Nitrogen, oxides of (EHC 188, 1997, 2nd edition)

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

The International Programme on Chemical Safety (IPCS) is a joint
venture of the United Nations Environment Programme, the International
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is to promote coordination of the policies and activities pursued by
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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 NO_x 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 NO_x
concentrations
3.3.2. Example case studies of NO_x 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 NO_x and NH_y
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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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
NH_y 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
NO_x nitric oxide plus nitrogen dioxide
NO_y 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

R_aw airway resistance
ROC reactive organic carbon
RUBISCO ribulose 1,5-biphosphate carboxylase
SD standard deviation
SES socioeconomic status
SG_aw specific airway conductance
SO₂ sulfur dioxide
SO_y sulfur oxides
SPM suspended particulate matter
SR_aw 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 NO_x. 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 NO_y. 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 NO_y 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, NO_x 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 NO_x 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, NO_x, total
reactive odd nitrogen (NO_y), 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. NH_y 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 NO_x 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 NO_x), 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 NO_x and NH_y 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 NO_x than for NH_y.

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). NO_x and NH_y 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 NO_x 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 NO_x 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 NO_x as a 24-h mean.

The critical level for NO_x (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 (NO_x and
NH_y) 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 NO_x 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 NO_x have been conducted. Of the NO_x 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 NO_x,
NO_y and NO_z are often employed. It is customary to refer to the sum
of NO and NO₂ emitted from a source as NO_x, the unit of measure for
NO_x being the NO₂ mass equivalent of the NO plus NO₂.

The term NO_y is frequently used to denote the sum of the gas
phase oxidized nitrogen species (except N₂O) and NO_z to denote the
sum of NO_y plus the oxidized nitrogen present as particulate matter.
Measurement of NO_z 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 NO_y rather than NO_x (or NO₂) concentrations.
This technique is used in most routine determinations of ambient NO_x
and NO₂ concentrations but the discrepancy between these values and
true NO_x 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 compounds^a

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)

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
NO_x 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 NO_x (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 (NH_y⁺) and hydroxyl (OH^-) ions. In the
atmosphere, NH₃ has been reported to be converted into NO_x 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 Methods^a Type^b Development Sample Performance Comments References
stage^c duration
Precision Accuracy MDL^d

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-h^e

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 ppb^e Purdue & Hauser (1980)

Table 2. (Con't)

Species Methods^a Type^b Development Sample Performance Comments References
stage^c duration
Precision Accuracy MDL^d

TEA I, A, IN L 24 h 15% 10% 0.2 ppb^e Interferences: Sickles et al. (1990)
filter PAN and HNO_2^f

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

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

TEA PSD I, P, IN L 24 h 30% - 30 ppb-h^e Similar to Palmes
Tube; interferences
as above^f

NO_y 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 ppt^e 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 ppt^e Sample collected Atlas (1988)
Nitrates on charcoal

Table 2. (Con't)

Species Methods^a Type^b Development Sample Performance Comments References
stage^c duration
Precision Accuracy MDL^d

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

Denuder I, A, IN R, RM 24 h 8% - 8 ppt^e Not subject to Sickles (1987);
above artifacts^f 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 ppt^e Annular denuder Sickles et al. (1989);

preferred^f 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 Methods^a Type^b Development Sample Performance Comments References
stage^c duration
Precision Accuracy MDL^d

NO₃ DOAS R, A, C R, C 12 min - 15% 2