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    UNITED NATIONS ENVIRONMENT PROGRAMME
    INTERNATIONAL LABOUR ORGANISATION
    WORLD HEALTH ORGANIZATION


    INTERNATIONAL PROGRAMME ON CHEMICAL SAFETY



    ENVIRONMENTAL HEALTH CRITERIA 188





    Nitrogen Oxides

    (Second Edition)



    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.


    First draft prepared by Drs J.A. Graham, L.D. Grant, L.J. Folinsbee,
    D.J. Kotchmar and J.H.B. Garner, US Environmental Protection Agency



    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 of the
    Inter-Organization Programme for the Sound Management of Chemicals.


    World Health Organization
    Geneva, 1997

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    WHO Library Cataloguing in Publication Data

    Nitrogen oxides - 2nd ed.

    (Environmental health criteria ; 188)

    1.Nitrogen dioxide                 2.Nitrogen oxides
    I.Series

    ISBN 92 4 157188 8                 (NLM Classification: WA 754)
    ISSN 0250-863X

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    CONTENTS

    ENVIRONMENTAL HEALTH CRITERIA FOR NITROGEN OXIDES

    Preamble

    1. SUMMARY

         1.1. Nitrogen oxides and related compounds
               1.1.1. Atmospheric transport
               1.1.2. Measurement
               1.1.3. Exposure
         1.2. Effects of atmospheric nitrogen species, particularly
               nitrogen oxides, on vegetation
         1.3. Health effects of exposures to nitrogen dioxide
               1.3.1. Studies of the effects of nitrogen compounds on
                       experimental animals
                       1.3.1.1    Biochemical and cellular mechanisms of
                                  action of nitrogen oxides
                       1.3.1.2    Effects on host defence
                       1.3.1.3    Effects of chronic exposure on the
                                  development of chronic lung disease
                       1.3.1.4    Potential carcinogenic or co-carcinogenic
                                  effects
                       1.3.1.5    Age susceptibility
                       1.3.1.6    Influence of exposure patterns
               1.3.2. Controlled human exposure studies on nitrogen
                       oxides
               1.3.3. Epidemiology studies on nitrogen dioxide
               1.3.4. Health-based guidance values for nitrogen dioxide

    2. PHYSICAL AND CHEMICAL PROPERTIES, AIR SAMPLING AND ANALYSIS,
         TRANSFORMATIONS AND TRANSPORT IN THE ATMOSPHERE

         2.1. Introduction
               2.1.1. The nomenclature and measurement of atmospheric
                       nitrogen species
         2.2. Nitrogen species and their physical and chemical properties
               2.2.1. Nitrogen oxides
                       2.2.1.1    Nitric oxide
                       2.2.1.2    Nitrogen dioxide
                       2.2.1.3    Nitrous oxide
                       2.2.1.4    Other nitrogen oxides
               2.2.2. Nitrogen acids
                       2.2.2.1    Nitric acid
                       2.2.2.2    Nitrous acid
               2.2.3. Ammonia
               2.2.4. Ammonium nitrate
               2.2.5. Peroxyacetyl nitrate
               2.2.6. Organic nitrites and nitrates

         2.3. Sampling and analysis methods
               2.3.1. Nitric oxide
                       2.3.1.1    Nitric oxide continuous methods
                       2.3.1.2    Passive samplers for NO
                       2.3.1.3    Calibration of NO analysis methods
                       2.3.1.4    Sampling considerations for NO
               2.3.2. Nitrogen dioxide
                       2.3.2.1    Chemiluminescence (NO + O3)
                       2.3.2.2    Chemiluminescence (luminol)
                       2.3.2.3    Laser-induced fluorescence and tuneable
                                  diode laser absorption spectrometry
                       2.3.2.4    Wet chemical methods
                       2.3.2.5    Other methods
                       2.3.2.6    Passive samplers
                       2.3.2.7    Calibration
               2.3.3. Total reactive odd nitrogen
               2.3.4. Peroxyacetyl nitrate
               2.3.5. Other organic nitrates
               2.3.6. Nitric acid
               2.3.7. Nitrous acid
               2.3.8. Dinitrogen pentoxide and nitrate radicals
               2.3.9. Particulate nitrate
               2.3.10. Nitrous oxide
               2.3.11. Summary
         2.4. Transport and transformation of nitrogen oxides in the air
               2.4.1. Introduction
               2.4.2. Chemical transformations of oxides of nitrogen
                       2.4.2.1    Nitric oxide, nitrogen dioxide and ozone
                       2.4.2.2    Transformations in indoor air
                       2.4.2.3    Formation of other oxidized nitrogen
                                  species
               2.4.3. Advection and dispersion of atmospheric nitrogen
                       species
                       2.4.3.1    Transport of reactive nitrogen species
                                  in urban plumes
                       2.4.3.2    Air quality models
                       2.4.3.3    Regional transport
         2.5. Conversion factor for nitrogen dioxide
         2.6. Summary

    3. SOURCES, EMISSIONS AND AIR CONCENTRATIONS

         3.1. Introduction
         3.2. Sources of nitrogen oxides
               3.2.1. Sources of NOx emission
                       3.2.1.1    Fuel combustion
                       3.2.1.2    Biomass burning
                       3.2.1.3    Lightning
                       3.2.1.4    Soils
                       3.2.1.5    Oceans

               3.2.2. Removal from the ambient environment
               3.2.3. Summary of global budgets for nitrogen oxides
         3.3. Ambient concentrations of nitrogen oxides
               3.3.1. International comparison studies of NOx
                       concentrations
               3.3.2. Example case studies of NOx and NO2
                       concentrations
         3.4. Occurrence of nitrogen oxides indoors
               3.4.1. Indoor sources
                       3.4.1.1    Gas-fuelled cooking stoves
                       3.4.1.2    Unvented gas space heaters and water
                                  heaters
                       3.4.1.3    Kerosene space heaters
                       3.4.1.4    Wood stoves
                       3.4.1.5    Tobacco products
               3.4.2. Removal of nitrogen oxides from indoor environments
         3.5. Indoor concentrations of nitrogen oxides
               3.5.1. Homes without indoor combustion sources
               3.5.2. Homes with combustion appliances
               3.5.3. Homes with combustion space heaters
               3.5.4. Indoor nitrous acid concentrations
               3.5.5. Predictive models for indoor NO2 concentration
         3.6. Human exposure
         3.7. Exposure of plants and ecosystems

    4. EFFECTS OF ATMOSPHERIC NITROGEN COMPOUNDS (PARTICULARLY NITROGEN
         OXIDES) ON PLANTS

         4.1. Properties of NOx and NHy
               4.1.1. Adsorption and uptake
               4.1.2. Toxicity, detoxification and assimilation
               4.1.3. Physiology and growth aspects
               4.1.4. Interactions with climatic conditions
               4.1.5. Interactions with the habitat
               4.1.6. Increasing pest incidence
               4.1.7. Conclusions for various atmospheric nitrogen
                       species and mixtures
                       4.1.7.1    NO2
                       4.1.7.2    NO
                       4.1.7.3    NH3
                       4.1.7.4    NH4+ and NO3- in wet and occult
                                  deposition
                       4.1.7.5    Mixtures
               4.1.8. Appraisal
                       4.1.8.1    Representativity of the data
               4.1.9. General conclusions
         4.2. Effects on natural and semi-natural ecosystems
               4.2.1. Effects on freshwater and intertidal ecosystems
                       4.2.1.1    Effects of nitrogen deposition on
                                  shallow softwater lakes

                       4.2.1.2    Effects of nitrogen deposition on lakes
                                  and streams
               4.2.2. Effects on ombrotrophic bogs and wetlands
                       4.2.2.1    Effects on ombrotrophic (raised) bogs
                       4.2.2.2    Effects on mesotrophic fens
                       4.2.2.3    Effects on fresh- and saltwater marshes
               4.2.3. Effects on species-rich grasslands
                       4.2.3.1    Effects of nitrogen on calcareous
                                  grasslands
                       4.2.3.2    Critical loads for nitrogen in
                                  calcareous grasslands
                       4.2.3.3    Comparison with other semi-natural
                                  grasslands
               4.2.4. Effects on heathlands
                       4.2.4.1    Effects on inland dry heathlands
                       4.2.4.2    Effects of nitrogen on inland wet
                                  heathlands
                       4.2.4.3    Effects of nitrogen on arctic and alpine
                                  healthlands
                       4.2.4.4    Effects on herbs of matgrass swards
               4.2.5. Effects of nitrogen deposition on forests
                       4.2.5.1    Effects on forest tree species
                       4.2.5.2    Effects on tree epiphytes, ground
                                  vegetation and ground fauna of forests
               4.2.6. Effects on estuarine and marine ecosystems
               4.2.7. Appraisal and conclusions

    5. STUDIES OF THE EFFECTS OF NITROGEN OXIDES ON EXPERIMENTAL ANIMALS

         5.1. Introduction
         5.2. Nitrogen dioxide
               5.2.1. Dosimetry
                       5.2.1.1    Respiratory tract dosimetry
                       5.2.1.2    Systemic dosimetry
               5.2.2. Respiratory tract effects
                       5.2.2.1    Host defence mechanisms
                       5.2.2.2    Lung biochemistry
                       5.2.2.3    Pulmonary function
                       5.2.2.4    Morphological studies
               5.2.3. Genotoxicity, potential carcinogenic or
                       co-carcinogenic effects
               5.2.4. Extrapulmonary effects
         5.3. Effects of mixtures containing nitrogen dioxide
         5.4. Effects of other nitrogen oxide compounds
               5.4.1. Nitric oxide
                       5.4.1.1    Endogenous formation of NO
                       5.4.1.2    Absorption of NO
                       5.4.1.3    Effects of NO on pulmonary function,
                                  morphology and host lung defence
                                  function

                       5.4.1.4    Metabolic effects
                       5.4.1.5    Haematological changes
                       5.4.1.6    Biochemical mechanisms for nitric oxide
                                  effects: reaction with iron and effects
                                  on enzymes and nucleic acids
               5.4.2. Nitric acid
               5.4.3. Nitrates
         5.5. Summary of studies of the effects of nitrogen compounds on
               experimental animals

    6. CONTROLLED HUMAN EXPOSURE STUDIES OF NITROGEN OXIDES

         6.1. Introduction
         6.2. Effects of nitrogen dioxide
               6.2.1. Nitrogen dioxide effects on pulmonary function and
                       airway responsiveness to bronchoconstrictive agents
                       6.2.1.1    Nitrogen dioxide effects in healthy
                                  subjects
                       6.2.1.2    Nitrogen dioxide effects on asthmatics
                       6.2.1.3    Nitrogen dioxide effects on patients
                                  with chronic obstructive pulmonary
                                  disease
                       6.2.1.4    Age-related differential susceptibility
               6.2.2. Nitrogen dioxide effects on pulmonary host defences
                       and bronchoalveolar lavage fluid biomarkers
               6.2.3. Other classes of nitrogen dioxide effects
         6.3. Effects of other nitrogen oxide compounds
         6.4. Effects of nitrogen dioxide/gas or gas/aerosol mixtures on
               lung function
         6.5. Summary of controlled human exposure studies of oxides of
               nitrogen

    7. EPIDEMIOLOGICAL STUDIES OF NITROGEN OXIDES

         7.1. Introduction
         7.2. Methodological considerations
               7.2.1. Measurement error
               7.2.2. Misclassification of the health outcome
               7.2.3. Adjustment for covariates
               7.2.4. Selection bias
               7.2.5. Internal consistency
               7.2.6. Plausibility of the effect
         7.3. Studies of respiratory illness
               7.3.1. Indoor air studies
                       7.3.1.1    St Thomas' Hospital Medical School
                                  Studies (United Kingdom)
                       7.3.1.2    Harvard University - Six Cities Studies
                                  (USA)
                       7.3.1.3    University of Iowa Study (USA)

                       7.3.1.4    Agricultural University of Wageningen
                                  (The Netherlands)
                       7.3.1.5    Ohio State University Study (USA)
                       7.3.1.6    University of Dundee (United Kingdom)
                       7.3.1.7    Harvard University - Chestnut Ridge
                                  Study (USA)
                       7.3.1.8    University of New Mexico Study (USA)
                       7.3.1.9    University of Basel Study (Switzerland)
                       7.3.1.10   Yale University Study (USA)
                       7.3.1.11   Freiburg University Study (Germany)
                       7.3.1.12   McGill University Study (Canada)
                       7.3.1.13   Health and Welfare Canada Study (Canada)
                       7.3.1.14   University of North Carolina Study (USA)
                       7.3.1.15   University of Tucson Study (USA)
                       7.3.1.16   Hong Kong Anti-Cancer Society Study
                                  (Hong Kong)
                       7.3.1.17   Recent studies
               7.3.2. Outdoor studies
                       7.3.2.1    Harvard University - Six City Studies
                                  (USA)
                       7.3.2.2    University of Basel Study (Switzerland)
                       7.3.2.3    University of Wuppertal Studies
                                  (Germany)
                       7.3.2.4    University of Tubigen (Germany)
                       7.3.2.5    Harvard University - Chestnut Ridge
                                  Study (USA)
                       7.3.2.6    University of Helsinki Studies (Finland)
                       7.3.2.7    Helsinki City Health Department Study
                                  (Finland)
                       7.3.2.8    Oulu University Study (Finland)
                       7.3.2.9    Seth GS Medical College Study (India)
         7.4. Pulmonary function studies
               7.4.1. Harvard University - Six City Studies (USA)
               7.4.2. National Health and Nutrition Examination Survey
                       Study (USA)
               7.4.3. Harvard University - Chestnut Ridge Study (USA)
               7.4.4. Other pulmonary function studies
         7.5. Other exposure settings
               7.5.1. Skating rink exposures
         7.6. Occupational exposures
         7.7. Synthesis of the evidence for school-age children
               7.7.1. Health outcome measures
               7.7.2. Biologically plausible hypothesis
               7.7.3. Publication bias
               7.7.4. Selection of studies
                       7.7.4.1    Brief description of selected studies
                       7.7.4.2    Studies not selected for quantitative
                                  analysis
               7.7.5. Quantitative analysis

         7.8. Synthesis of the evidence for young children
         7.9. Summary

    8. EVALUATION OF HEALTH AND ENVIRONMENT RISKS ASSOCIATED WITH
         NITROGEN OXIDES

         8.1. Sources and exposure
         8.2. Evaluation of the effects of atmospheric nitrogen species
               on the environment
               8.2.1. Guidance values - critical levels for air
                       concentrations of nitrogen oxides
               8.2.2. Environment-based guidance values - critical loads
                       for total nitrogen deposition
         8.3. Evaluation of health risks associated with nitrogen oxides
               8.3.1. Concentration-response relationships
               8.3.2. Subpopulations potentially at risk
               8.3.3. Derivation of health-based guidance values

    9. CONCLUSIONS AND RECOMMENDATIONS FOR PROTECTION OF HUMAN HEALTH
         AND THE ENVIRONMENT

    10. FURTHER RESEARCH

    REFERENCES

    RESUME

    RESUMEN
    

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    FIGURE 1

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    WHO TASK GROUP ON ENVIRONMENTAL HEALTH CRITERIA FOR NITROGEN OXIDES

     Members 

    Dr K. Bentley*, Health and Environment Policy Section, Department
         of Community Services and Health, Canberra ACT, Australia

    Dr S. Dobson, Institute of Terrestrial Ecology, Monks Wood
         Experimental Station, Abbots Ripton, Huntingdon, Cambridgeshire,
         United Kingdom

    Dr L. van der Eerden, Centre "De Bom"  Wageningen, The Netherlands

    Dr L. Folinsbee, Health Effects Research Laboratory, US Environmental
         Protection Agency, Research Triangle Park, North Carolina, USA
          (Rapporteur)

    Dr L. Grant*, National Center for Environmental Assessment, US
         Environmental Protection Agency, Research Triangle Park, North
         Carolina, USA

    Mr L. Heiskanen, Health and Environment Policy Section, Department of
         Community Services and Health, Canberra ACT, Australia

    Mr G.M. Johnson, CSIRO, Division of Coal and Energy Technology, Centre
         for Pollution Assessment and Control, North Ryde, NSW, Australia

    Dr J. Kagawa, Professor of Hygiene and Public Health, Tokyo Women's
         Medical College, Shinjuku-ku, Tokyo, Japan

    Dr R.R. Khan, Ministry of Environment and Forests, Paryavaran Bhawan,
         New Delhi, India

    Dr D.B. Menzel, University of California, Department of Community &
         Environment and Medicine, California, USA

    Dr L. Neas, Department of Environmental Health, Environmental
         Epidemiology Program, Harvard School of Public Health, Boston,
         Massachusetts, USA

    Dr S.E. Paulson, Department of Atmospheric Sciences, University of
         California, Los Angeles, California, USA

    Dr P.J.A. Rombout, Department for Inhalation Toxicology, National
         Institute of Public Health and Environmental Hygiene, Bilthoven,
         The Netherlands  (Chairman)

               

    *  Invited, but unable to attend

    Dr W. Tyler, Veterinary Anatomy and Cell Biology, University of
         California, California, USA

    Dr K. Victorin, Karolinska Institute, Institute of Environmental
         Medicine, Stockholm, Sweden

    Dr A. Woodward, Department of Community Medicine, University of
         Adelaide, Adelaide, Australia

    Dr R. Ye, Deputy Director, National Environmental Protection Agency,
         Xizhimennei Nanziaojie, Beijing, People's Republic of China

     Observers

    Professor M. Moore, National Research Centre for Environmental
         Toxicology, Nathan, Australia

    Dr M. Pain, Department of Thoracic Medicine, Royal Melbourne Hospital,
         Melbourne VIC, Australia

    Dr P. Psaila-Savona, WA Department of Health, Perth WA, Australia

    Mr B. Taylor, Policy and Planning Group, Public and Planning Group,
         Public Health Commission, Wellington, New Zealand

    Mr B. Saxby, AGL Gas Companies, North Sydney NSW, New  Zealand

     Secretariat

    Dr B.H. Chen, International Programme on Chemical Safety, World Health
         Organization, Geneva, Switzerland  (Secretary)

    Dr M. Younes, WHO European Centre for Environment & Health, Bilthoven,
         The Netherlands

    ENVIRONMENTAL HEALTH CRITERIA FOR NITROGEN OXIDES

         A WHO Task Group on Environmental Health Criteria for Nitrogen
    Oxides met in Melbourne, Australia from 14 to 18 November 1994.  The
    meeting was hosted by the Clean Air Society of Australia and New
    Zealand and the Victorian Departments of Health and Environment,
    Australia.  Dr B.H. Chen, IPCS, opened the meeting and welcomed the
    participants on behalf of the Director, IPCS, and the three IPCS
    cooperating organizations (UNEP/ILO/WHO).  The Task Group reviewed and
    revised the draft criteria monograph and made an evaluation of the
    risks for human health and the environment from exposure to nitrogen
    oxides. 

         The first draft of this monograph was prepared by Drs J.A.
    Graham, L.D. Grant, L.J. Folinsbee, D.J. Kotchmar and J.H.B. Garner,
    US EPA.  Drs W.G. Ewald, T.B. McMullen and B.E. Tilton, US EPA,
    contributed to the preparation of the first draft.  The second draft
    was prepared by Dr L.D. Grant incorporating comments received
    following the circulation of the first draft to the IPCS Contact
    Points for Environmental Health Criteria.  Drs R. Bobbink, L. Van der
    Eerden and S. Dobson prepared the final text of the environmental
    section.  Mr G.M. Johnson contributed to the final text of the
    chemistry section.

         Dr B.H. Chen and Dr P.G. Jenkins, both members of the IPCS
    Central Unit, were responsible for the overall scientific content and
    technical editing, respectively.

         The efforts of all who helped in the preparation and finalization
    of the document are gratefully acknowledged.

         Financial support for this Task Group meeting was provided by the
    Department of Community Services and Health, Australia, Victorian
    Departments of Health and Environment, Australia, and the Clean Air
    Society of Australia and New Zealand.

    ABBREVIATIONS

    ADP       adenosine diphosphate
    AM        alveolar macrophages
    AQG       Air Quality Guidelines
    BAL       bronchoalveolar lavage
    BHPN       N-bis (2-hydroxypropyl) nitrosamine
    CI        confidence interval
    CLM       chemiluminescence method
    COPD      chronic obstructive pulmonary disease
    ECD       electron capture detection
    FEF       forced expiratory flow
    FEV       forced expiratory volume
    FTIR      Fourier transformed infrared
    FVC       forced vital capacity
    GC        gas chromatography
    GDH       glutamate dehydrogenase
    (c)GMP    (cyclic) guanosine monophosphate
    GS        glutamine synthetase
    HNO2      nitrous acid
    HNO3      nitric acid
    LIF       laser-induced fluorescence
    MS        mass spectrometry
    N2        nitrogen (elemental)
    NH3       ammonia
    NH4+      ammonium ion
    NHy       the sum of NH3 and NH4+
    NiR       nitrate reductase
    NK        natural killer
    NO        nitric oxide
    NO2       nitrogen dioxide
    NO2-      nitrite ion
    NO3-      nitrate ion
    N2O       nitrous oxide
    N2O5      nitrogen pentoxide
    NOx       nitric oxide plus nitrogen dioxide
    NOy       gas-phase oxidized nitrogen species (except nitrous oxide)
    NPSH      non-protein sulfhydryl
    NR        nitrate reductase
    O3        ozone
    PAN       peroxyacetyl nitrate
    PBzN      peroxybenzoyl nitrate
    PEF       peak expiratory flow
    PFC       plaque-forming cell
    PMN       polymorphonuclear leukocyte
    ppb       parts per billion (10-9)
    ppm       parts per million (10-6)
    ppt       parts per trillion (10-12)
    pptv      parts per trillion (by volume)
    PSD       passive sampling device

    Raw       airway resistance
    ROC       reactive organic carbon
    RUBISCO   ribulose 1,5-biphosphate carboxylase
    SD        standard deviation
    SES       socioeconomic status
    SGaw      specific airway conductance
    SO2       sulfur dioxide
    SOy       sulfur oxides
    SPM       suspended particulate matter
    SRaw      specific airway resistance
    TDLAS     tuneable diode laser absorption spectrometry
    TSP       total suspended particulate
    VOC       volatile organic carbon

    1.  SUMMARY

    1.1  Nitrogen oxides and related compounds

         Nitrogen oxides can be present at significant concentrations in
    ambient air and in indoor air.  The types and concentrations of
    nitrogenous compounds present can vary greatly from location to
    location, with time of day, and with season.  The main sources of
    nitrogen oxide emissions are combustion processes.  Fossil fuel power
    stations, motor vehicles and domestic combustion appliances emit
    nitrogen oxides, mostly in the form of nitric oxide (NO) and some
    (usually less than about 10%) in the form of nitrogen dioxide (NO2). 
    In the air, chemical reactions occur that oxidize NO to NO2 and other
    products. There are also biological processes that liberate nitrogen
    species from soils, including nitrous oxide (N2O).  Emissions of N2O
    can cause perturbation of the stratospheric ozone layer.

         Human health may be affected when significant concentrations of
    NO2 or other nitrogenous species, such as peroxyacetyl nitrate (PAN),
    nitric acid (HNO3), nitrous acid (HNO2), and nitrated organic
    compounds, are present.  In addition, nitrates and HNO3 may cause
    health effects and significant effects on ecosystems when deposited on
    the ground.

         The sum of NO and NO2 is generally referred to as NOx.  Once
    released into the air, NO is oxidized to NO2 by available oxidants
    (particularly ozone, O3).  This happens rapidly under some conditions
    in outdoor air; in indoor air, it is generally a much slower process.
    Nitrogen oxides are a controlling precursor of photochemical oxidant
    air pollution resulting in ozone and smog formation; interactions of
    nitrogen oxides (except N2O) with reactive organic compounds and
    sunlight form ozone in the troposphere and smog in urban areas.

         NO and NO2 may also undergo reactions to form a range of other
    oxides of nitrogen, both in indoor and outdoor air, including HNO2,
    HNO3, nitrogen trioxide (NO3), dinitrogen pentoxide (N2O5), PAN
    and other organic nitrates.  The complex range of gas-phase nitrogen
    oxides is referred to as NOy.  The partitioning of oxides of nitrogen
    among these compounds is strongly dependent on the concentrations of
    other oxidants and on the meteorological history of the air.

         HNO3 is formed from the reaction of OH- and NO2.  It is a
    major sink for active nitrogen and also a contributor to acidic
    deposition.  Potential physical and chemical sinks for HNO3 include
    wet and dry deposition, photolysis, reaction with OH radicals, and
    reaction with gaseous ammonia to form ammonium nitrate aerosol.

         PANs are formed from the combination of organic peroxy radicals
    with NO2.  PAN is the most abundant organic nitrate in the
    troposphere and can serve as a temporary reservoir for reactive
    nitrogen, which may be regionally transported.

         The NO3 radical, a short-lived NOy species that is formed in
    the troposphere primarily by the reaction of NO2 with O3, undergoes
    rapid photolysis in daylight or reaction with NO.  Appreciable
    concentrations are observed during the night.

         N2O5 is primarily a night-time constituent of ambient air as it
    is formed from the reaction of NO3 and NO2.  In ambient air, N2O5
    reacts heterogeneously with water to form HNO3, which in turn is
    deposited.

         N2O is ubiquitous because it is a product of natural biological
    processes in soil.  It is not known, however, to be involved in any
    reactions in the troposphere.  N2O participates in upper atmospheric
    reactions contributing to stratospheric ozone (O3) depletion and is
    also a relatively potent greenhouse gas that contributes to global
    warming.

    1.1.1  Atmospheric transport

         The transport and dispersion of the various nitrogenous
    species in the lower troposphere is dependent on both meteorological
    and chemical parameters.  Advection, diffusion and chemical
    transformations combine to dictate the atmospheric residence times. 
    In turn, atmospheric residence times help determine the geographic
    extent of transport of given species.  Surface emissions are dispersed
    vertically and horizontally through the atmosphere by turbulent mixing
    processes that are dependent to a large extent on the vertical
    temperature structure and wind speed.

         As the result of meteorological processes, NOx emitted in the
    early morning hours in an urban area typically disperses vertically
    and moves downwind as the day progresses.  On sunny summer days, most
    of the NOx will have been converted to HNO3 and PAN by sunset, with
    concomitant formation of ozone.  Much of the HNO3 is removed by
    deposition as the air mass is transported, but HNO3 and PAN carried
    in layers aloft (above the nighttime inversion layer but below a
    higher subsidence inversion) can potentially be transported long
    distances in oxidant-laden air masses.

    1.1.2  Measurement

         There are a number of methods available to measure airborne
    nitrogen-containing species.  This document briefly covers
    methodologies currently available or in general use for  in situ

    monitoring of airborne concentrations in both ambient and indoor
    environments.  The species considered are NO, NO2, NOx, total
    reactive odd nitrogen (NOy), PAN and other organic nitrates, HNO3,
    HNO2, N2O5, the nitrate radical, NO3-, and N2O.

         Measuring concentrations of nitrogen oxides is not trivial. 
    While a straightforward, widely available method exists for measuring
    NO (the chemiluminescent reaction with ozone), this is an exception
    for nitrogen oxides.  Chemiluminescence is also the most common
    technique used for NO2; NO2 is first reduced to NO.  Unfortunately,
    the catalyst typically used for the reduction is not specific, and has
    various conversion efficiencies for other oxidized nitrogen compounds. 
    For this reason, great care must be taken in interpreting the results
    of the common chemiluminescence analyser in terms of NO2, as the
    signal may include many other compounds.  Additional difficulties
    arise from nitrogen oxides that may partition between the gaseous and
    particulate phases both in the atmosphere and in the sampling
    procedure.

    1.1.3  Exposure

         Human and environmental exposure to nitrogen oxides varies
    greatly from indoors to outdoors, from cities to the countryside, and
    with time of day and season.  The concentrations of NO and NO2
    typically present outdoors in a range of urban situations are
    relatively well established. The concentrations encountered indoors
    depend on the specific details of the nature of combustion appliances,
    chimneys and ventilation.  When unvented combustion appliances are
    used for cooking or heating, indoor concentrations of nitrogen oxides
    typically greatly exceed those existing outside.  Recent research has
    shown in these circumstances that HNO2 can reach significant
    concentrations. One report showed that HNO2 can represent over 10% of
    the concentrations usually reported as NO2.

    1.2  Effects of atmospheric nitrogen species, particularly nitrogen
         oxides, on vegetation

         Most of earth's biodiversity is found in (semi-)natural
    ecosystems, both in aquatic and terrestrial habitats.  Nitrogen is the
    limiting nutrient for plant growth in many (semi-)natural ecosystems. 
    Most of the plant species from these habitats are adapted to nutrient-
    poor conditions, and can only compete successfully on soils with low
    nitrogen levels.

         Human activities, both industrial and agricultural, have greatly
    increased the amount of biologically available nitrogen compounds,
    thereby disturbing the natural nitrogen cycle.  Various forms of
    nitrogen pollute the air: mainly NO, NO2 and ammonia (NH3) as dry
    deposition; and nitrate (NO3-) and ammonium (NH4+) as wet
    deposition.  NHy refers to the sum of NH3 and NH4+.  Another

    contribution is from occult deposition (fog and clouds).  There are
    many more nitrogen-containing air pollutants (e.g., N2O5, PAN, N2O,
    amines), but these are neglected here, either because their
    contribution to the total nitrogen deposition is believed to be small,
    or because their concentrations are probably far below effect
    thresholds.

         Nitrogen-containing air pollutants can affect vegetation
    indirectly, via photochemical reaction products, or directly after
    being deposited on vegetation, soil or water surface.  The  indirect
    pathway is largely neglected here although it includes very relevant
    processes, and should be taken into account when evaluating the entire
    impact of nitrogen-containing air pollutants: NO2 is a precursor for
    tropospheric O3, which acts both as a phytotoxin and a greenhouse
    gas.

         The impacts of increased nitrogen deposition upon biological
    systems can be the result of direct uptake by foliage or uptake via
    the soil.  At the level of individual plants, the most relevant
    effects are injury to the tissue, changes in biomass production and
    increased susceptibility to secondary stress factors.  At the
    vegetation level, deposited nitrogen acts as a nutrient; this results
    in changes in competitive relationships between species and loss of
    biodiversity.  The critical loads for nitrogen depend on (i) the type
    of ecosystem; (ii) the land use and management in the past and
    present; and (iii) the abiotic conditions (especially those that
    influence the nitrification potential and immobilization rate in the
    soil).

         Adsorption on the outer surface of the leaves takes place and may
    damage wax layers of the cuticle, but the quantitative relevance for
    the field situation has not yet been proved.  Uptake of NOx and NH3
    is driven by the concentration gradient between atmosphere and
    mesophyll.  It generally, but not always, is directly determined by
    stomatal conductance and thus depends on factors influencing stomatal
    aperture.  There is increasing evidence that foliar uptake of nitrogen
    reduces the uptake of nitrogen by the roots.  Uptake and exchange of
    ions through the leaf surface is a relatively slow process, and thus
    is only relevant if the surface remains wet for longer periods.

         NO is only slightly soluble in water, but the presence of other
    substances can alter the solubility.  NO2 has a higher solubility,
    while that of NH3 is much higher.  NO2- (the primary reaction
    product of NOx), NH3 and NH4+ are all highly phytotoxic, and could
    well be the cause of adverse effects of nitrogen-containing air
    pollutants.  The free radical *N=O may play a role in the phytotoxicity
    of NO.

         More-than-additive effects (synergism) have been found in nearly
    all studies concerning SO2 plus NO2.  With other NO2 mixtures (NO,
    O3 and CO2), interactive effects are the exception rather than the
    rule.

         When climatic conditions and supply of other nutrients allow
    biomass production, both NOx and NHy result in growth stimulation at
    low concentrations and growth reduction at higher concentrations. 
    However, the exposure level at which growth stimulation turns into
    growth inhibition is much lower for NOx than for NHy.

         Evidence exists that plants are more sensitive at low light
    intensity (e.g., at night and in winter) and at low temperatures (just
    above 0°C).  NOx and NHy can increase the sensitivity of plants to
    frost, drought, wind and insect damage.

         An interaction exists between soil chemistry and sensitivity of
    vegetation to nitrogen deposition; this is related to pH and nitrogen
    availability.

         The relative contribution of NO and NO2 to the NOx effect on
    plants is unclear.  The vast majority of information is on effects of
    NO2 but available information on NO suggests that NO and NO2 have
    comparable phytotoxic effects.

         Air quality guidelines refer to thresholds for adverse effects. 
    Two different types of effect thresholds exist: critical levels (CLEs)
    and critical loads (CLOs).  The critical level is defined as the
    concentration in the atmosphere above which direct adverse effects on
    receptors, such as plants, ecosystems or materials, may occur
    according to present knowledge.  The critical load is defined as a
    quantitative estimate of an exposure (deposition) to one or more
    pollutants below which significant harmful effects on specified
    sensitive elements of the environment do not occur according to
    present knowledge.

         According to current practice, critical levels have been derived
    from assessment of the lowest exposure concentrations causing adverse
    effects on physiology or growth of plants (biochemical effects were
    excluded), using a graphical method.

         To include the impact of NO, a critical level for NOx is
    proposed instead of one for NO2; for this purpose it has been assumed
    that NO and NO2 act in an additive manner.  A strong case can be made
    for the provision of critical levels for short-term exposure. However,
    currently there are insufficient data to provide these with sufficient
    confidence.  Current evidence suggests a critical level of about
    75 µg/m3 for NOx as a 24-h mean.

         The critical level for NOx (NO and NO2 added in ppb and
    expressed as NO2 in µg/m3) is considered to be 30 µg/m3 as an
    annual mean.

         Information on organisms in the environment is almost exclusively
    restricted to plants, with minimum data on soil fauna.  This
    evaluation and guidance values are, therefore, expressed in terms of
    nitrogen species effects on vegetation.  However, it is expected that
    plants will form the most sensitive component of natural systems and
    that the effect on biodiversity of plant communities is a sensitive
    indicator of effects on the whole ecosystem.

         Critical loads are derived from empirical data and steady-state
    soil models.  Estimated critical loads for total nitrogen deposition
    in a variety of natural aquatic and terrestrial ecosystems are given. 
    Possible differential effects of deposited nitrogen species (NOx and
    NHy) are insufficiently known to differentiate between nitrogen
    species for critical load estimation.

         The great majority of ecosystems for which there is sufficient
    information to estimate critical loads are from temperate climates. 
    The few arctic and montane ecosystems included, which might be
    expected to be representative of higher latitudes, have the least
    reliable basis.  There is no information on tropical ecosystems and
    little on estuarine or marine ecosystems in any climatic zone. 
    Nutrient-poor tropical ecosystems such as rain forests and mangrove
    swamps are likely to be adversely affected by nitrogen deposition. 
    The lack of both deposition data and effect thresholds make it
    impossible to make risk assessments for these climatic regions.

         The most sensitive ecosystems (ombrotrophic bogs, shallow soft-
    water lakes and arctic and alpine heaths) for which effects thresholds
    can be estimated show critical loads of 5-10 kg N.ha-1.year-1 based
    on decreased biological diversity in plant communities.  A more
    average value for the limited range of ecosystems studied is 15-20 kg
    N.ha-1.year-1, which applies to forest trees.

         The atmospheric chemistry of nitrogen oxides includes the
    capacity for ozone generation in the troposphere, ozone depletion in
    the stratosphere, and contribution to global warming as greenhouse
    gases.  Nitrogen oxides and ammonia contribute to soil acidification
    (along with sulfur oxides) and thereby to increased bioavailability of
    aluminium.

         The phytotoxic effects of nitrogen oxides on plants have little
    direct relevance to crop plants when concentrations marginally exceed
    the critical level. However, the role of NOx in the generation of
    ozone and other phytotoxic substances, e.g., organic nitrates leads to

    crop loss. Nitrogen deposited on growing crops will represent a very
    small increase in total available nitrogen compared to that added as
    fertilizer.

    1.3  Health effects of exposures to nitrogen dioxide

         A large number of studies designed to evaluate the health effects
    of NOx have been conducted.  Of the NOx compounds, NO2 has been
    most studied.  The discussion in this section focuses on NO2, NO,
    HNO2 and HNO3, while nitrates are mentioned briefly.

    1.3.1  Studies of the effects of nitrogen compounds on experimental
           animals

         Extrapolating animal data to humans has both qualitative and
    quantitative components.  As summarized below, NO2 causes a
    constellation of effects in several animal species; most notably,
    effects on host defence against infectious pulmonary disease, lung
    metabolism/biochemistry, lung function and lung structure.  Because of
    basic physiological, metabolic and structural similarities in all
    mammals (laboratory animals and humans), the commonality of the
    observations in several animal species leads to a reasonable
    conclusion that NO2 could cause similar types of effects in humans. 
    However, because of the differences between mammalian species, exactly
    what exposures would actually cause these effects in humans is not yet
    known.  That is the topic of quantitative extrapolation.  Limited
    modelling research on the dosimetric aspect (i.e., the dose to the
    target tissue/cell that actually causes toxicity) of quantitative
    extrapolation suggests that the distribution of the deposition of NO2
    within the respiratory tract of animals and humans is similar,
    without yet providing adequate values to use for animal-to-human
    extrapolation.  Unfortunately, very little information is available on
    the other key aspect of extrapolation, species sensitivity (i.e., the
    response of the tissues of different species to a given dose).  Thus,
    from currently available animal studies, we know which human health
    effects NO2 may cause. We are unable to assert with great confidence
    the effects that are  actually caused by a given inhaled dose of
    NO2.

         With the above issues in mind, the animal toxicology database
    for NO2 is summarized below according to major classes of effects
    and topics of special interest.  Although it is clear that the
    effects of NO2 exposure extend beyond the confines of the lung, the
    interpretation of these systemic effects relative to potential human
    risk is not clear.  Therefore they are not summarized further here,
    but are discussed in later chapters.  Although interactions of NO2
    and other co-occurring pollutants, such as O3 and sulfuric acid
    (H2SO4), can be quite important, especially if synergism occurs, the
    database does not yet allow conclusions that enable assessment of
    real-world potential interactions.

    1.3.1.1  Biochemical and cellular mechanisms of action of nitrogen
             oxides

         NO2 acts as a strong oxidant.  Unsaturated lipids are readily
    oxidized with peroxides as the dominant product.  Both ascorbic acid
    (vitamin C) and alpha-tocopherol (vitamin E) inhibit the peroxidation
    of unsaturated lipids.  When ascorbic acid is sealed within bilayer
    liposomes, NO2 rapidly oxidizes the sealed ascorbic acid.  The
    protective effects of alpha-tocopherol and ascorbic acid in animals
    and humans are due to the inhibition of NO2 oxidation.  NO2 also
    oxidizes membrane proteins.  The oxidation of either membrane lipids
    or proteins results in the loss of cell permeability control.  The
    lungs of NO2-exposed humans and experimental animals have larger
    amounts of protein within the lumen.  The recruitment of inflammatory
    cells and the changes in the lung are due to these events.

         The oxidant properties of NO2 also induce the peroxide
    detoxification pathway of glutathione peroxidase, glutathione
    reductase and glucose-6-phosphate dehydrogenase. Following NO2
    exposure the increase in the peroxide detoxification pathway in
    animals follows an exposure-response relationship.

         The mechanism of action of NO is less clear.  NO is readily
    oxidized to NO2 and peroxidation then occurs.  Because of the
    concurrent exposure to some NO2 in NO exposures, it is difficult to
    discriminate NO effects from NO2.  NO functions as an intracellular
    second messenger modulating a wide variety of essential enzymes, and
    it inhibits its own production (e.g., negative feedback).  NO
    activates guanylate cyclase which in turn increases intracellular cGMP
    levels.  A possible mechanism of action of nitrates may be through the
    release of histamine from mast cell granules.  Acidic nitrogenous air
    pollutants, particularly HNO3, may act by alteration of intracellular
    pH.

         PAN decomposes in water, generating hydrogen peroxide.  Little is
    known of the mechanism of action, but oxidative stress is likely for
    PAN and its congeners.

         Inorganic nitrates may act through alterations in intracellular
    pH.  Nitrate ion is transported into alveolar type 2 cells acidifying
    the cell.  Nitrate also mobilizes histamine from mast cells.  HNO2
    could also act to alter intracellular pH, but this mechanism is
    unclear.

         The mechanisms of action of the other nitrogen oxides are
    unknown.

         Acute exposure to NO2 at a concentration of 750 µg/m3 (0.4 ppm)
    can result in lipid peroxidation.  NO2 can oxidize polyunsaturated

    fatty acids in cell membranes as well as functional groups of proteins
    (either soluble proteins in the cell, such as enzymes, or structural
    proteins, such as components of cell membranes).  Such oxidation
    reactions (mediated by free radicals) are a mechanism by which NO2
    exerts direct toxicity on lung cells.  This mechanism of action is
    supported by animal studies showing the importance of lung antioxidant
    defences, both endogenous (e.g., maintenance of lung glutathione
    levels) and exogenous (e.g., dietary vitamins C and E), in protecting
    against the effects of NO2.  Many studies have suggested that various
    enzymes in the lung, including glutathione peroxidase, superoxide
    dismutase and catalase, may also serve to defend the lung against
    oxidant attack.

    1.3.1.2  Effects on host defence

         Although the primary function of the respiratory tract is to
    ensure an efficient exchange of gases, this organ system also provides
    the body with a first line of defence against inhaled viable and non-
    viable airborne agents.  An extensive database clearly shows that
    exposure to NO2 can result in the dysfunction of these host defences,
    increasing susceptibility to infectious respiratory disease.  The
    host-defence parameters affected by NO2 include the functional and
    biochemical activity of cells in lungs, alveolar macrophages (AMs),
    immunological competence, susceptibility to experimentally induced
    respiratory infections, and the rate of mucociliary clearance.

         Alveolar macrophages are affected by NO2.  These cells
    are responsible for maintaining the sterility of the pulmonary
    region, clearing particles from this region, and participating in
    immunological functions.  Functional changes that have been reported
    include the following: the suppression of phagocytic ability and
    stimulation of lung clearance at 560 µg/m3 (0.3 ppm) 2 h/day for
    13 days; a decrease in bactericidal activity at 4320 µg/m3 (2.3 ppm)
    for 17 h; and a decreased response to migration inhibition factor at
    3760 µg/m3 (2.0 ppm) 8 h/day, 5 days/week for 6 months.  The
    morphological appearance of these defence cells changes after chronic
    exposure to NO2.

         The importance of host defences becomes evident when animals have
    to cope with laboratory-induced pulmonary infections.  Animals exposed
    to NO2 succumb to bacterial or viral infection in a concentration-
    dependent manner.  Mortality also increases with increased NO2
    concentration or duration of exposure.  After acute exposure,
    effects are observed at concentrations as low as 3760 µg/m3 (2 ppm). 
    Exposure to concentrations as low as 940 µg/m3 (0.5 ppm) will cause
    effects in the infectivity model after 6 months.

         Both humoral and cell-mediated defence systems are changed by
    NO2 exposure.  In the cases in which the immune system has been
    investigated, effects have been observed after short-term exposure to

    concentrations > 9400 µg/m3 (5 ppm).  The effects are complex
    since the direction of the change (i.e., increase or decrease) is
    dependent upon NO2 concentration and the length of exposure.

    1.3.1.3  Effects of chronic exposure on the development of chronic
             lung disease

         Humans are chronically exposed to NO2.  Therefore, such
    exposures in animals have been studied rather extensively, typically
    using morphological and/or morphometric methods.  This research has
    generally shown that a variety of pulmonary structural and correlated
    functional alterations occur.  Some of these changes may be reversible
    when exposure ceases.

         Pulmonary function may be altered following chronic NO2 exposure
    of experimental animals. Impaired gas exchange occurred following
    exposure to 7520 µg/m3 (4.0 ppm) NO2 for four months and this was
    reflected in decreased arterial O2 tension, impaired physical
    performance and increased anaerobic metabolism.

         Although NO2 produces morphological changes in the respiratory
    tract, the database is sometimes confusing due to quantitative and
    qualitative variability in responsiveness between, and even within,
    species.  The rat, the most commonly used experimental animal in
    morphological assessments of exposure, appears to be relatively
    resistant to NO2.  Short-term exposures to concentrations of
    9400 µg/m3 (5.0 ppm) or less generally have little effect in the
    rat, where similar exposures in the guinea-pig may result in some
    centriacinar epithelial damage.

         Longer-term exposures result in lesions in some species with
    concentrations as low as 560 to 940 µg/m3 (0.3 to 0.5 ppm).  These
    are characterized by epithelial remodelling similar to that described
    above, but with the involvement of more proximal airways and
    thickening of the interstitium. Many of these changes, however, will
    resolve even with continued exposure, and long-term exposures to
    levels above about 3760 µg/m3 (2.0 ppm) are required for more
    extensive and permanent changes in the lungs.  Some effects are
    relatively persistent (e.g., bronchiolitis), whereas others tend to be
    reversible and limited even with continued exposure.  In any case, it
    seems that for either short- or long-term exposure, the response is
    more dependent upon concentration than duration of exposure.

         There is substantial evidence that long-term exposure of several
    species of laboratory animals to high concentrations of NO2 results
    in morphological lung lesions.  Destruction of alveolar walls, an
    essential additional criterion for human emphysema, has been reliably
    reported in lungs from animals in a limited number of studies.  The

    lowest NO2 concentration for the shortest exposure duration that will
    result in emphysematous lung lesions cannot be determined from these
    published studies.

    1.3.1.4  Potential carcinogenic or co-carcinogenic effects

         NO2 has been shown to be mutagenic in  Salmonella bacteria, but
    was not mutagenic in one study with a mammalian cell culture.  Other
    studies using cell cultures have demonstrated sister chromatid
    exchanges (SCE) and DNA single strand breaks.  No genotoxic effects
    have been demonstrated  in vivo concerning lymphocytes, spermatocytes
    or bone marrow cells, but two inhalation studies with high
    concentrations (50 760 and 56 400 µg/m3, 27 and 30 ppm) for 3 h and
    16 h, respectively, have demonstrated such effects in lung cells.

         Literature searches revealed no published reports of NO2 studies
    using classical whole-animal chronic bioassays for carcinogenesis. 
    Research with mice having spontaneously high tumour rates was
    equivocal.  In one study, NO2 at 18 800 µg/m3 (10 ppm) slightly
    enhanced the incidence of lung adenomas in a sensitive strain of mice
    (A/J).  Although several co-carcinogenesis investigations have been
    undertaken, conclusions are precluded because of problems with
    methodology and interpretation. Reports on whether NO2 facilitates
    the metastasis of tumours to the lung are also inadequate to form
    conclusions.  Other investigations have centred on whether NO2 could
    produce nitrates and nitrites that, by reacting with amines in the
    body, could produce nitrosamines.  A few studies suggest that
    nitrosamines are formed in animals treated with high doses of amines
    and exposed to NO2, but other studies have indicated that nitrosamine
    formation is unlikely.

    1.3.1.5  Age susceptibility

         Investigations into age dependency are inadequate and results so
    far are equivocal.

    1.3.1.6  Influence of exposure patterns

         Several animal toxicological studies have elucidated the
    relationships between concentration (C) and duration (T) of exposure,
    indicating that the relationship is complex.  Most of this research
    has used the infectivity model.  Early C × T studies demonstrated that
    concentration had more impact on mortality than did duration of
    exposure.  An evaluation of the toxicity of NO2 exposures cannot be
    delineated by C × T relationships.

    1.3.2  Controlled human exposure studies on nitrogen oxides

         Human responses to a variety of oxidized nitrogen compounds have
    been evaluated.  By far, the largest database and the one most

    suitable for risk assessment is that available for controlled
    exposures to NO2.  The database on human responses to NO, HNO3
    vapour, HNO2 vapour and inorganic nitrate aerosols is not as
    extensive. A number of sensitive or potentially sensitive subgroups
    have been examined, including adolescent and adult asthmatics, older
    adults, and patients with chronic obstructive pulmonary disease (COPD)
    and pulmonary hypertension.  Exercise during exposure increases the
    total uptake and alters the distribution of the deposited inhaled
    material within the lung. The relative proportion of NO2 deposited in
    the lower respiratory tract is also increased by exercise.  This may
    increase the effects of the above compounds in people who exercise
    during exposure.

         As is typical with human biological response to inhaled particles
    and gases, there is variability in the biological response to NO2. 
    Healthy individuals tend to be less responsive to the effects of NO2
    than  individuals with lung disease.  Asthmatics are clearly the most
    responsive group to NO2 that has been studied to date.  Individuals
    with COPD may be more responsive than healthy individuals, but they
    have limited capacity to respond to NO2 and thus quantitative
    differences between COPD patients and others are difficult to assess. 
    Sufficient information is not available at present to evaluate whether
    age and sex play a role in the response to NO2.

         Healthy subjects can detect the odour of NO2, in some cases at
    concentrations below 188 µg/m3 (0.1 ppm).  Generally, NO2 exposure
    did not increase respiratory symptoms in any of the subject groups
    tested.

         NO2 causes decrements in lung function, particularly increased
    airway resistance in resting healthy subjects at 2-h concentrations as
    low as 4700 µg/m3 (approx.2.5 ppm).  Available data are insufficient
    to determine the nature of the concentration-response relationship.

         Exposure to NO2 results in increased airway responsiveness to
    bronchoconstrictive agents in exercising healthy, non-smoking subjects
    exposed to concentrations as low as 2800 µg/m3 (approx.1.5 ppm) for
    1 h or longer.

         Exposure of asthmatics to NO2 causes, in some subjects,
    increased airway responsiveness to a variety of provocative mediators,
    including cholinergic and histaminergic chemicals, SO2 and cold air. 
    The presence of these responses appears to be influenced by the
    exposure protocol, particularly whether or not the exposure includes
    exercise.  These responses may begin at concentrations as low as
    380 µg/m3 (0.2 ppm).  A meta-analysis suggests that effects may occur
    at even lower concentrations.  However, an unambiguous concentration-
    response relationship is observed between 350 to 1150 µg/m3
    (approx.0.2 to 0.6 ppm).

         The implications of this overall trend are unclear, but increased
    airway responsiveness could potentially lead to increased response to
    aeroallergens or temporary exacerbation of asthma, possibly leading to
    increased medication usage or even increased hospital admissions.

         Modest increases in airway resistance may occur in COPD patients
    from brief exposure (15-60 min) to concentrations of NO2 as low as
    2800 µg/m3 (approx.1.5 ppm), and decrements in spirometric measures
    of lung function (3 to 8% change in FEV1 (forced expiratory volume
    in 1 second)) may also be observed with longer exposures (3 h) to
    concentrations as low as 600 µg/m3 (approx.0.3 ppm).

         Exposure to NO2 at levels above 2800 µg/m3 (approx.1.5 ppm) may
    alter the numbers and types of inflammatory cells in the distal
    airways or alveoli.  NO2 may alter the functioning of cells within
    the lungs and production of mediators that may be important in lung
    host defences.  The constellation of changes in host defences,
    alterations in lung cells and their activities, and changes in
    biochemical mediators is consistent with the epidemiological findings
    of increased host susceptibility associated with NO2 exposure.

         In studies on mixtures of NO2 with other pollutants, NO2 has
    not been observed to increase responses to other co-occurring
    pollutant(s) beyond that which would be observed for the other
    pollutant(s) alone.  A notable exception is the observation that
    pre-exposure to NO2 enhanced the ozone-induced change in airway
    responsiveness in healthy exercising subjects during a subsequent
    ozone exposure.  This observation suggests the possibility of delayed
    or persistent responses to NO2.

         Within an NO2 concentration range that may be of interest with
    regard to risk evaluation (i.e., 100-600 µg/m3), the characteristics
    of the concentration-response relationship for acute changes in lung
    function, airway responsiveness to bronchoconstricting agents or
    symptoms cannot be determined from the available data.

         On the basis of an effect at 400 µg/m3 and the possibility of
    effects at lower levels, based on a meta analysis, a one-hour average
    daily maximum NO2 concentration of 200 µg/m3 (approx.0.11 ppm) is
    recommended as a short-term guideline.

         NO is acknowledged as an important endogenous second messenger
    within several organ systems.  Inhaled NO concentrations above
    6000 µg/m3 (approx.5 ppm) can cause vasodilation in the pulmonary
    circulation without affecting the systemic circulation.  The lowest
    effective concentration has not been established.  Information on
    pulmonary function and lung host defences consequent to NO exposure
    are too limited for any conclusions to be drawn at this time.

    Relatively high concentrations (> 40 000 µg/m3) have been used in
    clinical applications for brief periods (< 1 h) without reported
    adverse reactions.

         Nitric acid levels in the range of 250-500 µg/m3 (97-194 ppb)
    may cause some pulmonary function responses in adolescent asthmatics,
    but not in healthy adults.

         Limited information on HNO2 suggests that it may cause eye
    inflammation at 760 µg/m3 (0.40 ppm).  There are currently no
    published data on human pulmonary responses to HNO2.

         Limited data on inorganic nitrates suggest that there are no lung
    function effects of nitrate aerosols at concentrations of 7000 µg/m3
    or less.

    1.3.3  Epidemiology studies on nitrogen dioxide

         Epidemiological studies on the health effects of nitrogen oxides
    have mainly focused on NO2.  Many indoor and outdoor epidemiological
    studies designed to evaluate the health effects of NO2 have been
    conducted.  Two health outcome measurements of NO2 exposure are
    generally considered: lung function measurements and respiratory
    symptoms and diseases.

         The evidence from individual studies of the effect of NO2 on
    lower respiratory symptoms and disease in school-aged children is
    somewhat mixed.  The consistency of these studies was examined and
    the evidence synthesized in a combined quantitative analysis
    (meta-analysis) of the subject studies.  Most of the indoor studies
    showed increased lower respiratory morbidity in children associated
    with long-term exposure to NO2.  Mean weekly NO2 concentrations
    in bedrooms in studies reporting NO2 levels were predominantly
    between 15 and 122 µg/m3 (0.008 and 0.065 ppm).  Combining the
    indoor studies as if the end-points were similar gives an estimated
    odds ratio of 1.2 (95% confidence limits of 1.1 and 1.3) for the effect
    per 28.3 µg/m3 (0.015 ppm) increase of NO2 on lower respiratory
    morbidity.  This suggests that, subject to assumptions made for the
    combined analysis, an increase of about 20% in the odds of lower
    respiratory symptoms and disease corresponds to each increase of
    28.3 µg/m3 (0.015 ppm) in estimated 2-week average NO2
    exposure.  Thus, the combined evidence is supportive for the effects
    of estimated exposure to NO2 on lower respiratory symptoms and
    disease in children aged 5 to 12 years.
    
         In individual indoor studies of infants 2 years of age or younger,
    no consistent relationship was found between estimates of NO2
    exposure and the prevalence of respiratory symptoms and disease.  Based

    on a meta-analysis of these indoor infant studies, subject to the
    assumptions made for the meta-analysis, the combined odds ratio for the
    increase in respiratory disease per increase of 28.2 µg/m3 (0.015 ppm)
    NO2 was 1.09 with a 95% confidence interval of 0.95 to 1.26, where
    mean weekly NO2 concentrations in bedrooms were predominantly between
    9.4 and 94 µg/m3 (0.005 and 0.050 ppm) in studies reporting levels.
    The increase in risk was very small and was not reported consistently
    by all studies.  We cannot conclude that the evidence suggests an effect
    in infants comparable to that seen in older children.  The reasons for
    these age-related differences are not clear.

         The measured NO2 studies gave a higher estimated odds ratio than
    the surrogate estimates, which is consistent with a measurement error
    effect.  The effect of having adjusted for covariates such as
    socioeconomic status, smoking and sex was that those studies that
    adjusted for a particular covariate found larger odds ratios than
    those that did not.

         Although many of the epidemiological studies that involved
    measured NO2 levels used measurements over only 1 or 2 weeks, these
    levels were used to characterize children's exposures over a much
    longer period.  The standard respiratory symptom questionnaire used by
    most of these studies summarizes information on health status over an
    entire year.  The 28.2 µg/m3 (0.015 ppm) difference in NO2 levels
    used in the meta-analyses relates to a difference in the household
    annual average exposure between gas and electric cooking stoves.
    Some studies measured NO2 levels only in the winter and may have
    overestimated annual average exposures.  This would tend to have
    underestimated the health effect of a 28.2 µg/m3 (0.015 ppm)
    difference in the annual NO2 exposure.  A study based on a household
    annual average exposure measured in both the winter and summer found a
    stronger health effect than many of the other studies.  The true
    biologically relevant exposure period is unknown, but these exposures
    extended over a lengthy period up to the entire lifetime of the child.

         The association between outdoor NO2 and respiratory health is
    not clear from current research.  There is some evidence that the
    duration of respiratory illness may be increased at higher ambient
    NO2 levels.  A major difficulty in the analysis of outdoor studies is
    distinguishing possible effects of NO2 from those of other associated
    pollutants.

         Several uncertainties need to be considered in interpreting the
    above studies and meta-analysis.  Error in measuring exposure is
    potentially one of the most important methodological problems in
    epidemiological studies of NO2.  Although there is evidence that
    symptoms are associated with indicators of NO2 exposure, the quality
    of these exposure estimates may be inadequate to determine a
    quantitative relationship between exposure and symptoms.  Most of the
    studies that measured NO2 exposure did so only for periods of 1 to

    2 weeks and reported the values as averages.  Few of the studies
    attempted to relate the observed effects to the pattern of exposure
    (e.g., transient NO2 peaks). Furthermore, measured NO2 concentration
    may not be the biologically relevant dose; estimating actual exposure
    requires knowledge of pollutant species, levels and related human
    activity patterns.  However, only very limited activity and aerometric
    data are available that examine such factors.  The extrapolation to
    possible patterns of ambient exposure is difficult.  In addition,
    although the level of similarity and common elements between the
    outcome measures in the NO2 studies provide some confidence in their
    use in the quantitative analysis, the symptoms and illnesses combined
    are to some extent different and could indeed reflect different
    underlying processes.  Thus, caution is necessary in interpreting the
    meta-analysis results.

         Other epidemiological studies have attempted to relate some
    measure of indoor and/or outdoor NO2 exposure to changes in pulmonary
    function.  These changes were marginally significant.  Most studies
    did not find any effects, which is consistent with controlled human
    exposure study data.  However, there is insufficient epidemiological
    evidence to draw any conclusions about the long- or short-term effects
    of NO2 on pulmonary function.

         On the basis of a background level of 15 µg/m3 (0.008 ppm) and
    the fact that significant adverse health effects occur with an
    additional level of 28.2 µg/m3 (0.015 ppm) or more, an annual
    guideline value of 40 µg/m3 (0.023 ppm) is proposed.  This value will
    avoid the most severe exposures.  The fact that a no-effect level for
    subchronic or chronic NO2 exposure concentrations has not yet been
    determined should be emphasized.

    1.3.4  Health-based guidance values for nitrogen dioxide

         On the basis of human controlled exposure studies, the
    recommended short-term guidance value is for a one-hour average NO2
    daily maximum concentration of 200 µg/m3 (0.11 ppm).  The recommended
    long-term guidance value, based on epidemiological studies of
    increased risk of respiratory illness in children, is 40 µg/m3
    (0.023 ppm) annual average.

    2.  PHYSICAL AND CHEMICAL PROPERTIES, AIR SAMPLING AND ANALYSIS,
        TRANSFORMATIONS AND TRANSPORT IN THE ATMOSPHERE

    2.1  Introduction

         Nitrogen oxides are produced by combustion processes and are
    emitted to the air mainly as NO together with some NO2.  Natural
    biological processes and lightning also emit NO and N2O.  In the
    atmosphere nitrogen oxides undergo complex chemical and photochemical
    reactions; NO is oxidized to NO2 and other products and eventually to
    HNO3 and nitrates.  Nitrogenous species are removed from the air to
    the ground by wet and dry deposition processes.  Oxidized nitrogen
    compounds can have impacts on human health and the environment, and
    are important to the formation of photochemical smog and tropospheric
    ozone.

         In this chapter the properties of nitrogen compounds are briefly
    described and techniques for their sampling and analysis outlined. 
    Atmospheric chemical reactions that cause the oxidation of NO to NO2
    and the production of ozone, organic nitrates and HNO3 are described.
    The differences between night-time and day-time chemistry and the
    composition of the atmosphere are discussed.  The nature of the
    nitrogen species and their chemical reactions in urban regions, in
    chimney plumes such as those from power stations, in air advected away
    from urban regions and in rural and remote areas are described.  The
    role of nitrogen oxides in photochemical smog production and the
    effects of nitrous oxide on stratospheric ozone are briefly discussed.

    2.1.1  The nomenclature and measurement of atmospheric nitrogen
           species

         There are several methods available for determining nitrogen
    species, but many of these techniques are nonspecific.

         To denote various mixtures of nitrogen species, the terms NOx,
    NOy and NOz are often employed.  It is customary to refer to the sum
    of NO and NO2 emitted from a source as NOx, the unit of measure for
    NOx being the NO2 mass equivalent of the NO plus NO2.

         The term NOy is frequently used to denote the sum of the gas
    phase oxidized nitrogen species (except N2O) and NOz to denote the
    sum of NOy plus the oxidized nitrogen present as particulate matter. 
    Measurement of NOz requires a combination of particulate and gas
    phase sampling and analysis.

         A confusion arises because one of the most commonly used methods
    for determining NO2 in ambient air (thermal conversion of NO2 to NO
    and measurement of the resultant NO by chemiluminescent reaction with
    O3) is nonspecific and responds to several gaseous species in
    addition to NO2.  These include organic nitrogen compounds and,

    depending on the converter, HNO3, although HNO3 can be readily lost
    to the sampling system.  Therefore, depending on the composition of
    the air being sampled, the results from this type of instrument can be
    representative of NOy rather than NOx (or NO2) concentrations. 
    This technique is used in most routine determinations of ambient NOx
    and NO2 concentrations but the discrepancy between these values and
    true NOx and NO2 can be considerable for air in which the pollutant
    emissions have undergone substantial exposure to sunlight.

         Nitrous oxide is ubiquitous in the atmosphere because it is a
    product of biological processes in soil as well as anthropogenic
    activities.  It is not involved to any appreciable extent in chemical
    reactions in the lower atmosphere, but it is an active "greenhouse"
    gas.  In the stratosphere N2O forms NO by reaction with excited
    oxygen atoms, and this NO then acts to deplete the stratospheric O3
    concentration.

         Although NO3, dinitrogen trioxide (N2O3), dinitrogen tetroxide
    (N2O4), and N2O5 may play a role in atmospheric chemical reactions
    leading to the transformation, transport, and ultimate removal of
    nitrogen compounds from ambient air, they are present in very low
    concentrations, even in polluted environments.

         NH3 is generated during decomposition of nitrogenous matter in
    natural ecosystems and may be locally produced in high concentrations
    by human activities such as intensive animal husbandry and feedlots. 
    Under suitable conditions NH3 can react with oxidized nitrogen
    species to form ammonium nitrate aerosol.

    2.2  Nitrogen species and their physical and chemical properties

         There are seven oxides of nitrogen that may be present in ambient
    air, namely: NO, NO2, N2O, NO3, N2O3, N2O4 and N2O5.  In
    addition these can be present as HNO2, HNO3 and various organic
    nitrogen species, such as PAN, other organic nitrates and particles
    containing oxidized nitrogen compounds (particularly adsorbed nitric
    acid).  Of these species, NO and NO2 are the ones most often measured
    and are present in the greatest concentrations in urban and industrial
    air.

         The chemical and physical properties of individual nitrogen
    species are given below and are summarized in Table 1.

        Table 1.  Some physical and thermodynamic properties of oxides of nitrogen and other nitrogen compoundsa
                                                                                                                                              

    Oxide               Relative         Melting point    Boiling point     Solubility in water            Thermodynamic functions
                        molecular        (°C)b,c,d        (°C)b,c           at 0°C (cm3 per 100 g)b        (Ideal gas, 1 atm, 25°C)
                        mass (g/mol)                                                                                                          
                                                                                                           Enthalpy of      Entropy
                                                                                                           formation        (cal/mol-deg)
                                                                                                           (kcal/mol)
                                                                                                                                              

    NO                  30.01            -163.6           -151.8            7.34                              21.58            50.35

    NO2                 46.01            -11.2            21.2              Reacts with H2O forming            7.91            57.34
                                                                            HNO2 and HNO3

    N2O                 44.01            -90.8            -88.5             130.52                            19.61            52.55

    N2O3                76.01            -102             47                Reacts with H2O forming           19.80            73.91
                                                          (decomposes)      HNO2

    N2O4                92.02            -11.3            21.2              Reacts with H2O forming            2.17            72.72
                                                                            HNO2 and HNO3

    N2O5                108.01           30               3.24              Reacts with H2O forming            2.7             82.8
                                                          (decomposes)      HNO2

    HNO2                47.01            -                -                 -                                  -                -

    HNO3                63.01            -42              83                                                 -32.1             63.7
                                                                                                                                              

    Table 1.  (Con't)
                                                                                                                                              

    Oxide               Relative         Melting point    Boiling point     Solubility in water            Thermodynamic functions
                        molecular        (°C)b,c,d        (°C)b,c           at 0°C (cm3 per 100 g)b        (Ideal gas, 1 atm, 25°C)
                        mass (g/mol)                                                                                                          
                                                                                                           Enthalpy of      Entropy
                                                                                                           formation        (cal/mol-deg)
                                                                                                           (kcal/mol)
                                                                                                                                              

    PAN                 121.06           -                -                 -                                  -                -
    (CH3COOONO2)

    NH4NO3              80.04            169.6            210 at            118.3 g/100 cm3                  -87.37            36.11
                                                          11 torr           H2O at 0°C
                                                                                                                                              

    a  Adopted from: US EPA (1993)
    b  Matheson Gas Data Book (Matheson Company, 1966)
    c  Handbook of Chemistry and Physics (Weast et al., 1986)
    d  At 0°C and 1 atm pressure
        2.2.1  Nitrogen oxides

    2.2.1.1  Nitric oxide

         NO is a colourless, odourless gas that is only slightly soluble
    in water.  It is a by-product of combustion processes, arising from
    (i) high temperature oxidation of molecular nitrogen from the
    combustion air, and (ii) from oxidation of nitrogen present in certain
    fuels such as coal and heavy oil.

    2.2.1.2  Nitrogen dioxide

         NO2 is a reddish-orange-brown gas with a characteristic pungent
    odour.  The boiling point is 21.1°C, but the low partial pressure of
    NO2 in the atmosphere prevents condensation.  NO2 is corrosive and
    highly oxidizing.  About 5 to 10% by volume of the total emissions of
    NOx from combustion sources is usually in the form of NO2, although
    substantial variations from one source type to another have been
    observed.

         In the atmosphere, photochemical reactions involving ozone
    and organic compounds convert NO to NO2.  NO2 is an efficient
    absorber of light over a broad range of ultraviolet (UV) and visible
    wavelengths.  Because of its brown colour, NO2 can contribute to
    discoloration and reduced visibility of polluted air.  Photolysis of
    NO2 by sunlight produces NO and an oxygen atom, which usually adds to
    an oxygen molecule to produce ozone.

    2.2.1.3  Nitrous oxide

         N2O is a colourless gas with a slight odour at high
    concentrations.  It is emitted to the atmosphere as a trace component
    from some combustion sources and from the consumption of nitrate by
    an ubiquitous group of denitrification bacteria that use nitrate as
    their terminal electron acceptor in the absence of oxygen (Delwiche,
    1970; Brezonik, 1972; Keeney, 1973; Focht & Verstraete, 1977).  At
    atmospheric concentrations N2O has no significant physiological
    effects in humans, although at higher concentrations it is employed as
    an anaesthetic.

         N2O does not play a significant role in atmospheric reactions in
    the lower troposphere.  In the stratosphere it reacts with singlet
    oxygen to produce NO, which participates in O3 decomposition in
    the stratosphere.  These reactions are of concern because of the
    possibility that increasing N2O concentrations resulting from fossil
    fuel use, and also from denitrification of excess fertilizer, may
    contribute to a decrease in stratospheric O3 (Council for
    Agricultural Science and Technology, 1976; Crutzen, 1976) with
    consequent potential for adverse impacts on ecosystems and human

    health.  Also of concern is the fact that N2O absorbs long-wave
    radiation, and therefore serves as a radiatively important greenhouse
    gas that may contribute to global warming.

    2.2.1.4  Other nitrogen oxides

         Other nitrogen oxides can be present in trace quantities in the
    air.  NO3 has been identified in laboratory systems containing
    NO2/O3, NO2/O and N2O5 as an important reactive transient
    (Johnston, 1966).  It is likely to be present in photochemical smog. 
    In the presence of sunlight, NO3 is rapidly converted to either NO or
    NO2 (Wayne et al., 1991).  Nitrogen trioxide is highly reactive
    towards both NO and NO2.  Its expected concentration in polluted air
    is very low (about 10-6 µg/m3).  However, traces of NO3 may play an
    important role in atmospheric chemistry, especially at night when it
    may serve as a reservoir for NOx (Wayne et al., 1991).  In the
    atmosphere N2O3 is in equilibrium with NO and NO2.  It reacts with
    water to form HNO2.  N2O4 is the dimer of NO2, formed in
    equilibrium with NO2 molecules, and it readily dissociates to NO2. 
    N2O5 can be a trace night-time component of the air because it is
    formed by a reaction between NO2 and NO3.  Since NO3 can exist in
    appreciable quantities only in the absence of sunlight, N2O5 is only
    important at night, when its reaction with water can be a significant
    source of nitric acid.

    2.2.2  Nitrogen acids

    2.2.2.1  Nitric acid

         HNO3 is the most oxidized form of nitrogen.  In the gaseous
    state it is colourless.  It is photochemically stable in the
    troposphere.  HNO3 is volatile, so that at typical concentrations and
    temperatures in the atmosphere the vapour does not coalesce into
    aerosol and is not retained on particles unless the aerosol contains
    reactants such as sodium chloride or ammonium salts to react with the
    acid, when it produces particulate nitrates (Wolff, 1984).

         In the aqueous phase (e.g., rain drops), HNO3 dissociates to
    form the nitrate ion (NO3-).  Because nitrate is chemically
    unreactive in dilute aqueous solution, nearly all of the
    transformations involving nitrate in natural waters result from
    biochemical pathways.  The nitrate salts of all common metals are
    quite soluble.

    2.2.2.2  Nitrous acid

         HNO2 is formed when NO and NO2 are present in the atmosphere,
    as a result of their reaction with water.  In sunlight, the dominant

    pathway for HNO2 formation is the reaction of NO with hydroxyl
    radicals.  During the daytime, atmospheric concentrations of HNO2 are
    limited by the photolysis of HNO2 to produce NO and hydroxyl radical.

         Nitrous acid is a weak reducing agent and is oxidized to nitrate
    only by strong chemical oxidants and by nitrifying bacteria.

    2.2.3  Ammonia

         NH3 is the completely reduced form of nitrogen.  It is a
    colourless gas with a pungent odour.  It is extremely soluble in
    water, forming ammonium (NHy+) and hydroxyl (OH-) ions.  In the
    atmosphere, NH3 has been reported to be converted into NOx by
    reaction with hydroxyl radicals (Soederlund & Svensson, 1976).  In the
    stratosphere, NH3 can be dissociated by irradiation with sunlight at
    wavelengths below 230 nm (McConnell, 1973).

    2.2.4  Ammonium nitrate

         Gas-phase ammonia reacts with nitric acid to form ammonium
    nitrate (NH4NO3).  Ammonium nitrate is a solid at room temperature. 
    Like ammonia, it is very soluble in water and hence will be absorbed
    by any water droplets present.  Thus it readily forms an aerosol in
    the atmosphere.  Pathways to aerosol formation include nucleation and
    condensation on existing particles.  The presence of NH4NO3
    particles can result in a visible haze.

    2.2.5  Peroxyacetyl nitrate

         Of the various peroxy nitrates found in ambient air, peroxyacetyl
    nitrate (CH3COOONO2), or PAN, is found at the highest concentrations.
    PAN undergoes a temperature-dependent decomposition to its precursors,
    NO2 and acetyl peroxy radicals.  At low ambient temperatures PAN
    can have a substantial lifetime in the atmosphere (Cox & Roffey, 1977).
    In polluted air PAN concentrations can reach several parts per billion.

    2.2.6  Organic nitrites and nitrates

         A wide variety of organic nitrites (RNO2) and nitrates (RNO3),
    where R denotes CH3, CH2CH3, benzyl, etc., may be found in ambient
    air.  Some of these are emitted directly while others are formed by
    photochemical reactions in the atmosphere.

    2.3  Sampling and analysis methods

         This section outlines methods for measuring nitrogen-containing
    species in the atmosphere.  The main focus is on methodologies
    currently available and in general use for monitoring concentrations
    in both ambient and indoor air.

         Table 2 summarizes sampling and analytical methods for selected
    species and addresses relevant characteristics, including the type of
    method (i.e.,  in situ, remote, active, passive, continuous or
    integrative), the stage of development of the method, sampling
    duration, precision, accuracy and detection limits.

    2.3.1  Nitric oxide

    2.3.1.1  Nitric oxide continuous methods

         Nitric oxide reacts rapidly with O3 to give NO2 in an excited
    electronic stage.  The transition of excited NO to the grand state can
    be accompanied by the emission of light in the red-infrared spectral
    range.  When this chemiluminescent reaction occurs under controlled
    conditions, the intensity of the emitted light is proportional to the
    concentration of the NO reactant.  This provides the basis of the
    chemiluminescence method (CLM) for analysis of NO.  This method is a
    continuous technique and is the most commonly used method for
    measuring NO in ambient air.  Commercial instruments for measuring NO
    and NO2 are available with detection limits of approximately 5 ppb
    and response times of the order of minutes.  CLM measurement of NO2
    can also be accomplished by firstly converting the NO2 of the sample
    to NO.  This is discussed in section 2.3.2.1.

         Other NO analytical methods include laser-induced fluorescence
    (LIF) (Bradshaw et al., 1985), absorption spectroscopy (e.g., tuneable
    diode laser absorption spectroscopy, TDLAS) and passive samplers.

    2.3.1.2  Passive samplers for NO

         Passive samplers are used for air with higher-than-typical
    ambient concentrations, which may be found indoors or in the
    workplace.  They are often used to obtain data at a large number of
    sites.  Sampling typically lasts a few hours.

         The Palmes tube is a passive sampler that relies on diffusion of
    an analyte molecule through a quiescent diffusion path of known length
    and cross-sectional area to a reactive surface where the molecule is
    captured by chemical reaction (Palmes et al., 1976).  The Palmes tube
    does not measure NO directly.  Two tubes are required; the first one
    has reactive grids coated with triethanolamine (TEA) to collect NO2,
    the second tube is similar but has an additional reactive surface
    coated with chromic acid to convert NO to NO2, which is in turn
    collected by the TEA-coated grids.  The NO concentration of the air is
    determined from the difference in the results from the two tubes.  The
    data is corrected for the effects of the different diffusivities of NO
    and NO2 molecules. To ensure reliable results, contact between the
    chromic-acid-coated surface and the TEA-coated grids for longer than
    24 h must be avoided.  Analysis of the material contained in the TEA

        Table 2.  Selected instruments and methods for determining oxides of nitrogen in ambient air (from: Sickles, 1992)
                                                                                                                                              

    Species        Methodsa   Typeb      Development  Sample                Performance           Comments                 References
                                         stagec       duration                                
                                                                 Precision  Accuracy   MDLd
                                                                                                                                              

    NO             CLM        I, A, C      C          5 min      < 10%      < 20%      < 9 ppb    -                    Finlayson-Pitts &
                   (NO + O3)                                                                                           Pitts (1986)

                   TP-LIF     I, A, C      R          30 sec     -          16%        10 ppt     -                    Bradshaw et al. (1985);
                                                                                                                       Davis et al. (1987)

                   TDLAS      I, A, C      R, C       60 sec     -          -          0.5 ppb    40-m path length     NASA (1983)

                   PSD        I, P, IN     C          24 h       -          -          70 ppb-he

    NO2            CLM        I, A, C      C          5 min      10%        20%        9 ppb      Commonly used        Finlayson-Pitts &
                   (NO + O3)                                                                      method; many         Pitts (1986)
                                                                                                  interferences

                   CLM        I, A, C      R          < 100 sec  20 ppt     30%        10-25 ppt  Uses thermal or      Helas et al. (1987);
                   (NO + O3)                                                                      photolytic           Fehsenfeld et al.
                                                                                                  converters           (1987)

                   CLM        I, A, C      C          100 sec    0.6 ppb    -          10 ppt     Interferences:
                   (Luminol)                                                                      PAN, HNO2, O3

                   TP-LIF     I, A, C      R          2 min      20 ppt     16%        12 ppt     -                    Davis (1988)

                   TDLAS      I, A, C      R, C       60 sec     -          15%        100 ppt    150-m path length    NASA (1983)

                   DOAS       R, A, C      R, C       12 min     -          10%        4 ppb      800-m path length    Platt & Perner (1983)

                   Bubbler    I, A, IN     RM         24 h       6 ppb      10%        8 ppbe                          Purdue & Hauser (1980)
                                                                                                                                              

    Table 2.  (Con't)
                                                                                                                                              

    Species        Methodsa   Typeb      Development  Sample                Performance           Comments                 References
                                         stagec       duration                                 
                                                                 Precision  Accuracy   MDLd
                                                                                                                                              

                   TEA        I, A, IN     L          24 h       15%        10%        0.2 ppbe   Interferences:       Sickles et al. (1990)
                   filter                                                                          PAN and HNO2f

                   Guaiacol   I, A, IN     L          1 h        4%         -          0.1 ppbe   Stability of         Buttini et al. (1987)
                   Denuder                                                                        extract uncertain

                   DPA        I, A, IN     L          8 h        8%         -          0.1 ppbe   DPA may volatilize;  Lipari (1984)
                   Cartridge                                                                      interferences:
                                                                                                  HNO2 and PAN

                   TEA PSD    I, P, IN     L          24 h       30%        -          30 ppb-he  Similar to Palmes
                                                                                                  Tube; interferences
                                                                                                  as abovef

    NOy           CLM        I, A, C      R          10 sec     -          15%        10 ppt     CO with Au           Fahey et al. (1986)
                   (NO + O3)                                                                      reducing catalyst

    PAN            GC-ECD     I, A, IN     R, RM      15 min     -          30%        10 ppte    Sensitivity can be   Vierkorn-Rudolph
                                                                                                  enhanced by using    et al. (1985)
                                                                                                  cryogenic sampling
                                                                                                  and capillary
                                                                                                  columns

                   GC-CLM     I, A, IN     L          -          -          -          -          CLM (NO + O3) and
                                                                                                  (Luminol) reported

    Other organic  GC-ECD/MS  I, A, C      R          24 h       -          -          1 ppte     Sample collected     Atlas (1988)
    Nitrates                                                                                      on charcoal
                                                                                                                                              

    Table 2.  (Con't)
                                                                                                                                              

    Species        Methodsa   Typeb      Development  Sample                Performance           Comments                 References
                                         stagec       duration                                
                                                                 Precision  Accuracy   MDLd
                                                                                                                                              

    NHO3           Filter     I, A, IN     R, RM      24 h       10%        20%        8 ppte     May be nylon or      Finlayson-Pitts &
                                                                                                  calcium chloride     Pitts (1986)
                                                                                                  impregnated filter;
                                                                                                  subject to
                                                                                                  artifactsf

                   Denuder    I, A, IN     R, RM      24 h       8%         -          8 ppte     Not subject to       Sickles (1987);
                                                                                                  above artifactsf     Sickles et al. (1989)

                   TDLAS      I, A, C      R, C       5 min      -          20%        100 ppt    150-m path length    NASA (1983)

    HNO2           Denuder    I, A, IN     R, RM      24 h       15%        -          10 ppte    Annular denuder      Sickles et al. (1989);
    
                                                                                                  preferredf           Vossler et al. (1988)

                   LIF        I, A, C      R          15 min     -          -          20 ppt     OH detected
                                                                                                  following photo-
                                                                                                  fragmentation

                   DOAS       R, A, C      R, C       12 min     -          30%        600 ppt    800-m path length    Biermann et al. (1988)
                                                                                                                                              

    Table 2.  (Con't)
                                                                                                                                              

    Species        Methodsa   Typeb      Development  Sample                Performance           Comments                 References
                                         stagec       duration                                
                                                                 Precision  Accuracy   MDLd
                                                                                                                                              

    NO3            DOAS       R, A, C      R, C       12 min     -          15%        2