probability function, 

 using a Weibull model to calculate the benchmark concentration, are 

 given in Tables 44, 45, and 46 and are illustrated in Figures 7 and 8. 

 Table 44. Benchmark concentration for rats after long-term exposure 

 to diesel exhaust by inhalation in study by Ishinishi et al. 

 (1988); end-point: hyperplastic lesions of the lung 

 

 Concentration (mg/m3) Rats that responded 

 (equivalent continuous 

 exposure of rats) Actal/observed Predicted Percent 

 numbers number 

 

 0 4/125 4.6 3.2 

 0.063 4/125 4.6 3.25 

 0.23 6/125 4.7 4.8 

 0.67 12/123 12.1 9.76 

 1.3 87/124 87.0 70.2 

 

 Probability function [p(conc)] - A0]/(1 - A0) = [1 - exp(-A1 * 

 Conc)K] 

 A0 = 3.7196 × 10-2

 A1 = 3.740 

 K = 4.3504 

 Lower confidence limit of the benchmark concentration (BC) for a given 

 risk: 

 

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 Risk Rat BC 

 (mg/m3) 

 

 0.1 0.634 

 0.05 0.511 

 0.01 0.313 

 

 The respective benchmark concentrations from the data sets for rats 

 are 0.634, 0.119, and 0.090 mg/m3, corresponding to a 10% response 

 (the lower 95% confidence limit on the exposure concentration for 

 hyperplastic lung injury and impaired lung clearance) or a 3% excess 

 of PMN in lavage fluid (the lower 95% confidence limit on the exposure 

 concentration for chronic alveolar inflammation). 

 The resulting human benchmark concentrations for the three 

 end-points were calculated from the model of Yu & Yoon (1990), 

 applying uncertainty factors of 10 to account for sensitive 

 subpopulations (human intraspecies differences) and 100.4 (2.5) for 

 potentially different toxicodynamics (see above), to be: 14 μg/m3

 for hyperplastic lung lesions, 3 μg/m3 for impaired lung clearance, 

 and 2 μg/m3 for chronic alveolar inflammation. Although the 

 mathematical description of the exposure-response relationships in 

 rats is very good for all three sets of data, they should be viewed as 

 hypothetical since they are based on dosimetric conversions from rats 

 to humans and on the application of uncertainty factors. 

 Table 45. Benchmark concentration for rats after long-term exposure 

 to diesel exhaust by inhalation in study by Creutzenberg 

 et al. (1990); end-point: impaired lung clearance 

 

 Concentration (mg/m3) Rats that responded 

 (equivalent continuous 

 exposure of rats) Actal/observed Predicted Percent 

 numbers number 

 

 0 0/6 0 0 

 0.45 2/8 1.7 25 

 1.34 3/6 3.0 50 

 3.74 5/6 5.2 83.3 

 

 Probability function 

 [p(conc)] - A0]/(1 - A0) = [1 - exp(-A1 * Conc - D0)A2] 

 A0 = 0.0 

 A1 = 0.522 

 A2 = 1.00 

 D0 = 0.0 (threshold) 

 Lower confidence limit of the benchmark concentration (BC) for a given 

 risk: 

 

 Risk Rat BC 

 (mg/m3) 

 

 0.1 0.119 

 0.05 0.058 

 0.01 0.011 

 

 The non-cancer guidance values and the benchmark concentrations 

 derived from these approaches are summarized in Table 47. 

 More sensitive end-points with respect to the adverse effects of 

 diesel exhaust on the lower respiratory tract are impaired clearance 

 in the deep lung and chronic alveolar inflammation, rather than 

 hyperplastic lung lesions. Chronic alveolar inflammation was also a 

 significant finding in the long-term study of rats exposed to diesel 

 exhaust by Henderson et al. (1988), who found a significantly 

 increased percentage of PMN in lavage fluid from the group with the 

 lowest exposure (0.35 mg/m3) after two years. For all three types of 

 end-points, however, there may be a threshold below which no change is 

 to be expected. The threshold concept is not included in the 

 mathematical model, and it would be difficult to do so at this point 

 in the absence of specific experimental data and data on variation 

 between human subjects. 

 These estimates are for the effects of long-term exposures, and 

 the concentrations are expressed as annual means over a lifetime. They 

 could apply to long-term effects on health, such as the association 

 between mortality from certain chronic conditions and exposure to 

 particulates in air pollution seen in a study in six cities in the 

 United States (Dockery et al., 1993). Their relevance to human 

 experience must also be considered in the context of particulate air 

 pollutants in general, however, and they have no direct bearing on the 

 acute effects of exposure to particulates, for which guidance values 

 are required in terms of 24-h mean concentrations. 

 B10.4 Neoplastic effects 

 B10.4.1 Hazard identification 

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 B10.4.1.1 Lung cancer: occupational exposure 

 In the 1970s and 1980s, the recognition that diesel exhaust 

 contains respirable particles and that known carcinogenic substances 

 are adsorbed on the surface of these particles led to the hypothesis 

 that inhalation of diesel exhaust could result in lung cancer in 

 humans. As lung cancer develops slowly, over many years, studies of 

 individuals with long, well-defined exposure and follow-up (> 20 

 years) were considered to be the most informative. Four studies of 

 occupationally exposed individuals meet these criteria (Garshick et 

 al., 1987, 1988; Gustavsson et al., 1990; Emmelin et al., 1993; see 

 Table 43). 

 Table 46. Benchmark concentration for rats after long-term exposure to 

 diesel exhaust by inhalation in study by Creutzenberg et al. 

 (1990); end-point: chronic alveolar inflammation 

 

 Concentration (mg/m3) PMN in lung lavage fluid (%) No. rats 

 (equivalent continuous responding 

 exposure of rats Actual/observed Predicted per no. 

 exposed 

 

 0 0.7 0 0/11 

 0.45 11.1 11.7 13/13 

 1.34 29.9 27.6 14/14 

 3.74 50.8 51.9 14/14 

 

 Dose-response function: F(dose) = Q(0) × (Dose - (Dose - D0)Q(2)

 Dose = log(1 + d) (d = rat exposure concentration) 

 Q(0) = 0.6.53 

 Q(1) = 77.010 

 Q(2) = 1.056 

 D0 = 0.0 (threshold) 

 Lower confidence limit of the benchmark concentration (BC) for a given 

 excess polymorphonuclear neutrophil (PMN) response (% of total lavaged 

 cells): 

 

 

 PMN in excess Rat BC 

 of control (%) (mg/m3) 

 

 3 0.090 

 2 0.059 

 1 0.029 

 

 Transition from steam to diesel locomotives occurred in the 

 American railroad industry during the 1950s. In a case-control study 

 of American railroad workers (Garshick et al., 1987), exposure was 

 estimated on the basis of yearly job (exposed or unexposed to diesel 

 exhaust) from 1959 to death or retirement; deaths were identified for 

 12 months in 1981-82. In an additional study of these workers 

 (Garshick et al., 1988), a retrospective cohort was defined on the 

 basis of work in a job with exposure to diesel exhaust in 1959, and 

 

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 deaths were recorded for 1959-80. Although the previous exposure 

 levels of the railroad workers were not available, the classification 

 of workers into groups on the basis of exposure was validated by an 

 industrial hygienist and a review of work practices. Air sampling was 

 conducted to establish current exposure levels in various jobs 

 (Hammond et al., 1988; Woskie et al., 1988a,b). 

 Gustavsson et al. (1990) studied lung cancer among bus garage 

 workers in Stockholm, Sweden, where all buses with internal combustion 

 engines have been diesel-fuelled since 1945. A cohort was established 

 of people who had worked in bus garages for at least six months 

 between 1945 and 1970, and mortality was determined for 1952-86. A 

 nested case-control study was performed within this cohort. Although 

 actual exposure was not measured, relative exposure to diesel exhaust 

 was graded on the basis of a scale established by an industrial 

 hygienist in a review of work practices, bus engine operation, and 

 shop ventilation. 

 Table 47. Summary of non-cancer guidance values and benchmark 

 concentrations 

 

 Approach Guidance value 

 or benchmark 

 concentration 

 (μg/m3) 

 

 NOAEL with dosimetric conversion from rats to humans 5.6a

 NOAEL without dosimetric conversion from rats to 2.3 

 humans 

 Benchmark concentration with dosimetric conversion 

 from rats to humans 

 Chronic alveolar inflammation 2a

 Impaired lung clearance 3a

 Hyperplastic lesions 14a

 Benchmark concentration without dosimetric 

 conversion from rats to humans 

 Chronic alveolar inflammation 0.9 

 Impaired lung clearance 1.2 

 Hyperplastic lesions 6.3 

 

 NOAEL, no-observed-adverse-effect level 

 Normalized for lung surface area in rats and humans; after 

 normalization for lung weight, the benchmark concentration increases 

 by a factor of 4. 

 Emmelin et al. (1993) studied Swedish stevedores in 15 ports 

 where diesel equipment had been introduced between 1957 and 1963; they 

 also performed a nested case-control study on cases of lung cancer 

 identified between 1960 and 1982. Exposure to diesel exhaust was 

 estimated on the basis of three indices derived from estimated diesel 

 fuel consumption and years of work after the introduction of diesel 

 equipment in each port. 

 All four studies showed an increased risk for lung cancer with 

 exposure to diesel exhaust. The relative risks reported ranged from 

 about 1.4 for railroad workers with the longest duration of exposure 

 in both studies of such populations to 1.3-2.4 for bus garage workers, 

 depending on the exposure category. The stevedores also had an 

 increased relative odds ratio for lung cancer with increasing exposure 

 with respect to all three indices of exposure examined, with an 

 increase of three- to sixfold in the highest exposure categories and 

 1.5-2.7-fold in the lowest exposure category. The point estimates 

 were, however, imprecise and had wide confidence intervals: for all 

 but one exposure category, the lower limit of the 90% confidence 

 intervals presented by the authors included 1.0. 

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 The effects of cigarette smoking could be adjusted for in the 

 case-control studies of railroad workers (Garshick et al., 1987) and 

 stevedores (Emmelin et al., 1993). The smoking histories of the 

 railroad workers were obtained from next-of-kin. Various regression 

 models (including both dose and duration of smoking) were examined in 

 detail in order to adjust adequately for the effects of smoking. No 

 matter how it was accounted for, the risk for lung cancer based on 

 work in a job with exposure to diesel exhaust was similar to the 

 unadjusted odds ratio. The study of stevedores (Emmelin et al., 1993) 

 was smaller than that of railroad workers, and in order to reduce the 

 number of strata for analysis workers were stratified only as smoker 

 or nonsmoker. In the two studies in which information on smoking was 

 not available (Garshick et al., 1988; Gustavsson et al., 1990), the 

 analysis was based on a comparison with workers in the same 

 occupational cohort, making confounding by smoking less likely. 

 The results of most of the other studies summarized in Tables 

 39-41 support those of the four studies discussed above. The relative 

 risks were generally in the range 1.2-1.9 but did not always achieve 

 statistical significance. Furthermore, exposure to diesel exhaust was 

 less precisely defined in these studies; it was usually based on 

 self-reporting, the report of a surrogate, or a census report of 

 occupation (Table 41). Self-reporting or the report of a surrogate 

 would reflect actual exposure to diesel exhaust or work in a job in 

 which exposure was likely; however, defining exposure in this less 

 precise fashion make it harder to detect an effect of the exposure and 

 leads to lower relative risks and wider confidence intervals. 

 In three other studies, job titles obtained from an employer were 

 used to define exposure. In the study of Howe et al. (1983), the job 

 held at the time of retirement from the railroads was used to 

 categorize exposure, and mortality was assessed for 1965-77. 

 Significantly elevated risks for lung cancer were noted among workers 

 who had probably been exposed to diesel exhaust (relative risk = 1.35) 

 and among those who had possibly been exposed (1.20); however, since 

 only retired workers were studied, actual exposure to diesel exhaust 

 would have been short for many workers. Rushton et al. (1983) and 

 Waller (1981) used job titles within the London Transport organization 

 to indicate potential exposure to diesel exhaust. Neither study showed 

 an elevated risk for lung cancer, but the study of Rushton and 

 coworkers was characterized by a short duration of exposure and 

 follow-up, whereas in the study of Waller, deaths occurring after 

 employment were not included. 

 The relative risks for lung cancer as a result of exposure to 

 diesel exhaust are generally low, and risks of this magnitude are more 

 susceptible to chance and to the effects of unmeasured confounding 

 factors and imprecision in adjusting for known confounding factors. As 

 discussed above, the elevated risk for lung cancer observed in the 

 four most informative studies is unlikely to be due to confounding by 

 cigarette smoking and is probably due to exposure to diesel exhaust. 

 Other studies, although limited primarily by the exposure 

 ascertainment, support this assessment. 

 B10.4.1.2 Urinary bladder cancer: occupational exposure 

 The hypothesis that exposure to diesel exhaust results in cancer 

 of the urinary bladder is based on the fact that individuals who smoke 

 cigarettes, a source of PAHs (as is diesel particulate), excrete 

 mutagenic substances in their urine, and cigarette smoking is 

 associated with an increased risk for bladder cancer. In a recent 

 study of railroad workers with current exposure to diesel exhaust 

 (median concentration of respirable particulates over a work shift, 

 54-113 μg/m3; adjusted for smoking), mutagenicity in urine at the 

 end of a shift was not associated with exposure (Schenker et al., 

 1992). 

 The evidence that bladder cancer is associated with exposure to 

 diesel exhaust is based on an association between work in industries 

 or occupations with potential exposure to diesel exhaust. The relative 

 risks reported (some of which are adjusted for smoking) are generally 

 in the range 1.2-2 (Hoar & Hoover, 1985; Silverman et al., 1986), 

 although higher risks have been reported. Exposure was assessed mainly 

 by self-reporting and reporting of occupation at interview. The main 

 occupation in which there was considered to be potential exposure to 

 diesel exhaust was truck driving. Measurements of exposure of truck 

 drivers by Zaebst et al. (1991) indicate that current exposure is 

 likely to be low, but there is no knowledge about past exposure 

 levels. 

 Thus, although work in occupations related to motor vehicles has 

 been associated with bladder cancer, the extent of exposure of these 

 workers to diesel exhaust is unknown. 

 B10.4.2 Dose-response assessment 

 B10.4.2.1 Lung cancer 

 Job category and work in an occupation with exposure to diesel 

 exhaust have been used as indicators of exposure. When years of 

 exposure and derived indices of exposure have been used, an 

 exposure-response relationship has generally been found. Measurements 

 of total and respirable dust in exposed workers do not reflect actual 

 exposure to diesel exhaust particles, however, since there are other 

 sources of dust in an occupational environment. The exposure of only 

 two occupational groups, American railroad workers (Woskie et al., 

 1988b) and truck drivers (Zaebst et al., 1991), to diesel exhaust 

 particles has been quantified (see section B5.2). Current exposure was 

 measured for both these groups, but past exposure levels could not be 

 determined (Woskie et al., 1988b), so that studies of workers do not 

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 permit determination of a dose-response relationship for inhaled 

 diesel particles. 

 B10.4.2.2 Urinary bladder cancer 

 Years of work in an occupation related to motor vehicles (mainly 

 truck driving) was examined in some, but not all, studies, but no 

 measurements were available to estimate exposure to diesel exhaust in 

 these settings. 

 B10.4.3 Exposure assessment 

 The ranges of exposures observed for workers are presented in 

 sections B5.2 and B10.2. 

 B10.4.4 Risk characterization 

 B10.4.4.1 Human lung cancer 

 Thus, historical measurements of exposure to diesel exhaust are 

 unreliable and exist only for current workers in two industries. A 

 quantitative risk assessment cannot be conducted on the basis of 

 epidemiological data in which job title was used as a surrogate of 

 exposure. Attempts to obtain estimates of risk (presented in section 

 B10.4.1) in the retrospective cohort study of American railroad 

 workers (Garshick et al., 1988) were not successful (see below for 

 discussion). Consequently, there are no human data suitable for 

 estimating unit risk. 

 B10.4.4.2 Human urinary bladder cancer 

 The risk for urinary bladder cancer cannot be assessed from the 

 available epidemiological data. 

 B10.4.4.3 Risk characterization based on studies in experimental 

 animals 

 (a) Introduction 

 Most human tumours arise in the bronchial region, and although 

 the frequency of adenocarcinomas has increased in recent years 

 (Martini, 1993), squamous bronchogenic carcinomas still represent the 

 majority (about 60%) of lung tumours in humans (Auerbach & Garfinkel, 

 1991; Devesa et al., 1991; Campobosso et al., 1993). The tumours 

 observed in rats are located almost exclusively in the bronchoalveolar 

 regions. This difference raises the question of whether the rat is the 

 appropriate species for extrapolating to humans. Although it may be 

 the wrong model, however, studies of hamsters and monkeys give 

 negative results, so the rat is the most appropriate model from a 

 conservative viewpoint and is therefore used for quantitative risk 

 extrapolation. 

 The objective is to assess quantitatively the potential risk for 

 lung cancer in humans posed by exposure to diesel exhaust emissions in 

 the ambient air. Ideally, human risk due to exposure to an 

 environmental pollutant should be predicted on the basis of human 

 experience. Although several epidemiological studies are available on 

 bus and railroad workers, these results alone are not adequate to 

 assess the potential risk of cancer in humans because of the lack of 

 reliable information on the conditions of exposure of these workers. 

 The challenge is to assess the risk of exposure to diesel exhaust on 

 the basis of all of the available information, for both experimental 

 animals and humans. In contrast to the sparse human data, there is a 

 rich pool of information on diesel-induced lung tumours in two strains 

 of rat. One approach to integrating this information is to make a 

 quantitative risk assessment on the basis of information from 

 bioassays and on the relevant biological mechanism and then to 

 evaluate these animal-based results against available human 

 experience. This approach was followed in this monograph. 

 Although, the available experimental data on the possible impact 

 of extractable organic matter and PAHs on the lung tumour response 

 associated with exposure to diesel soot are not strong (Heinrich et 

 al., 1991; Heinrich, 1994; Heinrich et al., 1995), a mathematical 

 approach to assessing the risk of exposure to diesel exhaust should 

 take into account the effects of both particles (carbon core) and 

 extractable organic matter, because: (i) organic compounds include a 

 variety of PAHs and nitroaromatic compounds, many of which are known 

 to be carcinogenic; (ii) the results of recent studies on inert 

 particles and carbon black in rats (Mauderly et al., 1991; Heinrich, 

 1994; Heinrich et al., 1994) strongly support the hypothesis that the 

 carbon cores of diesel particles are the component primarily 

 responsible for the induction of lung cancer; (iii) PAHs alone are 

 unlikely to be responsible for the tumour response; (iv) the 

 disproportionately high tumour incidence in animals with heavy 

 exposure coincides with a disproportionate increase in the cumulative 

 lung burden of diesel particles. Although a qualitative description of 

 the biological mechanism of diesel exhaust-induced tumours is 

 plausible, however, the lack of quantitative information on the 

 dynamics of tumour initiation, promotion, and progression vitiates the 

 construction of a biologically based dose-response model. 

 The crudest dose-response model is obtained by fitting observed 

 dose-response data to a mathematical function that is a monotonic, 

 non-decreasing function of exposure, using the inhaled concentration 

 and observed tumour incidence, without considering information on 

 pharmacokinetics and the mechanism of carcinogenesis. This approach 

 may result in uncertain estimates of risk at low doses, because, while 

 the model may adequately fit the dose-response data for high doses at 

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 which a tumour response is observed, it may greatly underestimate or 

 overestimate the risk at low doses. 

 Most previous risk estimates of diesel exhaust-induced cancer 

 risk were developed before the results of many of the bioassays became 

 available (Pepelko & Chen, 1993). Nevertheless, most of the estimates 

 are similar (within an order of magnitude), except for those 

 calculated on the basis of human data, which are higher than those 

 calculated from other databases. Because of great uncertainties 

 associated with the available human data, it is considered more 

 appropriate to calculate risk on the basis of animal data and then use 

 human data to evaluate their validity. 

 The approach adopted in this assessment is the linearized 

 multistage model (Anderson et al., 1983), in which burden per lung 

 surface area (milligrams per square centimetre) is used as an 

 equivalent dose in animals and humans. The use of lung (alveolar) 

 surface area is justified by the fact that the lung tumours observed 

 in rats are derived exclusively from epithelial cells in the alveolar 

 region of the lung. Normalization on the basis of lung weight can also 

 be done by using a factor of 4, for increasing the dose or decreasing 

 the risk, for the difference in the ratio of rat:human lung surface 

 area and lung weight. The risk prediction calculated by this approach 

 is presumably conservative (i.e. overpredicts the risk) because the 

 dose-response function is assumed to be non-threshold and linear at 

 low doses. 

 An alternative model that incorporates a biological mechanism is 

 constructed using statistically estimated parameters. The model 

 assumes that carcinogenic agents present in the organic fraction act 

 directly on the target cells, primarily via initiation. It is further 

 assumed that the majority of the particles are ingested by 

 macrophages. Particle-laden macrophages are then induced to secrete a 

 variety of mediators (e.g. reactive oxygen species and cytokines), 

 which diffuse to the target cells and induce initiation, 

 proliferation, and conversion of initiated cells to malignant cells. 

 This alternative model can be used only as a tool to evaluate the 

 impact of various biological assumptions and not for risk prediction, 

 because the parameters of the model are not measured in the 

 laboratory. 

 (b) Approaches to quantification of human risk from exposure to 

 diesel exhaust 

 Several issues must be addressed in estimating the risk of 

 exposure to diesel exhaust, including the critical target site, the 

 fraction of exhaust responsible for tumour induction, the availability 

 of dosimetric methods for accurately extrapolating dose from that for 

 experimental animals chronically exposed to high concentrations of 

 exhaust to that of humans exposed at ambient concentrations, and the 

 most suitable low-dose extrapolation model. 

 The critical target organ was considered to be the lung. Although 

 Iwai et al. (1986) reported induction of both malignant lymphomas and 

 lung tumours in rats exposed to diesel exhaust, the lung was the only 

 target site in other experimental studies of this species. Although 

 potentially carcinogenic agents present in diesel exhaust may be 

 absorbed from the lungs, enter the bloodstream, and be transported 

 systemically, no data are available to evaluate this possibility. 

 Organic compounds adsorbed on particles may also reach systemic 

 targets via the gastrointestinal tract, as particles deposited in the 

 conducting airways are cleared rapidly to the oropharynx and 

 swallowed. A considerable volume of particles is also likely to be 

 ingested as a result of grooming when the whole animal is exposed 

 (Wolff et. al., 1982); however, because the half-times for the elution 

 of organic compounds from particles are considerably longer than their 

 passage through the gastrointestinal tract, the fraction absorbed is 

 expected to be small. In any case, there is little evidence for any 

 systemic effects of diesel exhaust. 

 The site of action in the lungs is assumed to be the epithelial 

 lining of the alveoli and small airways. According to Mauderly et al. 

 (1987), inflammation and tumours appear to arise from this tissue. 

 Although interstitial events (e.g. fibrosis) have been suggested to be 

 associated with induction of lung tumours by particles (Kuschner, 

 1968), no data are available to support this view with respect to 

 diesel exhaust. 

 Accurate extrapolation of dose from studies of animals exposed to 

 high concentrations of exhaust to humans exposed to ambient 

 concentrations requires a variety of adjustments for species 

 differences in deposition efficiency and respiratory ventilation 

 rates. As the normal retention half-times in the alveolar region are 

 several times longer in humans than rats (Chan et al., 1981; Bohning 

 et al., 1982), the lung burden of humans may be underestimated if this 

 difference is not taken into account. The high exposure concentrations 

 used in some experimental studies, however, result in greatly slowed 

 or even completely inhibited clearance (Griffis et al., 1983). In 

 order to extrapolate dose accurately from experimental studies to 

 humans, the detailed dosimetric model developed by Yu et al. (1991) 

 was used, which accounts for species differences in respiratory 

 ventilation rates, deposition efficiency, normal particle clearance 

 rates, transport of particles to lung-associated lymph nodes, and lung 

 surface area. It also accounts for inhibition of particle clearance 

 due to lung overload. In this model, dose is estimated in terms of 

 particle concentration per unit of lung surface area. 

 Two approaches were used to derive unit risk estimates: the 

 linearized, multistage, low-dose extrapolation model and a model based 

 on the biological mechanism discussed above. In the linearized 

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 multistage model, the lung burden of carbon core per lung surface area 

 is used as the dosimetric parameter. A particle-based assessment was 

 considered to be reasonable for two principal reasons: (i) exposure to 

 the vapour phase alone did not result in detectable tumour induction 

 in rats (Brightwell et al., 1986; Iwai et al., 1986; Heinrich et al., 

 1986a); and (ii) exposure to carbon black, which is similar in 

 composition to the carbon core of whole diesel exhaust but contains 

 only negligible amounts of organic compounds, was about as effective 

 in inducing lung cancer as whole diesel exhaust (Mauderly et al., 

 1991; Nikula et al., 1994; Heinrich et al., 1995). Although use of the 

 carbon core as a dosimetric parameter implies that it is primarily the 

 insoluble carbon core of diesel particles that is responsible for the 

 carcinogenic effects of diesel exhaust, it can also be viewed simply 

 as a marker of exposure to diesel exhaust, with no biological 

 implication. Similarly, organic compounds could be used as markers of 

 exposure for the dose-response calculation. When this is done, the 

 resulting unit risk estimates (not presented here) are very similar 

 (within 25%) to those calculated with the carbon core as the surrogate 

 of exposure. 

 The second approach is based on the assumption that, even though 

 the concentration of carcinogenic compounds on diesel particles is 

 low, they nevertheless can act in concert with the particles to induce 

 carcinogenesis. An alternative low-dose extrapolation model was 

 therefore developed that allows for the possibility that various PAHs 

 and nitroaromatic compounds may induce organ-specific adducts that 

 contribute to cell initiation. This model is described in Appendix A1. 

 Both approaches incorporate the detailed dosimetric model of Yu 

 et al. (1991) to estimate dose at the airway and alveolar surfaces. 

 Risk is based on the assumption that an equivalent concentration 

 (dose) per unit of alveolar surface area results in equivalent risks 

 in humans and rats. 

 (c) Evidence to support a carcinogenic effect of the carbon core 

 The study of Heinrich et al. (1994) on carbon black and coal-tar 

 pitch provides information useful for evaluating the assumptions used 

 to construct the model that reflects current thinking about the 

 mechanism of action of diesel exhaust in inducing lung tumours. One 

 relevant question about diesel exhaust is whether lung tumours are 

 induced by the carbon core alone or in combination with organic 

 compounds. 

 In this study, female Wistar rats were exposed to carbon black or 

 tar pitch, or both for 10 months (43 weeks) or 20 months (86 weeks) 

 and followed until the end of the study, which lasted for 

 two-and-a-half years. No lung tumours were observed in the control 

 group. For each exposed group, the probability of dying from lung 

 cancer was calculated by a Kaplan-Meier survival analysis. Since these 

 data are used solely for interpretation and not for risk prediction, 

 it is statistically more appropriate to use only data on mortality, 

 excluding those tumours found at terminal sacrifice. Figure 9 shows 

 the probability of dying from lung cancer for the rats that were 

 exposed either to 6 mg/m3 of carbon black, or to coal-tar pitch 

 containing 50 μg/m3 of benzo[a]pyrene, or to a combination of the 

 two for 10 months, and then followed until the end of the study. In 

 Figure 10, each plot represents the time at which a tumour occurred. 

 To provide a better visual presentation, the probabilities at these 

 points are connected by straight lines. (Note: It is statistically 

 more appropriate to present these probabilities by a step function 

 rather than by interpolation when the Kaplan-Meier procedure is used.) 

 Two conclusions can be drawn from Figure 10: (1) Tumours appeared 

 much earlier in animals exposed to coal-tar pitch alone or in 

 combination with carbon black than in animals exposed to carbon black 

 alone. For instance, the first tumour occurred 665 days after the 

 start of exposure to carbon black, 406 days after exposure to coal-tar 

 pitch, and only 310 days after exposure to the combination. (2) Carbon 

 black and coal-tar pitch together caused a higher rate of mortality 

 from tumours than the sum of mortality caused by carbon black and 

 coal-tar pitch separately. The probability of dying from a lung tumour 

 before terminal sacrifice at 912 days was 0.28 for carbon black, 0.52 

 for coal-tar pitch, and 0.99 for the combination. These two 

 observations suggest that carbon black and coal-tar pitch act on 

 different stages of tumorigenesis. They are consistent with the 

 hypothesis that carbon black can increase the proliferation rates of 

 normal and cells at different stages of differentiation initiated 

 spontaneously or by coal-tar pitch. 

 When the rate of mortality from tumours among rats exposed to 

 diesel exhaust is compared with that of groups exposed to carbon 

 black, coal-tar pitch, or the combination (Figure 9), the rate among 

 the animals exposed to diesel exhaust is comaprable to that of rats 

 exposd to carbon black for 10 to 20 months. This implies that carbon 

 black alone can induce a tumour response similar to that induced by 

 diesel exhaust. Figure 9 also shows that doubling the duration of 

 exposure to carbon black from 10 to 20 months does not increase the 

 probability of dying from a lung tumour before terminal sacrifice; 

 however, doubling the duration of exposure to coal-tar pitch 

 significantly increases the probability of dying from a lung tumour. 

 Figure 11 shows that the shapes of the curves for age-dependent 

 mortality from cancer for animals exposed to diesel exhaust and 

 coal-tar pitch for 20 months are similar. It should be kept in mind 

 that the PAH content of the atmosphere containing both carbon black 

 and coal-tar pitch was about 1000 times higher than that of diesel 

 engine exhaust. These observations may have profound implications for 

 elucidating the mechanisms of induction of lung tumours by diesel 

 exhaust, but more refined analyses are necessary before any conjecture 

 can be made. 

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 (d) Data available for calculating risk 

 Seven bioassays have shown lung tumour responses in rats 

 (Brightwell et al., 1986; Heinrich et al., 1986b; Ishinishi et al., 

 1986; Iwai et al., 1986; Mauderly et al., 1987; Nikula et al., 1994; 

 Heinrich et al., 1995). Four studies were chosen for use in 

 calculating unit risk (Table 48) because they involved multiple 

 exposure groups. Data on time to event (death with or without a 

 tumour) are available in the studies of both Mauderly et al. (1987) 

 and Heinrich et al. (1995) and were used in all of the risk 

 calculations. 

 (e) Calculation of unit risks 

 The unit risk from exposure to an air pollutant is defined as the 

 95% upper bound of the increased lifetime cancer risk for an 

 individual continuously exposed to a concentration of 1 μg/m3 in 

 ambient air. Unit risk is a convenient tool for calculating lifetime 

 risk due to exposure to a pollutant when low-dose linearity is 

 assumed. Under this assumption, the risk due to exposure to d μg/m3

 of pollutant can be calculated from u × d if the pollutant has a 

 unit risk of u/μg per m3. This calculation is valid, however, only 

 when the level of risk is low. The results of unit risk calculations 

 are summarized in Table 49. 

 

 

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 Table 48. Incidence of lung tumours in rats exposed to diesel engine exhaust 

 

 Strain Exposure Dose metric Lung tumour Reference 

 (sex) incidence 

 Schedule Concentration Weekly exposure Lung particle burden 

 (mg/m3) (mg/m3 × h) (mg/cm2 lung surface)a

 

 Fischer 7 h/d, 0 0 0 2/230 Mauderly et al. 

 344 5 d/week 0.35 12 6.4 × 10-5 3/223 (1987) 

 (f+m) 3.50 122 2.8 × 10-3 8/222 

 7.08 248 6.0 × 10-3 29/227 

 Wistar 18 h/d, 0 0 0 1/217 Heinrich et al. 

 (f) 5 d/week, 0.84 76 5.8 × 10-4 0/198 (1995) 

 2 years, 2.50 225 5.2 × 10-3 11/200 

 < 6 months 6.98 628 1.5 × 10-2 22/100 

 follow-up 

 Fischer 16 h/d, 0 0 0 1/123 Ishinishi et al. 

 344 6 d/weekb 0.46 44 2.5 × 10-4 1/123 (1986) 

 (f+m) 0.96 92 2.0 × 10-3 0/125 

 1.84 177 4.2 × 10-3 4/123 

 3.72 357 8.8 × 10-3 8/124 

 Fischer 16 h/d, 0 0 0 4/250 Brightwell et al.

 344 5 d/week 0.7 56 3.5 × 10-4 1/112 (1986) 

 (f+m) 2.2 176 4.2 × 10-3 14/112 

 6.6 528 1.3 × 10-2 55/111 

 

 a Calculated from the model of Yu et al. (1991) 

 b Data on heavy-duty diesel engine exhaust used because those for light-duty engines showed no statistically significant difference 

 Particle-based model: The linearized multistage model, which is 

 used as a conservative approach to estimating risk, has the 

 mathematical form P = 1 exp(-Z), where Z is either q0 + q1 × d + ... 

 + qm × dm of a polynomial concentration d, or ( Q0 + Q1 × d + ... 

 + Qm × dm) × tk, a polynomial of concentration d multiplied by a time 

 factor, tk, when data on time to event are used. In this case, the 

 lifetime risk is calculated from actuarial life tables using the 

 survival probability of control Fischer 344 rats within the National 

 Toxicology Program, provided by Portier et al. (1986). The range of 

 extrapolation is about three orders of magnitude in the present 

 assessment. Denote P0 the lifetime cancer risk at concentration 0. 

 Because the extra risk (P-P0)/(1-P0) is dominated by the linear term 

 q1 × d at low concentrations, the 95% upper bound of q1 is used 

 to represent unit risk. 

 In extrapolating risk from animals to humans, a dose metric that 

 induces the same tumour incidence rate in animals and humans must be 

 assumed (i.e. dose equivalence). To calculate equivalent doses, a 

 mathematical model is used to adjust for the dosimetric parameters 

 that determine the lung burden of particulate matter in rats and 

 humans and to correct to dose per unit lung surface area. This dose is 

 considered to be equally potent in inducing lung tumours in animals 

 and in humans. The model accounts for differences between animals and 

 humans in regional deposition efficiency, particle clearance rates at 

 low doses and at doses that result in impaired clearance, and lung 

 surface area. In these calculations, the mass fraction of organic 

 compounds adsorbed on particles is assumed to be 20%; one-half of the 

 mass is assumed to be composed of slowly eluted organic compounds 

 (half-life, 30 days) and the other half of rapidly eluted organic 

 compounds (half-life, 1.3 h). The remainder is considered to be 

 inorganic carbon. At higher concentrations, particle clearance slows 

 and may even stop, and the lung particle burdens increase continually 

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 during exposure. The organic constituents, however, are eluted from 

 the particles fairly quickly and reach a steady state even during 

 continued exposure to high concentrations. The lung burdens of organic 

 compounds are therefore less affected by inhibition of clearance by 

 overloading. 

 In the linearized multistage model, determination of the dose of 

 the carbon core is problematic because the lung burdens after low and 

 high exposures differ drastically over time. This difference suggests 

 that use of a lung burden at a fixed time (e.g. one year after the 

 start of exposure) to represent dose may not be appropriate. In this 

 assessment, the average lung burden is used as the dose at the target 

 organ. The average lung burden is calculated by dividing the area 

 under the curve of lung burden over time by the corresponding period 

 of the experiment for which the curve was calculated. Figure 12 shows 

 a comparison of the lung burden predicted from the model and that 

 observed in the laboratory (Muhle et al., 1994) at specific times. It 

 suggests that the model used to calculate lung burden is adequate. 

 Table 49. Estimates of unit risk per microgram of particles per 

 cubic metre of diesel exhaust 

 

 Upper 95% confidence limit of cancer Study 

 risk due to exposure to 1 μg/m3 of 

 diesel particulate matter 

 

 3.4 × 10-5 Mauderly et al. (1987) 

 1.6 × 10-5a Ishinishi et al. (1988) 

 7.1 × 10-5 Brightwell et al. (1986) 

 3.4 × 10-5 Heinrich et al. (1995) 

 3.4 × 10-5 Geometric mean of 

 four studies 

 

 If milligrams per lung weight are used instead of milligrams per lung 

 surface as the equivalent dose, the risk estimates are reduced by a 

 factor of 4. 

 a Heavy-duty diesel engine 

 Biologically based model: A second approach to estimating risk 

 was used because it was considered more desirable to base risk on a 

 biologically based dose-response model. Although the data are at 

 present insufficient to replace the linearized multistage model, which 

 is considered more conservative, the implications of hypothetical 

 mechanisms of cancer induction by diesel particles can nevertheless be 

 investigated. The biological issues considered include the effects on 

 the carcinogenic process of particle-adsorbed organic compounds and of 

 a variety of mediators secreted by particle-laden macrophages. A 

 stochastic model was developed, which: 

 -- accounts for the possible effects of both the carbon particles 

 and their associated organic compounds: 

 -- allows evaluation of the contribution to tumour induction of 

 both carbon particles and organic compounds; 

 -- allows for changing parameters with increasing lung burden; 

 and 

 -- assumes that cell proliferation and tumour induction are 

 stochastic. (For instance, it is not appropriate to assume that 

 all cells divide at the same age.) 

 Unlike the linearized multistage model, this approach does not require 

 a constant dose metric but allows for varying lung burden over time. 

 

 The model, which is described in Appendix B10.3, allows for 

 initiation by both the carbon and the organic fraction and for the 

 proliferative effects of the carbon fraction. Although these 

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 mechanisms remain to be proven, it is assumed that carcinogenic agents 

 present in the organic fraction act directly on the target cells, 

 primarily by initiation. It is further assumed that most of the 

 particles are ingested by macrophages. Particle-laden macrophages are 

 then induced to secrete a variety of mediators (e.g. reactive oxygen 

 species and cytokines), which diffuse to the target cells, inducing 

 initiation, proliferation, and conversion of initiated cells to 

 malignant cells. 

 The results reported by Mauderly et al. (1987) for tumour 

 induction were used to estimate the model parameters. These are based 

 on the development of malignant tumours rather than all tumours as in 

 the first method. This was necessary in order to ensure that the data 

 used to estimate the parameters represented the same biological 

 mechanism. Lung burdens were calculated from the same dosimetry model 

 used in the linearized multistage model. 

 (f) Results of unit risk calculations 

 Particle-based model: Unit risks were derived from the linearized 

 multistage approach for the tumour incidences seen in four bioassays 

 (Brightwell et al., 1986; Ishinishi et al., 1986; Mauderly et al., 

 1987; Heinrich et al., 1995) and the corresponding equivalent doses 

 (Table 48). The resulting unit risk estimates, listed in Table 49, 

 range from 1.6 to 7.1 × 10-5/μg particles per m3 with a geometric 

 mean of 3.4 × 10-5/μg per m3. 

 In these calculations, the relationship between air concentration 

 (micrograms per cubic metre) and lung burden (milligrams) in humans is 

 used to determine the lung burden resulting from lifetime exposure to 

 1 g/m3 of diesel exhaust particulate matter. The particle burden in 

 terms of mass per unit lung surface area is then multiplied by the 

 slope derived from the bioassay data. For instance, when the data of 

 Mauderly et al. (1987) are used, the slope of the curve for 

 carcinogenicity in rats (i.e. the upper 95% confidence limit of the 

 linear coefficient in the multistage model), expressed in terms of 

 equivalent dose (micrograms of carbon particulate matter per square 

 centimetre) is 1.7 × 10-2/μg per cm2. According to the dosimetry 

 model, an air concentration of 1 μg/m3 of particulate matter 

 corresponds to a mass of 1230 μg of carbon particles per human lung. 

 Because the lung epithelial surface area, including the alveolar 

 region and conducting airways, is assumed to be 627 000 cm2, a unit 

 risk of 3.4 × 10-5/μg per m3 is derived from 1.7 × 10-2/μg per cm2

 × 1230 μg/627 000 cm2. 

 Biologically based model: The unit risk estimated by the 

 alternative model, based on the data on malignant tumours from the 

 study of Mauderly et al. (1987), is equal to 1.65 × 10-5/μg particles 

 per m3. This is lower than the estimate of 3.4 × 10-5/μg per m3

 derived from the same study with the linearized multistage approach. 

 Application of the linearized multistage model only to malignant 

 tumours seen in that study, rather than all lung tumours, resulted in 

 a unit risk estimate of 1.74 × 10-5/μg particles per m3 (Table 50). 

 Thus, the unit risk estimates obtained by the two approaches are 

 virtually identical. The estimated risks may differ somewhat with 

 increasing doses, because the slopes are not identical at all exposure 

 levels. It should be noted, however, that the unit risk predicted by 

 the alternative model is derived under the assumption that particles 

 continue to exert an effect on cell initiation or proliferation (or 

 both) at low doses. There is considerable uncertainty about the 

 effects of particles at low doses. It has been claimed that particles 

 do not induce initiation or proliferation at low doses (Vostal, 1986). 

 At present, the evidence is inadequate to support or refute this 

 claim. Moreover, even if macrophage overload is required, because of 

 uneven distribution of particles, some macrophages may become 

 overloaded even at low concentrations. Because of this uncertainty, 

 the biologically based model, like the linearized multistage model, 

 does not depart from linearity at low doses; however, if initiation 

 and proliferation do not occur at low doses, the risk may be much 

 smaller. 

 In an estimate of unit risk for rats, based on the results of 

 seven studies by inhalation and using linear interpolation and the 

 linearized multistage model, the risks were 7 × 10-5/μg of diesel 

 particles per m3 and 10 × 10-5/μg carbon core particles per m3

 (Csicsaky et al., 1993; Pott et al., 1993; Roller & Pott, 1994). 

 (g) Results and implications of the biologically based model 

 On the assumption that particles continue to affect cell 

 initiation or proliferation at low doses, the risks calculated with 

 this model are comparable to those obtained with the linearized 

 multistage model. Excess risks due to various exposures are shown in 

 Tables 50 and 51. Those in Table 50 are the risks predicted for humans 

 exposed continuously (24 h/day) from the two models: it is interesting 

 to note that the results are similar. Table 51 shows the excess risks 

 due to exposure to 2.6 μg/m3 of diesel particulate emission for 

 16 h/day on seven days per week and to 15 μg/m3 for 8 h/day on five 

 days per week. The first concentration was reported by the US 

 Environmental Protection Agency Office of Mobile Sources to be the 

 annual mean exposure of the American population to diesel particulate 

 matter in 1986; the second concentration was reported to be that to 

 which workers are exposed on urban freeways (Carey, 1987). The 

 retention half-time for insoluble particles after exposure to 

 Table 50. Comparison of excess risk for humans due to continuous exposure to 

 various concentrations of diesel exhaust emissions using two 

 different models 

 

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 Exposure concentration Biologically based (alternative) Linearized (μg/m3) 

 multistage 

 Maximum likelihood Upper 95% model 

 estimate bound estimate 

 

 0.01 7.68 × 10-8 1.35 × 10-7 1.71 × 10-7

 0.1 8.12 × 10-7 1.71 × 10-6 1.72 × 10-7

 1.0 (unit risk) 8.16 × 10-6 1.65 × 10-5 1.74 × 10-5

 100 5.58 × 10-4 9.63 × 10-4 1.74 × 10-4

 1000 2.60 × 10-2 4.22 × 10-2 3.33 × 10-2

 

 a Slope - 9.04 per mg/cm2 of lung surface, using carbon core as dosimetric. 

 Only malignant tumours are used in the calculations. 

 

 2.6 μg/m3 is shown to increase from 296 days for members of the 

 general population with normal respiratory function to 519 days for 

 those with a smoking history of 20 pack-years (Bohning et al., 1982). 

 This information was used to reduce the alveolar clearance rate for 

 the dosimetric calculations to that used for other risk calculations. 

 Interactive effects of smoking and diesel exhaust are not considered 

 in the risk calculations owing to lack of data. The studies of carbon 

 black and coal-tar pitch (Heinrich, 1994; Heinrich et al., 1994) 

 indicate that smokers have a higher risk for lung cancer than 

 nonsmokers when they are exposed to diesel exhaust. 

 The excess lifetime risks shown in Tables 50 and 51 are 

 standardized by the actuarial life-table approach, using the survival 

 probability of control animals in the US National Toxicology Program 

 provided by Portier et al. (1986). This approach gives a weighted 

 average of the probability of cancer occurrence over an entire 

 lifetime, weighted by survival probability. 

 Table 51. Excess lifetime risk for humans due to exposure to diesel 

 exhaust emissions under various exposure scenarios 

 

 Exposure pattern Biologically based model Linearized 

 multistage 

 Maximum Upper 95% modela

 likelihood bound 

 estimate estimate 

 

 General population (normal 1.41 × 10-5 2.44 × 10-5

 respiratory function; 

 nonsmoker): 2.6 μg/m3, 

 16 h/day, seven days 

 per week 

 General population 2.32 × 10-5 3.61 × 10-5 5.38 × 10-5

 (20-pack-year smoker)b: 

 2.6 μg/m3, 16 h/day, 

 seven days per week 

 Occupationally exposed: 3.12 × 10-5 5.17 × 10-5 6.18 × 10-5

 15 μg/m3 8 h/day, five 

 days per week 

 

 a Calculated using carbon core as dosimetric; only malignant 

 tumours are used. 

 b In this calculation, smoking affects only lung clearance rate; 

 biological interaction between smoking and exposure to diesel 

 exhaust is not considered. The retention half-times for 

 insoluble particles increased from 296 days for persons with 

 normal respiratory function to 519 days for 20-pack-year smokers 

 (Bohning et al., 1982). 

 Some implications of the alternative model are: 

 (1) At a low exposure concentration, the decrease in diesel-induced 

 initiation results in a greater reduction of risk; that is, the 

 number of initiated cells (cancer risk) is reduced more 

 efficiently with a low than with a high exposure. If only organic 

 compounds induce initiation when the concentration is low, they 

 play a more important role than particles in inducing tumours at 

 low concentrations, whereas the roles are reversed when the 

 concentration is high. 

 (2) Although cells initiated by diesel exhaust play an important role 

 in cancer induction, either organic compounds or the carbon core 

 alone could induce initiation by increasing their respective 

 proportions. Thus, although initiated cells are important for 

 tumour induction, they may be induced by any agent that initiates 

 tumours (e.g. smoking). 

 (3) A small change in the rate of proliferation induced by diesel 

 exhaust could disproportionately change cancer risk. As this 

 parameter is assumed to be a function of the dose of carbon core, 

 lung overloading has a significant effect on cancer incidence. In 

 the absence of better information, it is assumed in this 

 assessment that the carbon core continues to have a proliferating 

 effect at low doses. 

 These observations suggest that, although the effect of particle 

 overload on cell proliferation is important, initiation by the carbon 

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 core or organic compounds or both is also essential. Although this 

 conclusion is only tentative, because the model parameters are 

 estimated statistically on the basis of bioassays conducted at high 

 concentrations, it does suggest the importance of studying the role of 

 the carbon core and organic compounds in initiation and promotion at 

 low and high exposure concentrations. Does the relative initiation 

 potential of organic compounds and the carbon core differ with 

 concentration? These observations also suggest that a subcohort of 

 workers who were smokers and were exposed to high concentrations of 

 diesel exhaust for a long time would have a greater risk of dying from 

 lung cancer. 

 (h) Comparison of risk estimates derived from experimental studies 

 and human experience 

 The bioassay-based risk estimates, which range from 1.6 × 10-5 to 

 7.1 × 10-5, with a geometric mean of 3.4 x 10-5, can be compared with 

 human experience on the basis of three data sets: those of an 

 epidemiological study conducted on London Transport employees (Waller, 

 1981) and a subsequent analysis (Harris, 1983) and those on American 

 railroad workers (Garshick et al., 1987, 1988). Although these data 

 cannot be used to calculate unit risk, mainly because of a lack of 

 reliable information on exposure, they can be used to evaluate the 

 validity of unit risk estimates based on the results of experimental 

 studies. 

 Attempts have already been made to estimate the potential cancer 

 risk due to exposure to diesel exhaust on the basis of epidemiological 

 data. From the results of the study of London Transport workers, 

 Harris (1983) estimated that the increase in the relative risk for 

 lung cancer associated with exposure to 1 μg/m3-year of diesel exhaust 

 was 1.2 × 10-4, with an upper bound of the 95% confidence limit of 

 4.8 × 10-4. (Generally, when data from an epidemiological study with 

 negative results are used to estimate cancer risk, the upper bound is 

 used to calculate unit risk.) The resulting unit risk estimate is 2 × 

 10-3, which is about 60 times higher than the mean unit risk estimate 

 derived from bioassays, 3.4 × 10-5, and about 30 times higher than the 

 upper end of the range of unit risk estimates from bioassays, 7.1 × 

 10-5. Therefore, the risk estimate based on bioassays is not 

 inconsistent with that for humans, since 2 × 10-3 is the estimated 

 upper bound in an epidemiological study with negative results. 

 McClellan et al. (1989) reported risk estimates based on the 

 study of Garshick et al. (1987), in which lung cancers in railroad 

 workers were evaluated. Assuming exposure to concentrations of 500 and 

 125 μg/m3, the upper bounds of the 95% confidence interval for 

 lifetime cancer risk were estimated to be 6 × 10-4 and 2 × 10-3, 

 respectively. The lower of the two unit risk estimates is only about 

 one order of magnitude higher than the risk estimates based on 

 bioassays. 

 An epidemiological study potentially more suitable for 

 quantitative risk assessment was reported by Garshick et al. (1988), 

 which was based on a large number of subjects; a small but significant 

 increase in the rate of mortality from lung cancer was seen in some 

 subcohorts. The US Environmental Protection Agency has supported an 

 effort to derive a unit risk estimate from this study, and data on 

 exposure were estimated by Woskie et al. (1988a,b) and Hammond et al. 

 (1988). These data were analysed in a variety of ways, using relative 

 risk and absolute risk dose-response models and by classifying 

 individuals into various exposure categories, including job, duration 

 of employment, age, and exposure markers. Even though at least 50 

 analyses were carried out, an adequate dose-response relationship 

 could not be obtained; these data were therefore not used to estimate 

 unit risk. 

 The lack of a dose-response relationship is not totally 

 unexpected, given the low increase in mortality rate in the study of 

 Garshick et al. (1988) and the uncertain estimates of exposure. The 

 data on exposure were derived from air samples collected during a 

 limited period (1981-83) on four small railroads operating in a 

 limited geographical area (northern United States), in which 

 concentrations of respirable particulate matter were measured rather 

 than diesel exhaust per se; the measured concentrations were then 

 adjusted to derive markers of exposure. The data were used to estimate 

 exposure to diesel exhaust of railroad workers throughout the United 

 States 30 or more years earlier. Diesel equipment and working 

 conditions have, however, changed since the 1940s when diesel engines 

 first began to be used in large numbers. Woskie et al. (1988b) 

 summarized anecdotal reports of smoky working conditions in diesel 

 repair shops during the 1950s and 1960s and reported that the limited 

 data available on levels of nitrogen oxide during those periods 

 indicated high levels of diesel exhaust. By the time samples were 

 collected, however, the smoky conditions would have been largely 

 mitigated by improved ventilation and the advent of less smoky diesel 

 engines. The study of Garshick et al. (1988) gives the relative risks 

 for dying from lung cancer in exposed as opposed to unexposed railroad 

 workers classified into five subcohorts by age in 1959. The risks 

 ranged from 0.96 (95% CI, 0.74-1.33) to 1.45 (1.11-1.89). The highest 

 relative risk, 1.45, which was observed in workers who were 40-45 

 years old in 1959, was used here to evaluate the validity of unit risk 

 based on biossays results. Assuming that this subcohort of workers was 

 exposed to diesel exhaust for 8 h/day on five days per week from age 

 35 to age 65, the background mortality rate from lung cancer in this 

 subcohort would be 0.038 (0.63 × 0.06), as the unexposed workers in 

 the same age group had a relative risk of 0.63 and the corresponding 

 lifetime mortality rate from lung cancer in the general American white 

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 male population is about 0.06. If the lung cancer risk due to 

 1 μg/m3 is assumed to be 3.4 × 10-5, the concentration of diesel 

 exhaust in the working environment was at least 400 μg/m3, calculated 

 as follows: The risk due to 1 μg/cm2 of particles is 0.017 (which 

 results in a unit risk of 3.4 × 10-5). For a lower bound of the 

 relative risk of 1.1, a lung burden, d, that satisfies the 

 relationship 0.1 × 0.038 = 0.017 d would be needed; that is, d = 

 0.22 μg/cm2, which is equivalent to an air concentration of 

 0.4 mg/m3 by the dosimetry model of Yu et al. (1991). If the highest 

 unit risk estimate derived from Brightwell et al. (1986), 7.1 × 

 10-5, is used, the required minimal air concentration would be about 

 0.2 mg/m3. These calculations imply that a diesel exhaust 

 concentration of at least 0.2 mg/m3 was necessary to observe a 

 statistically significant increase in the mortality rate from lung 

 cancer in this study. This concentration appears to be reasonable in 

 the light of the working conditions described by Woskie et al. 

 (1988a). 

 Although the risk estimates derived from bioassays are lower than 

 those derived from human data and may possibly over-predict risk, 

 since the non-linearity of the human response is not considered in 

 this model, they are not inconsistent, for the following reasons: 

 (1) The risk estimates based on epidemiological studies are not 

 derived from all of the available data but on only a subset with 

 the highest response. The estimates are therefore higher than 

 those that would be derived from the whole data set. 

 (2) When a single data point (i.e. an overall relative risk and an 

 averaged exposure concentration) is used in the calculations, the 

 resulting slope for potency will be overestimated if the 

 dose-response relationship is not linear over all exposure 

 concentrations. Assume, for example, that the response follows 

 the simple multistage model P(d) = 1 - exp[-( q0 + qd + q2 d2)]. 

 The relative risk, R, at concentration d is R(d) = P(d)/P0. 

 Using this mathematical expression, it is easy to demonstrate 

 that the slope factor calculated from [ P(d) - 1] P0/ d is 

 greater at high doses (including the averaged concentration used 

 in the risk calculation) than at low doses where the 

 dose-response function is dominated by q1. Epidemiologists 

 have long had a similar (but not identical) concern about the use 

 of averaged data, since ecological associations are not 

 necessarily consistent with those measured at the individual 

 level (see Cohen, 1994; Greenland & Robins, 1994; Piantadosi, 

 1994). 

 (3) Some occupational groups were exposed to considerably higher 

 concentrations of diesel exhaust in the past than presently. For 

 example, the average particle concentration in a Finnish 

 roundhouse was reported to be 2 mg/m3 (Heino et al., 1978). The 

 lung burdens would thus be greater than those predicted on the 

 basis of current exposures, and the unit risk estimates would be 

 higher 

 (i) Summary and conclusions 

 A dosimetric model that accounts for differences between 

 experimental animals and humans in lung deposition efficiency, lung 

 particle clearance rates, lung surface area, ventilation, and the 

 rates of elution of organic chemicals from the particle surface was 

 used to calculate equivalent human doses as particle concentration per 

 unit lung surface area. After dosimetric adjustment, four risk 

 estimates were derived by a linearized multistage model from three 

 bioassays with Fischer 344 rats and one with female Wistar rats, which 

 ranged from 1.6 to 7.1 × 10-5/μg particles per m3, with a geometric 

 mean of 3.4 × 10-5. This quantitative assessment of the carcinogenic 

 risk due to exposure to diesel engine emissions is reasonable, 

 because: 

 -- The estimates are based on several well-designed, well-executed, 

 long-term bioassays. 

 -- Epidemiological studies indicate that humans are susceptible to 

 the induction of lung cancer after inhalation of diesel exhaust. 

 -- Dosimetry modelling, especially to account for inhibition of 

 particle clearance at high doses, has allowed accurate 

 extrapolation of doses from animals to humans. 

 -- The doses are based on actual concentrations of particulate 

 matter per unit of lung surface area. 

 -- Use of an alternative model that attempts to account for the 

 possible biological effects of the organic and carbon core 

 fractions did not appreciably change the unit risk estimate. 

 -- The risk estimates based on the results of bioassyas are not 

 inconsistent with the available human experience. 

 Nevertheless, a number of uncertainties remain, the most 

 significant of which are: 

 -- In any interspecies extrapolation there may be an inherent 

 difference in sensitivity to the agent being assessed. 

 -- The assumption of equivalent sensitivity across species is based 

 on concentration per unit of lung surface area, and use of other 

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 assumptions of dose equivalence may lead to different estimates 

 of risk; however, the estimates should not vary by more than one 

 order of magnitude. 

 -- Although linearized low-dose extrapolation methods are used, it 

 is still uncertain whether inflammatory cells secrete mediators 

 that induce cancer in lung epithelial cells when the particle 

 burden is smaller than that necessary to inhibit clearance. Even 

 if macrophages are activated at low particle burdens, it is 

 uncertain whether the responses of epithelial cells are linear at 

 very low concentrations; however, non-linear carcinogenic 

 responses have been observed in bioassays. 

 -- Although the unit risk estimate is corroborated in the 

 alternative model, uncertainty about the response at low doses 

 remains because the estimates in the alternative model are based 

 on the assumption that particles continue to induce cell 

 initiation and/or proliferation at low doses. The actual risk 

 would be much lower if this assumption does not hold. 

 The risk at low doses derived from the linearized multistage 

 model may thus be overestimated if particles no longer induce cell 

 initiation and/or proliferation. The model was selected for 

 calculating risk because a conservative model was needed in order to 

 ensure protection of public health and because adequate data were not 

 available to use fully the alternative model constructed for this 

 assessment. Thus, the risk derived from the bioassays should be viewed 

 as hypothetical. 

 These unit risk estimates should not be used to evaluate the 

 carcinogenic risk of other types of particulate matter present in 

 ambient air, which may have different solubilities, surface areas, and 

 free radical contents, which factors greatly affect carcinogenic 

 potency. 

 It could be argued that since the types and location of tumours 

 seen in rats after exposure to particles are different from those 

 found in humans, the experimental data are not relevant for humans. 

 The tumours diagnosed in rats after long-term exposure to carbon black 

 particles and diesel exhaust include benign adenomas and malignant 

 adenocarcinomas, squamous-cell carcinomas, adenosquamous carcinomas, 

 and squamous cysts (Mauderly et al., 1994; see section B7.3.2). After 

 injection into athymic mice, cells from 50-67% of squamous-cell 

 carcinomas and 25-40% of adenocarcinomas were found to grow (Table 

 35), whereas those from squamous cysts did not (Mauderly et al., 

 1994). 

 Squamous cysts have been defined by other authors as benign 

 cystic keratinizing squamous-cell tumours (Kittel et al., 1993; 

 Dungworth et al., 1994; Heinrich et al., 1995) and found not to grow 

 after transplantation (Heinrich et al., 1995). As pointed out by Mohr 

 (1992), there is, however, controversy about the correct terminology 

 of this type of lesion. In 1995, an international group of 

 pathologists re-evaluated lung tissue sections from rats exposed to 

 particles by inhalation and identified four distinct lesions: 

 squamous-cell metaplasia, pulmonary keratinizing cyst, cystic 

 keratinizing epithelioma (considered to be benign), and squamous-cell 

 carcinoma (G. Oberdörster, personal communication). 

 Regardless of the correct classification of lesions, the 

 important fact is that malignant tumours are induced in rats after 

 long-term inhalation of deisel exhaust and carbon black. The tumour 

 response of human beings may not, however, be the same, either 

 qualitatively or quantitatively. In fact, the response of rats to 

 long-term exposure to high concentrations of particles differs from 

 that of other species, including mice and hamsters. In the absence of 

 sufficient information about specific mechanisms unique to rats, 

 however, there is no justification for excluding data on this species 

 from extrapolations to the human situation (US Environmental 

 Protection Agency, 1986). 

 With respect to the mechanisms of induction of lung tumours by 

 particles in rats, it has been shown that particles devoid of 

 polyaromatic compounds can increase mutation rates in pulmonary 

 epithelial cells, which is an important step in tumour development via 

 cell transformation. In a recent study in which rats were exposed to 

 carbon black for 13 weeks, a significant influx of inflammatory cells 

 was seen at concentrations of 7 and 50 mg/m3 but not at 1 mg/m3

 (Oberdörster et al., 1995), and a significant, three- to fourfold 

 increase in the frequency of hprt mutations was seen in alveolar 

 epithelial cells (Driscoll et al., 1995 and in press; see section 

 B7.6). Thus, burdens of particles of low toxicity per se, similar to 

 those reached in long-term studies in rats, can be mutagenic, possibly 

 through the involvement of DNA damaging oxidants derived from 

 inflammatory cells. 

 Appendix B10.1 Construction of a biologically based (alternative) 

 model

 1. Preliminary considerations 

 In order to evaluate the effects of various biological 

 assumptions on the assessments of the risk of exposure to diesel 

 exhaust, a mathematical dose-response model must be constructed that 

 takes into account the proposed biological mechanisms. As a 

 significant issue in assessing the risk of diesel exhaust is the 

 effect of lung overloading on tumour induction, the model should have 

 the following properties: 

 -- It should depend on dose metrics for both organic compounds and 

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 the carbon core, and it should account for the contributions of 

 each to tumour induction and formation both separately and 

 jointly. 

 -- It should allow for changes in the model parameters with time due 

 to increasing lung burden during exposure. 

 -- It should view cell proliferation and tumour induction and 

 formation stochastically: it is not realistic to assume 

 deterministic clonal growth. For instance, it should not be 

 assumed that all cells divide at the same age. 

 It is therefore assumed that a normal cell can be initiated by 

 both organic compounds and the carbon core. The initiation rate is 

 denoted by μ1, which is a function of the background rate and that 

 induced by diesel exhaust (as specified below). Because an initiated 

 cell eventually either dies or enters the cell cycle (including cells 

 in quiescence, G0), it is reasonable to assume that the lifetime of 

 an initiated cell follows a certain probability distribution. In this 

 model, a cell in G0 phase is equivalent to one with a certain 

 probability of a very long lifetime (i.e. in the right-hand tail of 

 the distribution of the cell's lifetime). At the end of its lifetime, 

 it either dies (death) with probability b, divides into two daughter 

 cells (birth) with probability a, or divides into one initiated cell 

 and one malignant cell (second transition) with probability μ2; 

 alpha + ß + μ2 = 1. Instead of assuming that a single malignant cell 

 is equivalent to a tumour, as in the model proposed by Moolgavkar & 

 Venzon (1979) and Moolgavkar & Knudson (1981), it is assumed here that 

 a malignant cell has a certain probability of becoming a tumour; this 

 probability is assumed to be dose-dependent, thus allowing for an 

 evaluation of the effect of dose on tumour progression. It should be 

 noted that the proposed model does not exclude the possibility that 

 there may be more than one step in the 'initiation' of a normal cell. 

 The rate of initiation used in the model should be viewed as a net 

 rate that represents several genetic alterations and repairs. 

 2. Mathematical model and relationship of parameters to lung burden 

 A dose-response function P(t:d,D) is constructed for the 

 probability of cancer by time (age) t, which depends on both organic 

 compounds, d, and particles (carbon core), D, and incorporates the 

 biologically based concept discussed above. Because the model 

 parameters that are not observed directly in the laboratory can be 

 estimated statistically only from the results of bioassays at high 

 concentrations, the model should not be considered a real model of 

 diesel-induced carcinogenesis; uncertainty about extrapolation to low 

 doses remains. 

 A model with the features presented above was originally proposed 

 by Chen & Farland (1991) and was extended into one with time-variable 

 parameters by Tan & Chen (1992). This model was used as the basis for 

 constructing a biologically based dose-response model. A brief 

 mathematical description is presented in Appendix B10.3. 

 The data on time to event from Mauderly et al. (1987) were used 

 to estimate model parameters. These data are useful because they 

 contain information on natural mortality and serial sacrifice of 

 animals with and without (malignant) tumours, which is valuable for 

 estimating tumour latency. In order to use this information to 

 calculate maximum likelihood estimates of parameters, an 'E-M' 

 algorithm was derived. In the E-M algorithm, each iteration involves 

 an 'expectation' step (E) and a 'maximization' step (M) (see Appendix 

 B10.2). 

 (a) Model parameters and notations 

 The following parameters are incorporated into the dose-response 

 model, which includes the rate of initiation (μ1), the rate of 

 proliferation (gammaalpha), the rate of conversion (gammaμ2), and 

 the probability of progression ( q). The rate of death of the 

 initiated cells is implicitly defined by gamma(1-μ2-alpha). The 

 parameters are all dose dependent. 

 D: dose of carbon core in milligrams per square centimetre of 

 lung epithelial surface; varies over time; 

 d: dose of organic compounds in milligrams per square centimetre 

 of lung epithelial surface; 

 μ1: dose-related initiation rate (per cell per day); depends on 

 μ0 (background rate), d, and D by μ1 = μ0 (1 + ad + bD), where 

 a and b are parameters to be estimated statistically; 

 μ2: probability that a malignant cell will be produced by the end 

 of the lifetime of an initiated cell; 

 alpha: probability that an initiated cell will divide into two 

 daughter cells by the end of its lifetime; 

 q: probability that a single malignant cell will develop into a 

 malignant tumour; 

 gamma: 1/gamma is the mean lifetime of an initiated cell in days; the 

 lifetime ends when the cell goes into mitosis or dies. If it 

 is assumed that the probability that a cell will go into 

 mitosis is about the same as the probability that it will die, 

 the mean cell lifetime can be conveniently interpreted as time 

 to mitosis (i.e. cell turnover time); thus, a shorter cell 

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 lifetime implies more frequent cell division. Time to mitosis 

 is a random variable, not a fixed constant as in the 

 assumption of the model of Greenfield et al. (1984), which was 

 used by Cohen & Ellwein (1988) to analyse the results of 

 bioassays to dectect urinary bladder cancer. 

 N: number of (normal) target cells. 

 (b) Practical considerations 

 The E-M algorithm developed in Appendix B10.2 is an elegant 

 procedure that can be used by statistical theory alone to test 

 hypotheses about whether a particular parameter is influenced by 

 organic compounds and the carbon core, individually or together. For 

 instance, it could be postulated that the parameter the reciprocal of 

 which represents mean cell lifetime is given by gamma( d,Di) = gamma0 + 

 gamma11 d + gamma12 Di, and then proceed to test the null hypothesis 

 that gamma11 = 0, i.e. no effect of organic compounds on the cell 

 lifetime. This temptation must, however, be resisted, because too many 

 parameters would have to be be estimated. Therefore, the biologically 

 plausible assumption that parameters q and gamma depend only on the 

 lung burden of the carbon core, D,

 is used. 

 The study of Mauderly et al. (1987) lasted about 940 days. In 

 order to construct a dose-response model including time-dependent lung 

 burden, the time interval (0-940) is divided into five sub-intervals, 

 each spanning six months, except for the last, which spans 730-940 

 days. The deposition-retention model developed by Yu et al. (1991), 

 corresponding to a concentration of diesel exhaust emissions in 

 ambient air of milligrams per cubic metre, is used to calculate 

 ( d,Di), where i = 1, 2, ..., 5; the dose of organic compounds, 

 d, does not change with time because it reaches a steady state soon 

 after exposure begins; and Di is the lung burden of carbon core 

 during the ith sub-interval. 

 The assumptions for the dose-parameters relationship are: 

 -- The rate of initiation associated with a lung burden { d,Di, i

 = 1, 2, ..., 5} is given by μi( d,Di) = μ0(1 + a * d + b * Di) for 

 i = 1, 2, ..., 5. This is the only parameter that is assumed to 

 depend on both d and D.

 -- The probability of tumour formation from a malignant cell is 

 assumed to be dependent on lung burden, D, from q( Di) = q0

 q0 Di, i = 1, 2, ..., 5. In order to simplify calculation, the

 possibility that q0 is also dependent on organic compounds, d, is 

 not considered. 

 -- The cell lifetime, gamma, is assumed to be related nonlinearly to 

 lung burden, D, from gamma( Di) = gamma0 + gamma1 Log(1 + Di), 

 i = 1, 2, ..., 5. 

 In order to reduce the number of parameters that are to be 

 estimated from the data of Mauderly et al. (1987), some of the 

 background parameters for the dose-response model (μ0, q0, and 

 gamma0) are estimated from the historical control rates for Fischer 

 344 rats in the US National Toxicology Program (reconstructed from 

 Portier et al., 1986). The dose-related parameters are then estimated 

 with the E-M algorithm, which is described in Appendix B10.2. The 

 parameters estimated for the model resulting from the tumour response 

 data of Mauderly et al. (1987) and the corresponding dosimetric 

 parameters (Table 52) are given in Table 53. 

 Table 52. Dosimetric parameters (milligrams per square centimetre of lung surface) used 

 in modelling 

 

 Exposure d D1 D2 D3 D4 D5

 concn 

 (mg/m3) 

 

 0.35 2.5 × 10-6 6.2 × 10-5 8.8 × 10-5 9.0 × 10-5 9.0 × 10-5 9.0 × 10-5

 3.50 3.6 × 10-5 7.5 × 10-4 2.4 × 10-3 3.9 × 10-3 5.3 × 10-3 6.3 × 10-3

 7.08 7.3 × 10-5 2.0 × 10-3 5.5 × 10-3 8.6 × 10-3 1.1 × 10-2 1.4 × 10-2

 

 d, organic compounds; Di, i = 1, 2, ..., 5, are average lung burdens of carbon core over 

 five time intervals. Values calculated from the retention model of Yu et al. (1991) 

 

 Table 53. Maximum likelihood estimates for model parameters 

 

 Parameter Estimate 

 μ 1.033 × 10-7

 a 1.103 × 104

 b 3.214 × 102

 μ2 7.907 × 10-7

 q0 1.035 × 10-1

 q1 5.332 × 10-2

 gamma0 1.662 × 10-2

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 gamma1 2.647 × 10-2

 alpha 5.443 × 10-1

 N (given) 8.80 × 107

 

 For definitions of parameters, see text. Background parameters μ0, q0, 

 and gamma0 are estimated separately from historical control data from 

 the US National Toxicology Program. The number of target cells, N, is 

 assumed to be 10 times the number of type II cells in mice, which is 

 given by Kauffman (1974). It is not essential that N be given 

 accurately because Nμ0 appears as a single term in the model; the 

 estimated μ0 will compensate for the underestimation or overestimation 

 of N. 

 Appendix B10.2 E-M algorithm

 The E-M algorithm, derived below, was used to calculate maximum 

 likelihood estimates of the parameters for the alternative model. The 

 data used were taken from Mauderly et al. (1987) and include the time 

 when an animal died, naturally or at sacrifice, with or without 

 (malignant) tumours. The theory of the algorithm is given by Dempster 

 et al. (1977). 

 Assume that the distinct times at which animals died are t1

 < t2 < ...< tm. The observations can be classified as follows: 

 a1x (i): observed number of natural deaths without tumour at time

 ti in treatment group x (The four groups are x = 

 1, 2, 3, 4.) 

 a2x (i): observed number of natural deaths with tumour at time

 ti in treatment group x

 b1x (i): series sacrificed at time ti without tumour in

 treatment group x

 b2x (i): series sacrificed at time ti with tumours in

 treatment group x.

 Let Td represent the time an animal died and T the time a 

 tumour developed. 

 alphax (i) = Pr Td = ti | Td > ti, T > ti,, x} (conditional probability 

 of death without tumour) 

 ßx( i | u) = Pr Td = ti | Td > ti, T Epsolin ( tu-1, tu], x} (related 

 to deaths with tumours) 

 Define 

 

 and 

 Sx (t) = Pr T > t | x} = exp[- t0integralt h(x)dx]. 

 The function Sx (t) is the probability of being tumour-free by

 time t.

 The exact forms of the hazard function, h(x), and Sx (t) are

 given in Appendix B10.3. 

 Let 

 a2x( i | u) = number of natural deaths at ti, with a tumour 

 developing during ( tu-1, tu], in treatment group 

 x, u < i,

 b2x( i | u) = number of animals sacrificed at ti, with a tumour 

 developing during ( tu-1, tu], in treatment group 

 x, u < i.

 Then 

 

 Let 

 

 and 

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 where 

 

 Given a2x( x), { a2x( i | u), u = 1, ..., i} is an ( i-1)-dimension 

 multinomial with parameter { a2x( i), Px( i | u), u = 1, ..., i}. 

 Thus, 

 E[ a2x( i | u) | a2x( i)] = a2x( i) Px( i | u). 

 Similarly, { b2x( i | u), u = 1, ..., i}, is an ( i - 1)-dimension 

 multinomial with parameters { b2x( i), Qx( i | u), u = 1, ..., i}, and 

 E[ b2x( i | u) | b2x( i)] = b2x( i) Qx( i | u). 

 It can be shown that the likelihood function is proportional to 

 

 where 

 

 Let 

 

 Let 

 

 be a vector of parameters in function S;

 alphax = [alphax(1), alphax(2), ..., alphax( m)], and 

 ßx( u) = [ßx(1 | u), ßx(2 | u, ..., ßx( m | u)] 

 be vectors of parameters related to conditional probabilities of death 

 with and without tumours. These parameters and those in thetax were 

 estimated by the E-M algorithm described below. 

 The M step: 

 Given initial values a2x( i | u) and b2x( i | u), estimate 

 

 The E step: 

 Given the estimated values of alphax( i), ßx( i), and thetax from the M 

 step, compute Px( i | u) and Qx( i | u) and obtain estimates of 

 a2x( i | u) and b2x( i | u) by 

 

 With the estimated values of a2x( i | u) and b2x( i | u) available 

 from the E step, go back to the M step and repeat the process until 

 the estimates are stable. 

 Appendix B10.3 A tumour growth model

 A tumour growth model with piece-wise constant parameters taken 

 from Tan & Chen (1992) is an extension of a stochastic model developed 

 by Chen & Farland (1991). The biological justification of this model 

 is similar to that of the two-stage model proposed by Greenfield et 

 al. (1984), which was used by Cohen & Ellwein (1988) to analyse 

 urinary bladder tumour occurrence. The two models differ, however, 

 with respect to their mathematical formulations; the one adopted in 

 this report is a stochastic model, whereas the other is a 

 deterministic model and does not allow for estimation of parameters 

 because it does not have complete mathematical expression. 

 Although its most general form is not used here because of lack 

 of data, the stochastic model of Chen & Farland (1991) has two 

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 desirable features: (i) it allows for any cell growth distribution 

 (e.g. Gompertz), rather than only exponential distribution as in other 

 models; and (ii) it incorporates the birth and death of tumour cells, 

 rather than assuming that a tumour is born once a single tumour cell 

 occurs, as did Moolgavkar & Venzon (1979) and Moolgavkar & Knudson 

 (1981). Therefore, if information on cell lifetime distribution and 

 the progression of tumour development is available, a reasonably 

 realistic model can be constructed. 

 For completeness, a brief description of the model is presented 

 here. The following notations are required: 

 N(t): number of normal (target) cells at time t,

 μ1: rate of initiation, and 

 contour the probability density function for the lifetime of an 

 integral (t): an initiated cell. 

 At the end of its lifetime, an initiated cell either divides 

 (mitosis) or dies (programmed or nonprogrammed death). If it enters 

 mitosis, it either divides either into two initiated cells with 

 probability a or into one initiated cell and one malignant cell with 

 probability μ2. At the end of a cell's lifetime, the probability of 

 it dying is ß = 1 - alpha - μ2. A similar set-up (to allow for any 

 cell lifetime distribution) can be made for a malignant cell; however, 

 we confined ourselves to a simpler version, assuming that the lifetime 

 of a malignant cell follows an exponential distribution. Thus, we 

 assume that a malignant cell follows a simple birth-death process; it 

 can either divide into two malignant cells at a rate alpham or die 

 at a rate ßm. 

 When the parameters are constant over time (age), the hazard 

 function is given by 

 h(t) = μ1μ2 0integralt N(s)m( t - s) ds

 where 

 

 where y1 < y2 are two real roots of alpha y2 - (alpha + ß + μ2 q) y + 

 ß = 0; alpha + ß + μ2

 = 1; q = 1 - ßm/alpham; A(t) = / 0integralt a(x)d x, where a(t) =

 contour integral( t)/[1 - F(t)] is the hazard function of the cell 

 lifetime and F(t) is the cumulative function of contour integral (t).

 Two cases of special interest are a(t) = gamma when an exponential 

 distribution is assumed and a(t) = exp(-gamma t), when the Gompertz 

 distribution is assumed. 

 When an exponential distribution (i.e. a(t) = gamma or A(t) =

 gamma t) and q = 1 are assumed, the model is equivalent to the 

 model of Moolgavkar & Venzon (1979) and Moolgavkar & Knudson (1981). A 

 special case that may be more appropriate than the exponential 

 distribution is that when the Gompertz distribution is assumed (i.e. 

 A(t) = [1 - exp(-gamma t)]/gamma). 

 For the model with time-dependent parameters, assume that the 

 study begins at time t0. Divide the time scale ( t0, t] into 

 k sub-intervals Lj = ( tj-1, tj], j = 1, 2, ... k-1 and Lk = ( tk-1, tk] 

 where tk = t. (Note that these sub-intervals may not be the same as 

 those defined by deaths or sacrifice previously.) The parameters that 

 vary over sub-intervals ( ti-1, ti], i = 1, 2, ..., k are μ1j, alphaj, 

 ßj, μ2j, N, and those parameters related to contour integral( t). The 

 hazard functionis given by 

 

 where 

 

 and 

 

 where y1j < y2j are two real roots of a alpha y2 - (alphaj + ßj + 

 μ2j qj) y + ßj = 0; alphaj + ßj + μ2j = 1; qj = 1 - ßmj/alphamj, j = 1, 

 2, ..., k.

 When an exponential distribution (i.e. Aj( t) = gammaj( t) and 

 qj = 1) is assumed, the model is equivalent to the model of 

 Moolgavkar & Venzon (1979) and Moolgavkar & Knudson (1981), with 

 piece-wise constant parameters. A special case that may be more 

 appropriate than the exponential distribution is that when the 

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 Gompertz distribution is assumed (i.e. Aj( t) = {1 - exp[-gammaj t)]} 

 /gammaj). 

 In the alternative model for exposure to diesel exhaust, in which 

 the total time is divided into five (i.e. k = 5) sub-intervals, Tan 

 & Chen (1992) showed that, under the assumption of exponential cell 

 lifetime distribution, the tumour-free distribution function, Sx( t), 

 can be written: 

 

 where sj = tj if j < k and sj = t if j = k, and 

 

 where, 

 WI = [alpha + ß + μ2 q)2 - 4alphaß] ́

 ZI = alpha - ß - μ2 q, and 

 DeltaI( s,t) = gammai( t - s) if both s and t are in the same closed 

 sub-interval [ ti-1, ti] and 

 

 if sepsilon Li, tepsilon Lj with tj < tj. 

 B11. RECOMMENDATIONS

 B11.1 Recommendations for the protection of human health 

 Diesel exhaust contributes to the total effect of combustion 

 products on the environment. The data reviewed in this monograph 

 support the conclusion that inhalation of diesel exhaust is of concern 

 with respect to both neoplastic and non-neoplastic diseases. The 

 particulate phase appears to have the greatest effect on health, and 

 both the particle core and the associated organic materials have 

 biological activity, although the gas-phase components cannot be 

 disregarded. The following actions are recommended for the protection 

 of human health. 

 -- Diesel exhaust emissions should be controlled as part of the 

 overall control of atmospheric pollution, particularly in urban 

 environments. 

 -- Emissions should be controlled strictly by regulatory inspections 

 and prompt remedial action. 

 -- Urgent efforts should be made to reduce emissions, specifically 

 of particulates, by changing exhaust train techniques, engine 

 design, and fuel composition. 

 -- In the occupational environment, good work practices should be 

 encouraged, and adequate ventilation must be provided to prevent 

 excessive exposure. 

 B11.2 Recommendations for the protection of the environment 

 Too few data are available on which to base specific suggestions 

 with regard to diesel exhaust, except as part of the general control 

 of emissions. 

 B11.3 Recommendations for further research 

 The following recommendations are intended to help reduce the 

 uncertainty associated with assessing the risks of exposure to diesel 

 exhaust for human health. 

 -- Research is required on methods for determining concentrations of 

 diesel particulates in the presence of fine particles from other 

 sources, in order to improve assessments of the exposures of 

 occupational groups and the general population indoors and 

 outdoors. The quality and quantity of emissions from engines that 

 are not properly maintained or tuned should be investigated as 

 part of these studies. 

 -- The effects of diesel exhaust emissions on lung clearance should 

 be studied in animals and humans at concentrations including 

 those likely to be encountered by humans. 

 -- The mechanisms involved in the etiology of tumours induced in 

 rats exposed to particulate must be investigated by all available 

 techniques. 

 -- The relative roles of the gas and particulate phases of diesel 

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 exhaust in causing adverse effects after short- and long-term 

 exposure should be investigated. 

 -- Epidemiological investigations into the effects of diesel exhaust 

 should be continued in order to assess issues of dose and latency 

 in human populations with respect to lung cancer; and longer-term 

 studies should be conducted in populations exposed to diesel 

 exhaust with respect to noncarcinogenic effects. 

 -- Further steps should be undertaken to improve the combustion and 

 exhaust emission characteristics of diesel engines. 

 B12. PREVIOUS EVALUATIONS BY INTERNATIONAL BODIES

 The carcinogenic risks for human beings were evaluated by a 

 working group convened by the International Agency for Research on 

 Cancer in 1988 (International Agency for Research on Cancer, 1989b). 

 The conclusions were: 

 'There is sufficient evidence for the carcinogenicity in 

 experimental animals of whole diesel engine exhaust. 

 'There is inadequate evidence for the carcinogenicity in 

 experimental animals of gas-phase diesel engine exhaust (with 

 particles removed). 

 'There is sufficient evidence for the carcinogenicity in 

 experimental animals of extracts of diesel engine exhaust particles. 

 'There is limited evidence for the carcinogenicity in humans of 

 diesel engine exhaust. 

 'There is limited evidencefor the carcinogenicity in humans of 

 engine exhausts (unspecified as from diesel or gasoline engines). 

 'Overall evaluation 

 'Diesel engine exhaust is probably carcinogenic to humans (Group2A).' 

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 PARTIE A COMBUSTIBLE DIESEL

 A1. RESUME

 A1.1 Identité, propriétés physiques et chimiques et méthodes 

 d'analyse 

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 Le combustible diesel est un mélange complexe d'alcanes normaux 

 ramifiés ou cycliques (de 60 à plus de 90% de volume; longueur de la 

 chaîne hydrocarbonée, généralement comprise entre C9 et C30), de 

 composés aromatiques, surtout des alkyl benzènes, (5 à 40% en volume) 

 et de petites quantités d'alcènes (0 à 10% en volume) obtenu lors de 

 la distillation fractionnée du pétrole, à partir du distillat moyen 

 qui correspond à la fraction gazole. Le combustible diesel peut 

 contenir, à des concentrations de quelques parties par million, du 

 benzène, du toluène, de l'éthylbenzène, du xylène et des hydrocarbures 

 aromatiques polycycliques (HAP), en particulier du naphtalène et 

 certains de ses dérivés méthylés. La teneur en soufre du combustible 

 diesel dépend de l'origine du pétrole et du procédé de raffinage 

 utilisé. Dans un certain nombre de pays, elle est soumise à 

 réglementation et se situe en général entre 0,05 et 0,5% en poids. On 

 utilise un certain nombre d'additifs pour modifier la viscosité, la 

 conservation et la combustion, pour différencier les différents 

 produits et également pour satisfaire aux spécifications commerciales. 

 A la température ambiante, le combustible diesel est en général 

 modérément volatile, légèrement visqueux, inflammable et se présente 

 sous la forme d'un liquide brun à odeur de kérosène. L'intervalle 

 d'ébullition est habituellement de 140°C à 385°C (plus de 588°C pour 

 le carburant destiné aux moteurs marins); à 20°C, la densité est de 

 0,87-1,0 g/cm3 et la solubilité dans l'eau de 0,2-5 mg/litre. La 

 qualité et la composition du combustible diesel influent 

 considérablement sur l'émission de polluants par les moteurs diesel. 

 Les conditions d'allumage (exprimées au moyen de l'indice de cétane), 

 la densité, la viscosité et la teneur en soufre sont des variables 

 importantes. Les spécifications du combustible diesel commercial 

 varient fortement d'un pays à l'autre. 

 Les différents types de mazout destinés au chauffage ou de 

 kérosène pour avions à réaction produits lors du raffinage du pétrole 

 peuvent avoir une composition analogue à celle du combustible diesel, 

 mais avec des additifs différents. Les données biologiques relatives à 

 ces mélanges ont donc été prises en considération lors de l'évaluation 

 toxicologique et écotoxicologique. 

 En raison de la complexité du mélange, il n'existe pas de méthode 

 d'analyse spécifique pour le combustible diesel et les techniques 

 utilisées pour la plupart des études d'impact dur l'environnement ne 

 se prêtent qu'au dosage des hydrocarbures totaux. Elles consistent 

 tout d'abord à effectuer une extraction par solvant, puis à éliminer 

 les hydrocarbures d'origine naturelle et enfin à procéder au dosage 

 par gravimétrie, spectrophotométrie infrarouge ou chromatographie en 

 phase gazeuse. Ni la méthode gravimétrique, ni la spectrophotométrie 

 infrarouge ne donnent de renseignements qualitatifs ou quantitatifs 

 utiles et ne peuvent donc être utilisées que pour un premier tri. La 

 chromatographie en phase gazeuse couplée à des techniques de détection 

 telles que l'ionisation de flamme ou la spectrométrie de masse, est la 

 méthode classique d'analyse des échantillons prélevés dans 

 l'environnement. Il existe de nombreuses autres méthodes pour la 

 recherche et le dosage des divers hydrocarbures présents dans le 

 combustible diesel. 

 A1.2 Sources d'exposition humaine et environnementale 

 Le combustible diesel est produit par raffinage du pétrole brut. 

 Afin de satisfaire aux spécifications techniques relatives au 

 rendement des moteurs, ces combustibles sont généralement mélangés; 

 l'adjonction ultérieure d'additifs en améliore également l'adaptation 

 à diverses utilisations particulières. Ces combustibles sont largement 

 utilisés dans les transports. Les plus volatils d'entre eux, qui 

 présentent une faible viscosité, sont destinés aux moteurs tournant à 

 haut régime, les combustibles plus lourds étant réservés aux 

 transports ferroviaires et maritimes. Une grande partie des véhicules 

 lourds de transport routier sont mus par des moteurs diesel. Les cars 

 à moteur diesel destinés au transport des voyageurs se répandent de 

 plus en plus en Europe et au Japon (10 à 25%) alors qu'en Amérique du 

 Nord, la proportion de cars assurant les transports en commun est 

 d'environ 1 à 2%, et a même une légère tendance à se tasser. On 

 utilise également le combustible diesel pour alimenter les chaudières 

 et les moteurs fixes, qu'il s'agisse de moteurs à pistons, de turbines 

 à gaz, de pompes d'oléoducs, de compresseurs, de générateurs de vapeur 

 pour centrales thermiques, de brûleurs, et d'installations de 

 chauffage industriel par convection ou circulation d'eau. 

 La demande mondiale de combustible diesel a régulièrement 

 progressé au cours des 5 dernières années. En 1985, les chiffres de 

 consommation étaient les suivants: environ 170 000 kilotonnes par an 

 en Amérique du Nord, environ 160 000 kilotonnes par an, gazole y 

 compris, dans l'Union européenne, environ 46 000 kilotonnes par an en 

 Australie, au Japon et en Nouvelle-Zélande, soit l'équivalent de 

 1062 kilotonnes par jour. En 1990, la demande mondiale a été estimée à 

 environ 1110 kilotonnes par jour. 

 On ne dispose d'aucun renseignement sur les émissions qui se 

 produisent lors de la production des combustibles diesel; toutefois, 

 il semble que cette source soit d'importance secondaire, étant donné 

 que le raffinage s'effectue en vase clos. Si des émissions doivent se 

 produire, c'est surtout au cours du stockage et du transport. Ces 

 combustibles peuvent également être répandus dans l'environnement par 

 suite de déversements accidentels ou dans des stations service lorsque 

 l'on fait de plein des véhicules. L'atmosphère et l'hydrosphère sont 

 les compartiments du milieu les plus fortement affectés par ces 

 décharges accidentelles. Il peut y avoir contamination du sol par du 

 combustible diesel à la faveur d'accidents et ce type de contamination 

 pose également un problème dans les gares de triage. 

 Parmi les nombreuses techniques utilisables pour nettoyer les 

 sols contaminés par du combustible diesel, on peut citer l'excavation, 

Diesel fuel and exhaust emissions (EHC 171, 1996) Page 164 of 184

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 les méthodes biologiques et le confinement. 

 A1.3 Transport, distribution et transformation dans 

 l'environnement 

 On ne dispose que très rares données sur la destinée du 

 combustible diesel dans l'environnement mais on suppose que son mode 

 de distribution et de transformation est comparable à celui des huiles 

 lourdes destinées au chauffage comme le No 2 qui a été bien étudié. En 

 cas de déversement dans l'eau, il se forme presque immédiatement une 

 nappe de mazout. Les constituants polaires et ceux dont la masse 

 moléculaire est relativement faible se dissolvent et s'éliminent de la 

 nappe par lessivage; les constituants volatils s'évaporent en surface 

 et il y a un début de dégradation microbienne. Par attaque chimique et 

 biologique, la composition de la nappe se modifie. Ces processus 

 dépendent de la température; les déversements qui se produisent en 

 milieu arctique conduisent à des nappes plus durables que sous les 

 climats tempérés. En milieu marin, la plupart des composés aromatiques 

 de masse moléculaire relative faible se dissolvent dans la phase 

 aqueuse, mais les alcanes normaux, les alcanes ramifiés, les 

 cycloalcanes et les composés aromatiques restantes peuvent demeurer 

 dans les sédiments pendant plus d'un an. 

 Bien qu'on ne dispose d'aucune donnée sur la photo-oxydation du 

 combustible diesel dans l'air et l'eau, on sait que les composants qui 

 s'évaporent subissent une décomposition photochimique. Ainsi, on a 

 montré que l'huile lourde No 2 subissait une photo-oxydation rapide en 

 milieu aqueux dans les conditions naturelles. 

 Les différents constituants du combustible diesel sont 

 intrinsèquement biodégradables, mais à des degrés et à des 

 vitesses variables. Les alcanes normaux ainsi que les dérivés 

 n-alkylaromatiques et les molécules aromatiques simples en 

 C10-C22, sont les plus facilement dégradables. Les petites 

 molécules se métabolisent en général rapidement. Les n-alcanes à 

 longue chaîne sont plus lentement dégradés en raison de leur 

 hydrophobicité et du fait qu'ils sont visqueux ou solides à la 

 température ambiante. Les alcanes ramifiés et les cycloalcanes sont 

 relativement résistants à la décomposition biologique et les 

 hydrocarbures aromatiques polycycliques, franchement résistants. La 

 vitesse globale de dégradation des hydrocarbures est limitée par la 

 température, la teneur en eau et en oxygène, le pH, la présence de 

 nutriments inorganiques et la versatilité métabolique microbienne. 

 Les algues unicellulaires peuvent fixer et métaboliser les 

 hydrocarbures aliphatiques et aromatiques mais on connaît mal 

 l'ampleur de ce phénomène. Contrairement aux microorganismes qui 

 utilisent les hydrocarbures du pétrole comme source de carbone, le 

 métabolisme animal a généralement tendance à oxyder et à conjuguer les 

 produits pour les transformer en substances plus solubles et donc plus 

 faciles à excréter. Toutes les espèces animales étudiées sont capables 

 de fixer des hydrocarbures du pétrole. On sait que les hydrocarbures 

 aromatiques polycycliques, le pétrole brut et les produits pétroliers 

 raffinés induisent les enzymes du cytochrome P450 et chez de 

 nombreuses espèces de poissons de mer et d'eau douce, on constate 

 qu'il y a accroissement du métabolisme des hydrocarbures. 

 On n'a que peu de données sur la bioaccumulation du combustible 

 diesel dans les conditions du laboratoire mais il est largement 

 prouvé, par l'étude des nappes de mazout et d'autres études de 

 laboratoire consacrées à ce genre de produits, en particulier le No 2, 

 que les organismes aquatiques concentrent les hydrocarbures. Le 

 coefficient de partage du combustible diesel entre le n-octanol et 

 l'eau est égal à 3,3-7,06, ce qui incite à penser que son potentiel de 

 bioaccumulation est élevé; quoi qu'il en soit, de nombreux composés de 

 faible masse moléculaire relative sont facilement métabolisés et la 

 bioaccumulation effective des produits de masse moléculaire relative 

 plus élevée est limitée par leur faible solubilité dans l'eau et les 

 dimensions importantes de leur molécule. Il en résulte donc que la 

 bioaccumulation peut en réalité être faible. 

 On a constaté qu'après des déversements de combustible diesel, le 

 poisson pouvait devenir inconsommable. On ne dispose d'aucune donnée 

 sur la bioamplification du combustible diesel. 

 On ne possède non plus aucune donnée expérimentale sur le 

 déplacement du combustible diesel à travers le sol, encore qu'il ait 

 été avancé qu'il existait une corrélation directe entre ce déplacement 

 et la viscosité cinématique du produit. Le déplacement du kérosène 

 dans un sol dépend de la teneur en eau et de la nature de ce sol. 

 A1.4 Concentrations dans l'environnement et exposition humaine 

 Les divers types de combustible diesel étant constitués de 

 mélanges complexes, on n'en n'a pas mesuré la concentration dans 

 l'environnement. On peut mettre en évidence la présence de leurs 

 divers constituants dans presque tous les compartiments du milieu, 

 même s'il n'est pas possible d'en vérifier l'origine. Lorsqu'il y a 

 exposition de la population générale, elle se produit dans les 

 stations service ou par suite de déversements. 

 Il peut y avoir exposition professionnelle au combustible diesel 

 à la faveur d'un grand nombre d'activités. Du fait de leur faible 

 volatilité, ces combustibles ne devraient produire qu'une vapeur assez 

 ténue à la température normale mais si l'on opère à température 

 élevée, la concentration peut augmenter sensiblement. 

 A1.5 Effets sur les mammifères de laboratoire et les systèmes 

 d'épreuve in vitro 

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 Les combustibles diesel présentent une faible toxicité aiguë 

 après administration par voie orale, percutanée ou respiratoire. Chez 

 toutes les espèce étudiées (souris, lapin, rat, cobaye) on a obtenu 

 pour la DL50 par voie orale une valeur > 5000 mg/kg de poids 

 corporel. En application cutanée, on obtient une valeur de la DL50

 également > 5000 mg/kg de poids corporel chez la souris et le lapin, 

 mais des valeurs > 2000 mg/kg de poids corporel ont été relevées pour 

 certains types de kérosène et de distillats moyens, selon le protocole 

 d'application et la limite inférieure de la dose. Chez des rats 

 exposés par la voie respiratoire, on a obtenu une valeur de la CL50

 d'environ 5 mg/litre, sauf dans le cas d'un distillat moyen de 

 première distillation pour lequel on a obtenu une valeur de 

 1,8 mg/litre. 

 Chez des lapins badigeonnés avec du combustible diesel à des 

 doses allant jusqu'à 8000 μl/kg de poids corporel et par jour et chez 

 des souris traitées dans les mêmes conditions avec des doses 

 quotidiennes atteignant 40 000 mg/kg de poids corporel, on a observé 

 une acanthose et une hyperkératose dues à une grave irritation. Les 

 lapins se sont révélés plus sensibles que les souris. Chez la souris, 

 l'inhalation de combustible diesel a provoqué des effets 

 neurodépresseurs à des concentrations allant jusqu'à 0,2 mg/litre; en 

 revanche ces effets n'ont pas été observés chez des rats exposés à des 

 doses allant jusqu'à 6 mg/litre. Chez les rats, on a observé une 

 réduction du poids corporel et du poids du foie. 

 Après inhalation de doses de combustible diesel allant jusqu'à 

 1,5 mg/litre dans des conditions de subchronicité, des souris, des 

 rats et des chiens n'ont pas présenté de signes sensibles de toxicité 

 cumulative. Le syndrome néphropathique spécifique observé chez les 

 rats mâles est lié à l'accumulation intrinsèque d'inclusions hyalines 

 dans les tubules rénaux. 

 Les seuls effets de l'exposition à long terme ont été des 

 ulcérations après application cutanée de combustible diesel à des 

 souris (doses quotidiennes: 250 ou 500 mg/kg de poids corporel) et une 

 modification importante du poids des organes après inhalation par des 

 rats de ce même produit à la dose de 1 ou 5 mg/litre. Dans les deux 

 études, on a constaté une réduction du poids corporel moyen. 

 Les divers types de combustible diesel se révèlent légèrement à 

 fortement irritants pour la peau du lapin. Ils ne produisent pas 

 d'irritation oculaire mais dans le cas d'un certain nombre de 

 kérosènes, on a fait état d'un léger effet irritant. Il n'y a pas de 

 sensibilisation cutanée. 

 Le combustible diesel et les carburéacteurs (kérosène) ne se sont 

 révélés ni embryotoxiques, ni tératogènes lors de deux études 

 effectuées sur des rats à qui l'on avait fait inhaler ces produits aux 

 doses de 100 ou 400 ppm ainsi que dans une autre étude au cours de 

 laquelle des rats avaient reçu par gavage des doses quotidiennes de 

 ces produits allant jusqu'à 2000 mg/kg de poids corporel. Dans la 

 dernière étude, on a observé une réduction du poids des foetus. 

 Les épreuves effectuées sur Salmonella typhimurium n'ont pas 

 permis de prouver de manière nette l'existence d'une activité 

 mutagène. Des résultats positifs ont bien été observés chez 

 S. typhimurium ainsi que sur des cellules lymphomateuses de souris 

 mais leur caractère contradictoire les a fait considérer comme 

 équivoques. Les tests de génotoxicité effectués sur des souris 

 in vivo (induction de la formation de micronoyaux ou d'aberrations 

 chromosomiques) ont également donné des résultats équivoques ou 

 négatifs. 

 Les combustibles diesel présentent un faible pouvoir cancérogène 

 au niveau cutané. Dans l'état actuel de la recherche, on ne peut 

 déterminer si l'activité cancérogène de ces produits est due à leur 

 génotoxicité ou aux lésions chroniques qu'ils induisent dans le derme. 

 A1.6 Effets sur l'homme 

 Il peut y avoir exposition non professionnelle aux combustibles 

 diesel lors du remplissage manuel de citernes. C'est principalement 

 lors de déversements accidentels que la peau peut se trouver fortement 

 exposée à ces produits, encore que pour une brève durée. 

 A la suite de contacts directs avec le peau on a observé de 

 l'anurie, une insuffisance rénale, des symptômes gastro-intestinaux 

 ainsi qu'une hyperkératose cutanée. Des pneumopathies d'aspiration 

 d'origine toxique ont été observées par suite de l'ingestion 

 accidentelle de combustible diesel. Après inhalation, on peut observer 

 une toux grasse persistante. Lors d'une étude cas-témoins portant sur 

 des hommes exposés à du combustible diesel, on a constaté qu'ils 

 courraient un risque accru de cancers du poumon, autres que les 

 adénocarcinomes; on a également observé une association positive avec 

 le cancer de la prostate, encore que le risque ait été plus important 

 dans le groupe soumis à une exposition 'non substantielle' que dans 

 celui qui était soumis à une exposition 'substantielle'. 

 Lors d'une étude transversale portant sur des ouvriers d'une 

 usine exposés à des carburéacteurs, on a constaté qu'ils étaient plus 

 fréquemment sujets à des étourdissements, des maux de tête, des 

 nausées, des palpitations, une sensation d'oppression thoracique et 

 une irritation oculaire que les témoins non exposés. La concentration 

 moyenne pondérée par rapport au temps de la vapeur dégagée par le 

 combustible au niveau de la zone de respiration avait été estimée à 

 128-423 mg/m3. 

Diesel fuel and exhaust emissions (EHC 171, 1996) Page 166 of 184

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 A1.7 Effets sur les autres êtres vivants au laboratoire et dans 

 leur milieu naturel 

 Le combustible diesel est plus toxique que le pétrole brut pour 

 les animaux et les plantes aquatiques. L'écotoxicité du combustible 

 diesel est généralement attribuée à la présence de composés 

 aromatiques solubles, mais les hydrocarbures aliphatiques insolubles 

 peuvent également jouer un rôle. Parmi les composés aromatiques, les 

 dérivés monocycliques sont les moins toxiques, leur toxicité aiguë 

 augmentant avec la masse moléculaire jusqu'aux composés tétra- ou 

 pentacycliques, encore que ces derniers soient peu solubles dans l'eau 

 de mer. Certains animaux, comme les poissons et les oiseaux, peuvent 

 avoir le corps enduit de produit, avec des effets toxiques parfois 

 mortels. 

 On a étudié en laboratoire le combustible diesel et notamment ses 

 fractions solubles dans l'eau, les dispersions huile-eau et le pétrole 

 microencapsulé. Il apparaît que le combustible diesel ne réduit pas 

 sensiblement la croissance des cultures d'algues vertes du genre 

 Euglena gracilis, mais à faible concentration (0,1%), il inhibe 

 presque complètement la croissance de Scenedesmus quadricauda. Le 

 diesel léger (0,05%) stimule la croissance, la photosynthèse et la 

 synthèse de la chlorophylle a chez Chlorella salina, mais il en 

 inhibe légèrement la respiration. A concentration plus élevée, le taux 

 de croissance et la photosynthèse sont fortement réduits. Une 

 exposition de longue durée inhibe la croissance des algues benthiques 

 comme Ascophyllum nodosum et Laminaria digitata. Chez les algues 

 bleues, la photosynthèse est réduite par les fractions aromatiques et 

 asphaltiques, mais pas par la fraction aliphatique. 

 Le combustible diesel est fortement toxique pour les daphnies, 

 pour les larves de chironomidés et pour le mollusque Viviparus

 bengalensis (un gastéropode). A la concentration de 0,1 ml/litre, il 

 a provoqué la mort de copépodes du genre Tigriopus californicus,

 en l'espace de cinq jours. 

 Les moules du genre Mytilus edulis, accumulent le combustible 

 diesel, avec pour conséquence une réduction marquée de leur rythme 

 d'alimentation et de croissance; leur reproduction souffre également 

 d'une exposition de longue durée à ce produit. La CE50 relative au 

 frai des moules exposées pendant 30 jours à du combustible diesel, a 

 été trouvée égale à 800 μg/litre. La CL50 de gazole microencapsulé a 

 été égale à 5000 μg/litre pour des moules en maturation exposées 

 pendant 30 jours. Le gazole s'est révélé plus toxique pour les larves 

 que pour les jeunes moules: il avait un effet nocif sur la croissance 

 des larves à la dose de 10 μg/litre. 

 Des crabes d'eau douce (Barytelphusa cunicularis) exposés à des 

 concentrations sublétales de combustible diesel pendant des durées 

 allant jusqu'à 96 heures, ont généralement réduit leur consommation 

 d'oxygène, en particulier aux concentrations les plus faibles et pour 

 des durées d'exposition allant jusqu'à 8 heures. Lorsque l'exposition 

 se prolongeait, la consommation d'oxygène était égale ou supérieure à 

 celle des animaux témoins. 

 Lors d'épreuves de 96 heures visant à évaluer la toxicité aiguë 

 du produit sur des alevins de salmonidés dans des conditions 

 statiques, on a constaté que le combustible diesel était plus toxique 

 pour Onchorhychus gorbuscha (CL50: 32-123 mg/litre), que pour 

 O. kisutch (CL50: 2186-3017mg/litre) ou pour la truite arc-en-ciel 

 O. mykiss (CL50: 3333-33 216 mg/litre) quel que soit le type 

 d'eau. 

 Le seuil de détection des réactions comportementales de la morue 

 ( Gadus marhua L.), exposée à du combustible diesel dans de l'eau de 

 mer, a été trouvé égal à 100-400 ng/litre. Un poisson de 

 l'antarctique, Pagothenia borchgrevinki, a résisté pendant des 

 durées allant jusqu'à 72 heures à la fraction hydrosoluble non diluée 

 du combustible diesel, tout en présentant cependant des signes de 

 stress. 

 Dans le cas des oiseaux, il peut y avoir contamination externe ou 

 interne par les produits pétroliers. Le combustible diesel supprime 

 l'hydrophobicité du plumage et peut être ingéré lorsque l'oiseau lisse 

 ses plumes. Du combustible diesel et du mazout administrés par gavage 

 à des canards à la dose de 2 ml/kg de poids corporel, a provoqué au 

 bout de 24 heures une stéatose, une inflammation extrême des poumons, 

 une infiltration graisseuse du foie et une dégénérescence hépatique. 

 L'administration de combustible diesel ou de mazout à la dose de 

 1 ml/kg a également entraîné une grave irritation des voies digestives 

 et une néphrose toxique. A doses plus élevées, on a observé une 

 hypertrophie des surrénales (due principalement à une hyperplasie du 

 tissu cortical), une chute du taux de la cholinestérase plasmatique, 

 de l'ataxie et des tremblements. Jusqu'à 20 ml/kg de poids corporel, 

 la contamination n'a pas été mortelle pour les oiseaux en bonne santé 

 mais la DL50 s'abaissait à 3-4 ml/kg de poids corporel lorsque le 

 combustible diesel ou le mazout était administré à des oiseaux 

 stressés. 

 En cas de déversement de combustible diesel, le zooplancton se 

 révèle extrêmement vulnérable aux constituants dispersés ou dissous du 

 pétrole, mais moins aux nappes d'huile flottante. Pour les organismes 

 aquatiques, la nocivité de ces produits peut se manifester de diverses 

 manières: mortalité directe (oeufs de poisson, copépodes et plancton), 

 contamination externe (chorions des oeufs de poisson ou cuticules et 

 appendices buccaux des crustacés), contamination tissulaire par des 

 constituants aromatiques, développement anormal des embryons de 

 poisson et perturbation du métabolisme. 

Diesel fuel and exhaust emissions (EHC 171, 1996) Page 167 of 184

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 A1.8 Evaluation des risques pour la santé humaine 

 Il peut y avoir exposition de la population générale au 

 combustible diesel et à d'autres distillats moyens sur les lieux et 

 dans les circonstances suivants: dans les stations service, lors de 

 déversements accidentels, lors de la manipulation de ces combustibles 

 et lors de l'utilisation de pétrole lampant pour la cuisine ou le 

 chauffage. Il peut y avoir exposition des travailleurs à ces produits 

 lors de la manipulation et du transvasement du combustible dans les 

 terminaux, les citernes et les stations services; lors de la 

 fabrication, de la réparation, de l'entretien et de l'essai des 

 moteurs diesel et autres matériels; lors de l'utilisation de 

 combustible diesel pour le nettoyage ou comme solvant ou encore lors 

 de la manipulation des prélèvements de routine au laboratoire. En 

 raison de sa faible volatilité, le produit ne devrait pas émettre de 

 vapeurs très denses à la température ambiante, encore que dans un 

 espace confiné et à température élevée, la vapeur puisse être plus 

 concentrée. 

 Lors de la manipulation normale du combustible diesel, 

 l'exposition aux vapeurs est minime. L'effet le plus probable sur la 

 santé humaine consiste en une dermatite de contact. Le combustible 

 diesel est irritant pour la peau mais il ne semble pas irriter la 

 muqueuse oculaire. Des effets toxiques aigus au niveau rénal peuvent 

 s'observer après exposition cutanée, mais on ignore quels peuvent être 

 les effets à long terme d'une absorption percutanée de faibles 

 concentrations. 

 L'ingestion de combustible diesel peut avoir des effets toxiques 

 qui se traduisent quelquefois par une régurgitation et une aspiration 

 pouvant provoquer une pneumonie chimique, comme dans le cas de tout 

 hydrocarbure entre certaines limites de viscosité. 

 Chez des rongeurs exposés par la voie respiratoire à du 

 combustible diesel à des concentrations allant jusqu'à 0,2 mg/litre, 

 on a observé un effet neurodépresseur dans le cas de souris, mais pas 

 chez des rats, mêmes aux concentrations les plus élevées. Chez des 

 rats mâles, une exposition subchronique par la voie respiratoire à 

 divers distillats a produit une néphropathie spécifique à 

 alpha2-microglobulines; cette observation n'est pas considérée comme 

 transposable à l'homme. 

 Les combustibles diesel ne se sont révélés ni embryotoxiques ni 

 tératogènes chez les animaux exposés par la voie orale ou par la voie 

 respiratoire. 

 Rien n'indique de façon nette qu'il existe une activité mutagène 

 chez les bactéries, mais les résultats d'autres tests de génotoxicité 

 in vitro et in vivo sont plutôt équivoques. 

 Un étude cas-témoins portant sur des ouvriers exposés à du 

 combustible diesel incitent à penser qu'il existe un risque accru de 

 cancers du poumon n'appartenant pas au type épithélium glandulaire 

 ainsi que de ce cancer de la prostate. Il n'a pas été possible 

 d'établir de relation dose-réponse pour l'un ou l'autre de ces cas. En 

 raison du petit nombre d'études disponibles, du petit nombre de cas et 

 par voie de conséquence, de l'étendue de l'intervalle de confiance, il 

 n'est pas possible de tirer la moindre conclusion de ces données au 

 sujet de la cancérogénicité du produit pour l'homme. Chez la souris, 

 du combustible diesel administré par voie intradermique a présenté une 

 faible activité cancérogène. En raison de l'absence d'une activité 

 génotoxique avérée, il est possible d'invoquer un mécanisme non 

 génotoxique pour ces cancers; il pourrait s'agir par exemple d'une 

 irritation dermique chronique caractérisée par la répétition de 

 lésions cutanées entraînant une hyperplasie de l'épiderme. 

 A1.9 Evaluation des effets sur l'environnement 

 Il peut y avoir pollution de l'environnement par libération 

 accidentelle à grande échelle de combustible diesel, comme cela peut 

 se produire lors catastrophes affectant des réservoirs ou encore en 

 cas de fuites d'oléoduc ou, à plus petite échelle, lorsqu'il y a 

 contamination du sol aux alentours d'une usine ou d'un garage. Dans 

 l'eau, le combustible diesel s'étale presque immédiatement, les 

 composants polaires de masse moléculaire relative peu élevée se 

 dissolvent et disparaissent pas lessivage, les constituants volatils 

 s'évaporent et la décomposition microbienne s'amorece. L'élimination 

 des différents constituants dépend de la température et des conditions 

 climatiques. La composition chimique de la nappe varie dans le temps: 

 une fois répandues dans l'eau, certaines fractions s'évaporent et 

 subissent une décomposition photochimique; les fractions lourdes, 

 transportées par les particules qui se déposent, parviennent jusqu'aux 

 sédiments du fond; dans le sol les constituants du combustible diesel 

 migrent à des vitesses variables, en fonction de la nature de ce sol. 

 Les divers constituants du combustible diesel sont 

 intrinsèquement biodégradables mais leur vitesse de biodécomposition 

 dépend largement des conditions physiques et climatiques et de la 

 composition microbiologique du milieu. 

 Des organismes aquatiques et en particulier les mollusques, 

 accumulent les hydrocarbures à des degrés divers mais ceux-ci peuvent 

 être éliminés par passage dans l'eau claire. Le combustible diesel 

 peut subir une bioaccumulation; en revanche on ne dispose d'aucune 

 donnée sur une bioamplification éventuelle. 

 Tout déversement de combustible diesel a un effet nocif immédiat 

 sur l'environnement, qui se traduit par une mortalité notable pour la 

Diesel fuel and exhaust emissions (EHC 171, 1996) Page 168 of 184

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 faune et la flore. Il peut y avoir recolonisation au bout d'une année, 

 selon l'espèce animale ou végétale en cause et selon la composition 

 chimique et physique des résidus de produits pétroliers. 

 Les organismes aquatiques qui survivent aux déversements de 

 combustible diesel peuvent cependant subir une contamination externe 

 par ces produits et en accumuler dans leurs tissus: le stress qui en 

 résulte se traduit par un développement anormal et une modification du 

 métabolisme 

 PARTIE B GAZ D'ECHAPPEMENT DES MOTEURS DIESEL

 B1. RESUME

 B1.1 Identité, propriétés physiques et chimiques et méthodes 

 d'analyse 

 Les gaz d'échappement des moteurs diesel contiennent des 

 centaines de composés chimiques qui sont émis en partie dans la phase 

 gazeuse proprement dite et en partie dans la phase particulaire. Les 

 principaux produits gazeux de la combustion sont le dioxyde de 

 carbone, l'oxygène, l'azote et la vapeur d'eau: on trouve également du 

 monoxyde de carbone dixoyde de soufre, des oxydes d'azote et des 

 hydrocarbures et leurs dérivés. La phase gazeuse de la fraction 

 hydrocarbonée contient également un faible pourcentage en poids de 

 benzène et de toluène. Les autres constituants des gaz d'échappement 

 sont des hydrocarbures aromatiques polycycliques (HAP) de faible masse 

 moléculaire relative. 

 L'échappement des moteurs diesel est principalement caractérisé 

 par l'émission de particules dans une proportion environ 20 fois 

 supérieure à celle des moteurs à essence. Ces particules sont 

 composées de carbone élémentaire, de dérivés organiques adsorbés 

 provenant du combustible et de l'huile lubrifiante, de sulfates formés 

 à partir du soufre contenu dans le combustible et de dérivés 

 métalliques à l'état de traces. La granulométrie globale de ces 

 particules les situe en dessous du micron, entre 0,02 et 0,5 μm. Le 

 vieillissement peut conduire à une agglomération qui les amène à un 

 diamètre maximal de 30 μm. Les particules émises ont une aire 

 superficielle importante. Les composés organiques constituent 

 généralement 10 à 30% des particules totales mais avec des moteurs mal 

 conçus et mal entretenus cette proportion peut atteindre 90%. Dans 

 cette fraction on trouve également des hydrocarbures aromatiques 

 polycycliques de masse moléculaire élevée, entre autres, sous forme 

 oxygénée et nitrée, à des concentrations de l'ordre de plusieurs 

 parties par million. 

 Pour mesurer les émissions des véhicules on travaille en régime 

 transitoire ou stationnaire. L'échantillonnage peut se faire à partir 

 de gaz d'échappement dilués ou non dilués. Il est difficile d'obtenir 

 des échantillons débarrassés de tout artéfact car les constituants 

 peuvent subir des réactions chimiques, être adsorbés ou désorbés, ou 

 encore soumis à une condensation ou à une diffusion. Les hydrocarbures 

 aromatiques polycycliques d'importance toxicologique qui sont présents 

 dans les particules émises par les moteurs diesel sont généralement 

 dosées selon la procédure suivante: extraction au Soxhlet, 

 purification et fractionnement puis analyse finale par chromatographie 

 liquide à haute performance ou chromatographie en phase gazeuse 

 couplée à la spectométrie de masse. 

 B1.2 Sources d'exposition humaine et environnementale 

 Les gaz d'échappement des moteurs diesel proviennent 

 essentiellement des véhicules à moteur; parmi les autres source on 

 peut citer les installations fixes, le matériel de traction 

 ferroviaire et les machines de navires. Les émissions de ces véhicules 

 à moteurs diesel ont été bien décrites mais les résultats obtenus pour 

 chaque catégorie particulière ne sont souvent pas comparables en 

 raison de différences concernant certains paramètres comme le cycle de 

 fonctionnement, le type de moteur et la composition du combustible. 

 Les divers constituants sont émis dans les proportions suivantes: 

 dioxyde de carbone, environ 1 kg/km; monoxyde de carbone, oxydes 

 d'azote, hydrocarbures gazeux totaux et particules 0,1-20 g/km; 

 dérivés aliphatiques, alcools, aldédhydes, hydrocarbures aromatiques 

 légers et hydrocarbures aromatiques polycycliques, quelques 

 microgrammes/km. Dans un certain nombre de pays, il y a réglementation 

 des émissions de monoxyde de carbone, d'oxyde d'azote, d'hydrocarbures 

 gazeux totaux et de particules. 

 En principe, il n'y a aucune différence entre les moteurs de 

 faible ou de forte puissance pour ce qui est de la nature et de la 

 quantité des émissions, encore que les véhicules lourds aient tendance 

 à dégager une quantité relativement plus importante de particules. Les 

 émissions dépendent du cycle de fonctionnement du moteur (régime 

 transitoire ou régime stationnaire), du type et de l'état du moteur 

 (injection ou aspiration, entretien, kilométrage total) et de la 

 composition du combustible (teneur en soufre, teneur en composés 

 aromatiques, volatilité); le réglage du moteur jour un rôle très 

 important. 

 Le dégagement de particules augmente en raison inverse du rapport 

 air/combustible, mais en raison directe de la charge et de la 

 température. Les moteurs vieillissants, soumis à une utilisation 

 intense, libèrent plus de particules que les moteurs récents, qui ont 

 peu de kilométrage, probablement du fait de la plus grande 

 consommation d'huile lubrifiante. Dans le cas des véhicules légers à 

 moteur diesel, il y a également une corrélation entre l'émission de 

 particules et la teneur en soufre du combustible, car la formation de 

 sulfates métalliques accroît la masse des particules. Dans le cas des 

 véhicules lourds, ce type de corrélation n'a pas encore été établi. 

Diesel fuel and exhaust emissions (EHC 171, 1996) Page 169 of 184

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 Entre outre, plus la teneur du combustible en dérivés aromatiques est 

 élevée, plus le moteur dégage de particules. 

 Les hydrocarbures aromatiques polycycliques, oxygénés ou non, 

 émis par les moteurs diesel et les moteurs à allumage commandé, sont 

 de nature similaire. Des hydrocarbures aromatiques polycycliques 

 oxygénés ou nitrés sont émis à raison de quelques microgrammes/km, 

 mais la concentration effective de ces composés n'est pas connue avec 

 certitude car il peut y avoir décomposition ou formation lors de 

 l'échantillonnage. Les émissions de HAP augmentent avec la charge et 

 la température ainsi qu'avec l'âge du moteur, probablement du fait 

 d'une consommation plus importante d'huile lubrifiante. Les émissions 

 d'HAP dépendent également de la technique d'injection utilisée dans le 

 moteur: ces émissions sont proportionnelles au rapport air/combustible 

 dans les moteurs à injection directe mais la situation est inversée 

 dans le cas des moteurs à injection indirecte. La teneur en dérivés 

 aromatiques et la volatilité du combustible sont directement liées aux 

 émissions de HAP. En cas de mauvais fonctionnement de certains 

 éléments du moteur, en particulier des injecteurs, il y a augmentation 

 de l'émission des principaux constituants des gaz d'échappement. On ne 

 possède guère de données sur la contribution des moteurs diesel aux 

 émissions totales de produits de combustion d'origine artificielle. 

 Les émissions des moteurs diesel peuvent être réduites moyennant 

 une meilleure conception du moteur, la pose de pièges à particules 

 (pièges oxydants) et de convertisseurs catalytiques. Alors que les 

 pièges à particules éliminent la suie et les composés organiques 

 solubles adsorbés sur les particules, les convertisseurs catalytiques 

 réduisent principalement la teneur en oxyde de carbone et 

 hydrocarbures gazeux. En pratique, il est difficile de régénérer les 

 pièges à particules. Les convertisseurs catalytiques nécessitent 

 l'utilisation de combustibles à faible teneur en soufre car le soufre 

 empoisonne les centres actifs du catalyseur. 

 B1.3 Transport, distribution et transformation dans l'environnement 

 C'est principalement l'atmosphère qui est affectée par les 

 émissions de moteurs diesel. L'hydrosphère et la géosphère peuvent 

 être contaminées indirectement par des dépôts secs ou humides. La 

 destinée environnementale des divers constituants des gaz 

 d'échappement des moteurs diesel est en général bien connue: les 

 particules se comportent comme les molécules de gaz non réactives pour 

 ce qui est de leur transport mécanique dans l'atmosphère; elles 

 peuvent être transportées sur de longues distances et même pénétrer 

 dans la stratosphère. On pense que leur vitesse d'élimination est 

 faible, ce qui fait qu'elles séjournent plusieurs jours dans 

 l'atmosphère. Avec le temps, ces particules peuvent s'agglomérer, et 

 leur vitesse de chute augmentant, la quantité restante aéroportée 

 diminue. Le carbone élémentaire présent dans des particules émises par 

 les moteurs diesel peut catalyser la formation d'acide sulfurique par 

 oxydation du dioxyde de soufre. Les constituants organiques adsorbés à 

 la surface des particules de carbone élémentaire peuvent subir un 

 certain nombre de transformations et de rections chimiques avec 

 d'autres composés atmosphériques ou par exposition à la lumière 

 solaire. 

 B1.4 Concentrations dans l'environnement et exposition humaine 

 Etant donné que les gaz d'échappement des moteurs diesel sont des 

 mélanges complexes contenant des composés très divers, on ne peut pas 

 définir de 'concentration dans l'environnement'. On devrait pouvoir 

 mettre en évidence la présence de ces divers constituants dans tous 

 les compartiments de l'environnement, encore qu'il ne soit pas 

 généralement possible d'en déterminer l'origine. On connaît la 

 concentration dans l'environnement de la plupart de ces constituants. 

 C'est le plus probablement dans les rues très passantes ou dans 

 les parkings, en particulier souterrains, que la population générale a 

 le plus de chances d'être exposée aux émissions des moteurs diesel. Il 

 est difficile d'identifier les sources de pollution et on calcule 

 généralement la contribution des gaz d'échappement des moteurs diesel 

 à la pollution totale due à la circulation des véhicules à moteur, sur 

 la base des facteurs d'émission et du pourcentage de véhicules à 

 moteur diesel dans le parc automobile général. Le niveau d'exposition 

 de la population générale et des travailleurs aux particules émises 

 par les moteurs diesel est toxicologiquement significatif. 

 Les concentrations quotidiennes moyennes ambiantes de particules 

 à proximité des voies de communication sont de 8-42 μg/m3. On a 

 calculé que les concentrations annuelles moyennes de particules 

 étaient de 5 à 10 μg/m3 dans les zones urbaines et < 1,5 μg/m3

 dans les zones rurales d'Allemagne et de 1 à 2 μg/m3 dans les zones 

 urbaines et 0,6-1 μg/m3 dans les zones rurales des Etats-Unis 

 d'Amérique. Ces concentrations sont directement corrélées à la densité 

 de la circulation automobile et diminuent à mesure qu'on s'éloigne des 

 routes. 

 Il peut être également difficile de déterminer l'origine de la 

 pollution sur les lieux de travail, en particulier dans les mines où 

 la quantité totale de poussière est élevée. Le dosage du carbone 

 particulaire a permis de déterminer l'exposition spécifique aux 

 émissions de moteurs diesel sur les lieux de travail et il en ressort 

 que les travailleurs seraient exposés à des concentrations de 

 particules de l'ordre de 0,04 à 0,134 mg/m3 pour les camionneurs et 

 de 0,004 à 0,192 mg/m3 pour les cheminots. On a également eu recours 

 au dosage des particules respirables totales et des particules totales 

 en suspension pour évaluer l'exposition professionnelle. 

 B1.5 Cinétique et métabolisme chez les animaux de laboratoire et 

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 l'homme 

 B1.5.1 Dépôt 

 Les particules émises par les moteurs diesel, dont le diamètre 

 aérodynamique médian massique est égal à environ 0,2 μm, sont quelque 

 peu filtrés par le nez et leur aptitude au dépôt dans les poumons 

 n'est que légèrement supérieure à la valeur minimale trouvée pour les 

 particules de diamètre aérodynamique médian massique égal à environ 

 0,5 μm. Autrement dit, lorsque les particules de suie émises par les 

 moteurs diesel sont inhalées, 10 à 15% d'entre elles se déposent au 

 niveau des alvéoles chez le rat et le cobaye, le dépôt au niveau des 

 alvéoles étant d'environ 10% chez l'homme. 

 B1.5.2 Rétention et élimination des particules 

 L'élimination des particules par l'ascenseur muco-ciliaire est 

 pratiquement complète au bout de 24 heures. L'élimination à long terme 

 des particules déposées dans la zone alvéolaire a fait l'objet de 

 plusieurs études sur des rats qui avaient été exposés par la voie 

 respiratoire à deux types de particules: les particules émises par un 

 moteur diesel et les particules servant de référence. Dans le cas des 

 témoins chez lesquels la charge pulmonaire était faible (< 1 mg par 

 poumon), on a obtenu des temps de demi-élimination de l'ordre de 60 à 

 100 jours, alors que chez les rats présentant une charge pulmonaire 

 allant de 1 à 60 mg/poumon, le temps de demi-élimination était de 

 l'ordre de 100 à 600 jours. Dans plusieurs études, on a constaté que 

 les effets observés étaient dus à une surcharge en particules, 

 laquelle a été décrite chez diverses espèces et pour un certain nombre 

 de matériaux particulaires. Ce phénomène s'observe généralement 

 lorsque la vitesse de dépôt des particules de faible solubilité et de 

 faible toxicité aiguë reste supérieure à leur vitesse d'élimination 

 pendant une très longue durée. Chez l'homme, le temps de 

 demi-élimination alvéolaire normal est de plusieurs centaines de 

 jours, c'est-à-dire plus long que chez le rat. 

 On a mis au point un modèle pulmonaire dosimétrique sur la base 

 des données de dépôt et de rétention des particules diesel chez le rat 

 après inhalation de longue durée et des mêmes données chez l'homme. Ce 

 modèle peut être utilisé pour prévoir la rétention des particules 

 diesel et des composés organiques adsorbés dans les poumons de 

 personnes d'âges divers. On ne dispose d'aucune donnée sur la manière 

 dont la rétention de différents composés évolue après une exposition 

 prolongée aux gaz d'échappement de moteurs diesel. 

 B1.5.3 Rétention et élimination des hydrocarbures aromatiques 

 polycycliques adsorbés sur la suie de moteurs diesel 

 Les hydrocarbures aromatiques polycycliques présents dans la suie 

 émise par les moteurs diesel adhèrent fortement à la surface des 

 particules. Environ 50% des HAP adsorbés sur les particules sont 

 éliminés par les poumons dans l'espace d'une journée, mais le temps de 

 demi-rétention de la fraction restante s'est révélé égal à 18-36 

 jours. Des études portant sur du 3H-benzo[ a]pyrène et du 

 14C-nitropyrène ont montré que lorsqu'ils sont associés à des 

 particules, les HAP sont sensiblement plus longs à être éliminés des 

 poumons que leurs homologues libres. 

 B1.5.4 Métabolisme 

 Déposé sur des particules émises par un moteur diesel, du 

 benzo[ a]pyrène a subi une métabolisation oxydative au niveau du 

 poumon et dans des cultures cellulaires de macrophages pulmonaires 

 aboutissant à la formation de phénols, de diols et de quinones 

 substituant le noyau benzo[ a]pyrène. Du nitropyrène adsorbé sur des 

 particules diesel a été métabolisé en acétylaminopyrène-phénol après 

 inhalation. Chez des rats exposés à des émissions de moteur diesel on 

 a constaté, dans les poumons et les cellules de type II, un 

 accroissement des adduits de l'ADN par rapport aux témoins. Le 

 métabolisme oxydatif de certains composés organiques qui conduit à des 

 époxydes pourrait être responsable de la formation des adduits, mais 

 il est vrai qu'on ne les trouve qu'après exposition à des particules. 

 Certains dérivés organiques présents dans les émissions de moteur 

 diesel se sont révélés capables de former des adduits avec l'ADN; 

 toutefois le noyau carboné lui-même (sans composés organiques 

 extractibles) peut également conduire à la formation d'adduits, en 

 provoquant des lésions chroniques au niveau des cellules épithéliales. 

 B1.6 Effets sur les mammifères de laboratoire et les systèmes 

 d'épreuve in vitro 

 Les quelques données disponibles incitent à penser que les 

 émissions de moteur diesel ne présentent qu'une faible toxicité aiguë. 

 Des souris auxquelles on avait administré par voie intratrachéale, des 

 particules émises par un moteur diesel, sont mortes des suites d'une 

 oedème du poumon. La DL50 était égale à environ 20 mg/kg de poids 

 corporel. Des particules du même type, extraites au méthanol, n'ont 

 entraîné aucune mortalité jusqu'à une concentration d'environ 33 mg/kg 

 de poids corporel. Chez le hamster, on a obtenu une DL50 de 

 1280 mg/kg de poids corporel après administration par voie 

 intrapéritonéale. On ne dispose d'aucune donnée concernant 

 l'exposition par la voie respiratoire. 

 Après exposition de rats, de cobayes et de chats pendant environ 

 quatre semaines à des émissions de moteur diesel ayant une teneur en 

 particules de 6 mg/m3, on a observé une altération de la fonction 

 pulmonaire, et notamment une augmentation de 35% de la résistance 

 ventilatoire chez les cobayes et une diminution de 10% de la capacité 

 vitale chez les chats. Du point de vue histopathologique, on a observé 

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 un épaississement focal des parois alvéolaires, un accroissement 

 significatif de l'indice de marquage des cellules de type II et des 

 accumulations de macrophages chargés de particules. Ces accumulations 

 se situaient au niveau des bronchioles terminales et elles ont 

 augmenté de volume lors de la période de récupération postérieure à 

 l'expérience en raison de la fixation des macrophages (séquestration). 

 Après avoir inhalé pendant de longues périodes des émissions de 

 moteur diesel à des concentrations atteignant 4 mg/m3, des rats, des 

 souris, des hamsters, des chats et des singes n'ont pas présenté de 

 chute spectaculaire de leur poids corporel ni de réduction de leur 

 longévité. Les effets toxiques liés à la dose qui ont été observés 

 chez toutes les espèces après une longue période d'inhalation étaient 

 les suivants: augmentation du poids des poumons pouvant aller jusqu'à 

 400%; inflammation pulmonaire objectivée par des paramètres 

 biochimiques (marqueurs enzymatiques cytoplasmiques, collagène) et 

 cytologiques (augmentation des neutrophiles polynucléaires); 

 perturbation de la mécanique pulmonaire; accroissement du nombre de 

 macrophages chargés de particules avec accumulations focales 

 (séquestration) dans des conditions de surcharge; enfin, altérations 

 prolifératives des cellules épithéliales et début de fibrose. 

 D'après les données limitées dont on dispose sur la toxicité des 

 émissions de moteurs diesel pour la fonction de reproduction et le 

 développement, on peut penser qu'il n'y a pas d'effets toxiques 

 déterminants. Dans la plupart des expériences, on n'a pas constaté 

 d'effets chez des souris, des rats, des hamsters, des lapins ou des 

 singes; toutefois, après injection par voie intrapéritonéale, on a 

 observé chez des souris qui avaient reçu de particules émises pas des 

 moteurs diesel, des anomalies touchant les spermatozoïdes et constaté 

 une certaine embryotoxicité chez des hamsters auxquels on avait 

 administré des extraits d'émissions de ces mêmes moteurs. 

 La plupart des épreuves de génotoxicité in vitro ont été 

 réalisées avec des extraits d'émissions de moteurs diesel plutôt 

 qu'avec les émissions totales elles-mêmes et l'on a obtenu des 

 réactions positives en l'absence d'activation métabolique. Autrement 

 dit, il semble que ces effets génotoxiques soient indépendants de la 

 présence d'HAP. Environ 50% des études in vivo ont donné des

 résultats négatifs; les seuls résultats positifs obtenus consistaient 

 en échanges de chromatides soeurs dans le cas des émissions totales et 

 des extraits organiques, et dans la présence de micronoyaux dans le 

 cas des extraits organiques. 

 On n'a généralement pas observé d'effets immunotoxiques après 

 inhalation d'émissions de moteurs diesel; toutefois on a observé dans 

 une étude une augmentation du titre des immunoglobulines 

 anti-ovalbumine et deux autres expériences ont mis en évidence un 

 accroissement de la sensibilité aux infections chez des souris. 

 Des études effectuées sur des rats incitent à penser que 

 l'inhalation de gaz d'échappement de moteurs diesel affecte l'état 

 comportemental et neurophysiologique. 

 Lors d'études sur la cancérogénicité des émissions de moteur 

 diesel, au cours desquelles des rats étaient exposés à ces émissions 

 par la voie respiratoire, on a constaté que la phase gazeuse 

 (c'est-à-dire dépourvue de particules) n'était pas cancérogène. Toutes 

 les études sur des rats qui ont été validées ont montré que les 

 émissions de moteurs diesel avaient un effet cancérogène lorsque la 

 concentration en particules était supérieure à 2 mg/m3, soit 

 l'équivalent d'une exposition continue à une concentration d'environ 

 1 mg/m3. Aucun effet n'a été observé en revanche chez les hamsters 

 et les souris. Lors d'études au cours desquelles on a pratiqué une 

 instillation intratrachéale, on a constaté que les particules 

 présentes dans les émissions de moteurs diesel et le noir de fumée 

 produisaient des tumeurs; en outre on a observé l'existence d'une 

 corrélation entre l'aire superficielle des particules carbonées et 

 leur activité tumorigène. 

 L'inhalation, pendant une longue période, de noir de fumée 

 pratiquement dépourvu d'hydrocarbures aromatiques polycycliques à ces 

 concentrations, a également provoqué des tumeurs pulmonaires chez le 

 rat. 

 On ne sait pas avec certitude si la cancérogénicité des émissions 

 de moteurs diesel est due à un mécanisme faisant intervenir ou non des 

 réactions au niveau de l'ADN (ou à un mécanisme mixte). Différents 

 modèles ont été proposés pour élucider la cancérogénicité des 

 émissions de moteurs diesel. 

 B1.7 Effets sur l'homme 

 Les émissions de moteurs diesel contribuent à la pollution 

 globale de l'air. Les études toxicologiques, qu'elles cherchent à 

 mettre en évidence des effets aigus ou des effets chroniques, ne 

 permettent pas d'assigner un rôle particulier à ces particules mais il 

 apparaît qu'elles pourraient être en partie responsables d'un certain 

 nombre d'effets attribués à la pollution de l'air. 

 Les émissions de moteur diesel ont des caractéristiques qu'un 

 certain nombre de personnes trouvent agressives, en particulier à 

 fortes concentrations. Les symptômes observés après exposition de 

 brève ou de longue durée à ce type d'émissions ont été décrits dans un 

 certain nombre d'études et de rapports concernant des personnes 

 exposées de par leur profession. Les effets aigus consistent en 

 irritation des muqueuses oculaires et nasales et l'on a observé dans 

 les cohortes professionnelles une augmentation de la fréquence des 

 symptômes respiratoires; toutefois on ignore qu'elle est la 

 contribution exacte des particules émises par les moteurs diesel à ce 

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 type de symptômes. Aucun effet à court terme n'a été régulièrement 

 observé au niveau de fonction pulmonaire, mais on a signalé des crises 

 d'asthme. 

 Lors d'une étude contrôlée au cours de laquelle huit volontaires 

 non fumeurs, en bonne santé, ont été exposés à des émissions diluées 

 de moteurs diesel, pendant 60 minutes dans une chambre fermée, on a 

 constaté une réduction du taux de phagocytose chez des macrophages 

 alvéolaires recueillis par lavage broncho-alvéolaire. 

 Un certain nombre d'études transversales et longitudinales 

 portant sur des ouvriers longtemps exposés de part leur profession à 

 des émissions de moteur diesel, ont révélé une altération de la 

 fonction pulmonaire et une augmentation de la prévalence des symptômes 

 respiratoires, toutefois la brièveté des épisodes d'exposition limite 

 la portée de ces études. Aucune surmortalité n'a été constatée lors 

 d'études de cohorte au cours desquelles on s'est efforcé d'étudier des 

 décès par maladie cardio-vasculaire ou accident vasculaire cérébral, 

 imputables à l'exposition des émissions de moteurs diesel. 

 Lors d'un certain nombre d'études épidémiologiques on a tenté 

 d'établir des relations entre certains cancers du poumon et de la 

 vessie et une exposition professionnelle à des émissions de moteurs 

 diesel. Seules les études jugées utiles pour l'évaluation des effets 

 cancérogènes de ces émissions ont été prises en considération dans la 

 présente monographie. Celles qui sont les plus intéressantes pour ce 

 qui est du cancer du poumon, concernent des cheminots, des personnes 

 travaillant dans des garages de cars et des débardeurs qui constituent 

 des cohortes dont les membres sont effectivement exposés aux émissions 

 de moteur diesel. Les quatre études les plus informatives font toutes 

 état d'un risque accru de cancer du poumon, avec un risque relatif 

 allant de 1,4 pour les cheminots, et de 1,3-2,4 pour les ouvriers des 

 garages (selon le type d'exposition), jusqu'à un risque trois à six 

 fois plus élevé pour les débardeurs (en fonction du mode d'évaluation 

 de l'exposition, mais avec un large intervalle de confiance). Il a été 

 possible de tenir compte du tabagisme dans une étude cas-témoins sur 

 des cheminots et dans une étude sur des débardeurs. Dans les deux cas, 

 cette correction pour tenir compte du tabagisme n'a eu aucune 

 influence sur l'effet de l'exposition aux émissions diesel. Dans les 

 trois études pour lesquelles on n'a pas pu tenir compte du tabagisme, 

 l'analyse était basée sur des comparaisons entre les différents 

 sous-groupes de ces cohortes, de sorte que l'effet de confusion créé 

 par le tabagisme avait moins de chance d'être gênant qu'en cas de 

 comparaison avec des groupes extérieurs. 

 Plusieurs études cas-témoins ont été menées afin d'examiner la 

 relation pouvant exister entre les cancers de la vessie et une 

 exposition supposée à des émissions de moteurs diesel. On a constaté 

 un accroissement du risque, en particulier pour le chauffeurs de 

 camion; toutefois toutes ces études souffrent d'une caractérisation 

 insuffisante de l'exposition. De la sorte, il n'est pas possible 

 d'affirmer qu'une exposition aux émissions de moteurs diesel entraîne 

 un risque accru de cancer vésical. 

 B1.8 Effets sur les autres êtres vivants au laboratoire et dans 

 leur milieu naturel 

 Les effets des émissions de moteur diesel n'ont été abordés que 

 dans une seule étude, portant sur des algues vertes. 

 B1.9 Evaluation des risques pour la santé humaine 

 L'évaluation des risques de cancer et de maladies non malignes a 

 été menée conformément au modèle d'évaluation des risques établi par 

 l'Académie nationale des sciences des Etats-Unis (National Research 

 Council, 1983). Ce modèle d'évaluation comporte quatre étapes: (1) 

 identification du danger; (2) évaluation de la relation dose-réponse; 

 (3) évaluation de l'exposition et (4) caractérisation du risque. 

 On estime que les travaux les plus intéressants sont les études 

 épidémiologiques de longue durée dans lesquelles l'exposition est bien 

 définie et le suivi supérieur à 20 ans. Quatre études portant sur le 

 cancer du poumon chez des personnes professionnellement exposées 

 satisfont à ces critères. Il apparait que le risque relatif de cancer 

 du poumon lié à une exposition à des émissions de moteur diesel est 

 généralement faible et qu'il est influencé par les circonstances, les 

 effets des facteurs de confusion non évalués et la difficulté de tenir 

 suffisamment compte des facteurs de confusion reconnus. D'autres 

 études, où l'exposition est définie avec une moindre précision, 

 corroborent les conclusions des études précédentes. Globalement, on 

 estime que les émissions de moteurs diesel sont probablement 

 cancérogènes pour l'homme; toutefois on ne dispose d'aucune donnée 

 quantitative permettant d'évaluer le risque. 

 B.1.9.1 Effets non néoplasiques 

 Pour caractériser le risque, on a procédé de deux manières: 

 premièrement une concentration sans effets nocifs observables que l'on 

 divise par un coefficient d'incertitude; deuxièmement, une 

 concentration de référence. Dans les deux cas, on a utilisé un modèle 

 dosimétrique élaboré qui permet de réduire l'imprécision due à 

 l'extrapolation interspécifique des doses. 

 La dose de particules sans effet pour l'homme a été estimée à 

 0,139 mg/m3. La valeur guide pour la population générale calculée 

 d'après le modèle dosimétrique a été établie à 5,6 μg/m3, la valeur 

 calculée sans recours au modèle étant de 2,3 μg/m3. 

 La méthode basée sur l'utilisation d'une concentration de 

 référence prend en compte l'ensemble de la relation exposition-réponse 

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 de préférence aux données ponctuelles fournies par les études 

 d'inhalation, comme c'est le cas dans la méthode de la dose sans 

 effets observables. On a identifié trois paramètres biologiques 

 sensibles: l'inflammation alvéolaire chronique, la diminution 

 d'efficacité de l'ascenseur mucociliaire et les lésions pulmonaires 

 hyperplasiques. Les concentrations de référence calculées à partir du 

 même modèle dosimétrique que dans le cas de la méthode de la dose sans 

 effets observables, étaient de 0,9 à 2 μg/m3 pour l'inflammation, de 

 1,2 à 3 2 μg/m3 pour la dégradation de l'ascenseur muco-ciliaire et 

 de 6,3 à 14,2 μg/m3 pour les lésions hyperplasiques. 

 B1.9.2 Effets néoplasiques 

 Pour évaluer le risque d'une exposition aux émissions de moteur 

 diesel, on a eu recours à un modèle linéarisé en plusieurs étapes. 

 Comme les résultats des études épidémiologiques avaient été jugés 

 insuffisants pour une évaluation quantitative du risque unitaire, on a 

 eu recours à des données provenant de plusieurs études d'inhalation à 

 long terme chez des rats, études qui montraient l'existence d'une 

 cancérogénèse à partir de 2 mg/m3. 

 On a ainsi établi par le calcul que le risque unitaire était 

 de 3,4 × 10-5 μg/m3 (moyenne géométrique de quatre estimations). 

 Un autre modèle de type biologique a fourni une valeur similaire pour 

 le risque unitaire, en prenant pour hypothèse que les particules 

 émises par les moteurs diesel agissent à faibles concentrations sur la 

 prolifération cellulaire ou l'initiation du processus de 

 transformation. 

 B1.10 Evaluation des effets sur l'environnement 

 On ne dispose pas d'informations suffisantes pour évaluer les 

 effets spécifiques des émissions de moteurs diesel. La combustion du 

 carburant diesel devrait avoir des effets similaires à celle des 

 autres combustibles fossiles, effets qui sont liés à la consommation 

 de ce type de combustible. 

 PARTE A DIESEL

 A1. RESUMEN

 A1.1 Identidad, propiedades físicas y químicas y métodos 

 analíticos 

 El diesel es una mezcla compleja de alcanos normales, ramificados 

 y cíclicos (60%-> 90% en volumen; hidrocarburos de longitud de cadena 

 comprendida entre C9 y C30); compuestos aromáticos, especialmente 

 alquilbencenos (5%-40% en volumen), y pequeñas cantidades de alquenos 

 (0%-10% en volumen) obtenidos a partir de la fracción de gasóleo del 

 destilado medio durante la separación del petróleo. El diesel puede 

 contener benceno, tolueno, etilbenceno, y xilenos e hidrocarburos 

 aromáticos policíclicos (HAP), sobre todo naftaleno y derivados del 

 mismo con metilos sustituyentes, a niveles de partes por millón. El 

 contenido de azufre de los combustibles diesel depende del origen del 

 crudo y del proceso de refino. En un cierto número de países está 

 reglamentado por ley, y suele estar comprendido entre 0,05% y 0,5% en 

 peso. Se utilizan aditivos para influir en el flujo, el almacenamiento 

 y la combustión del diesel, para diferenciar productos y para 

 satisfacer las especificaciones comerciales. A temperatura ambiente, 

 los combustibles diesel suelen ser líquidos de color marrón 

 moderadamente volátiles, ligeramente viscosos, inflamables y de olor 

 parecido al del queroseno. Los márgenes de ebullición están 

 comprendidos por lo general entre 140°C y 385°C (> 588°C en el caso 

 del diesel marino); a 20°C la densidad es de 0,87-1,0 g/cm3, y la 

 hidrosolubilidad de 0,2-5 mg/litro. La calidad y composición del 

 diesel influye considerablemente en los contaminantes emitidos por los 

 motores diesel. Otras variables importantes son el proceso de 

 encendido (expresado en términos del índice de cetano), la densidad, 

 la viscosidad y el contenido de azufre. Las especificaciones del 

 diesel comercial varían considerablemente de un país a otro. 

 Los combustibles de calefacción y algunos combustibles de 

 aviación a base de queroseno producidos durante el proceso de refino 

 tienen a veces una composición parecida a la del diesel, aunque con 

 distintos aditivos. Por ello, a la hora de evaluar la toxicidad y la 

 ecotoxicidad se han tenido también en cuenta los datos biológicos 

 sobre estas mezclas. 

 Debido a la complejidad de las mezclas diesel, no existe un 

 método analítico específico para ellas, y las técnicas analíticas 

 empleadas en la mayoría de las evaluaciones ambientales sólo permiten 

 determinar la mezcla total de hidrocarburos de petróleo. Los métodos 

 consisten en una extracción previa con solventes, un proceso de 

 limpieza para eliminar los hidrocarburos naturales, y la posterior 

 detección mediante gravimetría, espectroscopía infrarroja o 

 cromatografía de gases. 

 Ni la gravimetría ni la técnica infrarroja proporcionan 

 información cualitativa o cuantitativa de utilidad sobre los 

 contaminantes, por lo que sólo pueden usarse con fines de cribado. 

 El método utilizado habitualmente para analizar muestras 

 ambientales es la cromatografía de gases unida a técnicas de detección 

 tales como la ionización por conductor y la espectrometría de masas. 

 Existen otros muchos métodos para analizar hidrocarburos particulares 

 en los combustibles diesel. 

 A1.2 Fuentes de exposición humana y ambiental 

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 Los combustibles diesel se producen por refinación del petróleo bruto. 

 Para satisfacer las especificaciones técnicas en cuanto al 

 rendimiento, normalmente se combinan varios componentes para 

 obtenerlos; la ulterior inclusión de aditivos mejora sus propiedades 

 para usos específicos. Los combustibles diesel son muy utilizados con 

 fines de transporte. En los motores de alta velocidad se deben emplear 

 los más volátiles y de menor viscosidad, y los de cadena más larga se 

 reservan para los motores diesel de ferrocarriles y barcos. Una gran 

 parte del transporte pesado por carretera está propulsado por motores 

 diesel. 

 Los automóviles para pasajeros propulsados por motores diesel son 

 cada vez más frecuentes en Europa y el Japón (10%-25%), mientras que 

 en América del Norte el porcentaje de ese tipo de automóviles es de 

 aproximadamente 1%-2%, con una ligera tendencia a la baja. El diesel 

 es utilizado en motores fijos y en calderas, como por ejemplo motores 

 de pistones, turbinas de gas, bombas de oleoductos, compresores de 

 gas, unidades de procesamiento de vapor de centrales de energía 

 eléctrica, quemadores e instalaciones industriales de calefacción de 

 espacios y de agua. 

 En los últimos cinco años la demanda mundial de combustibles 

 diesel ha aumentado constantemente. En 1985 se consumieron las 

 siguientes cantidades: unas 170 000 kilotoneladas al año en América 

 del Norte; unas 160 000 kilotoneladas al año, gasóleos incluidos, en 

 la Unión Europea; y aproximadamente 46 000 kilotoneladas anuales en 

 Australia, el Japón y Nueva Zelandia, lo que equivale a un total de 

 1062 kilotoneladas diarias. En 1990 se notificó que la demanda mundial 

 ascendía aproximadamente a 1110 kilotoneladas al día. 

 No se dispone de información sobre las emisiones a que da lugar 

 la producción de combustibles diesel; no obstante, al parecer esta 

 fuente tiene una importancia secundaria, dado que el proceso de 

 refinación se lleva a cabo en sistemas cerrados. Las emisiones se 

 producen sobre todo durante el almacenamiento y el transporte. Se 

 libera diesel como resultado de derrames y durante el reabastecimiento 

 de los vehículos en las gasolineras. 

 La atmósfera y la hidrosfera son los compartimentos ambientales 

 más gravemente afectados. En algunos accidentes se produce 

 contaminación del suelo por combustibles diesel, problema que también 

 afecta a las playas ferroviarias. Entre las numerosas técnicas 

 empleadas para limpiar los suelos contaminados por diesel, cabe citar 

 la excavación, los métodos biológicos y el confinamiento. 

 A1.3 Transporte, distribución y transformación en el medio 

 ambiente 

 Apenas hay datos sobre el destino ambiental de los combustibles 

 diesel, pero se considera que los mecanismos de su distribución y 

 transformación son comparables a los de combustibles de calefacción 

 que han sido bien estudiados, como por ejemplo el fuel-oil No 2. Los 

 derrames de diesel en agua se extienden casi de inmediato para formar 

 una 'capa aceitosa'. Los componentes polares y de bajo peso molecular 

 relativo se disuelven y se separan por lixiviación de dicha capa, 

 mientras que los componentes volátiles se evaporan a partir de la 

 superficie; además da comienzo la degradación microbiana. La 

 degradación química y biológica altera la composición del derrame. 

 Estos procesos dependen de la temperatura; así, los derrames que se 

 producen en el Artico duran más que los que se producen en zonas de 

 clima templado. En entornos marinos, la mayoría de los agentes 

 aromáticos de bajo peso molecular relativo se disuelven en la fase 

 acuosa, pero los alcanos ramificados, los cicloalcanos y los restantes 

 compuestos aromáticos primarios pueden persistir en los sedimentos 

 durante más de un año. 

 No se dispone de información sobre la fotooxidación de los 

 combustibles diesel en el agua y el aire, pero se sabe que los 

 componentes del petróleo evaporados se degradan fotoquímicamente. Se 

 ha demostrado que el fuel-oil No 2 se fotooxida rápidamente en el agua 

 en condiciones ambientales. 

 Los distintos componentes del diesel son de por sí 

 biodegradables, en diversa medida y a distinta velocidad. Los 

 n-alcano, los compuestos n-alquilaromáticos y las moléculas 

 aromáticas simples comprendidas en el margen de C10 a C22 son los 

 que más fácilmente se degradan. Las moléculas más pequeñas son 

 metabolizadas por lo general rápidamente. Los n-alcanos de cadena 

 larga se degradan más lentamente, debido a su hidrofobicidad y a que 

 son viscosos o sólidos a temperatura ambiente. Los alcanos ramificados 

 y los cicloalcanos son relativamente resistentes a la degradación 

 biológica, y los HAP son resistentes. La velocidad global de 

 degradación de los hidrocarburos depende de la temperatura, el 

 contenido de agua, el oxígeno, el pH, los nutrientes inorgánicos y la 

 variabilidad metabólica microbiana. 

 Las algas unicelulares pueden incorporar y metabolizar 

 hidrocarburos tanto alifáticos como aromáticos, pero no se sabe con 

 seguridad en qué medida ocurre realmente tal cosa en la naturaleza. A 

 diferencia de los microorganismos que utilizan carbonos de petróleo 

 como fuente de carbono, los animales generalmente oxidan y conjugan 

 los productos, generando productos finales que son más solubles y por 

 consiguiente más fáciles de excretar. Todas las especies animales 

 analizadas pueden incorporar hidrocarburos de petróleo. Se sabe que 

 los HAP, el petróleo bruto y los productos refinados derivados del 

 petróleo son inductores de las enzimas del citocromo P450 y aumentan 

 el metabolismo de los hidrocarburos en numerosas especies de peces 

 marinos y de agua dulce. 

 Hay pocos datos disponibles sobre la bioacumulación de diesel en 

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 condiciones de laboratorio, pero diversos estudios sobre derrames y 

 estudios de laboratorio sobre otros tipos de petróleo, en particular 

 el fuel-oil No 2, han aportado pruebas abundantes de que los 

 organismos acuáticos bioconcentran los hidrocarburos. El coeficiente 

 de reparto n-octanol-agua para el diesel es de 3,3-7,06, valores que 

 indican una alta bioacumulación potencial; no obstante, muchos de los 

 compuestos de bajo peso molecular relativo son metabolizados 

 fácilmente, y la bioacumulación real de los compuestos de mayor peso 

 molecular relativo se ve limitada por su escasa hidrosolubilidad y su 

 gran tamaño molecular. Así pues, la bioacumulación real posiblemente 

 es baja. 

 Se han descubierto peces envenenados por diesel después de 

 derrames, pero no se dispone de datos sobre la biomagnificación del 

 combustible. No hay datos experimentales sobre el movimiento del 

 diesel a través del suelo, aunque se ha señalado que existe quizá una 

 correlación directa entre el movimiento y la viscosidad cinemática. El 

 movimiento del queroseno a través del suelo depende del contenido de 

 humedad y de las características del suelo. 

 A1.4 Niveles ambientales y exposición humana 

 Debido a su carácter de mezclas complejas, no se han determinado 

 los niveles ambientales de los combustibles diesel. Se pueden detectar 

 componentes individuales del diesel en casi todos los compartimentos 

 del medio ambiente, pero no es posible averiguar su origen. La 

 población general puede verse expuesta al diesel en las gasolineras y 

 de resultas de los derrames. 

 Hay muchas actividades que acarrean exposición ocupacional al 

 diesel. Dada su escasa volatilidad, en principio estos combustibles 

 sólo suelen generar bajas concentraciones de vapores a temperaturas 

 normales, pero a temperaturas altas las concentraciones pueden llegar 

 a ser importantes. 

 A1.5 Efectos en mamíferos de laboratorio y en sistemas de pruebas 

 in vitro 

 La toxicidad aguda de los combustibles diesel es baja en caso de 

 exposición oral o cutánea o de inhalación. El valor de la DL50 oral 

 fue superior a 5000 mg/kg de peso corporal en todas las especies 

 analizadas (ratón, conejo, rata, cobayo). La DL50 del producto 

 aplicado a nivel cutáneo fue superior a 5000 mg/kg de peso corporal en 

 el ratón y el conejo, si bien se notificaron valores de más de 

 2000 mg/k de peso corporal para algunos querosenos y destilados 

 medios, con distintos protocolos y dosis límite menores. La CL50

 observada en ratas expuestas por inhalación fue de aproximadamente 

 5 mg/litro, con excepción de un destilado medio directo para el que se 

 halló un valor de 1,8 mg/litro. 

 En conejos y en ratones tratados cutáneamente con cantidades 

 diarias de hasta 8000 μl/kg de peso corporal y hasta 40 000 mg/kg de 

 peso corporal respectivamente, se observó la aparición de acantosis e 

 hiperqueratosis como consecuencia de una irritación grave. Los conejos 

 eran más sensibles que los ratones. La inhalación de diesel tuvo 

 efectos neurodepresivos en ratones a concentraciones de hasta 

 0,2 mg/litro, pero no así en ratas expuestas a concentraciones de 

 hasta 6 mg/litro. En ratas se observó una disminución del peso 

 corporal y del peso del hígado. 

 No se observaron signos importantes de toxicidad acumulativa en 

 ratones, ratas y perros que habían inhalado hasta 1,5 mg/litro de 

 forma subcrónica. El síndrome de nefropatía específico observado en 

 ratas macho se asocia a una acumulación inherente de gotas hialinas en 

 los túbulos renales. 

 Los únicos efectos de las exposiciones a largo plazo fueron la 

 ulceración por aplicación cutánea en ratones (250 ó 500 mg/kg de peso 

 corporal al día) y alteraciones importantes del peso de los órganos 

 tras la inhalación de 1 ó 5 mg/litro en ratas. En los dos estudios el 

 peso corporal medio disminuyó. 

 Diversos tipos de diesel se revelaron entre leves y gravemente 

 irritantes para la piel del conejo. Los combustibles diesel no son 

 irritantes para el ojo, si bien se ha observado que algunos querosenos 

 tienen un ligero efecto de esa naturaleza. Los combustibles diesel no 

 causan sensibilización cutánea. 

 El diesel y los combustibles de avión (queroseno) no tuvieron 

 efectos embriotóxicos ni teratogénicos en dos estudios realizados en 

 ratas expuestas por inhalación a concentraciones de 100 ó 400 ppm y en 

 un estudio en que las ratas recibieron hasta 2000 mg/kg de peso 

 corporal diarios mediante sonda. En este último estudio se observó una 

 disminución del peso fetal. 

 Las pruebas realizadas con Salmonella typhimurium no aportaron 

 indicios claros de mutagenicidad. Algunos datos positivos obtenidos 

 con S. typhimurium y en células de linfoma de ratón se consideraron 

 equívocos dada la incoherencia de los resultados. Las pruebas de 

 genotoxicidad realizadas con ratones in vivo (inducción de 

 micronúcleos o aberraciones cromosómicas) también dieron resultados 

 equívocos o negativos. 

 Se ha observado la inducción de un bajo nivel de carcinogenicidad 

 cutánea por combustibles diesel. En el estado actual de las 

 investigaciones, es imposible discernir si la actividad carcinogénica 

 del diesel se debe a un mecanismo genotóxico o a la aparición de 

 lesiones cutáneas crónicas. 

 A1.6 Efectos en el ser humano 

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 Una posible fuente de exposición no ocupacional al combustible 

 diesel es el llenado manual de depósitos de combustible. La fuente 

 principal de exposición cutánea son los derrames accidentales, que dan 

 lugar de inmediato a niveles altos de exposición, si bien de corta 

 duración. 

 Como efectos del contacto cutáneo accidental se han notificado 

 anuria, insuficiencia renal, síntomas gastrointestinales e 

 hiperqueratosis cutánea. Se ha observado un cuadro pulmonar tóxico 

 tras la ingestión accidental de diesel y su sucesiva aspiración. Se ha 

 notificado el desarrollo de tos productiva persistente tras la 

 inhalación del producto. 

 En un estudio de casos y testigos realizado en hombres expuestos 

 al diesel, se observó un aumento del riesgo de cáncer de pulmón 

 distinto del adenocarcinoma; se detectó asimismo una correlación 

 positiva con el cáncer de próstata, si bien se halló un riesgo mayor 

 para el grupo sometido a una exposición 'no considerable' que para el 

 sometido a una exposición 'considerable'. 

 En un estudio transversal realizado entre obreros expuestos a 

 combustibles de avión a base de queroseno se observó que los 

 trabajadores presentaban mareos, cefaleas, náuseas, palpitaciones, 

 presión torácica e irritación ocular con mayor frecuencia que los 

 testigos no expuestos. Se calculó que la concentración promedio 

 ponderada por el tiempo del vapor desprendido por el combustible en la 

 zona en que se respiraba era de 128-423 mg/m3

 A1.7 Efectos en otros organismos en el laboratorio y en el medio 

 ambiente 

 El diesel es más tóxico que el petróleo bruto para los organismos 

 y las plantas acuáticas. La ecotoxicidad del diesel se atribuye por lo 

 general a compuestos aromáticos solubles, pero es posible que también 

 intervengan hidrocarburos alifáticos insolubles. Entre los compuestos 

 aromáticos, los monoaromáticos son los menos tóxicos, y su toxicidad 

 aguda aumenta con el peso molecular hasta los compuestos de cuatro a 

 cinco anillos, si bien estos últimos son escasamente solubles en agua 

 de mar. En algunos animales, como por ejemplo peces y aves, el 

 recubrimiento físico de la superficie corporal por el combustible 

 puede ser causa de toxicidad y mortalidad. 

 Se han llevado a cabo experimentos de laboratorio con combustible 

 diesel, fracciones hidrosolubles, dispersiones de petróleo-agua y 

 petróleo microencapsulado. El diesel no redujo significativamente el 

 crecimiento en cultivo del alga verde Euglena gracilis, mientras que 

 una concentración baja (0,1%) inhibió casi por completo el crecimiento 

 de Scenedesmus quadricauda. La presencia de diesel a baja 

 concentración (0,05%) estimuló el crecimiento, la fotosíntesis y la 

 síntesis de clorofila a de Chlorella salina, pero inhibió 

 ligeramente su respiración; a concentraciones superiores el ritmo de 

 crecimiento y la fotosíntesis se vieron considerablemente reducidos. 

 La exposición prolongada inhibió el crecimiento de las algas 

 bentónicas Ascophyllum nodosum y Laminaria digitata. En algas 

 verdeazuladas, la fotosíntesis se vio reducida por las fracciones 

 aromática y asfáltica, pero no por la fracción alifática. 

 El diesel tuvo efectos tóxicos agudos en Daphnia, en larvas de 

 quironómidos, y en el molusco Viviparus bengalensis (gasterópodos). 

 Una concentración de 0,1 ml/litro causó la muerte de copépodos de 

 charca Tigriopus californicus en el término de cinco días. 

 Los mejillones Mytilus edulis acumulan diesel, presentan 

 índices de alimentación y crecimiento considerablemente reducidos y 

 acusan efectos de toxicidad reproductiva tras la exposición crónica a 

 dicho combustible. La CE50 para el desove en mejillones expuestos 

 durante 30 días fue de aproximadamente 800 μg/litro. La CL50 de 

 gasóleo microencapsulado en mejillones en fase de maduración expuestos 

 durante 30 días al producto fue de unos 5000 μg/litro. El gasóleo fue 

 más tóxico para las larvas que para los ejemplares jóvenes: 

 10 μg/litro tenían efectos adversos para el crecimiento de las larvas. 

 Cangrejos de agua dulce (Barytelphusa cunicularis) expuestos a 

 concentraciones subletales de diesel por espacio de hasta 96 horas 

 redujeron por lo general su consumo de oxígeno, sobre todo a 

 exposiciones bajas de hasta ocho horas. A exposiciones más largas el 

 consumo de oxígeno fue similar o superior al de los controles. 

 En las pruebas de toxicidad aguda de 96 horas llevadas a cabo en 

 salmónidos jóvenes en condiciones estáticas, el diesel tuvo efectos 

 más tóxicos para el salmón rosado Onchorhychus gorbuscha

 (CL50: 32-123mg/litro) que para el salmón plateado O. kisutch

 (CL50: 2186-3017 mg/litro) o para la trucha arco iris O. mykiss

 (CL50: 3333-33216 mg/litro), con independencia del tipo de agua. 

 El umbral de detección de efectos comportamentales en bacalaos 

 ( Gadus morhua L.) expuestos a diesel en agua de mar fue de 

 100-400 ng/litro. El pez antártico Pagothenia borchgrevinki soportó 

 una fracción hidrosoluble no diluida de combustible diesel durante 

 72 horas, si bien mostró signos de estrés. 

 Las aves se ven afectadas externa e internamente por los 

 petróleos contaminantes. El diesel destruye la impermeabilidad del 

 plumaje de las aves y éstas lo ingieren cuando se limpian las plumas. 

 El diesel y el fuel-oil administrados mediante sonda a razón de 

 2 ml/kg de peso corporal a patos causó neumonía lipídica, inflamación 

 extrema de los pulmones, infiltración grasa del hígado y degeneración 

Diesel fuel and exhaust emissions (EHC 171, 1996) Page 177 of 184

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 hepática al cabo de 24 horas. La administración de diesel o fuel-oil a 

 dosis de 1 ml/kg causó irritación grave del tracto digestivo y 

 nefrosis tóxica. Dosis mayores causaron aumento de las glándulas 

 suprarrenales (debido sobre todo a una hiperplasia del tejido 

 cortical), disminución de los niveles plasmáticos de colinesterasa, 

 ataxia y temblores. La administración de estos productos a dosis de 

 hasta 20 ml/kg de peso corporal no tuvieron efectos mortales en 

 pájaros sanos, pero la DL50 del diesel y el fuel-oil administrados a 

 aves estresadas fue de 3-4 ml/kg de peso corporal. 

 Tras los derrames de diesel, el zooplancton parece altamente 

 vulnerable a los componentes dispersos y disueltos del petróleo, pero 

 no tanto al petróleo flotante. Los organismos acuáticos pueden verse 

 afectados de varias formas: mortalidad directa (huevos de pescados, 

 copépodos y plancton mixto), contaminación externa por petróleo 

 (corion de huevos de pescados y cutículas y apéndices de alimentación 

 de los crustáceos), contaminación tisular por componentes aromáticos, 

 desarrollo anormal de embriones de peces, y alteración de las tasas 

 metabólicas. 

 A1.8 Evaluación de los riesgos para la salud humana 

 La población general puede verse expuesta al diesel y a otros 

 destilados medios en las gasolineras de resultas de derrames 

 accidentales, durante la manipulación de dichos combustibles y con 

 motivo del uso de queroseno en la cocina o la calefacción domésticas. 

 Los trabajadores pueden verse expuestos al diesel o a otros destilados 

 medios al manipular y descargar el combustible en las terminales, los 

 tanques de almacenamiento y las gasolineras; durante la fabricación, 

 la reparación, el mantenimiento y el ensayo de motores y demás equipo 

 a base de diesel; durante la utilización del diesel como agente 

 limpiador o disolvente; y durante el manejo y el muestreo sistemáticos 

 de combustible diesel en el laboratorio. Debido a su baja volatilidad 

 a temperatura ambiente sólo suelen producirse concentraciones bajas de 

 vapor, si bien en espacios cerrados y a altas temperaturas se pueden 

 alcanzar niveles importantes. 

 La exposición al vapor desprendido es mínima durante la 

 manipulación habitual del diesel. El efecto más probable en la salud 

 humana es la dermatitis resultante del contacto cutáneo. El diesel es 

 irritante para la piel, pero al parecer no para el ojo. La exposición 

 cutánea puede dar lugar a efectos tóxicos agudos a nivel renal, pero 

 se desconoce qué efectos tiene la absorción cutánea prolongada de 

 bajas concentraciones. 

 La ingestión de combustibles diesel tiene efectos tóxicos, y en 

 ocasiones se produce regurgitación y aspiración, posible causa de 

 neumonía química, al igual que puede ocurrir con cualquier 

 hidrocarburo que tenga un determinado grado de viscosidad. 

 En roedores, la exposición por inhalación a concentraciones de 

 diesel de hasta 0,2 mg/litro tuvo efectos neurodepresivos en ratones, 

 pero no en cambio en ratas a las concentraciones más altas. La 

 exposición subcrónica por inhalación a diversos destilados 

 combustibles indujo una nefropatía específica para la 

 alpha2-microglobulina en ratas macho; se consideró que este efecto era 

 irrelevante para el hombre. 

 No se observaron efectos embriotóxicos ni teratogénicos en 

 animales expuestos oralmente o por inhalación a combustibles diesel. 

 No hay indicios claros de una actividad mutagénica en bacterias, 

 y los resultados de otras pruebas de genotoxicidad 

 in vitro e in vivo fueron ambiguos. 

 Los resultados de un estudio de casos y testigos realizado entre 

 trabajadores expuestos a diesel llevaron a pensar en un aumento del 

 riesgo de cáncer de pulmón distinto del adenocarcinoma y de cáncer de 

 próstata. En ninguno de los casos se observó una relación exposición- 

 respuesta. En vista de los pocos estudios disponibles, del reducido 

 número de casos y de la consiguiente amplitud de los intervalos de 

 confianza, no es posible extraer conclusión alguna acerca de la 

 carcinogenicidad del diesel para el hombre. 

 En ratones, la administración cutánea de combustibles diesel fue 

 débilmente carcinógena. Dado que no existe una genotoxicidad clara, es 

 posible que la inducción de cáncer se deba a mecanismos no 

 genotóxicos, por ejemplo a una irritación cutánea crónica 

 caracterizada por ciclos repetidos de lesiones cutáneas, con la 

 consiguiente hiperplasia epidérmica. 

 A1.9 Evaluación de los efectos en el medio ambiente 

 El medio puede contaminarse de resultas de la liberación 

 accidental de diesel en gran escala, como la asociada a desastres en 

 depósitos o escapes en oleoductos, o a menor escala como resultado de 

 la contaminación del suelo de las inmediaciones de fábricas o garajes. 

 En el agua, el diesel se propaga de forma casi inmediata, los 

 componentes polares y de bajo peso molecular relativo se disuelven y 

 se separan por lixiviación, los componentes volátiles se evaporan a 

 partir de la superficie del agua, y da comienzo la degradación 

 microbiana. La intensidad de la degradación depende de la temperatura 

 y de las condiciones climáticas. La composición química de los 

 derrames cambia con el tiempo: después de un vertido al agua, algunas 

 fracciones se evaporan, y los componentes de diesel evaporados se 

 degradan fotoquímicamente; en el sedimento, parece ser que el diesel 

 es transportado en general a los sedimentos del fondo por las 

 partículas que se depositan; en el suelo, los componentes del diesel 

 migran a distintas velocidades, en función del tipo de suelo. 

Diesel fuel and exhaust emissions (EHC 171, 1996) Page 178 of 184

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 Los componentes individuales son de por sí biodegradables, pero 

 la velocidad de biodegradación depende estrechamente de las 

 condiciones físicas y climáticas y de la composición de la población 

 microbiana. 

 Los organismos acuáticos, en particular los moluscos, bioacumulan 

 hidrocarburos en diversa medida, pero se produce una depuración de los 

 hidrocarburos al transferirlos a agua limpia. Puede darse una 

 bioacumulación de diesel; ahora bien, no hay datos sobre su 

 biomagnificación. 

 Los derrames de diesel tienen efectos nocivos inmediatos en el 

 medio, donde causan una considerable mortalidad de la biota. Puede 

 producirse una recolonización al cabo de aproximadamente un año, en 

 función de la especie de animal o planta y del contenido químico y 

 físico de los restos del derrame. Los organismos acuáticos que 

 sobreviven a los derrames de diesel pueden verse afectados por la 

 contaminación externa y por la acumulación del producto en los 

 tejidos: un desarrollo anormal y la presencia de tasas metabólicas 

 alteradas son indicios del estrés resultante. 

 PARTE B EMISIONES DE GASES DE ESCAPE DE MOTORES DIESEL

 B1. RESUMEN

 B1.1 Identidad, propiedades físicas y químicas y métodos 

 analíticos 

 Las emisiones de gases de escape de los motores diesel contienen 

 cientos de compuestos químicos, que son emitidos en parte en la fase 

 gaseosa y en parte en la fase de materia particulada de los gases de 

 escape. Los principales productos gaseosos de la combustión son los 

 siguientes: dióxido de carbono, oxígeno, nitrógeno y vapor de agua; 

 hay también monóxido de carbono, dióxido de azufre, óxidos de 

 nitrógeno, e hidrocarburos y sus derivados. Se detectan benceno y 

 tolueno en el margen porcentual correspondiente a los compuestos de 

 menor peso en la parte gaseosa de la fracción de hidrocarburos. Otros 

 componentes de los gases de escape son los hidrocarburos aromáticos 

 policíclicos (HAP) de bajo peso molecular relativo. 

 Una importante característica de las emisiones de estos gases de 

 escape es que la liberación de partículas es 20 veces más intensa que 

 en los vehículos propulsados por gasolina. Las partículas están 

 compuestas de carbono elemental, compuestos orgánicos adsorbidos del 

 combustible y el aceite lubricante, sulfatos derivados del azufre del 

 combustible, y cantidades mínimas de componentes metálicos. La mayor 

 parte de la materia particulada total tiene al parecer dimensiones del 

 orden de la submicra: entre 0,02 y 0,5 μm. Con el paso del tiempo 

 puede producirse aglomeración, hasta un diámetro máximo de 30 μm. Las 

 partículas emitidas presentan una gran superficie. Los compuestos 

 orgánicos representan por lo general un 10%-30% de la materia 

 particulada total, pero los motores mal diseñados o mantenidos pueden 

 generar hasta un 90%. En esta fracción se encuentran también, a 

 concentraciones de partes por millón, HAP, HAP oxigenados y nitro-HAP 

 de alto peso molecular relativo. 

 Para medir las emisiones de los vehículos se utilizan ciclos de 

 pruebas transitorios y estables específicos. Pueden tomarse muestras 

 de gases de escape diluidos o no diluidos. Es difícil conseguir 

 muestras sin artefactos, ya que los componentes de los gases de escape 

 pueden sufrir reacciones químicas, procesos de adsorción y desorción, 

 y condensación y difusión. Los HAP de mayor interés toxicológico de la 

 materia particulada del diesel se determinan por lo general mediante 

 la extracción de Soxhlet, limpieza y fraccionamiento, seguidos de 

 análisis por cromatografía líquida de alta resolución o cromatografía 

 de gases unida a espectrometría de masas. 

 B1.2 Fuentes de exposición humana y ambiental 

 La principal fuente de gases de escape de motores diesel son los 

 vehículos de motor; otras fuentes son los motores diesel fijos, de 

 locomotoras de ferrocarril y de barco. Las emisiones de los vehículos 

 de motor diesel han sido bien caracterizadas, pero a menudo los 

 resultados de los estudios no se prestan a comparación, debido a 

 diferencias que afectan a parámetros tales como los ciclos de pruebas, 

 el tipo de motor y la composición del combustible. Las cantidades 

 emitidas de los diversos componentes son las siguientes: dióxido de 

 carbono, aproximadamente 1 kg/km; monóxido de carbono, óxidos de 

 nitrógeno, hidrocarburos gaseosos totales y materia particulada, 

 0,1-20 g/km; y compuestos alifáticos, alcoholes, aldehídos, compuestos 

 aromáticos ligeros y HAP, microgramos por kilómetro. Las emisiones de 

 monóxido de carbono, óxidos de nitrógeno, hidrocarburos gaseosos 

 totales y materia particulada están reglamentadas por ley en varios 

 países. 

 En lo que respecta a la calidad y cantidad de los gases de 

 escape, no suele haber diferencias entre los motores de baja y de gran 

 potencia, si bien los vehículos pesados liberan cantidades 

 relativamente mayores de materia particulada. La naturaleza de los 

 gases de escape depende del ciclo de pruebas (transitorio o estable), 

 de las características del motor (técnicas de inyección y de 

 aspiración, mantenimiento, kilometraje), y de la composición del 

 combustible (contenido de azufre, aromaticidad, volatilidad); el 

 ajuste del motor es muy importante en este sentido. 

 La liberación de materia particulada aumenta con la disminución 

 de la proporción aire/combustible, el aumento de la carga y el aumento 

 de la temperatura. Emiten más partículas los motores viejos y muy 

 usados que los nuevos y de bajo kilometraje, probablemente debido a un 

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 mayor consumo de aceites lubricantes. La emisión de partículas por los 

 vehículos diesel de poca potencia también está correlacionada con el 

 contenido de azufre del combustible, ya que la formación de sulfatos 

 de metal se traduce en un aumento de la masa de partículas; no se ha 

 determinado la emisión de partículas por parte de vehículos de gran 

 potencia. El aumento de la aromaticidad del combustible también 

 conlleva una mayor emisión de partículas. 

 Los HAP y los HAP oxigenados emitidos por los motores diesel y de 

 encendido por chispa son parecidos cualitativamente. Los HAP 

 oxigenados y nitrados se emiten a niveles del orden de pocos 

 microgramos por kilómetro, pero no se sabe con seguridad qué 

 concentración real alcanzan estos compuestos, ya que pueden 

 descomponerse y formarse durante el muestreo. Las emisiones de HAP 

 aumentan con la carga y con la temperatura, así como con a antigüedad 

 del motor, a causa probablemente de un mayor consumo de aceites 

 lubricantes. La emisión de HAP depende también de la técnica de 

 inyección del motor: las emisiones de HAP aumentan al mismo tiempo que 

 la proporción aire/combustible en los motores de inyección directa, 

 mientras que disminuyen en los motores de inyección indirecta. La 

 aromaticidad y la volatilidad del combustible guardan relación directa 

 con la emisión de HAP. El mal funcionamiento de los dispositivos del 

 motor, sobre todo del sistema de inyección de combustible, aumenta la 

 emisión de los principales componentes de escape. Se dispone de pocos 

 datos sobre la contribución de las emisiones de los motores diesel a 

 la liberación total de productos de combustión por el hombre. 

 Es posible reducir las emisiones de gases de escape producidos 

 por el diesel mejorando el diseño de los motores, los captores de 

 partículas (oxidantes de captores) y los catalizadores. Mientras que 

 los captores de partículas eliminan tanto el hollín como los 

 compuestos orgánicos solubles adsorbidos en las partículas, los 

 catalizadores reducen sobre todo los niveles de monóxido de carbono y 

 de hidrocarburos gaseosos. En la práctica es difícil regenerar los 

 captores de partículas. Los catalizadores exigen combustibles de bajo 

 contenido de azufre, ya que este elemento daña los centros activos del 

 catalizador. 

 B1.3 Transporte, distribución y transformación en el medio 

 ambiente 

 El compartimento que antes se ve afectado por las emisiones de 

 gases de escape de los motores diesel es la atmósfera. La hidrosfera y 

 la geosfera se ven contaminadas indirectamente por depósitos secos y 

 húmedos. El destino ambiental de los distintos componentes de estos 

 gases de escape es en general bien conocido: las partículas se 

 comportan como moléculas de gas (no reactivas) por lo que se refiere a 

 su transporte mecánico en la atmósfera; pueden ser transportadas a 

 gran distancia y penetrar incluso en la estratosfera. 

 Se estima que el índice global de eliminación de las partículas 

 diesel es bajo, lo que se traduce en una permanencia de varios días en 

 la atmósfera. Con el tiempo se puede producir una coagulación de las 

 partículas, con lo que aumenta la precipitación de las mismas y 

 disminuye su concentración total en el aire. El carbono elemental de 

 las partículas diesel puede actuar como catalizador de la formación de 

 ácido sulfúrico por oxidación del dióxido de azufre. Los componentes 

 orgánicos adsorbidos en el carbono elemental pueden experimentar 

 varias reacciones físicas y químicas con otros compuestos atmosféricos 

 y durante la exposición a la luz solar. 

 B1.4 Niveles ambientales y exposición humana 

 Dado que los gases de escape diesel son una mezcla compleja de 

 gran diversidad de compuestos, por lo general no es posible precisar 

 los 'niveles ambientales'. Los distintos componentes de los gases de 

 escape diesel se pueden detectar en principio en todos los 

 compartimentos del medio ambiente, aunque por lo general no es posible 

 averiguar su origen. Se conocen los niveles ambientales de la mayoría 

 de los distintos componentes. 

 La exposición de la población general a los gases de escape de 

 motores diesel se produce especialmente en las calles transitadas y en 

 los aparcamientos, sobre todo los subterráneos. La identificación de 

 las fuentes resulta difícil, y la contribución de esos gases a la 

 contaminación total por productos de combustión del tráfico se calcula 

 en general a partir de los coeficientes de emisión y del porcentaje de 

 vehículos propulsados por diesel. Los niveles de exposición de la 

 población general y de los trabajadores a la materia particulada de 

 los motores diesel tienen importancia toxicológica. Las 

 concentraciones ambientales diarias de partículas diesel cerca de las 

 carreteras oscilan como promedio entre 8 y 42 μg/m3. Las 

 concentraciones promedio anuales estimadas fueron de 5-10 μg/m3 en 

 zonas urbanas y < 1,5 μg/m3 en zonas rurales de Alemania, y de 

 1-2 μg/m3 en zonas urbanas y 0,6-1 μg/m3 en zonas rurales de los 

 Estados Unidos de América. Las concentraciones están directamente 

 relacionadas con la densidad del tráfico y son tanto menores cuanto 

 más lejos están las carreteras. 

 La identificación de las fuentes también puede revestir 

 dificultad en los lugares de trabajo, sobre todo en las minas, donde 

 la carga total de polvo es elevada. Se han hecho análisis de muestras 

 de carbono para determinar la exposición específica a gases de escape 

 de motores diesel en el lugar de trabajo y, según se ha notificado, 

 los niveles de materia particulada a que están expuestos los 

 trabajadores son del orden de 0,04-0,134 mg/m3 para los conductores 

 de camiones y de 0,004-0,192mg/m3 para los ferroviarios. Como 

 medidas de la exposición ocupacional se han utilizado también las 

 partículas respirables totales y las partículas suspendidas totales. 

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 B1.5 Cinética y metabolismo en animales de laboratorio y en el 

 hombre 

 B1.5.1 Depósito 

 Las partículas de los gases de escape de motores diesel, con un 

 diámetro aerodinámico mediano de aproximadamente 0,2 μm, son filtradas 

 en cierta medida por la nariz, y la eficiencia de depósito en el 

 pulmón es sólo ligeramente superior al valor mínimo hallado para las 

 partículas que tienen un diámetro aerodinámico mediano de 

 aproximadamente 0,5 μm. Así, un 10%-15% de las partículas de hollín 

 diesel inhaladas se depositan en la región alveolar de los pulmones de 

 la rata y el cobayo; en el hombre se deposita en la región alveolar un 

 10%. 

 B1.5.2 Retención y eliminación de las partículas 

 La eliminación mucociliar de partículas en las vías respiratorias 

 ciliadas es casi completa en un plazo de 24 horas. La eliminación a 

 largo plazo de las partículas diesel en la región alveolar se ha 

 determinado mediante varios estudios realizados en ratas expuestas por 

 inhalación a partículas diesel o control marcadas. Se notificaron 

 periodos de semieliminación de 60-100 días en testigos con cargas 

 pulmonares bajas (< 1 mg/pulmón), mientras que los periodos de 

 semieliminación aumentaron a 100-600 días en ratas con cargas 

 pulmonares crecientes de 1 a 60 mg/pulmón. En varios estudios se halló 

 que los efectos se debían a una sobrecarga de partículas, fenómeno 

 descrito en diversas especies y con varios tipos de materia 

 particulada. Este hecho se observa por lo general cuando la velocidad 

 de depósito de las partículas de baja solubilidad y baja toxicidad 

 aguda supera su velocidad de eliminación durante un tiempo 

 considerable. El periodo de semieliminación alveolar libre en el 

 hombre es de varios cientos de días, mayor que en la rata. 

 Se desarrolló un modelo pulmonar dosimétrico a partir de datos 

 relativos al depósito y retención de las partículas diesel en ratas 

 sometidas a inhalación prolongada, así como de datos referentes al 

 depósito y retención de partículas en el hombre. Este modelo puede 

 utilizarse para predecir la retención de partículas diesel y de 

 material orgánico adsorbido en los pulmones de personas de diferentes 

 edades. No se dispone de datos sobre la variación de la retención de 

 distintos componentes tras la exposición prolongada a gases de escape 

 de motores diesel. 

 B1.5.3 Retención y eliminación de hidrocarburos aromáticos 

 policíclicos adsorbidos en hollín de diesel 

 Los HAP del hollín de diesel se adhieren fuertemente a la 

 superficie de las partículas. Aproximadamente un 50% de los HAP 

 adsorbidos en las partículas diesel desaparece de los pulmones en el 

 plazo de un día, pero los periodos de semieliminación de los restantes 

 HAP fueron del orden de 18-36 días. Estudios realizados con 

 3H-benzo[ a]pireno y 14C-nitropireno han demostrado que, cuando 

 los HAP están asociados a materia particulada, su eliminación de los 

 pulmones se retrasa significativamente en comparación con los HAP 

 inhalados no asociados a materia particulada. 

 B1.5.4 Metabolismo 

 Se ha observado que el benzo[ a]pireno adsorbido en partículas 

 de gases de escape de motores diesel se metaboliza por oxidación en 

 fenoles, dioles y quinonas de benzo[ a]pireno en el pulmón y en 

 cultivos celulares de macrófagos pulmonares. 

 El nitropireno adsorbido en partículas diesel se metabolizó en 

 acetilaminopirenofenol después de su inhalación. Se han hallado más 

 aductos de ADN en los pulmones y las células de tipo II de ratas 

 expuestas a gases de escape de motores diesel que en las testigo. El 

 metabolismo oxidativo de algunos compuestos orgánicos en epóxidos 

 podría ser la causa de la formación de esos aductos, pero únicamente 

 se hallaron aductos tras la exposición a partículas. Se ha demostrado 

 que algunas sustancias orgánicas de los gases de escape de motores 

 diesel dan lugar a la formación de aductos de ADN; sin embargo, el 

 núcleo carbonáceo por sí mismo (sin material orgánico extraíble) 

 también puede inducir aductos, por lesión crónica de las células 

 epiteliales. 

 B1.6 Efectos en mamíferos de laboratorio y en sistemas de pruebas 

 in vitro 

 Los escasos datos disponibles parecen indicar que la toxicidad 

 aguda de los gases de escape de motores diesel es escasa. Ratones 

 tratados intratraquealmente con partículas de tales gases murieron de 

 edema pulmonar; la DL50 fue de aproximadamente 20 mg/kg de peso 

 corporal. Partículas extraídas con metanol no tuvieron efectos letales 

 a concentraciones de hasta aproximadamente 33 mg/kg de peso corporal. 

 En hámsters, la DL50tras administración intraperitoneal fue de 

 1280 mg/kg de peso corporal. No hay datos respecto a la exposición por 

 inhalación. 

 La exposición de ratas, cobayos y gatos a gases de escape de 

 motores diesel con un contenido de partículas de 6 mg/m3 durante 

 aproximadamente cuatro semanas alteró la función pulmonar, causando en 

 particular un aumento del 35% de la resistencia al flujo pulmonar en 

 los cobayos y una disminución del 10% de la capacidad vital (flujo 

 espiratorio) en los gatos. El análisis histopatológico reveló un 

 espesamiento focal de las paredes alveolares, un aumento significativo 

 del índice de marcaje de las células de tipo II, y acumulaciones de 

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 macrófagos cargados de partículas. Estas acumulaciones se hallaban 

 cerca de los bronquiolos terminales, y aumentaron de tamaño, debido a 

 la adhesión (secuestro) de macrófagos, durante el periodo ulterior de 

 recuperación. 

 No se observaron disminuciones importantes del peso corporal ni 

 acortamiento alguno del tiempo de supervivencia en ratones, ratas, 

 hámsters, gatos y monos después de un periodo prolongado de inhalación 

 de concentraciones de hasta 4 mg/m3. En todas las especies sometidas 

 a inhalación prolongada de gases de escape de motores diesel se 

 observaron los siguientes efectos tóxicos relacionados con la dosis: 

 aumentos de hasta un 400% del peso pulmonar; inflamación pulmonar 

 cuantificable mediante parámetros bioquímicos (enzimas citoplasmáticas 

 marcadoras, colágeno) y citológicos (aumento de los neutrófilos 

 polimorfonucleares); trastornos de la mecánica pulmonar; aumento del 

 número de macrófagos cargados de partículas con acumulaciones focales 

 (secuestro) en condiciones de sobrecarga; y ulteriores cambios 

 proliferativos de las células epiteliales, con inicio de fibrosis. 

 La limitada información disponible sobre la toxicidad para la 

 reproducción y el desarrollo lleva a pensar que la inhalación de gases 

 de escape de motores diesel no reviste gran importancia. En la mayoría 

 de los experimentos no se observaron efectos en ratones, ratas, 

 hámsters, conejos o monos; no obstante, tras inyección intraperitoneal 

 se observaron anomalías en el semen de ratones sometidos a partículas 

 de esos gases de escape, y embriotoxicidad en hámsters sometidos a 

 extractos de tales gases. 

 La mayoría de las pruebas de genotoxicidad in vitro se han 

 llevado a cabo con extractos de gases de escape de motores diesel en 

 lugar de con la mezcla total de tales gases; se detectaron respuestas 

 positivas en ausencia de activación metabólica, es decir: los efectos 

 genotóxicos eran al parecer independientes de los HAP. Aproximadamente 

 la mitad de las investigaciones in vivo arrojaron resultados 

 negativos; los únicos resultados positivos fueron la inducción del 

 intercambio de cromátides hermanas en respuesta a la mezcla total de 

 gases de escape y a extractos orgánicos, y la inducción de 

 micronúcleos en respuesta a extractos orgánicos. 

 Por lo general no se observaron efectos inmunotóxicos después de 

 la inhalación de gases de escape de motores diesel; sin embargo, en un 

 estudio se halló un mayor título de anticuerpos IgE antiovoalbúmina, y 

 en dos experimentos, una mayor susceptibilidad a las infecciones en 

 ratones. Algunos estudios realizados en la rata parecen indicar que la 

 inhalación de estos gases de escape tiene efectos sobre el 

 comportamiento y el estado neurofisiológico. 

 En estudios de determinación de la carcinogenicidad de los gases 

 de escape de motores diesel administrados por inhalación a ratas se 

 observó que la fase gaseosa (sin la fracción particulada) no era 

 carcinogénica. En todos los estudios válidos realizados en la rata se 

 halló que los gases eran carcinogénicos a concentraciones de 

 partículas superiores a 2 mg/m3, lo que equivale a una exposición 

 continua de aproximadamente 1 mg/m3. No se observaron efectos ni en 

 el hámster ni en el ratón. En estudios realizados mediante instilación 

 intratraqueal, tanto las partículas de los gases de escape como el 

 negro de humo indujeron la aparición de tumores, y se observó una 

 aparente correlación entre la superficie de las partículas carbonosas 

 y la actividad tumorigénica. La inhalación prolongada de negro de humo 

 prácticamente desprovisto de HAP a concentraciones similares también 

 provocó la aparición de tumores pulmonares en ratas. 

 No está claro si en los mecanismos de carcinogenicidad de los 

 gases de escape de motores diesel intervienen reacciones del ADN o de 

 otro tipo (o quizá ambas). Se han utilizado diversos modelos para 

 dilucidar la carcinogenicidad de esos gases. 

 B1.7 Efectos en el ser humano 

 Los gases de escape de los motores diesel contribuyen a la 

 contaminación atmosférica en general. Aunque en los estudios agudos o 

 crónicos no es posible diferenciar el papel de las partículas diesel, 

 éstas podrían ser parcialmente responsables de los diversos efectos 

 sobre la salud asociados a la contaminación atmosférica. 

 Los gases de escape habituales de los motores diesel tienen un 

 olor peculiar, que algunas personas consideran desagradable, sobre 

 todo a altas concentraciones. Los síntomas que siguen a la exposición 

 aguda y crónica a esos gases han sido descritos en estudios y en 

 referencias anecdóticas de personas expuestas en el lugar de trabajo. 

 Se ha observado la aparición de irritación de las membranas mucosas 

 oculares y nasales en respuesta a la exposición aguda a tales gases, 

 así como un aumento de la frecuencia de síntomas respiratorios en 

 cohortes ocupacionales; no obstante, se ignora la contribución de las 

 partículas diesel. No se han detectado efectos sistemáticos a corto 

 plazo en la función pulmonar, pero se han notificado ataques de asma. 

 En un estudio controlado en el que se expuso a ocho voluntarios 

 sanos no fumadores en una cámara durante 60 minutos a gases de escape 

 de motores diesel diluidos, se detectó una disminución de la 

 fagocitosis en los macrófagos alveolares del líquido de lavado 

 broncoalveolar. 

 En algunos estudios transversales y longitudinales realizados 

 entre trabajadores expuestos de forma prolongada en su entorno laboral 

 a esos gases se han hallado decrementos de la función pulmonar y una 

 mayor frecuencia de síntomas respiratorios, pero estos estudios 

 presentan la limitación de haberse realizado con una exposición breve. 

 No se observaron aumentos importantes en estudios de cohortes 

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 realizados para investigar las defunciones por trastornos 

 cardiovasculares y/o cerebrovasculares debidos a las emisiones diesel. 

 En varios estudios epidemiológicos se ha evaluado la asociación 

 entre cánceres de pulmón y de la vejiga urinaria y la exposición 

 ocupacional a gases de escape de motores diesel. En esta monografía se 

 incluyen sólo los estudios considerados pertinentes para evaluar los 

 efectos carcinogénicos de esos gases. Los estudios más importantes por 

 lo que se refiere al cáncer de pulmón son los realizados en 

 ferroviarios, trabajadores de garajes de autobuses y estibadores, esto 

 es, cohortes de individuos cuya actividad laboral no deja lugar a 

 dudas sobre la exposición a gases de escape diesel. La totalidad de 

 los cuatro estudios más informativos pusieron de manifiesto un mayor 

 riesgo de cáncer de pulmón, con riesgos relativos que van desde 1,4 

 para los ferroviarios, pasando por 1,3-2,4 para los trabajadores de 

 garajes de autobuses (según el grado de exposición), hasta 3-6 para 

 los estibadores (según el método empleado para evaluar la exposición, 

 pero con amplios intervalos de confianza). En un estudio de casos y 

 testigos realizados entre ferroviarios y en el estudio de los 

 estibadores fue posible introducir ajustes en función del consumo de 

 tabaco. En los dos casos, el efecto de la exposición al diesel no se 

 vio materialmente alterado por el ajuste realizado en función del 

 consumo de tabaco. En los tres estudios en que no pudo hacerse ese 

 ajuste, el análisis se basó en comparaciones de subgrupos de las 

 cohortes, de manera que la probabilidad de influencia del tabaco como 

 factor de confusión fue menor que al utilizar grupos de comparación 

 externos. 

 Se han llevado a cabo varios estudios de casos y testigos para 

 examinar la relación entre el cáncer de vejiga urinaria y la presunta 

 exposición a gases de escape de motores diesel. Se detectó un aumento 

 del riesgo, sobre todo para los conductores de camión; no obstante, 

 todos estos estudios adolecían de una deficiente caracterización de la 

 exposición. Por ello, no es posible establecer una asociación causal 

 entre la exposición a los gases de escape diesel y un aumento del 

 riesgo de cáncer de vejiga urinaria 

 B1.8 Efectos en otros organismos en el laboratorio y en el medio 

 ambiente 

 El único estudio sobre los efectos de las emisiones de motores 

 diesel propiamente dichas es un trabajo realizado con algas verdes. 

 B1.9 Evaluación de los riesgos para la salud humana 

 Se utilizó el paradigma de evaluación de riesgos de la Academia 

 Nacional de Ciencias de los Estados Unidos (National Research Council, 

 1983) para evaluar los riesgos asociados a variables de valoración 

 relacionadas y no relacionadas con el cáncer. Este proceso consta de 

 los cuatro pasos siguientes: 1) identificación del riesgo, 2) 

 evaluación de la relación dosis-respuesta, 3) evaluación de la 

 exposición, y 4) caracterización del riesgo. 

 Se considera que los estudios más informativos son los 

 epidemiológicos de larga duración realizados con una exposición bien 

 definida y con seguimiento ulterior (> 20 años). Satisfacían esos 

 criterios cuatro estudios sobre el cáncer de pulmón en personas 

 expuestas en su entorno de trabajo. Los riesgos relativos de cáncer de 

 pulmón asociado a la exposición a gases de escape de motores diesel 

 fueron por lo general bajos y podían haberse debido al azar, a los 

 efectos de factores de confusión no determinados y a la dificultad 

 para corregir con precisión la influencia de los factores de confusión 

 conocidos. Las conclusiones de estos estudios están avaladas por los 

 resultados de otros estudios menos precisos en cuanto a la definición 

 de la exposición. Globalmente se considera que los gases de escape de 

 los motores diesel son probablemente carcinogénicos para el hombre; 

 sin embargo, no se dispone de datos cuantitativos que permitan estimar 

 el riesgo para el ser humano. 

 B1.9.1 Efectos no neoplásicos 

 Para caracterizar los riesgos se utilizaron dos métodos 

 generales: el nivel sin efectos adversos observados (NOAEL) dividido 

 por un factor de incertidumbre y una concentración de referencia. En 

 los dos casos se empleó un sofisticado modelo dosimétrico para reducir 

 la incertidumbre asociada a la extrapolación interespecies de las 

 dosis. 

 Se calculó que el nivel sin efecto de las partículas de los gases 

 de escape de los motores diesel en el hombre era de 0,139 mg/m3. El 

 valor orientativo para la población general calculado a partir del 

 modelo dosimétrico fue de 5,6 μg/m3, y el calculado sin el modelo, 

 de 2,3 μg/m3. 

 El método de la concentración de referencia tiene en cuenta la 

 totalidad de la relación exposición-respuesta en lugar de puntos 

 únicos obtenidos en estudios de inhalación, como ocurre con el método 

 del NOAEL. Se identificaron tres variables de evaluación sensibles: 

 inflamación alveolar crónica, eliminación pulmonar alterada, y 

 lesiones pulmonares hiperplásicas. Las concentraciones de referencia, 

 calculadas mediante el mismo modelo dosimétrico utilizado para el 

 método del NOAEL, fueron de 0,9-2 μg/m3 para la inflamación, 

 1,2-3 μg/m3 para la disminución de la eliminación pulmonar, y 

 6,3-14 μg/m3 para las lesiones hiperplásicas. 

 B1.9.2 Efectos neoplásicos 

 Se utilizó un modelo polietápico linearizado para hacer 

 estimaciones del riesgo unitario asociado a la exposición a gases de 

 escape de motores diesel. Se consideró que los resultados de los 

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 estudios epidemiológicos disponibles eran insuficientes para hacer una 

 estimación cuantitativa del riesgo unitario, por lo que se decidió 

 utilizar datos de varios estudios de inhalación prolongada en los que 

 se había detectado carcinogénesis a concentraciones superiores a 

 2 mg/m3. Se calculó un riesgo unitario de 3,4 × 10-5 μg/m3

 (media geométrica de cuatro estimaciones del riesgo) para las 

 partículas de los gases de escape. Usando otro modelo biológico se 

 obtuvo un riesgo unitario parecido, en el supuesto de que las 

 partículas diesel influyen en la iniciación y/o proliferación celular 

 a bajas concentraciones. 

 B1.10 Evaluación de los efectos en el medio ambiente 

 No se disponía de suficiente información para evaluar los efectos 

 específicos de las emisiones de gases de escape de motores diesel. Los 

 efectos del combustible diesel quemado deben de ser parecidos a los de 

 otros combustibles fósiles y están relacionados con el consumo de 

 diesel. 

 

 See Also: 

 Toxicological Abbreviations

Diesel fuel and exhaust emissions (EHC 171, 1996) Page 184 of 184

http://www.inchem.org/documents/ehc/ehc/ehc171.htm 3/8/2011