ASSESSMENT REPORT ON
NITROGEN
DIOXIDE
FOR DEVELOPING
AMBIENT AIR QUALITY
OBJECTIVES
ASSESSMENT REPORT ON
NITROGEN DIOXIDE
FOR DEVELOPING AMBIENT AIR QUALITY OBJECTIVES
Prepared by
Toxico-Logic Consulting Inc.
for
Alberta Environment
October 2007
ISBN No. 978-0-7785-9958-6 (printed version)
ISBN No. 978-0-7785-9959-3 (on-line version)
Web Site: http://www.environment.alberta.ca/
Although prepared with funding from Alberta Environment (AENV), the contents of this
report/document do not necessarily reflect the views or policies of AENV, nor does mention of
trade names or commercial products constitute endorsement or recommendation for use.
Any comments, questions, or suggestions regarding the content of this document may be
directed to:
Air Policy Branch
Alberta Environment
11th Floor, Baker Centre
100254– 106th Street
Edmonton, Alberta T5J 1G4
Fax: (780) 644-8946
Additional copies of this document may be obtained by contacting:
Information Centre
Alberta Environment
Main Floor, Oxbridge Place
9820 – 106th Street
Edmonton, Alberta T5K 2J6
Phone: (780) 427-2700
Fax: (780) 422-4086
Email: [email protected]
FOREWORD
Alberta Environment maintains Ambient Air Quality Objectives to support air quality
management in Alberta. Alberta Environment currently has ambient objectives for more
than thirty substances and five related parameters. These objectives are periodically updated
and new objectives are developed as required.
With the assistance of the Clean Air Strategic Alliance, a multi-stakeholder workshop was
held in October 2004 to set Alberta’s priorities for the next three years. Based on those
recommendations to Alberta Environment, a three-year work plan was developed to review
four existing objectives, and create three new objectives.
This document is one in a series of documents that presents the scientific assessment for
these substances.
Laura Blair
Project Manager
Air Policy Branch
Assessment Report on Nitrogen Dioxide for Developing Ambient Air Quality Objectives
i
ACKNOWLEDGEMENTS
The authors of this Assessment Report for nitrogen dioxide would like to thank Laura Blair
of the Environmental Policy Branch of Alberta Environment for her input. Toxico-Logic
Consulting Inc. would also like to acknowledge and thank the following authors who
participated in the completion of this report:
Dr. Warren Kindzierski
WBK & Associates Inc.
St. Albert, Alberta
Dr. Selma Guigard
Edmonton, Alberta
Jason Schulz
Calgary, Alberta
Dr. John Vidmar
Edmonton, Alberta
Colleen Purtill
Toxico-Logic Consulting Inc.
Calgary, Alberta
Assessment Report on Nitrogen Dioxide for Developing Ambient Air Quality Objectives
ii
TABLE OF CONTENTS
FOREWORD.................................................................................................................... i
ACKNOWLEDGEMENTS............................................................................................... ii
LIST OF TABLES ........................................................................................................... v
GLOSSARY ................................................................................................................... vi
SUMMARY................................................................................................................... viii
1.0
INTRODUCTION .................................................................................................. 1
2.0
GENERAL SUBSTANCE INFORMATION........................................................... 2
2.1
Physical, Chemical and Biological Properties .........................................................2
2.2
Environmental Fate..................................................................................................3
2.2.1 Formation and Conversion of Nitrogen Dioxide in Air...............................4
2.2.2 Relationship between NOx and the Formation of Ozone .............................4
2.2.3 Formation of Nitric Acid and Removal of NOx from the Atmosphere .........5
3.0
EMISSION SOURCES AND INVENTORY........................................................... 6
3.1
Natural Sources........................................................................................................6
3.2
Anthropogenic Sources............................................................................................6
3.3
Ambient Levels........................................................................................................9
4.0
EFFECTS ON HUMANS AND ANIMALS .......................................................... 14
4.1
Overview of Chemical Disposition........................................................................14
4.2
Genotoxicity...........................................................................................................15
4.3
Acute Toxicity .......................................................................................................16
4.3.1 Acute Toxicity in Humans ..........................................................................16
4.3.1.1 Healthy Individuals ............................................................................... 16
4.3.1.2 Sensitive Individuals ............................................................................ 17
4.3.1.3 Epidemiological Studies ...................................................................... 18
4.4
4.5
4.6
4.3.2 Acute Toxicity in Animals ..........................................................................19
Subchronic and Chronic Toxicity ..........................................................................27
4.4.1 Subchronic and Chronic Toxicity in Humans............................................28
4.4.2 Subchronic and Chronic Toxicity in Animals ............................................29
Fetal and Developmental Toxicity.........................................................................33
Carcinogenicity......................................................................................................35
5.0
EFFECTS ON VEGETATION............................................................................. 37
5.1
Plant Uptake...........................................................................................................37
5.2
Plant Metabolism ...................................................................................................37
5.3
Effects of Nitrogen Dioxide on Plants ...................................................................38
6.0
EFFECTS ON MATERIALS ............................................................................... 43
7.0
AIR SAMPLING AND ANALYTICAL METHODS .............................................. 44
7.1
Chemiluminescence Methods ................................................................................44
Assessment Report on Nitrogen Dioxide for Developing Ambient Air Quality Objectives
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7.2
7.3
7.4
7.5
7.6
7.7
7.1.1 Gas-Phase Chemiluminescence .................................................................44
7.1.2 Liquid-Phase Chemiluminescence .............................................................45
Passive Samplers....................................................................................................45
Colourimetric Samplers .........................................................................................46
Electrochemical Sensors ........................................................................................47
Thick Film Sensors ................................................................................................47
Spectroscopic Methods ..........................................................................................47
Fourier Transform Infrared Spectrometry .............................................................48
8.0
AMBIENT OBJECTIVES IN OTHER JURISDICTIONS ..................................... 50
8.1
Canadian Nitrogen Dioxide Air Quality Guidelines and Objectives.....................50
8.2
United States Nitrogen Dioxide Air Quality Guidelines and Objectives ..............50
8.3
International Nitrogen Dioxide Air Quality Guidelines and Objectives ...............51
9.0
LITERATURE CITED ......................................................................................... 54
APPENDIX A ................................................................................................................ 65
Assessment Report on Nitrogen Dioxide for Developing Ambient Air Quality Objectives
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LIST OF TABLES
Table 1
Identification of Nitrogen Dioxide (HSDB, 2007; Genium, 1999) ........................ 2
Table 2
Physical and Chemical Properties of Nitrogen Dioxide ......................................... 3
Table 3
Summary of Nitrogen Oxides (NOx) Emissions (tonnes) in Canada and in
Alberta (adapted from EC, 2007a,b)....................................................................... 7
Table 4
Nitrogen oxides (NOx) Emissions in Alberta According to the 2005 NPRI
Database (EC, 2007d) (in tonnes, ranked by total emissions) .............................. 10
Table 5
Acute Respiratory Effects Following Human Exposure to NO2: Clinical
Exposure Studies................................................................................................... 20
Table 6
Acute Respiratory Effects Following Animal Exposure to NO2 .......................... 24
Table 7
Subchronic/Chronic Respiratory Effects Following Animal Exposure to NO2.... 30
Table 8
Reproductive Effects Reported Following Animal Exposure to NO2 .................. 34
Table 9
Effects Following Plant Exposure to NO2 ............................................................ 39
Table 10
Advantages and Disadvantages of Sampling and Analytical Methods ................ 49
Table 11
Summary of Ambient Air Quality Objectives and Guidelines for Nitrogen
Dioxide.................................................................................................................. 52
Assessment Report on Nitrogen Dioxide for Developing Ambient Air Quality Objectives
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GLOSSARY
AAQC
Ambient Air Quality Criterion
AENV
Alberta Environment
ATSDR
Agency for Toxic Substances and Disease Registry
CASA
Clean Air Strategic Alliance
CAL/EPA
California Environmental Protection Agency
CO
Carbon monoxide
COPD
Chronic Obstructive Pulmonary Disorder
d
day
DEM
Department of Environmental Management
DEP
Department of Environmental Protection
DEQ
Department of Environmental Quality
DES
Department of Environmental Services
DNR
Department of Natural Resources
DIAL
Differential Absorption Lidar
DOAS
Differential Optical Absorption Spectrometry
DOE
Department of Ecology
DOH
Department of Health
EC
Environment Canada
ENR
Environment and Natural Resources
EPHC
Environment Protection and Heritage Council
FEV1
Forced Expiratory Volume in 1 second
FVC
Forced Vital Capacity
FTIR
Fourier Transform Infrared Spectrometry
hr
hour
HSDB
Hazardous Substances Database
IPCS
International Programme on Chemical Safety
LOAEL
Lowest Observable Adverse Effect Level
mg m-3
milligram per cubic meter
mo
month
MOE
Ontario Ministry of the Environment
MW
Molecular Weight
Assessment Report on Nitrogen Dioxide for Developing Ambient Air Quality Objectives
vi
NAPS
National Air Pollution Surveillance Network
NIST
National Institute of Standards and Technology
NIOSH
National Institute for Occupational Safety and Health
NO
Nitrogen Oxide
NO2
Nitrogen Dioxide
NOx
Nitrogen Oxides (NO + NO2)
NOAEL
No Observable Adverse Effect Level
NPRI
National Pollutant Release Inventory
O3
Ozone
OECD
Organization for Economic Cooperation and Development
OEL
Occupational Exposure Limit
OSHA
Occupational Safety and Health Administration
PAN
Peroxyacetyl Nitrate
SO2
Sulphur Dioxide
Raw
pulmonary airway resistance
sRaw
specific airway resistance
TDLAS
Tunable Diode Laser Absorption System
TEA
Triethanolamine
µg m-3
microgram per cubic meter
US EPA
United States Environmental Protection Agency
VOC
Volatile Organic Compound
WHO
World Health Organization
wk
week
yr
year
Assessment Report on Nitrogen Dioxide for Developing Ambient Air Quality Objectives
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SUMMARY
Nitrogen dioxide is an irritating gas with an acrid, pungent odour. It is corrosive, highly
oxidizing and non-combustible. Nitrogen dioxide is prepared by the oxidation of nitric acid or as
an intermediate in the oxidation of ammonia to nitric acid. It can be released directly to the
atmosphere but is often produced by the conversion of nitric oxide released from combustion
processes. In the presence of sunlight, nitrogen dioxide can lead to the formation of ozone, nitric
acid and nitrate-containing respirable particles.
Nitrogen dioxide exists as a gas in the atmosphere and will decompose to nitric acid in water and
soil water. It occurs naturally in the environment as a result of forest fires, atmospheric lightning
discharges and biogenic oxidation of nitrogen compounds present in soil. Anthropogenic
emissions of nitrogen dioxide are mainly due to combustion processes, including vehicle
exhaust, coal, oil, and natural gas, with some emissions occurring as a result of use in industrial
processes. Anthropogenic emissions are mostly in the form of nitric oxide with some (less than
10%) nitrogen dioxide, which are typically considered together as oxides of nitrogen (NOx). In
Canada, anthropogenic emissions of NOx are tracked by the Environment Canada National
Pollutant Release Inventory program. The main emission sources of NOx in Canada in 2005
were transportation (53%), upstream oil and gas industry (19%) and electric power generation
(10%), with the remaining emissions (18%) attributed to other sources. In Alberta, air emissions
of NOx are predominantly the result of stack or point source emissions; the principal industrial
emitter is the upstream oil and gas sector, with contributions also coming from the electric power
generating sector, the natural gas processing sector, oil sands, and other industries.
Ambient air concentrations of nitrogen dioxide were reported in 2004 for 120 rural and urban
sites in Canada with annual mean concentrations ranging from 1 to 26 ppb. A similar
concentration range was reported for Alberta, with nitrogen dioxide concentrations ranging from
1 to 24 ppb. The Clean Air Strategic Alliance, which monitors nitrogen dioxide concentrations
at stations across Alberta, reported a decrease in concentrations in urban areas of Alberta from
1982 to 2000 (e.g., decreased by 32% in Edmonton and by 38% in downtown Calgary). At other
urban stations in Alberta, average nitrogen dioxide concentrations have decreased by up to 17%
over the period of 1982 to 2000.
In healthy adults, acute exposure to nitrogen dioxide concentrations greater than those generally
observed in outdoor air (i.e., >1000 ppb) were required to induce changes in pulmonary function,
respiratory symptoms, or airway responsiveness. Airway inflammation and alterations in
lymphocytes (host defense) appear to be sensitive responses of healthy individuals acutely
exposed to nitrogen dioxide concentrations of 1000 to 2000 ppb. Individuals with asthma,
chronic obstructive pulmonary disorder or chronic bronchitis have a greater sensitivity to acute
nitrogen dioxide exposures, with pulmonary effects and increased airway responsiveness
reported in asthmatics exposed to concentrations as low as 110 ppb.
Epidemiological studies have reported associations between daily (acute) changes in nitrogen
dioxide concentrations and aggravation of asthma and asthma morbidity in children; in addition
to, cardiac arrhythmias and mortality in adults. Studies investigating the effects of chronic
Assessment Report on Nitrogen Dioxide for Developing Ambient Air Quality Objectives
viii
nitrogen dioxide exposure on children have reported positive associations between outdoor
concentrations of nitrogen dioxide and an increased incidence of bronchitic symptoms in
asthmatic children, deficits in lung function growth, and allergic sensitization. Fetal effects (low
birth weight, intrauterine growth retardation, sudden infant death syndrome) have also been
associated with exposure to nitrogen dioxide in epidemiological studies on traffic-related air
pollution.
Acute exposure to nitrogen dioxide concentrations ranging from 470 to 1000 ppb produced
epithelial cell damage in mice, guinea pigs, and rats. Morphological effects were observed in the
lungs of rats exposed to 800 ppb nitrogen dioxide while concentrations ranging from 300 to 1000
ppb affected lung clearance of mice and rabbits. Acute exposure to 300 to 5000 ppb nitrogen
dioxide produced structural, biochemical and functional effects in the alveolar macrophages of
rabbits, rats, and mice. Numerous studies reported adverse effects on host defense as a result of
the interaction of nitrogen dioxide with infectious microorganisms, including increased infection,
impaired immune response, and/or increased mortality in animals infected with A/PR/8 virus,
Mycoplasma pulmonis, Streptococcus, Klebsiella pneumoniae, or Staphylococcus aureus and
acutely exposed to nitrogen dioxide concentrations ranging from 1000 to 10,000 ppb.
Subchronic or chronic exposures of rats to 400 or 500 ppb nitrogen dioxide (including
intermittent peak exposures to 1000 or 1500 ppb) produced morphological changes in the lung.
Chronic exposure of mice to nitrogen dioxide produced alveolar cell hyperplasia (250 to 300
ppb) and structural changes in the alveolar macrophage (500 ppb). Morphological effects were
reported in the lungs of ferrets subchronically exposed to 500 ppb nitrogen dioxide. The
interaction of nitrogen dioxide exposure and infectious microorganisms (A/PR/8 virus,
Mycoplasma pulmonis, Streptococcus, or Klebsiella pneumoniae) was reported in several
subchronic and chronic exposure studies in mice and guinea pigs with an increase in mortality
due to infection reported following exposure to concentrations ranging from 200 to 1000 ppb. In
mice, the cell-mediated immune response was suppressed following subchronic and chronic
exposure to 250 to 500 ppb nitrogen dioxide, while subchronic exposure to 400 ppb suppressed
the humoral immune response system. No adverse effect was reported for cell-mediated
immunity in rats following chronic exposure to 500 ppb nitrogen dioxide. Pulmonary function
effects (alterations in bronchial responsiveness, vital capacity, and lung volume) were reported in
rodents following subchronic/chronic exposure to nitrogen dioxide concentrations ranging from
500 to 1000 ppb.
Gestational exposure of rats to 50 ppb nitrogen dioxide produced changes in motor behavior
while reduced birth weight was reported in mice and rats following gestational exposure to 250
to 5000 ppb nitrogen dioxide. Pulmonary inflammation and injury were reported following
exposure of newborn mice to 250 to 300 ppb nitrogen dioxide, developing rats to 500 to 14000
ppb nitrogen dioxide, 6 week old ferrets to 500 ppb nitrogen dioxide, and 1.5 to 2 month old
guinea pigs to 2000 ppb nitrogen dioxide.
Epidemiological studies have reported on the association of lung cancer in Europe with exposure
to nitrogen oxides (including nitrogen dioxide); however, traffic-related pollution, which
includes carcinogenic components (benzene, diesel particulate, and PAH) was the primary
exposure source considered. A detailed carcinogenicity study conducted in rats did not report an
Assessment Report on Nitrogen Dioxide for Developing Ambient Air Quality Objectives
ix
increased incidence in respiratory tract or non-pulmonary organ tumors following continuous,
chronic exposure to nitrogen dioxide concentrations ranging from 40 to 4000 ppb.
Plants are relatively resistant to nitrogen dioxide with no visible foliar injury occurring at air
concentrations below 200 ppb. Acute exposure to high nitrogen dioxide concentrations produced
intercostal lesions in broad-leaf plants, necrosis at or below the leaf blade tips of narrow-leaf
plants, and dulling of the needle tip in coniferous plants. Plants susceptible to nitrogen dioxide ­
induced foliar injury include the common juniper, Scots pine and Norway spruce, corn, pinto
bean, and sunflower. The box elder, elm, Norway maple, willow, asparagus and bush bean were
resistant to NO2-induced foliar injury. Many studies have been conducted on the effects of
nitrogen dioxide exposure on plant growth and yield with no clear pattern emerging; however,
pasture grasses, white ash, sweet gum, loblolly pine, and potato plants demonstrated reduced
growth or yield following exposure (from 2 to 33 weeks) to relatively low levels of nitrogen
dioxide (100 to 200 ppb).
Nitrogen dioxide is the precursor for nitric acid which is a large contributor to acid deposition
and thus indirectly impacts most materials, including structures, metals, paints and coatings, and
everyday items such as leather and paper. Limestone, marble and sandstone are particularly
vulnerable to acidity and all types of metals exposed to acid rain can corrode, tarnish, crack, and
lose thickness. Acid deposition may discolour and then destroy automobile paint, eventually
tarnishing the metal frame of the automobile. Widely employed and accepted methods for
monitoring nitrogen dioxide have been developed, tested and reported by the United States
Environmental Protection Agency, National Institute of Occupational Safety and Health, and
Occupational Safety and Health Administration. The chemiluminescent analyzer is widely used
for continuous monitoring of nitrogen dioxide concentrations. It is the reference method of
choice for many regulatory agencies and jurisdictions, including Alberta and Canada, and for
many researchers. Other methods of measurement, such as passive samplers, colourimetric
methods, electrochemical sensors, thick film sensors, various spectroscopic methods, and FTIR
analyzers are also available.
Ambient (outdoor) objectives of 400 µg m-3 (212 ppb) as a 1-hr average, 200 µg m-3 (106 ppb) as
a 24-hr average, and 60 µg m-3 (32 ppb) as an annual average have been developed for nitrogen
dioxide by Alberta Environment. The Canadian government has developed National Ambient
Air Quality Objectives (NAAQO) for nitrogen dioxide ranging from of 60 µg m-3 (32 ppb)
(maximum desirable level as an annual average) to 1,000 µg m-3 (532 ppb) (maximum acceptable
level as a 1-hour average). The US Environmental Protection Agency has established a National
Ambient Air Quality Standard (NAAQS) for nitrogen dioxide of 100 µg m-3 (53 ppb) (annual
average). Eighteen US state agencies have adopted this NAAQS in their regulatory programs.
The California Environmental Protection Agency also uses a 1-hour standard of 470 µg m-3 (250
ppb). Other international environment agencies (Australia, New Zealand, UK, the European
Commission, and the World Health Organization) have established ambient guidelines for
nitrogen dioxide ranging from 200 to 226 µg m-3 (106 to 120 ppb)(1-hour average) and from 40
to 56 µg m-3 (21 to 30 ppb) (annual average). The UK and the European Commission have also
established an annual guideline of 30 µg m-3 (16 ppb) to protect vegetation.
Assessment Report on Nitrogen Dioxide for Developing Ambient Air Quality Objectives
x
1.0
INTRODUCTION
Alberta Ambient Air Quality Objectives (AAQO) are established by Alberta Environment under
Section 14 (1) of the Environmental Protection and Enhancement Act (EPEA) (AENV, 2007).
The purpose of this assessment report is to provide a review of scientific and technical
information to assist in evaluating the basis and background for an ambient air quality objective
for nitrogen dioxide. The following aspects were examined as part of the review:
•
•
•
•
•
Physical-chemical properties and environmental fate;
Existing and potential anthropogenic emissions sources in Alberta;
Effects on humans, animals, and vegetation;
Effects on materials and air monitoring techniques, and;
Ambient air guidelines and objectives in other jurisdictions.
The physical and chemical properties identified for nitrogen dioxide include chemical structure,
molecular weight, melting and boiling points, water solubility, density, and vapor pressure. A
discussion of the behaviour of nitrogen dioxide in the environment was also presented. Existing
and potential natural and anthropogenic sources of nitrogen dioxide emissions in Alberta and
Canada were examined. Nitrogen oxides are reportable substances on Environment Canada’s
National Pollutant Release Inventory.
Scientific information on the effects of nitrogen dioxide on humans, animals, and vegetation
were identified. Toxicity and epidemiology studies were located in peer reviewed evaluations by
the California Environmental Protection Agency and the World Health Organization. The
effects of nitrogen dioxide on vegetation were identified following a comprehensive search of
the Web of Science database and using data from the US and California Environmental
Protection Agencies.
The effects of nitrogen dioxide on materials were reviewed as atmospheric nitrogen dioxide is
the precursor for nitric acid which is a large contributor to acid deposition. Air sampling and
analytical methods used by regulatory agencies for nitrogen dioxide were identified and
reviewed for this assessment. Widely employed and accepted reference air monitoring methods
reported by the United States Environmental Protection Agency (US EPA), National Institute of
Occupational Safety and Health (NIOSH), and Occupational Safety and Health Administration
(OSHA) were reviewed and air monitoring methods used by Alberta Environment were
identified.
Ambient air guidelines for nitrogen dioxide have been established by a number of jurisdictions in
North America, Europe, Australia, and New Zealand for different averaging time periods. The
basis for how these guidelines were developed and used by different jurisdictions was
investigated in this report.
Assessment Report on Nitrogen Dioxide for Developing Ambient Air Quality Objectives
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2.0
GENERAL SUBSTANCE INFORMATION
Nitrogen dioxide (NO2) is a reddish-orange-brown gas with an irritating, acrid, characteristic
pungent odour (O’Neil, 2006; Genium, 1999; IPCS, 1997). At temperatures below 21.15ºC,
nitrogen dioxide exists as a brown liquid and at temperatures below -11ºC, as a colourless solid
(Lewis, 2002). Nitrogen dioxide is corrosive, highly oxidizing (IPCS, 1997) and non­
combustible (Lewis, 2002). The commercial pressurized liquid form is an equilibrium mixture
of NO2 and N2O4, sold as nitrogen tetroxide (O’Neil, 2006).
Nitrogen dioxide is prepared by the oxidation of nitric acid or as an intermediate in the oxidation
of ammonia to nitric acid (Lewis, 2002). Nitrogen dioxide is used as a chemical intermediate in
the production of nitric acid, as a nitrating agent, as an oxidizing agent, as a catalyst (in the
production of sulphuric acid for example), as an oxidizer for rocket fuels and as a polymerization
inhibitor for acrylates (Lewis, 2002; Genium 1999). It has also been used in the manufacturing of
oxidized cellulose compounds (hemostatic cotton) and in bleaching flour (ONeil, 2006; Genium,
1999).
Table 1 provides a list of important identification numbers and common synonyms for nitrogen
dioxide.
Table 1
Identification of Nitrogen Dioxide
Property
Value
Formula
NO2
Structure
O=N=O
CAS Registry Number
10102-44-0
RTECS number
QW9800000
UN Number
UN 1067
Common Synonyms/Trade names azote, azoto, dinitrogen tetroxide, nitrite, nitro,
nitrogen dioxide (liquid), nitrogen oxide, nitrogen
peroxide, nitrogen peroxide liquid, nitrogen
tetroxide.
Hazardous Substances Database (HSDB), 2007; Genium, 1999
2.1
Physical, Chemical and Biological Properties
The physical and chemical properties of nitrogen dioxide are summarized in Table 2.
Assessment Report on Nitrogen Dioxide for Developing Ambient Air Quality Objectives
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Table 2
Physical and Chemical Properties of Nitrogen Dioxide
Property
Value
Reference
Molecular weight
46.01 g.mol-1
Lide, 2007; O’Neil, 2006
Physical state
Clear colourless volatile liquid
Lide, 2007; O’Neil, 2006
Melting Point
-9.3ºC
Lide, 2007; O’Neil, 2006
Boiling Point
21.15ºC
Lide, 2007; O’Neil, 2006
Density (liquid)
1.448 (at 20ºC)
O’Neil, 2006
Density (gas) (air=1)
1.58
O’Neil, 2006
Vapour pressure
58.66 kPa at 10°C
121 kPa at 25°C
RSC, 2007
HSDB, 2007
Solubility in water
reacts with water, decomposes
forming nitric acid and nitric
oxide
Lide, 2007; O’Neil, 2006
Solubility
soluble in concentrated
sulphuric acid, nitric acid,
carbon disulphide, chloroform
RSC, 2007; Lewis, 2000
Conversion factors for vapour (at
25 °C and 101.3 kPa)
1 mg.m-3= 0.532 ppm
1 ppm = 1.88 mg.m-3
HSDB, 2007
2.2
Environmental Fate
Since nitrogen dioxide exists as a gas at ambient temperatures (greater than 21.15ºC) and
pressures, most releases of nitrogen dioxide to air will occur as a gas. If nitrogen dioxide is
released to water, it will decompose to nitric acid (HSDB, 2007). If nitrogen dioxide is released
to soil, it will decompose to nitric acid in soil water and it may volatilize into air from dry soil
surfaces (HSDB, 2007).
Nitrogen dioxide can be directly released to air but more often, it is produced by the conversion
of nitric oxide released from combustion processes (California EPA, 2007). In sunlight, nitrogen
dioxide can lead to the formation of ozone, nitric acid and nitrate-containing particles (California
EPA, 2007).
A brief description of the chemical reactions involved in the transformation of nitrogen dioxide
in the atmosphere is presented below. For a detailed presentation on the atmospheric chemistry
of nitrogen dioxide, please refer to Finlayso-Pitts and Pitts (2000), Seinfeld and Pandis (1998)
and Warneck (2000) (cited in California EPA, 2007).
Assessment Report on Nitrogen Dioxide for Developing Ambient Air Quality Objectives
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2.2.1
Formation and Conversion of Nitrogen Dioxide in Air
As mentioned previously, NO2 can be released directly to air or it can be formed by the reaction
of hydroperoxy radicals (HO2·), alkylperoxy radicals (RO2·) or ozone (O3) radicals with NO
according to the following reactions (Manahan, 2000):
HO2· + NO
NO2 + HO·
(1)
RO2· + NO
NO2 + RO·
(2)
O3 + NO
NO2 + O2
(3)
Production of NO2 from NO occurs rapidly in the troposphere (Manahan, 2000) however NO2
can rapidly photodissociate (at wavelengths below 398 nm) to reproduce NO:
NO2 + hv
NO + O
(4)
According to Jaffe and Weiss-Penzias (2003), a steady state between NO and NO2 is rapidly
reached and this steady state depends on the oxidants present and on the available light. Because
of this relationship between NO and NO2, these two compounds are often grouped together as
NOx (Jaffe and Weiss-Penzias, 2003).
2.2.2
Relationship between NOx and the Formation of Ozone
In Equation (3), the produced atomic oxygen (O) reacts with oxygen (O2) to produce ozone (O3)
according to the following reaction (CAL/EPA, 2007; Manahan, 2000):
O + O2 + M
O3 + M
(5)
where M is a molecule (often nitrogen or oxygen in air) that can absorb energy from the reaction.
The ozone formed can then in turn react with NO to convert NO back to NO2 according to
Equation 3 (CAL/EPA, 2007; Manahan, 2000).
It should be noted that, in urban areas, the concentration of ozone predicted by Equations (4) and
(5) is less than that which has been observed, suggesting additional pathways for the production
of O3 from NOx (CAL/EPA, 2007). It has been suggested that the oxidation of volatile organic
compounds (VOCs) in the atmosphere leads to the formation of RO2· and HO2·(peroxy radicals)
which in turn react with NO to produce NO2 (see Equations (1) and (2)). The produced NO2 then
undergoes the chemical reaction given in Equation 4 to produce atomic oxygen and thus leads to
the formation of additional O3.
Assessment Report on Nitrogen Dioxide for Developing Ambient Air Quality Objectives
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2.2.3
Formation of Nitric Acid and Removal of NOx from the Atmosphere
Nitrogen dioxide is removed from the atmosphere by reaction with the hydroxyl free radical
(OH·) and forming nitric acid (HNO3) according to the following reaction (CAL/EPA, 2007;
Manahan, 2000):
NO2 + OH·
HNO3
(6)
Nitric acid is a temporary sink for NO2 since it can react with OH radicals to produce nitrate
(Manahan, 2000):
OH· + HNO3
H2O + NO3
(7)
or with light to produce NO2 (Manahan, 2000):
HNO3 + hv
OH· + NO2
(8)
Nitric acid is removed from the atmosphere by precipitation (acid rain), or by reaction with
ammonia to produce ammonium nitrate (NH4NO3) (CAL/EPA, 2007):
HNO3 + NH3
NH4NO3
(9)
Ammonium nitrate readily condenses to produce particulate nitrates (IPCS, 1997).
Assessment Report on Nitrogen Dioxide for Developing Ambient Air Quality Objectives
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3.0
EMISSION SOURCES AND INVENTORY
3.1
Natural Sources
Nitrogen dioxide occurs naturally in the environment as a result of forest fires, atmospheric
lightning discharges and biogenic oxidation of nitrogen containing compounds present in soil
(HSDB, 2007).
3.2
Anthropogenic Sources
Anthropogenic emissions of nitrogen dioxide are mainly the result of combustion processes, such
as the combustion of fuel for vehicles or the combustion of coal, oil and natural gas for industrial
processes (HSDB, 2007). Emissions from these sources are mostly in the form of nitric oxide
(NO) with some (less than 10%) nitrogen dioxide (IPCS, 1997) and are typically considered
together as oxides of nitrogen (NOx). Emissions of nitrogen dioxide may also result from its use
in industrial processes, for example when it is used as an intermediate in the manufacturing of
nitric acid or as an oxidizing agent (HSDB, 2007).
Nitrogen oxides (NOx) are Criteria Air Contaminants (CAC) and detailed NOx emissions data
(Table 3) are provided by Environment Canada as part of their CAC Emission Summaries (EC,
2007a,b). The NOx emissions data provided by Environment Canada consists of nitric oxide
(NO) and nitrogen dioxide (NO2) and are reported as NOx on a NO2 mass basis.
For comparison purposes, the data for Alberta for 2005 (EC, 2007b) is also presented in Table 3.
According to Environment Canada (2007a,b), the total NOx emissions in Canada in 2005 were
2,377,485 tonnes (not including forest fires, prescribed burning and other open sources listed in
Table 3) or 2,444,044 (including open sources). The main emission sources of NOx in 2005
were transportation (53% of the total emissions, not including open sources), the upstream oil
and gas industry (19% of the total emissions, not including open sources) and electric power
generation (10% of the total emissions, not including open sources), with the remaining
emissions (18% of the total emissions, not including open sources) being attributed to other
sources (EC, 2007c).
Industrial emissions of oxides of nitrogen (NOx) in Canada are provided in the 2005 National
Pollutant Release Inventory (NPRI) database (EC, 2007d). The 2005 data were used since at the
time of writing this report, the 2006 data were preliminary and had not undergone review. Table
4 summarizes NOx emissions to air in Alberta alone. Due to the number of industrial facilities
emitting NOx, only industrial facilities reporting NOx emissions to air of greater than 500 tonnes
in 2005 are reported. It should also be noted that the NPRI reported emissions of NOx in Alberta
are exclusively to air.
Assessment Report on Nitrogen Dioxide for Developing Ambient Air Quality Objectives
6
Table 3
Summary of Nitrogen Oxides (NOx) Emissions (tonnes) in Canada and in Alberta
(adapted from EC, 2007a,b)
CATEGORY / SECTOR
INDUSTRIAL SOURCES
Abrasives Manufacture
1995
Canada
2005
2000
2010
Alberta
2005
2015
192
96
2
25
27
0
Aluminum Industry
Asbestos Industry
Asphalt Paving Industry
Bakeries
Cement and Concrete Industry
Chemicals Industry
1,020
240
598
5
47,295
30,451
1,442
151
178
4
37,049
33,481
1,041
86
12
0
45,924
22,091
1,327
88
253
5
38,329
32,273
1,392
104
279
5
35,585
35,066
0
0
9
0
4,674
13,479
Clay Products Industry
Coal Mining Industry
Ferrous Foundries
Grain Industries
Iron and Steel Industries
Iron Ore Mining Industry
Mining and Rock Quarrying
103
3,198
96
0
24,826
10,136
13,436
85
1,596
290
0
14,933
10,117
10,757
34
2,094
324
0
12,406
12,759
12,186
197
1,817
581
2
14,592
17,026
22,713
222
2,117
632
2
14,755
17,883
23,985
0
358
2
0
215
0
0
Non-Ferrous Mining and Smelting Industry
Oil Sands
Other Petroleum & Coal Products Industry
Paint & Varnish Manufacturing
Petrochemical Industry
Petroleum Refining
3,682
48,518
271
23
8,592
33,019
3,421
40,700
158
47
8,022
31,423
3,778
71,178
513
9
5,566
31,204
2,756
157,000
129
30
12,115
29,745
2,760
196,000
136
33
13,181
30,247
0
70,680
0
0
4,866
4,513
1,419
55,364
279,364
14,378
54,443
423
49,429
379,554
15,021
39,468
229
44,932
461,540
11,282
65,195
350
57,646
414,902
16,805
47,561
403
59,500
435,998
17,617
51,201
0
5,026
366,155
2,745
7,388
630,669
677,844
804,382
868,265
939,131
480,129
27,091
259,578
36,880
9,895
30,246
297,156
36,943
10,248
34,498
244,691
35,088
10,262
39,636
267,774
35,193
11,213
40,569
267,081
36,168
11,635
5,110
84,913
6,605
398
333,444
374,593
324,540
353,816
355,454
97,027
Plastics & Synthetic Resins Fabrication
Pulp and Paper Industry
Upstream Oil and Gas Industry
Wood Industry
Other Industries
TOTAL
NON-INDUSTRIAL FUEL
COMBUSTION
Commercial Fuel Combustion
Electric Power Generation (Utilities)
Residential Fuel Combustion
Residential Fuel Wood Combustion
TOTAL
TRANSPORTATION
Air Transportation
Heavy-duty diesel vehicles
Heavy-duty gasoline trucks
49,981
61,647
62,223
78,352
83,610
7,884
312,101
34,104
311,407
26,487
276,167
25,753
188,913
17,966
97,588
11,147
50,516
6,607
Assessment Report on Nitrogen Dioxide for Developing Ambient Air Quality Objectives
7
CATEGORY / SECTOR
Light-duty diesel trucks
1995
4,641
2000
4,868
Canada
2005
4,898
2010
3,702
2015
2,328
Alberta
2005
1,511
Light-duty diesel vehicles
Light-duty gasoline trucks
Light-duty gasoline vehicles
Marine Transportation
Motor cycles
Off-road use of diesel
1,489
149,540
271,355
124,645
777
388,414
1,630
138,307
184,275
111,266
979
389,627
1,405
114,481
105,011
117,096
1,539
368,194
922
92,728
77,496
118,999
1,368
318,123
408
62,763
48,636
124,009
1,020
239,436
90
20,832
12,398
0
220
82,828
Off-road use of gasoline
Rail Transportation
Tire wear & Brake lining
41,288
118,150
52,645
109,289
50,490
117,170
33,079
96,537
27,003
85,211
10,940
16,263
0
TOTAL 1,496,484 1,392,427 1,244,428 1,028,185
783,160
210,088
INCINERATION
Crematorium
Industrial & Commercial Incineration
Municipal Incineration
Wood Waste Incineration
Other Incineration & Utilities
TOTAL
25
22
36
26
27
4
738
1,298
318
1,109
348
1,478
0
4,621
254
1,451
0
2,342
369
1,723
0
4,755
386
1,762
0
4,999
0
0
NA
0
3,487
6,469
4,083
6,873
7,175
19
MISCELLANEOUS
Cigarette Smoking
0
6
0
7
7
0
Dry Cleaning
Fuel Marketing
General Solvent Use
Printing
Structural Fires
Surface Coatings
1
1
0
71
0
0
2
13
0
86
2
0
0
27
0
25
0
0
2
5
6
61
2
84
2
5
6
64
2
90
0
0
0
0
0
0
TOTAL
OPEN SOURCES
Agriculture Tilling and Wind Erosion
Construction Operations
Dust from Paved Roads
Forest Fires
74
108
52
168
177
0
0
236
0
44,195
0
0
0
15,496
0
14
0
64,593
0
0
14
23,144
232
0
0
15,292
0
0
0
2,338
Landfills Sites
Mine Tailings
Prescribed Burning
10,594
0
3,710
10,620
169
3,942
1,099
0
853
42,274
274
579
5,625
244
4,793
9
0
77
58,735
30,229
66,559
66,285
26,186
2,425
2,522,893 2,481,670 2,444,044 2,323,591 2,111,283
2,464,158 2,451,441 2,377,485 2,257,307 2,085,097
789,688
787,264
TOTAL
TOTAL
With open sources
Without open sources
Assessment Report on Nitrogen Dioxide for Developing Ambient Air Quality Objectives
8
The results in Table 4 show that, in Alberta, the air emissions of NOx are predominantly the
result of stack or point source emissions and some other non-point sources. As indicated in both
Tables 3 and 4 and as highlighted in MacDonald and Bietz (1999), the industrial sectors that
contribute to NOx emissions in Alberta are principally the upstream oil and gas sector, the
electric power generating sector, the natural gas processing sector, oil sands and other industries.
3.3
Ambient Levels
Extensive ambient air concentration data for nitrogen dioxide are presented in HSDB (2007) and
IPCS (1997). For Canada, ambient air levels of nitrogen dioxide at several rural and urban
Canadian sites are available through annual reports from the National Air Pollution Surveillance
(NAPS) Network (see http://www.etc-cte.ec.gc.ca/NAPS/index_e.html). Nitrogen dioxide has
been monitored as part of the NAPS program since 1970 (EC, 2007e). In 2004, nitrogen dioxide
concentrations in ambient air were reported for 120 sites in Canada (EC, 2007f). Annual mean
nitrogen dioxide concentrations at these sites ranged from 1 ppb (on Sable Island, Nova Scotia
and in Fort Chipewayan, Alberta) to 26 ppb (in Toronto, Ontario) (EC, 2007f). For monitoring
stations in Alberta, nitrogen dioxide concentrations ranged from 1 ppb (in Fort Chipewayan at an
undeveloped rural site) to 24 ppb (in Calgary at a commercial site) (EC, 2007f).
EC (2004) also provides a summary of NAPS Network data from 1990 to 2001. The nitrogen
dioxide concentrations at all Canadian sites in 2001 were below 53 ppb (the maximum
acceptable annual mean National Ambient Air Quality Objective) (EC, 2004). The highest
concentrations were observed at urban sites. EC (2004) also notes that the ratio of NO
concentrations to NO2 concentrations was greater at urban sites (0.95) than at rural sites (0.20).
This trend is as expected since, in urban areas, oxides of nitrogen are released from
anthropogenic sources as NO and reactions in the atmosphere cause NO to oxidize to NO2 (EC,
2004). Therefore, as air moves from urban areas to rural areas, less NO is released and the NO
in the atmosphere is being transformed into NO2 (EC, 2004).
The Clean Air Strategic Alliance (CASA) also monitors nitrogen dioxide concentrations at
stations across Alberta. According to CASA (2007a), nitrogen dioxide concentrations in urban
areas of Alberta have decreased from 1982 to 2000. More specifically, these concentrations have
decreased by 32% in Edmonton and by 38% in downtown Calgary (CASA, 2007a). For
example, in central Edmonton, the annual mean nitrogen dioxide concentration decreased from
26.6 to 21.3 ppb from 1990 to 2006 (CASA, 2007b). Over the same time period, in central
Calgary, the annual mean nitrogen dioxide concentration decreased from 34.2 to 24.0 ppb
(CASA, 2007b). At other urban stations in Alberta, average nitrogen dioxide concentrations
have decreased by as much as 17% over the period of 1982 to 2000 (CASA, 2007a).
Assessment Report on Nitrogen Dioxide for Developing Ambient Air Quality Objectives
9
Table 4
Nitrogen oxides (NOx) Emissions in Alberta According to the 2005 NPRI Database (EC, 2007d) (in tonnes,
ranked by total emissions)
NOx Emissions (in tonnes)
Duffield
Stack/Point
25786.9
Other NonPoint
0
Total
25786.9
Genesee Thermal Generating Station
Warburg
13635.01
0
13635.01
Syncrude Canada
Mildred Lake Plant Site
Fort McMurray
11602.93
0
11602.93
2286
Transalta Utilities
Keephills Generating Facility
Duffield
11008.11
0
11008.11
2230
Suncor Energy
Suncor Energy Inc. Oil Sands
Fort McMurray
10900.89
0
10900.89
1036
Alberta Power (2000) Ltd.
Sheerness Generating Station
Hanna
10287
0
10287
1033
Alberta Power (2000) Ltd.
Battle River Generating Station
Forestburg
9926
0
9926
442
Imperial Oil
Cold Lake Heavy Oil Plants
Grande Centre
5084.326
0
5084.326
2282
Transalta Utilities
Wabamun Generating Station
Wabamun
3985.96
0
3985.96
5291
Lafarge Canada Inc.
Exshaw Plant
Exshaw
3423
0
3423
424
Imperial Oil
Bonnie Glen Gas Plant
Thorsby
2981.8
0
2981.8
2132
Sherritt International Corporation Fort Saskatchewan
Fort Saskatchewan
2665.563
0
2665.563
1779
NOVA Chemicals Corporation
280
NPRI ID
Company
2284
Transalta Utilities
Facility Name
Sundance Generating Facility
267
EPCOR Generation
2274
City
County of Lacombe
2380.978
0
2380.978
Dow Chemical Canada Inc.
Joffre Site; Olefins and Polyethylene
Manufacturing
Western Canada Operations
Fort Saskatchewan
2182.844
0.156
2183
4136
Canadian Natural Resources
Wolf Lake and Primrose Plant
NA
2129.18
0
2129.18
3707
Imperial Oil
Strathcona Refinery
Edmonton
2039.042
0
2039.042
1039
Milner Power Inc.
H.R.Milner Generating Stn
Grande Cache
1831
0
1831
3821
Canadian Fertilizers
Canadian Fertilizers Limited
Medicine Hat
1759.102
4.466
1763.568
3903
Petro-Canada
Edmonton Refinery
Edmonton
1671.4
0
1671.4
1
Alberta Pacific Forest Industries
Alberta Pacific Forest Industries
Boyle
1380.37
0
1380.37
5243
Lehigh Inland Cement
Inland Cement
Edmonton
1245.65
5.66
1251.31
5337
Duke Energy Midstream Services Nevis Gas Plant
Canada Corporation
Apache Canada
Nevis Gas Plant
1246.9
0
1246.9
1244.947
0
1244.947
15369
Assessment Report on Nitrogen Dioxide for Developing Ambient Air Quality Objectives
Stettler
N/A
10
Agrium
ConocoPhillips Canada
Anadarko Canada Corporation
Taylor Processing Inc.
ATCO Electric Ltd.
Agrium
Pengrowth Corporation
Burlington Resources
Paramount Energy Operating
Corporation
Shell Canada Limited
Inter Pipeline Extraction Ltd.
Weyerhaeuser Company Limited
Trilogy Energy Trust LP
Celanese Canada
West Fraser Mills Ltd.
KEYERA Energy Ltd.
Agrium
KEYERA Energy Ltd.
Devon Canada Corporation
Daishowa Marubeni International Peace River Pulp Division
Shell Canada
BP Canada
NAL Resources Management
2134
4928
15229
3941
19926
3269
440
15638
17409
5248
2875
3754
1162
2991
1372
4874
1362
106
223
2960
15587
6559
Edmonton
N/A
Grande Prairie
Cochrane
Fort Saskatchewan
N/A
Baptiste River
Swan Hills
Calgary
Jasper National Park
Didsbury
N/A
Grande Prairie
Redwater
Balzac
City
Swan Hills
Sylvan Lake Gas Processing Plant
11-8-74-5W4
Shell Scotford Refinery
Dunvegan Sour Gas Plant
Brazeau River Gas Plant
Ft Saskatchewan
14-32-37-3-W5
n/a
Fort Saskatchewan
MD of Northern Lights
Fairview
Drayton Valley
Ft Saskatchewan
HINTON PULP, A Division of West Fraser Hinton
Mills Ltd.
Rimbey Gas Plant
Rimbey
Edmonton Facility
Kaybob Gas Plant
Weyerhaeuser Grande Prairie Operations Pulpmill/Sawmill
Cochrane Extraction Plant
Scotford Upgrader
Legend 12-31
Ferrier 13-17
Judy Creek Gas Conservation Plant
Carseland Nitrogen Operations
Palisades Generating Station
Harmattan Gas Plant
Knopcik Gas Group 09-10
Elmworth Gas Plant
Assessment Report on Nitrogen Dioxide for Developing Ambient Air Quality Objectives
6546
Balzac Gas Plant
Nexen Inc.
1902
Redwater Fertilizer Operations
Facility Name
Judy Creek Production Complex
NPRI ID
Company
4566
Pengrowth Corporation
788.606
799.09
802.6
824.482
830.032
838.51
847.39
849.02
850.29
888.912
888.92
896.145
910.146
927.9
938.311
950.19
1032.16
1037.968
1104.481
1142.94
1186.329
1186.99
1196.3
1233.543
Stack/Point
1244.345
0
0
0
0
0
0
0
0
0
0
0
0
0
0
0
0
0
0
0
0
0
0
0
0
Other NonPoint
0
NOx Emissions (in tonnes)
11
788.606
799.09
802.6
824.482
830.032
838.51
847.39
849.02
850.29
888.912
888.92
896.145
910.146
927.9
938.311
950.19
1032.16
1037.968
1104.481
1142.94
1186.329
1186.99
1196.3
1233.543
Total
1244.345
NOx Emissions (in tonnes)
City
Exshaw Plant
Exshaw
Stack/Point
755.643
Other NonPoint
0
Total
755.643
Cancarb Ltd.
Cancarb Ltd.
Medicine Hat
741.656
0
741.656
17935
Signalta Resources
Birch Lake Ranfurly West
04-05-50-11-4
738.71
0
738.71
16562
Encana
Countess Makepeace Sweet Gas Plant
n/a
738.23
0
738.23
6647
Albian Sands Energy
Muskeg River Mine
Ft. McMurray
732.446
0
732.446
15744
Primewest Energy
Wilson Creek Comp 6-18-43-4W5
6-18-43-4W5
725.23
0
725.23
3939
Exxonmobil Canada
Lone Pine Creek Gas Plant
Carstairs
722.385
0
722.385
15818
Canadian Natural Resources
Liege 03-29
N/A
720.732
0
720.732
NPRI ID
Company
6826
Graymont Western Canada Inc.
5357
Facility Name
16521
Encana
Monogram Comp Stn 13-14
n/a
706.61
0
706.61
5284
Talisman Energy
Edson Gas Plant
Edson
702.36
0
702.36
16654
Encana
Paddle Prairie South Comp Stn 15-12
n/a
698.81
0
698.81
15247
Anadarko Canada Corporation
Wild River 14-36
N/A
696.457
0
696.457
432
Devon Canada Corporation
Wapiti Deep-Cut Gas Plant
Grovedale
692.444
0
692.444
15584
BP Canada
10-25-73-5W4
n/a
683.338
0
683.338
18023
Talisman Energy
Petromet Bigstone West Fir 14-28-59-22
n/a
674.59
0
674.59
6576
City of Medicine Hat
Medicine Hat
673.15
0
673.15
15792
N/A
671.436
0
671.436
15567
Canadian Natural Resources
Limited
BP Canada
City of Medicine Hat, Electric Utility ­
Generation
Edson W. 01-24-052-20w5
Chinchaga Gas Plant
n/a
668.006
0
668.006
4140
Primewest Energy
East Crossfield Gas Plant
9-14-28-1-W5M
667.869
0
667.869
1374
KEYERA Energy Ltd.
Strachan Gas Plant
Rocky Mountain House
624.42
0
624.42
16739
Encana
Suffield Koomati Comp Stn 04-04
n/a
622.35
0
622.35
16009
Canadian Natural Resources
Galloway Plant 14-14
N/A
616.587
0
616.587
6622
ConocoPhillips Canada
Alder Flats Gas Plant
Drayton Valley
607.43
0
607.43
6591
NOVA Chemicals Corporation /
ATCO Power / EPCOR
SemCAMS
Joffre Site; Cogeneration
County of Lacombe
606.457
0
606.457
West Whitecourt Plant
Whitecourt
603.93
0
603.93
4138
Assessment Report on Nitrogen Dioxide for Developing Ambient Air Quality Objectives
12
NOx Emissions (in tonnes)
Stack/Point
600.83
Other NonPoint
0
Total
600.83
598.94
0
598.94
N/A
589.954
0
589.954
Princess
N/A
586.77
0
586.77
NAL Resources Management
Medicine River 10-4
10-4-39-4-5
586.182
0
586.182
19830
Shiningbank Energy
Sousa (7-4)
7-4-113-4-6
578.313
0
578.313
17328
Nexen Inc.
Many Islands 04-16
N/A
577.891
0
577.891
15241
Anadarko Canada Corporation
Hays Gas Plant 11-31
N/A
572.369
0
572.369
5285
Apache Canada
Zama Gas Processing Complex
ZAMA
571.596
0
571.596
19008
NAL Resources Management
5-11 Plant
05-11-34-12-4
570.546
0
570.546
17019
Husky Energy
Muskwa River G.P.
Wabasca-Desmarais
567
0
567
15449
Baytex Energy Trust
Baytex Darwin Gas Plant
Darwin
558.4
0
558.4
17876
Shell Canada
Waterton Complex–Compressor Station W
Pincher Creek
553.605
0
553.605
16850
Enerplus Resources
Bantry 05-08-019-13 W4
N/A
530.31
0
530.31
19585
Enermark
Trochu 11-11-034-20W4
NA
530.31
0
530.31
16532
Encana
Redland Sweet Gas Plant
n/a
526.03
0
526.03
6628
ConocoPhillips Canada
Wolf Creek Sweet Gas Plant
Edson
519.98
0
519.98
6626
ConocoPhillips Canada
Viking Sweet Gas Plant
Viking
514.51
0
514.51
15437*
ATCO Gas and Pipelines Ltd.
Carbon Plant
Carbon
509.74
0
509.74
15416
ARC Resources
Ante Creek 10-7 Battery
MD #16
504.97
0
504.97
683
SemCAMS
Kaybob South #3 Gas Plant
Fox Creek
504.08
0
504.08
2227
Suncor Energy
Simonette Production Complex
Valleyview
503.627
0
503.627
EOG Resources Canada
Twining 12-10-31-24W4
North
501.939
0
501.939
501.129
0
501.129
NPRI ID
Company
4150
SemCAMS
Facility Name
Kaybob Amalgamated Sour Gas Plant
City
Fox Creek
16864
EOG Resources Canada
Swalwell 14-35-29-24W4-01
North
17956
Suncor Energy
Browncreek
6731
Transcanada Pipelines
17239
16865
§
17422
Trilogy Energy Trust LP
Summit Two Creek 07-04
N/A
reported in database but not in on-line data search (at http://www.ec.gc.ca/pdb/querysite/query_e.cfm, September 2007)
§
reported in on-line data search (at http://www.ec.gc.ca/pdb/querysite/query_e.cfm, September 2007) but not in database
Note: Storage/Handling, Fugitive and Spills had 0 (zero) emissions so were not included in the table.
*
Assessment Report on Nitrogen Dioxide for Developing Ambient Air Quality Objectives
13
4.0
EFFECTS ON HUMANS AND ANIMALS
Nitrogen dioxide is a contaminant of concern due to its ability to directly affect respiratory health
and its role in the formation of ozone and respirable particulate matter. The following is a
discussion of the respiratory effects of nitrogen dioxide inhalation in animals and humans, with a
focus on recent studies in assessments completed by the World Health Organization (WHO,
2006; IPCS, 1997) and the California Environmental Protection Agency (CAL/EPA, 2007).
4.1
Overview of Chemical Disposition
A study in humans reported 81 to 90% absorption of inhaled NO2 (0.29 to 7.2 ppm) by the lower
respiratory tract, with exercise increasing the amount absorbed to 91 to 92% (Wagner, cited in
IPCS, 1997 and HSDB, 2005). An increase in exercise (and mouth breathing) resulted in a
higher amount of NO2 absorbed by the lower respiratory tract in studies of controlled human
exposure to NO2 (Bauer et al.; Miller et al.; Wagner, cited in WHO, 2006). Rhesus monkeys
retained 50 to 60% of inhaled NO2 (0.3 to 0.9 ppm) in the lungs in original form or as
intermediates for prolonged periods following exposure; NO2 transport following absorption
occurred via the blood stream (Goldstein et al.; Clayton and Clayton, cited in HSDB, 2005). An
average uptake of 65% was reported for an isolated perfused rat lung model (Postlethwait and
Mustafa, cited in CAL/EPA (2007).
Inhaled NO2 is partly dissolved in the mucus of the upper airways and can be removed by the
nasopharynx (Linvall, cited in HSDB, 2005; Wagner, cited in WHO, 2006). Nasal breathing
(versus mouth breathing) resulted in greater amounts (~85%) of NO2 absorbed in the upper
respiratory tract (above the larynx) of dogs exposed to 1.0 or 5.0 ppm NO2; an increased
ventilation rate reduced the uptake of NO2 by the upper respiratory tract (Kleinman and Mautz,
cited in IPCS, 1997). In dogs and rabbits exposed though the nose to NO2 concentrations
ranging from 4.0 to 41.0 ppm, 42.1% of NO2 inhaled was removed by the upper airway
(Yokoyama, cited in IPCS, 1997).
Modelling studies in humans, rats, guinea-pigs, and rabbits indicate that NO2 is maximally
distributed to the centriacinar region (junction between the conducting and respiratory airways);
this is supported by the observation of morphometric lesions in this region following NO2
exposure of various animal species (Rom, cited in HSDB, 2005; Miller et al. and Overton et al.,
cited in WHO, 2006). A recent study which simulated the transport of inhaled NO2 in the
airways of rats, dogs, and humans, reported higher NO2 concentrations in the upper and lower
airways of humans compared to rats and dogs. However rats were predicted to have higher NO2
concentrations within the alveoli. Factors affecting airway concentrations between the species
included differences in tidal volume, respiratory rate, and surface area (Tsujino et al., cited in
CAL/EPA, 2007).
Assessment Report on Nitrogen Dioxide for Developing Ambient Air Quality Objectives
14
Following deposition to the lower airway, NO2 dissolves and reacts in lung fluids to produce
reaction products (nitrous and nitric acids) which are taken up and translocated via the
bloodstream and other body fluids (Goldstein et al.; Moncada et al., cited in IPCS, 1997).
Animal studies indicate that inhalation exposure to NO2 produced nitrates and nitrites in the
blood which were then excreted in the urine (Saul and Archer; Clayton and Clayton, cited in
HSDB, 2005; Oda et al., cited in IPCS, 1997). The conversion of NO2 to nitrite (NO2-) was
reported in an in vitro study exposing perfused rat lung to NO2 (Sullivan and Krieger, cited in
HSDB, 2005).
In an in vitro rat model, NO2 did not penetrate the epithelial liquid lining to react directly with
the epithelial tissue suggesting that NO2 chemical reaction products are formed in the epithelial
liquid lining (Postlethwait et al.; Postlethwait and Bidani, cited in CAL/EPA, 2007).
Subsequent studies identified glutathione and ascorbate as NO2 substrates associated with the
generation of reactive oxygen species in the epithelial liquid lining and cellular injury
(Postlethwait et al.; Velsor and Postlethwait, cited in CAL/EPA, 2007). These findings suggest
that the extrapolation of animal health effects of NO2 to humans may be limited, due to speciesspecific variations in the levels of anti-oxidant and other constituents that react with NO2 in
surface liquid lining (Postlethwait and Bidani, cited in CAL/EPA, 2007).
4.2
Genotoxicity
Positive results for NO2 mutagenicity (alone or combined with NO) have been reported in in
vitro bacterial assays (Victorin and Stahlberg; Aroyo et al., cited in CAL/EPA, 2007). A recent
study by Kelman et al. suggests NO2 may be directly mutagenic, although base pair mutations
were only observed in bacterial DNA exposed to a reaction product (N2O3) of NO and NO2
(CAL/EPA, 2007). Chromatid-type aberrations, sister chromatid exchanges, or DNA strand
breaks occurred in V79 hamster cells exposed in vitro to NO2 (1 ppm and higher) (Tsuda et al.;
Gorsdorf et al.; Shiraishi and Bandow, cited in CAL/EPA, 2007); sister-chromatid exchange did
not occur in cells exposed to 0.5 ppm NO2 Shiraishi and Bandow, cited in CAL/EPA, 2007). An
in vitro study of rat alveolar macrophage (AM) reported DNA single strand breaks following
exposure to 20 ppm NO2 (Walles et al., cited in CAL/EPA, 2007).
Acute in vivo exposure of rats (3 hours) to NO2 increased lung cell chromosome aberrations (8
ppm NO2) and mutation frequency to ouabain resistance (15 ppm NO2) (Isomura et al., cited in
CAL/EPA, 2007). No significant increase in DNA single strand breaks or in the activity of DNA
repair enzyme poly (ADP-ribose)synthetase in lavaged AMs was reported following the
continuous, in vivo exposure of rats (3 days) to 1.2 ppm NO2 (Bermudez et al.; Bermudez, cited
in CAL/EPA, 2007). No genotoxic effects were observed in the bone marrow (micronucleus
assay) of mice following in vivo exposure for 23 hours to 20 ppm NO2 (Victorin et al., cited in
CAL/EPA, 2007) and in spermatocytes and lymphocytes (non-pulmonary) of mice after 6 hours
exposure to 0.1 to 10 ppm NO2 (Gooch, cited in CAL/EPA, 2007).
Assessment Report on Nitrogen Dioxide for Developing Ambient Air Quality Objectives
15
4.3
Acute Toxicity
The toxicity of NO2 following acute exposure of humans and animals is discussed below. Acute
toxicity refers to adverse effects occurring after short-term (acute) exposures, which in the
current assessment ranged from 15 minutes to intermittent daily exposures for up to 3 weeks.
4.3.1
Acute Toxicity in Humans
An extensive number of studies have been conducted on the response of humans to acute clinical
NO2 exposure. An overview of select studies is provided below and in Table 5. Further details
for these studies can be found in assessments published by WHO (2006) and CAL/EPA (2007).
4.3.1.1
Healthy Individuals
In healthy adult individuals, acute exposure to NO2 concentrations greater than those observed in
outdoor air (i.e., >1 ppm or 1880 µg m-3) were required to induce changes in pulmonary
function, respiratory symptoms, or airway responsiveness (WHO, 2006). The majority of
clinical studies indicated that exposure of healthy volunteers to NO2 concentrations up to 4.0
ppm (7520 µg m-3) for up to 5 hours will not cause respiratory symptoms or alter lung function
(CAL/EPA, 2007). Several recent studies reported no effects on symptoms or lung function
following clinical exposure to up to 2 ppm (3760 µg m-3) NO2 for 4 to 6 hours (Azadniv et al.;
Blomberg et al.; Devlin et al., cited in CAL/EPA, 2007).
Airway inflammation and alterations in lymphocytes (host defense) appear to be sensitive
responses of healthy individuals acutely exposed to NO2 concentrations of 2 ppm or lower.
Earlier studies conducted by Sandstrom and colleagues found no airway inflammation but
reported an increase in lymphocytes in bronchoalveolar lavage fluid following 20 minute
exposure to 2.25 to 5.5 ppm (4230 to 9400 µg m-3) NO2 (CAL/EPA, 2007). Several studies
reported airway inflammation following acute exposure of healthy individuals to 1.0 ppm NO2
(Jörres et al., cited in CAL/EPA, 2007), 1.5 ppm (2820 µg m-3) NO2 (Frampton et al., cited in
CAL/EPA, 2007) and 2.0 ppm NO2 (Azadniv et al., Blomberg et al.; Devlin et al.; Pathmanathan
et al., cited in CAL/EPA, 2007). Alterations in lymphocytes were reported in studies of healthy
individuals acutely exposed to NO2 concentrations ranging from 1.5 to 2.0 ppm (Frampton et al.;
Solomon et al., cited in CAL/EPA, 2007).
Limited data were available on the clinical effects of NO2 in the elderly. In healthy seniors (61
years old), exposure to 0.3 ppm (560 µg m-3) NO2 for 4 hours with light exercise did not affect
lung function, however, a slight decrease in forced expiratory volume (FEV1) during NO2
exposure was observed for smokers compared to nonsmokers (Morrow et al., cited in CAL/EPA,
2007). More recently, a study reported no effects on pulmonary function in seniors (mean age of
68 years) exposed to 0.4 ppm (752 µg m-3) NO2 for 2 hours with intermittent exercise (Gong et
al., cited in CAL/EPA, 2007). One study reported a significant decrease in cardiac output in
elderly individuals following acute (2 hour) exposures to mixtures of 0.45 ppm ozone plus 0.6
Assessment Report on Nitrogen Dioxide for Developing Ambient Air Quality Objectives
16
ppm (1130 µg m-3) NO2 with intermittent exercise; these effects were not observed with
individual exposure to ozone or NO2 (Drechsler-Parks, cited in CAL/EPA, 2007).
4.3.1.2
Sensitive Individuals
Individuals with asthma, chronic obstructive pulmonary disorder (COPD) or chronic bronchitis
have a greater sensitivity to acute NO2 exposures compared to healthy individuals (WHO, 2006).
Direct, albeit inconsistent, pulmonary effects were reported in asthmatics exposed to NO2
concentrations as low as 0.3 ppm (560 µg m-3) NO2 for 2 to 2.5 hours (Roger et al.; Bauer et al.;
Avol et al., cited in WHO, 2006). Several clinical studies conducted by Linn and colleagues
reported no adverse effects on the pulmonary response of asthmatics acutely exposed (1 hour)
with intermittent exercise to NO2 concentrations ranging from 1 to 4 ppm (1880 to 7520 µg m-3)
(WHO, 2006). No effects on lung function were observed in asthmatics acutely exposed (30
minutes to 3 hours) to NO2 concentrations ranging from 0.26 to 0.4 ppm (488 to 752 µg m-3)
(Solomon et al.; Strand et al.; Vagaggini et al., cited in CAL/EPA, 2007) or in COPD subjects
acutely exposed (2 hours) with intermittent exercise to 0.4 ppm NO2 (Gong et al., cited in
CAL/EPA, 2005). Two studies reported decrements in forced vital capacity (FVC) and FEV1 in
individuals with COPD following acute exposure (3.75 to 4 hours) to 0.3 ppm (560 µg m-3) NO2
with exercise (Morrow and Utell; Morrow et al., cited in WHO, 2006). Von Nieding and
colleagues conducted several studies on individuals with COPD and reported an increase in
airway reactivity following brief exposures (15 minutes) to 1.6 ppm (3000 µg m-3) NO2 (WHO,
2006). This response was not observed in another study of individuals with COPD exposed 1
hour (with intermittent exercise) to 0.5 to 2.0 ppm (940 to 3760 µg m-3) NO2 (Linn et al., cited in
WHO, 2006). Acute exposure (1 hour) of COPD subjects to 0.3 ppm (560 µg m-3) NO2 with
intermittent exercise decreased FEV1 (Vagaggini et al., cited in CAL/EPA, 2007).
NO2 exposure has been demonstrated to intensify airway responsiveness in asthmatics (WHO,
2006). Acute (30 min) exposure to 0.26 ppm (488 µg m-3) NO2 increased bronchial
responsiveness of asthmatics to histamine (Bylin et al.; Strand et al., cited in WHO, 2006). Avol
and colleagues reported an increase in the cold air airway constriction response of asthmatics
exposed for 2 hours to 0.3 ppm (560 µg m-3) NO2 but not to 0.6 ppm (1130 µg m-3) NO2; further
studies by the same group did not observe any changes in the cold air response of asthmatics
exposed 2.5 hours to 0.3 ppm (560 µg m-3) NO2 (WHO, 2006). Several studies reported a lack of
effect on airway responsiveness of asthmatics acutely exposed (30 minutes to 1 hour) to 0.1 ppm
(190 µg m-3) NO2 (Ahmed et al.; Hazucha et al.; Tunnicliffe et al.; Svartengren et al., Orehek et
al., cited in WHO, 2006). Folinsbee reported an increase in the bronchoconstriction response of
asthmatics exposed to NO2 concentrations greater than 0.11 ppm (200 µg m-3) NO2 following a
meta-analysis of 20 studies (WHO, 2006).
Pre-exposure to NO2 concentrations ranging from 0.16 to 0.43 ppm (300 to 800 µg m-3)
increased the responsiveness of mildly asthmatic individuals to inhaled allergens (house dust
mite, pollen) (Svartengren et al.; Tunnicliffe et al.; Strand et al., cited in WHO, 2006; Barck et
al.; Solomon et al., cited in CAL/EPA, 2007). Exposure of individuals with mild asthma to NO2
(0.38 ppm or 720 µg m-3) plus sulfur dioxide (7000 µg m-3) enhanced airway response to an
Assessment Report on Nitrogen Dioxide for Developing Ambient Air Quality Objectives
17
inhaled allergen, with the maximum response reported 24 hours post-exposure and lasting until
the following day (Rusznak et al.; Devalia et al., cited in WHO, 2006).
4.3.1.3
Epidemiological Studies
Unlike animal and clinical human exposure studies, epidemiological studies are observational by
nature, do not involve controlled measured exposures, and are susceptible to biases from
confounding variables. An important characteristic of NO2 is that it is strongly correlated with
particulate matter (PM) as both originate from the same combustion sources. NO2 is also
converted to nitrates and thus contributes to fine particle mass, making it very difficult to
differentiate the effects of NO2 from other pollutants (WHO, 2006). Another important
consideration is that epidemiological studies mainly rely on outdoor ambient monitoring data to
characterize population exposure. This is a questionable method for characterizing exposure of
individuals who spend a majority of their time indoors, exposed to indoor sources of NO2.
Despite these drawbacks, many epidemiological studies have been conducted for NO2 and have
reported associations between NO2 levels and adverse health effects (CAL/EPA, 2007).
Numerous short-term exposure, outdoor community-based studies have been conducted
worldwide and have reported associations between daily changes in NO2 concentrations and
daily counts of mortality (Ostro; Kelsall; Simpson; Toulomi; Borja Aburto; Burnett; Michelozzi;
Morgan; Fairley; Hong; Gwynn; Hoek; Lippmann; Mar; Samet; Dominici; Katsouyanni; Kwon;
Anderson; Biggeri; Roemer; Sunyer; Wong; Saez; Siteb; Le Tertre; Hong; Wong; Samoli; and
Simpson, cited in CAL/EPA, 2007). In summary, daily concentrations of NO2 were significantly
associated with increased mortality from respiratory causes, cardiovascular causes, and allcauses. Stieb and colleagues conducted a meta-analysis of 109 studies from Canada, the U.S.,
Mexico, South America, Europe, Asia, Australia and New Zealand and determined, using a
single pollutant model, that mortality from all-causes was increased by 2.8% for every 24 ppb
(45 µg m-3) increase in NO2 concentrations. Use of a multi-pollutant model, which included
particulates, carbon monoxide, ozone, and sulphur dioxide, decreased the estimate to a 0.9% for
every 24 ppb increase in NO2. This attenuation of the effect of NO2 exposure on morbidity with
the addition of PM was also observed in other studies; PM and NO2 are strongly correlated
making it difficult to separate out the independent effects of NO2 (CAL/EPA, 2007). Short-term,
community-based studies have reported associations between adult morbidity and daily changes
in NO2 concentrations (Morris; Schwartz; Burnett; Poloniecki; Anderson; Sunyer; Spix; Morgan;
Tenias; Prescott; Burnett; Atkinson; Wong; Fusco; Petroeschevsky; Mann; Koken; Oftedal;
Galan; D’Ippoliti; Tsai; Yang; Metzger; Barnett; Peel; Rich; Wellenius; and Simpson, cited in
CAL/EPA, 2007). In summary, several time-series studies associated NO2 with hospital
admissions/emergency room visits for respiratory and cardiovascular diseases, after accounting
for exposure to other pollutants. Other studies found NO2 had a reduced or insignificant effect
on morbidity after controlling for other pollutants (CAL/EPA, 2007).
The effect of daily NO2 concentrations on asthma morbidity in children has been examined in
time-series studies (Buchdahl; Median; Sunya; Morgan; Anderson; Atkinson; Hajat; Norris;
Gouveia; Fusco; Petroeschevsky; Thompson; Wong; Braga; Lee; and Lin, cited in CAL/EPA,
2007). Several studies reported a strong association between NO2 and hospital admissions or
Assessment Report on Nitrogen Dioxide for Developing Ambient Air Quality Objectives
18
emergency room visits for asthma in children, which remained after adjusting for exposure to
other pollutants. The association of NO2 with asthma morbidity in children appeared more
robust than associations with mortality or adult respiratory/cardiovascular diseases (CAL/EPA,
2007).
Field studies have been conducted on small groups of subjects to determine the effect of shortterm NO2 exposure on respiratory health, with a focus on symptoms in asthmatic children
(Segala; Roemer; van der Zee; Boezen; Linaker; Ostro; Mortimer; Delfino; Just; Schildcrout,
cited in CAL/EPA, 2007) and cardiac arrhythmias in adults (Peters; Pekkanen; Dockery, cited in
CAL/EPA, 2007). Several studies further evaluated the effect of NO2 on changes in medication
use in asthmatic children (Roemer; Segala; Schildcrout, cited in CAL/EPA, 2007) and on
changes in lung function in asthmatic children (Roemer; Segala; Boezen; van der Zee; Jalaludin;
Timonen; Delfino; Moshammer; Lagorio, cited in CAL/EPA, 2007). The majority of studies
reported an association between NO2 and the aggravation of asthma in children that was stronger
than that observed for other pollutants and remained robust to the inclusion of pollutants such as
PM, ozone, or volatile organic compounds. The available evidence also suggests an association
between NO2 and the occurrence of cardiovascular outcomes in adults (CAL/EPA, 2007).
For details on the short-term exposure epidemiological studies cited above, please refer to the
Technical Support Document for the Review of the California Ambient Air Quality Standard for
Nitrogen Dioxide (CAL/EPA, 2007).
4.3.2
Acute Toxicity in Animals
Acute exposure to NO2 produced morphological changes in the rat lung, inflammatory and
permeability changes in the lung of rats, mice, and guinea pigs, affected pulmonary function of
the guinea pig, and altered host defense of the rabbit, rat, mouse, hamster, and squirrel monkey
through interaction with infectious agents. A summary of these effects is provided below,
further study details including exposure concentration and duration and species exposed are in
Table 6.
The lowest observed adverse effect level (LOAEL) for morphological effects (increased
proliferation of bronchiolar epithelium) in the lungs of rats acutely exposed (24 h/d for 1 or 3
days) to NO2 was 0.8 ppm (1504 µg m-3) (Barth et al., cited in CAL/EPA, 2007). The same
exposure concentration (and duration) was identified as the no observed adverse effect level
(NOAEL) for increased interstitial thickness and cell infiltration in the lung (Muller et al., cited
in CAL/EPA, 2007). A NOAEL of 0.6 ppm (1130 µg m-3) was reported for morphological
effects in rats exposed for 3 hr to NO2 (Mautz et al., cited in CAL/EPA, 2007).
An increase in lung permeability, indicative of epithelial cell damage, was reported in mice,
guinea pigs, and rats acutely exposed to NO2 concentrations ranging from 0.47 to 1.0 ppm (885
to 1880 µg m-3) (Sherwin and Carlson; Selgrade et al.; Robison et al.; Hubbard et al.; Muller et
al.; Hälinen et al.; Robison and Kim, cited in CAL/EPA, 2007). The NOAEL values reported
for pulmonary inflammation in rats acutely exposed to NO2 ranged from 0.6 to 0.8 ppm (1130 to
Assessment Report on Nitrogen Dioxide for Developing Ambient Air Quality Objectives
19
Table 5
Acute Respiratory Effects Following Human Exposure to NO2: Clinical
Exposure Studies
Effects Reported
Healthy Individuals
Increased BAL neutrophils, decreased blood CD8+ and null
T lymphocytes (18 h PE). No effects on symptoms or
pulmonary function.
Increased neutrophils and interleukin-8 in bronchial wash.
Increases in specific lymphocyte subsets in BAL fluid.
Symptoms, pulmonary function not reported.
After 4 days of NO2, increased neutrophils in bronchial
wash but decreased neutrophils in bronchial biopsy. 2%
decrease in FEV1 after first exposure to NO2, attenuated
with repeated exposure. Symptoms not reported.
Increased bronchial lavage neutrophils, IL-6, IL-8, alpha1antitrypsin, and tissue plasminogen activator. Decreased
alveolar macrophage phagocytosis and superoxide
production. No effects on pulmonary function. Symptoms
not reported.
Significant reduction in cardiac output during exercise,
estimated using noninvasive impedance cardiography,
symptoms, pulmonary function not reported.
Dose-related decrease in hematocrit, hemoglobin, blood
lymphocytes, and T lymphocytes. Mild increase in
neutrophils recovered in bronchoalveolar lavage. In vitro
viral challenge of bronchial epithelial cells showed
increased cytotoxicity after 1.5 ppm NO2. No effects on
symptoms/pulmonary function.
No effects on symptoms and pulmonary function. No
change in induced sputum samples. Small decrease in
diastolic blood pressure and increase in heart rate 4 h and 22
h PE.
Changes in eicosanoids, but not inflammatory cells, in BAL
fluid. No change in lung function. Symptoms not reported.
Results diminished compared with results of 12 asthmatics
in same study.
No symptoms or pulmonary function effects for group as a
whole. Smokers showed a 2.3 % decline in FEV1 with NO2
that was statistically different from nonsmokers.
Epithelial expression of IL-5, IL-10, IL-13, and ICAM-1
increased following NO2 exposure. Symptoms, pulmonary
function not reported.
Increase in BAL mast cells and lymphocytes 4-24 h after
exposure. No change in neutrophil counts. Odor and mild
upper airway symptoms. No effects on pulmonary function.
Increased in BAL mast cells (all concentrations) and
lymphocytes (4.0 and 5.5 ppm) 24 h after exposure. No
change in neutrophil counts. Odor and throat irritation. No
Exposure
Period
6 h,
intermittent
exercise
4 h,
intermittent
exercise
4 h on 4 d,
intermittent
exercise
Air
Concentration
ppm (µ
µg m-3)
Reference
2 (3760)
Azadniv et al.
1998a
2 (3760)
Blomberg et al.
1997a
2 (3760)
Blomberg et al.
1999a
4 h,
intermittent
exercise
2 (3760)
Devlin et al.
1999a
2h,
intermittent
exercise
3 h,
intermittent
exercise
0.60 (1130)
NO2 + 0.45
ppm O3
0.6 (1130)
1.5 (2820)
Drechsler­
Parks 1995a
2 h,
intermittent
exercise
0.4 (752)
Gong et al.
2005a
3 h,
intermittent
exercise
1 (1880)
Jörres et al.
1995a
4 h,
intermittent
exercise
0.3 (560)
Morrow et al.
1992a
4 h on 4 d,
intermittent
exercise
20 m with 15
m exercise
2 (3760)
Pathmanathan
et al. 2003a
4 (7520)
Sandstrom et
al. 1990a
20 m, light
exercise
2.25 (4230)
4.0 (7520)
5.5 (10340)
Sandstrom et
al. 1991a
Assessment Report on Nitrogen Dioxide for Developing Ambient Air Quality Objectives
Frampton et al.
2002a
20
Effects Reported
Exposure
Period
Air
Concentration
ppm (µ
µg m-3)
Reference
effects on pulmonary function.
Sensitive individuals
No effect on lung function in elderly subjects with COPD.
No effects on pulmonary function in mild asthmatics
exposed to allergen. Decrease in eosinophils 6 hr PE.
No effect on pulmonary function of mild asthmatics;
decrease in FEV1 in subjects with COPD.
Increased histamine reactivity in mild asthmatics, 5 h PE.
No effect on pulmonary function.
Increased airway inflammatory response to allergen in mild
asthmatics (19 h PE). No effect on symptom or pulmonary
function.
Increased eosinophilic response to allergen in mild
asthmatics. Tendency to increased sneezing after allergen
exposure.
No airway inflammation or increase in eosinophils in mild
asthmatics in response to nasal allergen (1, 4, or 18 h PE).
No effect on specific airway conductance (SGaw), FEV1 or
reactivity to ragweed in asthmatics. Variable effect (non­
significant trend) on carbachol reactivity.
No effects on function or methacholine response in
asthmatics.
No effect on FEV1. 752 Jg/m3 increased early (P<0.009)
and late (P<0.02) response (decline in FEV1) of asthmatics
to house dust mite allergen.
Subjective symptoms not pronounced. Increased specific
Raw (SRaw) (P=0.025) and thoracic gas volume (P=0.01)
following allergen exposure of asthmatics. Lower lung
function (P=0.04) and more asthma symptoms (0.016)
during late phase.
No change in SRaw or grass pollen reactivity in three allergic
asthmatics and four allergic subjects.
Decline in SRaw over time unrelated to nitrogen dioxide.
Tendency to increased histamine reactivity in 14 out of 20
asthmatic subjects at 140 Jg m-3 only.
No effect on SRaw or thoracic gas volume or early asthmatic
reaction to birch or timothy pollen and histamine. During the
late response decreased peak expiratory flow (P=0.016) and
FEV1 (P=0.06). No effect on differential cell counts or
eosinophil cationic protein.
No effect on function in asthmatics. Enhanced early
2 h,
intermittent
exercise
3 h,
intermittent
exercise
1 h,
intermittent
exercise
0.4 (752)
Gong et al.
2005a
0.4 (752)
Solomon et al.,
2004a
0.3 (560)
Vagaggini et
al., 1996a
0.26 (488)
Strand et al.,
1996a
0.26 (488)
Barck et al.
2002a
15 min on day 0.26 (488)
1 and 2 sets of
15 min on day
2.
30 min
0.26 (488)
Barck et al.
2005a
30 min,
intermittent
exercise
30 min
Barck et al.
2005ba
Ahmed et al.
1983a; 1983bb
1h
0.1 (188)
1h
0.1 (188)
1h
0.1 (188)
0.4 (752)
Hazucha et al.
1982; 1983b
Tunnicliffe et
al. 1994b
30 m
0.11-0.25
(207-462)
Svartengren et
al. 2000b
1h
0.11 (207)
30 m
30 m
0.14 (260)
0.27 (500)
0.54 (1015)
0.26 (488)
Orehek et al.
1981b
Bylin et al.
1988b
30 m
0.27 (500)
Assessment Report on Nitrogen Dioxide for Developing Ambient Air Quality Objectives
Strand et al.
1997b
Strand et al.
21
Effects Reported
Exposure
Period
Air
Concentration
ppm (µ
µg m-3)
1998b
(P=0.02) and late (P=0.01) airway response (decline in
FEV1) to birch and grass pollen. Tendency towards
increased night-time symptoms after nitrogen dioxide and
allergen (P=0.07).
No significant effects on SRaw in asthmatics. Possible
increased cold air response at 560 Jg m-3 only.
At 60 min, decreased in FEV1, FVC and peak expiratory
flow in asthmatics. Increase in SRaw. No change in cold air
response. No effect after 2.5 hours’ exposure.
No effect at rest. Nitrogen dioxide increased cold air
response of asthmatics.
No effects on function or reactivity to cold air in asthmatics.
Decreased FEV1 in asthmatics after first 10 min of exercise;
smaller change later. No effect on FEV1 or SRaw. No change
in methacholine reactivity 2 hours after exposure.
Reference
2 h (1 h
exercise at 40­
41 litres/min)
2.5 h (1.5 h
exercise at 30
litres/min)
0.5 h (10 min
exercise at 30
litres/min)
1 h (30 min
exercise at 41
litres/min
110 min
(1 h exercise
at 42 L/min)
75 min
(30 min
exercise at 42
L/min)
No effect on SRaw symptoms in asthmatics, heart rate or skin 75 min (15
conductance. Small decrease in systolic blood pressure.
min exercise
at 25 or 49
litres/min)
225 min (21
Decreased FVC (after exposure) and FEV1 (> 4 hr PE) in
individuals with COPD.
min exercise
at 25
litres/min)
4 h (exercise)
Progressive decrements in FVC and FEV1 in individuals
with COPD. Subgroup analyses suggested responsiveness
decreased with severity of COPD.
No change in spirometry of COPD subjects. SRaw tended to 1 h (30 min
increase after the first exercise period. No symptom change. exercise at 16
No change in arterial oxygen saturation.
litres/min)
0.3 (560)
0.6 (1130)
Avol et al.
1988b
0.3 (560)
Avol et al.
1989b
0.3 (560)
Bauer et al.
1986b
0.3 (560)
1.0 (1880)
3.0 (5640)
0.3 (560)
0.15 (282)
0.30 (560)
0.60 (1130)
Linn et al.
1986b
Roger et al.
1990b
4.0 (7520)
Linn &
Hackney 1984b
0.3 (560)
Morrow &
Utell 1989b
0.3 (560)
Morrow et al.
1992b
0.5 (940)
1.0 (1880)
2.0 (3760)
Linn et al.
1985b
Decreased earlobe oxygen tension in COPD patients above
7520 Jg m-3. Increased Raw above 3000 Jg m-3.
15 min
0.5-5 (940­
9400)
Von Nieding et
al. 1970; 1971b
Increased Raw in COPD subjects above 2820 Jg m-3.
Decreased earlobe oxygen tension.
30 breaths (15
min)
1h
5-60 min
1-5 (1880­
9400)
5 (9400)
1-8
(1880-15040)
Von Nieding et
al. 1973b
At 7520-9400 Jg/m3 for 15 min, decreased arterial oxygen
pressure in COPD patients. At 2 3000 Jg/m3, increased
Raw.
a
Cited in CAL/EPA, 2007
b
Cited in WHO, 2006
Assessment Report on Nitrogen Dioxide for Developing Ambient Air Quality Objectives
Von Nieding &
Wagner 1979b
22
1504 µg m-3) (Barth et al.; Mautz et al., cited in CAL/EPA, 2007). Bronchoconstriction was
induced in guinea pigs exposed for 1 hour to 1.0 ppm (1880 µg m-3) NO2 combined with 10
minutes to cold dry air; this response was not observed in the same species of guinea pig
simultaneously exposed to 1.0 ppm NO2 with cold or warm air for 1 hour, likely due to adaptive
mechanisms against prolonged bronchoconstriction (Hälinen et al., cited in CAL/EPA, 2007).
An increase in alveolar clearance of the rabbit lung was induced by acute exposure to NO2
concentrations ranging from 0.3 to 1.0 ppm (560 to 1880 µg m-3) (Vollmuth et al., cited in
CAL/EPA, 2007; Schlesinger & Gearhart, cited in IPCS, 1997). Acute exposure to 1.0 ppm
(1880 µg m-3) NO2 increased mucociliary clearance in mice (Davis et al., cited in CAL/EPA,
2007). Adverse effects on alveolar macrophages (structural, biochemical and functional) in
exposed rabbits, rats, and mice were reported following acute exposure to NO2 concentrations
ranging from 0.3 to 5.0 ppm (560 to 9400 µg m-3) (Schlesinger and Robison et al., cited in
CAL/EPA, 2007; Hooftman et al.; Suzuki et al.; Lefkowitz et al., cited in IPCS, 1997). Alveolar
macrophages and the alveolar/mucociliary clearance processes play important roles in the
clearance of inhaled debris and particles from the lung (CAL/EPA, 2007).
Numerous studies have reported adverse effects on host defense as a result of the interaction of
NO2 with infectious microorganisms, including increased infection, impaired immune response,
and/or increased mortality (CAL/EPA, 2007). A LOAEL of 10 ppm (18800 µg m-3) NO2 was
reported for acute host defense effects in mice infected with A/PR/8 virus (Ito, cited in IPCS,
1997). In mice infected with Mycoplasma pulmonis and acutely exposed to NO2, a LOAEL
value of 5 ppm (9400 µg m-3) NO2 (Parker et al., cited in IPCS, 1997) and a NOAEL value of 1.0
ppm (1880 µg m-3) NO2 (Nisizawa et al.; Davis et al., cited in CAL/EPA, 2007) was reported for
effects on host defense. No adverse effects on host defense were reported in mice infected with
cytomegalovirus following intermittent, acute exposure to 1.0 ppm (1880 µg m-3) NO2 (Rose et
al., cited in CAL/EPA, 2007). In mice infected with Streptococcus and acutely exposed to NO2,
LOAEL values ranging from 1 to 4.5 ppm (1880 to 8460 µg m-3) NO2 (Gardner; Gardner et al.;
Graham et al.; Illing et al.; Ehrlich et al.; Ehrlich; Sherwood et al., cited in IPCS, 1997) and a
NOAEL of 0.1 ppm (188 µg m-3) NO2 (Gardner; Gardner et al.; Graham et al., cited in IPCS,
1997) was reported for effects on host defense. Adverse effects on host defense in mice,
hamsters, and squirrel monkeys infected with Klebsiella pneumoniae were reported following 2
hours exposure to 3.5 ppm (6580 µg m-3) NO2 (Purvis and Ehrlich; Ehrlich, cited in IPCS, 1997).
In mice infected with Staphylococcus aureus and acutely exposed to NO2, LOAEL values
ranging from 1 to 2.5 ppm (1880 to 4700 µg m-3) NO2 (Goldstein et al.; Jakab, cited in IPCS,
1997) and a NOAEL of 1 ppm (1880 µg m-3) NO2 (Jakab, cited in IPCS, 1997) were reported for
effects on host defense.
Additional acute effects of nitrogen dioxide (not in the table) include alterations in lung
biochemistry and in the immune response of animals sensitized to allergens. Changes observed
in lung metabolism include the levels and activity of antioxidants and enzymes associated with
cell injury. Biochemical changes occurring in the lung following acute exposure to NO2 were
often manifested at higher concentrations and can indicate mechanisms of toxic action or
protection and repair. Cellular injury (as measured by extracellular lactose dehydrogenase)
following acute in vitro exposure was observed in alveolar macrophage (AM) exposed to 20 ppm
NO2 but not in AM exposed to 1 ppm NO2 (Robison et al., Robison and Forman, cited in
Assessment Report on Nitrogen Dioxide for Developing Ambient Air Quality Objectives
23
Table 6
Acute Respiratory Effects Following Animal Exposure to NO2
Effect
Morphological
focal lung lesions; increased
number of nuclei in walls of
alveolar ducts and septae in
centriacinar units of lung
interstitial thickness;
mononuclear cell infiltration in
central acini
Increased proliferation of
bronchiolar epithelium
Centriacinar region: edema,
inflammatory cells, plasma
protein accumulation, sloughed
epithelial cells
Increased active ion transport
across tracheobronchial
epithelial monolayers
Change in transepithelial
resistance (fluid leakage)
Pulmonary function
Bronchoconstriction
Bronchoconstriction
Species
Reference1
3 hr
(with exercise)
NOAEL = 0.6 (1130)
Rat, male
Sprague-Dawley
Mautz et al.,
1988
1 or 3 d,
24 hr/d
NOAEL = 0.8 (1504)
Rat, male
Sprague-Dawley
Muller et al.,
1994
1 or 3 d,
24 hr/d
LOAEL = 0.8 (1504)
Rat, male
Sprague-Dawley
Barth et al., 1994
LOAEL = 0.4 (752)
Guinea pig, male
White, short-hair
Mouse, male
Inflammation and Lung Permeability Changes
Increased protein content of lung 7 d, 24 h/d
Changes in BAL fluid cell
number/type
Air Concentration
ppm (µ
µg m-3)
Exposure
Period
NOAEL = 0.4 (752)
LOAEL = 1.0 (1880)
NOAEL = 0.5 (940)
Guinea Pig, male
Hartley COBS
Rat, male
Sprague-Dawley
Sherwin and
Carlson, 1973
Sherwin and
Layfield, 1976
Selgrade et al.,
1981
Robison et al.,
1993
NOAEL = 0.7 (1316)
Mouse, male
C57BL/6
Rat, male
Sprague-Dawley
Guinea pig, male
Dunkin-Hartley
Hubbard et al.,
2002
Muller et al.,
1994
Hälinen et al.,
2000
Rat, male
Sprague-Dawley
Rat, male
Sprague-Dawley
Barth et al.,1994
NOAEL = 0.5 (940)
LOAEL = 1 (1880)
Guinea Pig, male
Hartley
Robison and
Kim, 1995
1 or 4 hr
(in vitro)
NOAEL = 1 (1880)
Guinea Pig, male
Hartley
Robison and
Kim, 1995
1 hr
(with 10 min
exp to cold air)
LOAEL = 1 (1880)
Guinea pig, male
Dunkin-Hartley
Hälinen et al.,
2000a
1 hr
(with 60 min
exp to cold or
warm air)
NOAEL = 1 (1880)
Guinea pig, male
Dunkin-Hartley
Hälinen et al.,
2000b
10, 12, or 14 d,
24 hr/d
24 h/d
for 3 or 7 d
4 or 8 hr/d, 5
d/wk for
5 or 10 d
2 hr
LOAEL = 0.47 (884)
24 hr/d
for 1 or 3 d
1 hr
(combined with
cold (-30ºC)
air)
24 h/d
for 1 or 3 d
3 hr with
exercise
NOAEL = 0.8 (1504)
1 or 4 hr
(in vitro)
LOAEL = 1.0 (1660)
(
AM/PMN ratio)
NOAEL = 0.8 (1504)
NOAEL = 0.6 (1130)
Assessment Report on Nitrogen Dioxide for Developing Ambient Air Quality Objectives
Mautz et al.,
1988
24
Exposure
Period
Effect
Host Defense
Increased clearance
2 hr
Reference1
Rabbit, male
New Zealand
Mouse
C57BL/6N
Vollmuth et al.,
1986
Davis et al., 1991
2 hr/d, 14 d
Rabbit, male
New Zealand
Rabbit
2 hr/d, 2d
LOAEL = 0.3 (560)
4 or 8 hr
LOAEL = 0.5 (940)
(ex vivo response)
LOAEL = 0.5 (940)
(ex vivo response)
LOAEL = 4 (7520)
Rabbit, male
New Zealand
Rat, male
Sprague-Dawley
Rat, male
Sprague-Dawley
Rat
Vollmuth et al.,
1986
Schlesinger &
Gearhart, 1987a
Schlesinger, 1987
LOAEL = 4 (7520)
Rat
7d
NOAEL = 5 (9400)
(phagocytosis)
Mouse
4 hr
NOAEL = 1 (1880)
(M. pulmonis)
Mouse
C57/BL/6N
Davis et al., 1991
24 h/d
for 7 or 14d
NOAEL = 1 (1880)
(M. pulmonis)
Mouse, female
SPF ddY
Nisizawa et al.
1988
4h
LOAEL = 5 (9400)
(M. pulmonis)
Mouse
Parker et al.,
1989a
6 hr/d, 6d
NOAEL = 1 (1880)
(cytomegalovirus)
Mouse
CD-1
Rose et al., 1989
2 h/d for 1, 3,
and 5 d
LOAEL = 1 (1880)
(A/PR/8 virus)
Mouse, female
Ito, 1971a
1, 3.5, or 7 h
LOAEL = 4.5 (8460)
(Streptococcus)
Mouse
3h
(with exercise)
3h
LOAEL = 3 (5640)
(Streptococcus)
LOAEL = 2 (3760)
(Streptococcus)
Mouse
48 h
LOAEL = 1 (1880)
(Streptococcus)
LOAEL = 1.5 (2820)
(Streptococcus)
LOAEL = 1.5 (2820)
(Streptococcus)
Mouse
Gardner, 1980;
Gardner et al.,
1982; Graham et
al., 1987a
Illing et al.,
1980a
Ehrlich et al.,
1977; Ehrlich,
1980a
Sherwood et al.,
1981a
Gardner et al.,
1982a
Gardner et al.,
1979a
2 hr/d, 14 d
8 hr/d, 5 d/wk,
for 5 or 10 d
6 h/d for 7, 14,
or 21 d
Up to 10 d
Interaction with infectious
agents: increased infection;
impaired response; mortality
from infection
Species
LOAEL = 0.3 (560)
(alveolar)
NOAEL = 0.5 (940)
LOAEL = 1 (1880)
(mucociliary)
LOAEL = 1 (1880)
(alveolar)
LOAEL = 0.3 (560)
4 hr
Structural, biochemical, and
functional changes in alveolar
macrophage
Air Concentration
ppm (µ
µg m-3)
7 h/d for 7 d
24 h/d for 1 wk
or
Mouse
Mouse
Mouse
Assessment Report on Nitrogen Dioxide for Developing Ambient Air Quality Objectives
Robison et al.,
1993
Robison et al.,
1993
Hooftman et al.,
1988a
Suzuki et al.,
1986a
Lefkowitz et al.,
1986a
25
Exposure
Period
Effect
7 h/d for 2 wk
1.5 ppm, 60 h
with 1 peak of
4.5 ppm for 3.5,
or 7 h followed
by 1.5 ppm for
18h
0.05-0.5 ppm
daily with two
1 hr peaks to
0.1-1ppm; 5
d/wk, 15 d
2h
a
Species
Reference1
LOAEL = 1.5-4.5
(2820-8460)
(Streptococcus)
Mouse
Gardner, 1980;
Gardner et al.,
1982; Graham et
al., 1987a
NOAEL = 0.05-0.1
(94-188)
LOAEL = 0.5-1.0
(940-1880)
(Streptococcus)
LOAEL = 3.5 (6580)
(K. pneumoniae)
Mouse
Gardner, 1980;
Gardner et al.,
1982; Graham et
al., 1987a
Mouse
Purvis and
Ehrlich, 1966;
Ehrlich, 1979a
2h
LOAEL = 3.5 (6580)
(K. pneumoniae)
Mouse, Hamster,
Squirrel monkey
Ehrlich, 1975a
17 h
NOAEL = 1.0 (1880)
LOAEL = 2.3 (4324)
(Staphylococcus
aureus)
LOAEL = 1.0-2.5
(1880-4700)
(Staphylococcus
aureus)
Mouse
Goldstein et al.,
1974a
Mouse
Jakab, 1988a
4h
1
Air Concentration
ppm (µ
µg m-3)
cited in CAL/EPA, 2007 unless otherwise noted
cited in IPCS, 1997
CAL/EPA, 2007). The inhibition of the membrane bound enzyme Na, K-adenosine
triphosphatase following in vitro NO2 exposure (1 ppm) of guinea pig tracheobronchial epithelial
monolayers was associated with oxidative stress (Robson and Kim, cited in CAL/EOA, 2007).
At high air concentrations (>3 ppm), NO2 was demonstrated to interact with lung surfactants
(proteins and phospholipids) overlying the alveolar epithelium, resulting in impaired lung surface
tension which could impair lung function; however, these responses were not observed at lower
concentrations (0.8 ppm) which better reflect ambient concentrations (Muller et al., cited in
CAL/EPA, 2007). The production of toxic aldehydes following oxidation of cellular membranes
(polyunsaturated fatty acids) by NO2 (0.5 to 1 ppm) was demonstrated following in vitro
exposure of rat AM and pig airway epithelial monolayers. In the case of AM, the release of
aldehydes was correlated to a loss of essential function (Robison et al., cited in CAL/EPA,
2007).
Subtle effects on the lung which could impair lung development and growth have been reported
following exposure to NO2. Increased lung collagen synthesis in the developing lung of the
ferret was observed following acute exposure to high NO2 air concentrations (10 ppm or 18800
µg m-3) but not at lower air concentrations (0.5 ppm or 940 µg m-3) (Rasmussen and McClure,
cited in CAL/EPA, 2007). Intermittent exposure for 6 weeks to 0.25 ppm NO2 produced changes
Assessment Report on Nitrogen Dioxide for Developing Ambient Air Quality Objectives
26
in the elastin content of alveolar tissue in the developing mouse lung (Sherwin and Richters,
cited in CAL/EPA, 2007).
Studies involving the exposure of allergen-sensitized animal models to NO2 have been conducted
to determine the effect of NO2 on sensitive human asthmatics (CAL/EPA, 2007). Intermittent
exposure to 5 ppm (9400 µg m-3) NO2 for 6 weeks enhanced the allergenic respiratory disease of
guinea pigs sensitized to Candida albicans (Kitabatake et al., 1995). Intermittent exposure to 6
ppm (11280 µg m-3) NO2 for 13 days increased tracheal epithelium injury in guinea pigs
sensitized by anti-benzylpenicilloil bovine gamma globulin guinea pig serum (Ohashi et al., cited
in CA/EPA, 2007). Acute intermittent NO2 exposure to 0.7, 2.0, or 5 ppm (1316, 3760, or 9400
µg m-3) did not enhance the effect of ovalbumin (OVA) sensitization of mice with allergic
airway disease (i.e., pre-exposed to OVA) (Poynter et al.; Hussain et al., cited in CAL.EPA,
2007), or result in an attenuation of OVA-induced effects (Hubbard et al.; Proust et al., cited in
CAL/EPA, 2007), which was contrary to observations made in humans. The contrasting results
may be due to a wider range of risk factors in clinical studies (including multiple pollutants and
respiratory tract infections), variations in the timing of NO2 and OVA exposures, and/or the
developmental stage at the time of exposure (Hubbard et al., CAL/EPA, 2007). Exposure to
NO2 may also reduce the ability of AM to respond to allergens (Proust et al., cited in CAL/EPA,
2007).
Fujimaki et al. (cited in CAL/EPA, 2007) studied the pulmonary immune response (production
of antibodies and cytokines in BAL fluid) of mice continuously exposed to 0.5 or 1.0 ppm (940
or 1880 µg m-3) NO2 for 12 weeks and intermittently exposed to OVA at 3 week intervals. Prior
to NO2 exposure, half of the mice were pre-immunized with OVA. Antibody and cytokine
production were suppressed in mice not pre-immunized to OVA and exposed to 1.0 ppm (1880
µg m-3) NO2 and ovalbumin over the 12 week period. These results suggest the timing of NO2
and OVA exposures affects the response of the antigen-specific immune system (CAL/EPA,
2007). No effect on the allergic immune response (serum IgE levels) of mice sensitized to 2,4­
dinitrochlorobenzene was observed following induction of oxidative stress by acute NO2
inhalation (5-6 ppm for 2 weeks) (Mi et al., cited in CAL/EPA, 2007). Acute in vitro exposure
to NO2 did not affect the response of bronchial smooth muscle isolated from allergic guinea pigs
(Chitano et al., cited in CAL/EPA, 2007). Mi and colleagues observed the effects of NO2
inhalation (5-6 ppm for 2 weeks) on the allergic immune response of mice sensitized to 2,4­
dinitrochlorobenzene or trimellitic anhydride (TMA) with or without oxidative stress induced by
Vitamin E deficiency. Acute NO2 exposure increased the allergic response (increased serum IgE
levels) of TMA-sensitized mice with or without Vitamin E deficiency (CAL/EPA, 2007). An
increase in the allergic immune response of Brown Norway rats sensitized to house dust mite
allergen was reported following 3-hours exposure to 5 ppm (9400 µg m-3) NO2 (Gilmour et al.,
cited in CAL/EPA, 2007).
4.4
Subchronic and Chronic Toxicity
The toxicity of NO2 following subchronic and chronic exposure of humans and animals is
discussed below. Subchronic and chronic toxicity refers to the adverse effects occurring
Assessment Report on Nitrogen Dioxide for Developing Ambient Air Quality Objectives
27
following mid- to long-term exposures, which in the current assessment ranged from 6 weeks to
over 10 years.
4.4.1
Subchronic and Chronic Toxicity in Humans
Epidemiological studies have attempted to characterize the effects of chronic human exposure to
NO2. As mentioned previously, epidemiological studies are observational by nature, do not
involve controlled measured exposures, and are susceptible to biases from confounding
variables. In particular, NO2 is strongly correlated with PM making it difficult to differentiate
the effects of NO2 from other pollutants in epidemiological studies (WHO, 2006). The majority
of epidemiological studies rely on outdoor ambient monitoring data to characterize population
exposure, which is likely inadequate for individuals who spend the majority of their time
indoors, potentially exposed to indoor sources of NO2. In addition, the mobility of populations
over time and variability in the methodologies used in the collection of outdoor ambient air data
over the long-term introduce further uncertainty to the characterization of long-term exposures
(CAL/EPA, 2007). Informative and recently conducted studies of chronic NO2 exposure were
selected for review by the California EPA, a brief summary of their findings is provided below.
Several studies investigated the association of chronic NO2 exposure to the incidence and
prevalence of asthma, respiratory diseases and lung function in children (Dockery; BraunFahrländer; Studnika; Peters; McConnell, cited in CAL/EAP, 2007). Studies conducted by
Peters and McConnell on the southern California cohort reported positive associations between
outdoor NO2 concentrations and the incidence of bronchitic symptoms in asthmatic children
playing team sports and in deficits in lung function growth (a serious risk factor for chronic
disease and early mortality) in children over an 8-year period. Studies conducted in Europe
associated allergic sensitization in children with exposure to traffic-related pollutants, including
NO2 (CAL/EPA, 2007).
Using data collected by Dockery and colleagues in the Harvard Six Cities study, which assessed
all-cause mortality over a 14-16 year exposure period, Krewski et al. reported an association
between NO2 exposure and increased mortality (all-causes and cardiopulmonary-related);
however, multi-pollutant models were not used in this assessment and NO2 was highly correlated
with other air pollutants (PM, TSP, and sulphur dioxide) limiting a direct association with
exposure to NO2 alone (CAL/EPA, 2007). European studies have also associated all-causes and
cardiopulmonary-related mortality with exposure to traffic-related pollutants, including but not
limited to NO2 (Hoek et al.; Nafstad et al.; and Gehring, cited in CAL/EPA, 2007). A study by
the American Cancer Society found no association between NO2 exposure and increased
mortality (all-cause, cardiopulmonary- related, lung cancer) (Pope et al., cited in CAL/EPA,
2007).
Further details on the chronic exposure epidemiological studies cited above are available in the
Technical Support Document for the Review of the California Ambient Air Quality Standard for
Nitrogen Dioxide (CAL/EPA, 2007).
Assessment Report on Nitrogen Dioxide for Developing Ambient Air Quality Objectives
28
4.4.2
Subchronic and Chronic Toxicity in Animals
Effects reported following subchronic and chronic exposures to NO2 are similar to those reported
following acute exposures (inflammation, changes in morphology, and altered host defense). In
addition, effects on pulmonary function have been reported as a result of subchronic and chronic
exposure to NO2. A summary of these effects is provided below, further study details including
exposure concentration and duration and species exposed are in Table 7.
Subchronic or chronic exposures of rats to 0.4 or 0.5 ppm (752 to 954 µg m-3) NO2 produced
morphological changes in the lung, including increased thickness of pleura, alveolar or septal
wall, epithelial and alveolar cell hyperplasia and hypertrophy, and interstitial edema (Hayashi et
al.; Mercer et al.; Ichinose et al.; Tepper et al.; and Kubota et al., cited in CAL/EPA, 2007).
Two of these studies (Mercer et al. and Tepper et al.) included intermittent (1-2) peak exposures
to 1.0 or 1.5 ppm (1880 or 2820 µg m-3) for 1 or 2 hours (CAL/EPA, 2007). In mice, subchronic
to chronic exposure to NO2 produced alveolar cell hyperplasia (0.25 to 0.30 ppm or 470 to 560
µg m-3) (Sherwin and Richters, cited in CAL/EPA, 2007), microthrombus formation in lung
capillary endothelium (0.35 ppm or 658 µg m-3) (Richters and Richters, cited in CAL/EPA,
2007), and structural changes in the alveolar macrophage (0.5 ppm NO2 plus a 2 hour peak
exposure to 1.0 ppm NO2) (Aranyi et al., cited in IPCS, 1997).
Exposure of ferrets to 0.5 ppm (940 µg m-3) NO2 for 15 weeks produced morphological effects in
the lung (increased septal wall thickness), increased inflammatory and necrotic cells in the lung,
and increased particle clearance (Rasmussen and McClure; Rasmussen et al., cited in CAL/EPA,
2007). No alterations in AM (biochemical effects) were reported for rats continuously exposed
for 12 weeks to 0.4 ppm (752 µg m-3) NO2 (Mochitate et al., cited in CAL/EPA, 2007).
The interaction of NO2 exposure and infectious microorganisms was reported in several
subchronic and chronic exposure studies in mice and guinea pigs (CAL/EPA, 2007). A/PR/8
virus infection in mice was not increased by continuous exposure 0.3 ppm (560 µg m-3) NO2 for
6 months (Motomiya et al., cited in IPCS, 1997) but was increased by continuous exposure to 0.5
to 1.0 ppm (940 to 1880 µg m-3) NO2 for 39 days (Ito, cited in IPCS, 1997). No adverse effects
were reported in mice infected with M. pulmonis and continuously exposed to 1.0 ppm (1880 µg
m-3) NO2 for up to 28 days (Nisizawa et al., cited in CAL/EPA, 2007). An increase in mortality
was reported in mice infected with streptococcus and chronically exposed to NO2 concentrations
ranging from 0.2 to 0.8 ppm (376 to 1504 µg m-3) (Miller et al.; Ehrlich et al., cited in
CAL/EPA, 2007) and in mice infected with K. pneumoniae and chronically exposed for 0.5 ppm
(940 µg m-3) NO2 (Ehrlich and Henry, cited in CAL/EPA, 2007). An increase in mortality was
also reported following chronic exposure of guinea pigs infected with K. pneumoniae to NO2 (1
ppm or 1880 µg m-3) (Kosmider et al., cited in IPCS, 1997).
Subchronic to chronic exposure of mice to 0.25 to 0.5 ppm (470 to 940 µg m-3) NO2 was reported
to suppress the cell-mediated immune response (decreased splenic lymphocytes) (Richters and
Damji; Kuraitis and Richters; Maigaetter et al., cited in CAL/EPA, 2007) while subchronic
exposure of mice to 0.4 ppm (752 µg m-3) NO2 suppressed the humoral immune system (splenic
primary antibody response) (Fujimaki et al., cited in CAL/EPA, 2007). In rats, no adverse effect
Assessment Report on Nitrogen Dioxide for Developing Ambient Air Quality Objectives
29
on cell-mediated immunity was reported following chronic exposure to 0.5 ppm (940 µg m-3)
with a two hour weekly peak exposure to 1.5 ppm (2820 µg m-3) (Selgrade et al., cited in
CAL/EPA, 2007).
Pulmonary function effects of subchronic to chronic exposure of rodents to NO2 include
alterations in bronchial responsiveness, vital capacity, and lung volume (CAL/EPA, 2007). In
guinea pigs continuously exposed for 12 weeks to 1 ppm (1880 µg m-3) NO2, bronchial
hyperresponsiveness to histamine was increased, whereas pulmonary specific airway resistance
was not affected (Kobayashi and Miura, cited in CAL/EPA, 2007). A decrease in the lung vital
capacity of mice was reported following exposure to 0.2 ppm (376 µg m-3) NO2 (5 days/week)
with intermittent peak exposures (2 hours/day) to 0.8 ppm (1504 µg m-3) NO2 over the period of
a year (Miller et al., cited in CAL/EPA, 2007). A LOAEL of 0.5 ppm (940 µg m-3) was reported
for adverse effects on lung volume following subchronic exposure (4 hours/day, 5 days/week for
15 weeks) of ferrets to NO2 (Rasmussen and McClure, cited in CAL/EPA, 2007). NOAEL
values ranging from 0.25 to 1.5 ppm (470 to 2820 µg m-3) were reported for lung volume effects
in mice and rats following subchronic and chronic exposure to NO2 (Sherwin and Richters;
Tepper et al., cited in CAL/EPA, 2007).
Table 7
Subchronic/Chronic Respiratory Effects Following Animal Exposure to NO2
Effect
Morphological Effects
Increased alveolar wall thickness
Increased septal wall thickness
Structural changes in alveolar
macrophage
Fibrous thickening of pleura
Alveolar or bronchiolar epithelial
cell hyperplasia
Histopathological changes in
epithelial cell make-up and
characteristics in proximal alveolar
Exposure Period
Air
Concentration
ppm (µ
µg m-3)
9, 18, or 27 mo,
24 hr/d
NOAEL = 0.04 (75)
LOAEL = 0.4 (752)
Rat, male
Sprague­
Dawley
Kubota et al.,
1987
24 h/d, 6 mo
LOAEL = 0.5 (940)
Rat
Wistar
Hayashi et al.,
1987
4 hr/d, 5 d/wk,
15 wks
LOAEL = 0.5 (940)
Ferret
Rasmussen and
McClure, 1992
0.5 ppm daily with
two 1 hr peaks to
1.5 ppm; 7 d/wk,
9 wks
0.5 ppm daily with
one 2 hr peak to
1.0 ppm; 5 d/wk,
24 wk
24 h/d, 19 mo
NOAEL = 0.5-1.5
(940-2820)
Rat, male
Fischer 344
Mercer et al., 1995
NOAEL = 0.5-1.0
(940-1880)
(morphology)
Mouse
Aranyi et al.,
1976a
LOAEL = 0.5 (940)
Rat
Wistar
Rat, male
Wistar
Rat, male
Fischer 344
Hayashi et al.,
1987
Ichinose et al.,
1991
Tepper et al., 1993
17 mo, continuous NOAEL = 0.4 (752)
0.5 ppm daily with NOAEL = 0.5-1.5
one 2 hr peak to
(940-2820)
1.5 ppm; 5 d/wk,
Species
Assessment Report on Nitrogen Dioxide for Developing Ambient Air Quality Objectives
Reference1
30
Effect
region
Type II alveolar cell hyperplasia
and hypertrophy (32 wks PE)
Type II alveolar cell hypertrophy
(4 mo PE)
Type II alveolar cell hyperplasia
(immediately PE)
Exposure Period
1, 3, 13, 52, or 78
wks
7 hr/d, 5 d/wk,
6 wks
24 h/d, 4 mo
6 hr/d, 5 d/wk,
6 wks
(begun last wk of
gestation)
Microthrombus formation in lung
7 hr/d, 5 d/wk,
capillary endothelium
6 wks
Pinocytotic vesicles in the capillary 24 h/d, 2 to 4 mo
endothelial cells followed by
interstitial edema in the alveolar
wall
interstitial edema in the alveolar
24 h/d, 12 mo
wall
Inflammation and Lung Permeability Changes
Increased inflammatory and
4 hr/d, 5 d/wk,
necrotic cells in alveolar lumen 15 wks
and interstitium
Host Defense
Increased clearance
Structural, biochemical, and
functional changes in alveolar
macrophage
Interaction with infectious
agents: increased infection;
mortality from infection
4 hr/d, 5 d/wk
for 8 or 15 wks
24 hr/d, 12 wks
24 h/d, 6 mo
24 h/d for 39 d
0.2 ppm daily with
two 1 hr peaks to 0.8
ppm;
5 d/wk, 1 yr
3 hr/d, 5 d/wk for 3
or 6 mo
(base exposure of 0.1
ppm)
6, 18, or 24 hr/d, 7
d/wk, for 6 or 12 mo
6 mo
Air
Concentration
ppm (µ
µg m-3)
Species
Reference1
LOAEL = 0.25 (470)
Mouse, male
Swiss Webster
Sherwin and
Richters, 1995
LOAEL = 0.5 (940)
Rat
Wistar
Mouse, male
Swiss Webster
Hayashi et al.,
1987
Sherwin and
Richters, 1995
Mouse, male
C57BL/6J
Rat
Wistar
Richters and
Richters, 1989
Hayashi et al.,
1987
LOAEL = 0.5 (940)
Rat
Wistar
Hayashi et al.,
1987
LOAEL = 0.5 (940)
Ferret
Rasmussen and
McClure, 1992
LOAEL = 0.3 (560)
LOAEL = 0.35 (658)
LOAEL = 0.5 (940)
NOAEL = 0.5 (940)
(thoracic and head
airways)
NOAEL = 0.4 (752)
(biochemical)
Ferret
Rasmussen et al.,
1994
Rat, male
Jcl: Wistar
Mochitate et al.,
1992
NOAEL = 0.3 (560)
(A/PR/8 virus)
LOAEL = 0.5-1.0
(940-1880)
(A/PR/8 virus)
LOAEL = 0.2-0.8
(376-1504)
(Streptococcus)
Mouse
Motomiya et al.,
1973a
Ito, 1971a
Mouse, female
Mouse, female
CD-1
Miller et al., 1987
Mouse, female
CD2F1
Ehrlich et al., 1979
LOAEL = 0.5 (940) Mouse, female
(K. pneumoniae)
Swiss Albino
LOAEL = 1.0 (1880) Guinea-pig
(K. pneumoniae)
Ehrlich and Henry,
1968
Kosmider et al.,
1973a
LOAEL = 0.5 (940)
(Streptococcus)
Assessment Report on Nitrogen Dioxide for Developing Ambient Air Quality Objectives
31
Effect
Cell-mediated immunity
(decreased splenic lymphocyte
response)
Exposure Period
24 hr/d
for 21 or 28 d
7 hr/d, 5 d/wk, 181 d
8 hr/d, 5 d/wk,
12 or 16 wk
7 h/d, 5 d/wk, 7wk
7 h/d, 5 d/wk, 12 wk
24 h/d, 3 to 12 mo
Humoral immunity (splenic
primary antibody response)
24 h/d, 5 d/wk,
0.5 ppm daily with
one 2 hr peak
to 1.5 ppm each wk
24 h/d, 4 wk
Air
Concentration
Species
ppm (µ
µg m-3)
NOAEL = 1.0 (1880) Mouse, female
(M. pulmonis)
SPF ddY
LOAEL = 0.25 (470) Mouse, female
AKR/cum
LOAEL = 0.25-0.35 Mouse, male
(470-658)
C57BL/6J
LOAEL = 0.25 (470) Mouse, female
AKR/cum
LOAEL = 0.35 (658) Mouse, male
C57BL/6j
LOAEL = 0.5 (940) Mouse, male
CD-1
NOAEL = 0.5-1.5
Rat, male
(940-2820)
Fisher 344
Reference1
Nisizawa et al.
1988
Richters and Damji,
1990
Kuraitis and
Richters, 1989
Richters and Damji,
1988
Richters and Damji,
1988
Maigaetter et al.,
1978
Selgrade et al.,
1991
LOAEL = 0.4 (752)
Mouse, male
BALB/c
Fujimaki et al.,
1982
24 hr/d, 6 or 12 wks
NOAEL = 1 (1880)
Kobayashi and
Mura, 1995
Airway responsiveness
(histamine challenge)
24 hr/d, 12 wks
LOAEL = 1 (1880)
Decreased vital capacity
0.2 ppm daily with
two 1 hr peaks to 0.8
ppm;
5 d/wk, 1 yr
7 hr/d, 5 d/wk,
6 wks
4 hr/d, 5 d/wk,
15 wks
0.5 ppm daily with
one 2 hr peak to 1.5
ppm; 5 d/wk, 1, 3,
13, 52, or 78 wks
LOAEL = 0.2-0.8
(376-1504)
Guinea Pig,
male
Hartley
Guinea Pig,
male
Hartley
Mouse, female
CD-1
Pulmonary function
Pulmonary specific airway
resistance (sRAW)
Lung volume
NOAEL = 0.25 (470) Mouse, male
(up to 32 wks PE)
Swiss Webster
LOAEL = 0.5 (940) Ferret
NOAEL = 0.5-1.5
(940-2820)
Rat, male
Fischer 344
Kobayashi and
Mura, 1995
Miller et al., 1987
Sherwin and
Richters, 1995
Rasmussen and
McClure, 1992
Tepper et al., 1993
PE: Post-Exposure
1
cited in CAL/EPA, 2007 unless otherwise noted
a
cited in IPCS, 1997
Additional subchronic and chronic effects of nitrogen dioxide (not in the table) include
alterations in lung biochemistry and in the immune response of animals sensitized to allergens.
Chronic exposure (9 months) to low NO2 concentrations (0.04 ppm or 75 µg m-3) initiated lipid
peroxidation of unsaturated fatty acids in epithelial cell membranes, leading to cell injury or
Assessment Report on Nitrogen Dioxide for Developing Ambient Air Quality Objectives
32
death (Sagai et al., cited in CAL/EPA, 2007). There were no adverse effects on alpha-1­
proteinase inhibitor (protects lung from proteolysis) as a result of chronic (12 to 18 mo) exposure
to NO2 concentrations of 0.5 ppm (background) with daily 2 hour exposures to peaks of 1.5
ppm (2820 µg m-3) NO2 (Johnson et al., cited in CAL/EPA, 2007).
The interaction of NO2 and allergens on the development of the immune system of rabbits was
examined by Douglas et al. (CAL/EPA, 2007). Intermittent exposure of neonatal rabbits (24
hours old) immunized with house dust mite to 4 ppm (7520 µg m-3) NO2 for 3 months did not
affect total and differential cell counts in BAL fluid or airway hyperresponsiveness to histamine
or methacholine; the authors suggested the mode of antigen exposure (IP injection versus
inhalation) may have contributed to the lack of an observed effect of NO2 on the allergic immune
response (CAL/EPA, 2007).
4.5
Fetal and Developmental Toxicity
Epidemiological studies have associated fetal effects (low birth weight, intrauterine growth
retardation, sudden infant death syndrome) with exposure to traffic related air pollution (Ha; Liu;
Wilhelm; Dales; Lin, cited in CAL/EPA, 2007). Although estimates of outdoor NO2 exposure
were provided for the majority of these studies, it is unlikely the effects can be attributed to NO2
alone (CAL/EPA, 2007). The effect of NO2 exposure on development was examined in rats,
mice, guinea pigs and ferrets. A summary of these effects is provided below, further study
details including exposure concentration and duration and species exposed are in Table 8.
Gestational exposure to NO2 reduced birth weight in mice (22 ppm or 41360 µg m-3) NO2)
(Singh et al., cited in CAL/EPA, 2007) and rats (5 ppm or 9400 µg m-3 NO2) (Tabacova et al.,
cited in CAL/EPA, 2007). Reduced body weights were reported for newborn mice exposed 12
weeks to 0.25 ppm or 470 µg m-3 NO2 (Richters et al., cited in CAL/EPA, 2007). Rats exposed
to very low NO2 concentrations (0.05 ppm or 94 µg m-3) during gestation resulted in motor
behavioral changes (Tabacova et al., cited in CAL/EPA, 2007).
Sherwin and Richters exposed newborn mice to 0.25 to 0.3 ppm (470 to 560 µg m-3) NO2 for 4 to
6 weeks after birth and reported evidence of pulmonary inflammation and injury (CAL/EPA,
2007). Similar effects were observed in developing rats at higher exposure concentrations (0.5 to
14 ppm NO2) (Rasmussen and McClure; Rasmussen; Rasmussen et al.; Kyono and Kawai ;
Chang et al.; Azoulay-Dupuis et al.; and Stevens et al., cited in CAL/EPA, 2007), in 6 week old
ferrets exposed to 0.5 ppm or 940 µg m-3 NO2 (Rasmussen and McClure; Rasmussen; Rasmussen
et al., cited in CAL/EPA, 2007) and 1.5 to 2 month old guinea pigs exposed to 2 ppm or 376 µg
m-3 NO2 (Azoulay-Dupuis et al., cited in CAL/EPA, 2007). Exposure to 2 ppm (376 µg m-3)
NO2 (with two daily 1-hour exposures to 6 ppm NO2) over a 6 week period or 9.5 ppm (17860
µg m-3 ) over a 6 month period, produced adverse effects on the pulmonary function of juvenile
rats (Stevens et al.; Mauderly et al., cited in CAL/EPA, 2007). Subchronic exposure to 0.35 ppm
(670 µg m-3) NO2 increased spleen weight and spleen cell numbers in newborn mice (Kuraitis et
al., CAL/EPA, 2007).
Assessment Report on Nitrogen Dioxide for Developing Ambient Air Quality Objectives
33
Table 8
Reproductive Effects Reported Following Animal Exposure to NO2
Effect
Exposure Period
Reduced body weight 6 h/d, day 1 to 21 of
gestation
24 h/d, day 7 to 18 of
gestation
8 h/d, 5 d/wk, 1 to 12
wks
Motor behavioural
changes (postural,
gait, righting reflex,
aerial righting)
Pulmonary
inflammation and
injury; alveolar type
II cell hyperplasia/
hypertrophy
6 h/d, day 1 to 21 of
gestation
24 h/d for 1 month
(post-natal)
7 hr/d, 5 d/wk, 6 wks
6 hr/d, 5 d/wk, 6 wks
begun last week of
gestation
Increased spleen
weight and spleen
cell numbers
1
Species
Reference1
LOAEL = 5 (9400) Rat
Wistar
LOAEL = 22
Mouse
(41360)
CD-1
LOAEL = 0.25
Mouse, male
(470)
Swiss-Webster
(newborn)
LOAEL = 0.05
Rat
(94)
Wistar
Tabacova et al., 1985
LOAEL = 3 (5600) Rat, female
JCL-SD
(1 mo old)
LOAEL = 0.25
Mouse, male
(470)
Swiss-Webster
(32 wks PE)
( 3 wks old)
LOAEL = 0.3
Mouse, male
(560)
Swiss-Webster
Kyono and Kawai, 1982
Singh et al., 1988
Richters et al., 1987
Tabacova et al., 1985
Sherwin and Richters,
1995
Sherwin and Richters,
1985
0.5 ppm for 7 d/wk
with two daily 1 hr
peaks to 1.5 ppm for
5 d/wk over 6 wks
4 hr/day 5 days/wk,
8 or 15 weeks
LOAEL = 0.5-1.5
(940-2820)
Rat, male
F344
( 1 d and 6 wks old)
Chang et al., 1986
LOAEL = 0.5
(940)
Ferret
(6 wks old)
24 h/d, 3 d
NOAEL = 2 (3760) Rat
Wistar
(5 to 60 d old)
Rasmussen and
McClure, 1992;
Rasmussen, 1994;
Rasmussen et al., 1994
Azoulay-Dupuis et al.,
1983
24 h/d, 3d
LOAEL = 2 (3760) Guinea Pig
Dunkin Hartley
(45 to 60 d old)
LOAEL = 14
Rat
(26320)
Sprague-Dawley
(1- 40 d old)
LOAEL = 2 (3760) Rat, male
F344
( 6 wks old)
Azoulay-Dupuis et al.,
1983
NOAEL = 9.5
(17860)
LOAEL = 0.35
(658)
Mauderly et al., 1987
24 h/d, 1-3d
Changes in lung
compliance or
functional efficiency
Air Concentration
ppm (mg m-3)
2 ppm for 7 d/wk
with two daily 1 hr
peaks to 6 ppm for 5
d/wk over 6 wks
7 hr/d, 5 d/wk, 6 mo
8 hr/d, 5 d/wk, 6 wks
Rat, male, F344
(1 d or 6 mo old)
Mouse, male
Swiss-Webster
(newborn)
Stevens et al., 1978
Stevens et al., 1988
Kuraitis et al., 1981
cited in CAL/EPA, 2007, 2005
Assessment Report on Nitrogen Dioxide for Developing Ambient Air Quality Objectives
34
4.6
Carcinogenicity
Epidemiological studies have reported on the association of lung cancer in Europe with exposure
to nitrogen oxides (including NO2) (Feychting et al.; Filleul et al.; Nyberg et al., cited in WHO,
2006 and Nafstad et al.; Raaschou-Nielsen et al., cited in CAL/EPA, 2007). Three of these
studies presented statistical associations between NO2 exposure and cancer.
A case-referent study conducted in Sweden by Feychting and colleagues reported an increased
risk of childhood cancer with exposure to motor vehicle exhaust. Using an NO2 exposure
estimate equal to the 99th percentile outdoor air concentrations (1-hour averages over 1 year), the
study reported a relative risk estimate of 2.7 for total cancer at NO2 concentrations of 50 µg m-3
or higher (compared to 39 µg m-3 NO2 or lower) (WHO, 2006).
A registry-based case-control study conducted in Denmark reported an increased risk of
childhood cancer (Hodgkin’s lymphoma) as a result of exposure to NO2 and benzene in motor
vehicle exhaust (Raaschou-Nielsen et al., cited in CAL/EPA, 2007). Street configuration, traffic
patterns, meteorological variables, and background air concentrations were used to model
children’s exposure to NO2. A relative risk of 6.7 was reported for children (under the age of 15
years) in the highest category of residential exposure to NO2 (CAL/EPA, 2007), indicating that
the risk of developing Hodgkin’s lymphoma for children in this exposure group was 6.7-fold
higher than for children in the control group.
Nyberg and colleagues conducted a population-based case-control study of lung cancer patients
and controls residing in Stockholm from 1950 to 1990. Using air dispersion models to link
residential addresses to N02 exposure, the study estimated that lung cancer was associated with
an increase in 10 µg m-3 traffic-related NO2 exposure over 10 years (odds ratio = 1.10) and
provided evidence for a response threshold of 30 µg m-3 (WHO, 2006).
Traffic-related pollution is a major source of NO2 and was the primary exposure source
considered for epidemiological studies of cancer. This pollution source involves a complex
mixture of carcinogenic components (i.e., benzene, diesel particulate, and PAH) which likely
contributed to the observed cancer occurrences (WHO, 2006; CAL/EPA, 2007).
There was no increased incidence of respiratory tract tumours or tumours of non-pulmonary
organs in rats continuously exposed to 0.04, 0.4, or 4 ppm (75, 752, or 7520 µg m-3 ) NO2 for 17
months (Ichinose et al., cited in CAL/EPA, 2007). A slight, but significant, increase in the
frequency and incidence of lung adenomas in A/J mice exposed to 10 ppm NO2 for 6 months, but
not in mice exposed to 1 or 5 ppm (1880 or 9400 µg m-3 ) NO2 (Adkins et al., cited in CAL/EPA,
2007). Drawbacks to this study include an apparent lack of a dose-response effect and large
variability in the development of lung adenomas among unexposed (control) A/J mice groups
which suggests ambiguity in the response data (CAL/EPA, 2007).
A beneficial response attributed to the cytotoxicity of NO2 was the inhibition of spontaneous
AKR lymphoma formation in AKR mice exposed to 0.25 ppm (470 µg m-3) NO2 for up to 181
days; NO2 exposure also reduced splenic T-lymphocyte subpopulations (which give rise to AKR
Assessment Report on Nitrogen Dioxide for Developing Ambient Air Quality Objectives
35
lymphoma formation), suggesting a direct effect on cells of the immune system (Richters and
Damji, cited in CAL/EPA, 2007).
Several studies have reported an increased in vivo formation of carcinogens following coexposure to NO2 (at ambient air concentrations) plus nitrosamine precursors (Kanoh et al.;
CARB; Rubenchik et al.; Kosaka et al.; Van Steel et al., cited in CAL/EPA, 2007) and the in
vivo formation of mutagenic nitrated PAH following co-exposure to NO2 and various non­
mutagenic or weakly mutagenic PAH (Kanoh et al.; Miyanishi et al., cited in CAL/EPA, 2007).
The potential for atmospheric formation of mutagenic nitro-PAHS and nitro-alkenes has been
demonstrated through reactions, in the presence of photoirradiation, of various PAHs with 10
ppm NO2 and various alkenes with 0.2 to 0.25 pm NO2 (Hisamatsu et al.; Sasaki et al,; Ishii et
al.; Victorin and Stahlberg, cited in CAL/EPA, 2007).
Assessment Report on Nitrogen Dioxide for Developing Ambient Air Quality Objectives
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5.0
EFFECTS ON VEGETATION
Literature on the biological effects of nitrogen dioxide on terrestrial vegetation was reviewed.
The Web of Science database was searched using key words nitrogen dioxide with plant, and
vegetation, in addition, information was summarized from the U.S. EPA Air Quality Criteria for
Oxides of Nitrogen (EPA, 1993), and the Review of the California Ambient Air Quality Standard
for Nitrogen Dioxide (CAL/EPA, 2007) reports.
Nitrogen is the fourth most abundant element in plants after carbon, oxygen and hydrogen and
represents 2-6% plant dry matter. It is the principal factor limiting plant growth (Good et al.,
2004). Nitrogen is a component of amino acids, proteins, a number of heterocyclic compounds
(purines and pyrimidines), coenzymes, plant pigments, and a number of secondary metabolites.
5.1
Plant Uptake
The uptake of nitrogen dioxide by plants occurs predominately by foliar deposition. The mode of
entry responsible for the majority of gaseous NO2 is the leaf through the stomatal openings
(Darrall; Saxe; Thoene et al., and Okano et al., cited in CAL/EPA, 2007) with a minority
absorbed through the cuticle (Kisser-Priesak et al., 1987). Okano and colleagues evaluated the
transport of NO2 (containing the stable isotope of nitrogen 15N) transport into the plant of 8
herbaceous plant species (Helianthus annus, Raphanus sativus, Lycopersicon esculentum,
Nicotiana tabacum, Cucumis sativus, Phaseolus vuglaris, Zea mays and Sorghum vulgare).
Plants were exposed to 0.5 ppm of NO2 (940 µg m-3) for 14 d, resulting in an uptake range of
0.16 to 0.57 mg nitrogen/dm/d with stomatal resistance being the determining factor for NO2
entry into the plants (CAL/EPA, 2007).
5.2
Plant Metabolism
Zeevaart (1976) hypothesized that once NO2 entered the substomatal cavity of the leaf, NO2
dissolves in water to form NO2- and NO3-, where these two inorganic nitrogen compounds are
absorbed into the cell wall spaces. Nitrate and nitrite, are then transported into the plant cell,
through high and/or low affinity transporters (active transport) (Crawford and Glass 1998). Once
in the cytoplasm of the cell nitrate is reduced to nitrite by the enzyme nitrate reductase or
transported to the vacuole (storage). Nitrite is then transported to the chloroplast where it is
further reduced to ammonium. Ammonium is assimilated into amino acids by glutamine
synthase/glutamine oxoglutarate aminotranferase cycle and then used as a nitrogen donor for
other biochemical processes.
Assessment Report on Nitrogen Dioxide for Developing Ambient Air Quality Objectives
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5.3
Effects of Nitrogen Dioxide on Plants
Foliar injuries due to NO2 have only been observed at spill sites or near strong point sources
(Taylor and McLean, cited in CAL/EPA, 2007; Wellburn 1990; Bytnerowiz et al. 1998). At
ambient NO2 concentrations, no visible symptoms have been reported in the field. The effect of
acute levels of NO2 on plants have been summarized from US EPA (1993) and CAL/EPA (2007)
reports. In broad-leaf (dicotyledonous) plants under high experimental exposures 3.5 -10,000
ppm of NO2 (3.29 – 18,800 mg m-3), for short duration (10 h or less)) results in early symptoms
of irregularly shaped intercostal lesions, resulting from tissue collapse, extending from the upper
to lower surface. The lesions are distributed on the entire leaf surface in between the veins.
Lesions attributed to NO2 toxicity are indistinguishable from those produced by SO2. It has been
observed in narrow leaf (monocotyledonous) plants that acute NO2 exposures resulted in necrosis
at or below the leaf blade tips. The necrotic lesions (margins and strips) also occur between the
veins. The development of longitudinal necrotic strips between veins has been observed in
grains (wheat, barley and rye). In evergreens (coniferous) plants foliar injury develops with
initial stage of dulling of the needle tip (going from green to gray-green to brown to red-brown).
In actively growing needles injury is localized to the tips; whereas, in mature needles damage
occurs in the medial or basal portions of the needle. NO2 induced lesions are irreversible.
Bytnerowicz et al. (1998) reported that when exposed to NO2, near a fertilizer plant in Poland,
the most susceptible woody plants (for foliar injury) were common juniper, Scots pine and
Norway spruce; whereas, box elder, elm, Norway maple and willow were resistant. Taylor and
McLean reported that corn, pinto bean and sunflower were susceptible to NO2 foliar injury, but
asparagus and bush bean were resistant (CAL/EPA, 2007). A meta-analysis of over 50 peerreviewed reports on the effects of NO2 on foliar injury indicated that plants are relatively
resistant to NO2, with no visible effects under 0.2 ppm concentration (376 µg m-3) (US EPA,
1993).
Increased and decreased plant photosynthesis has been associated with NO2 treatment (US EPA,
1993; CAL/EPA, 2007). The reduction of photosynthesis is thought to be attributed to nitrite
toxicity in the chloroplasts. Saxe exposed horticultural plants to NO and NO2 at 1 ppm (1,880
µg m-3) for 12 hours and found that NO toxicity was 22 times greater than NO2 (CAL/EPA,
2007). Sabaratnam et al. found that 0.2 ppm (376 µg m-3) NO2 exposure 7 hours/day for 5 days
increased net photosynthesis in soybean, whereas exposure to 0.5 ppm resulted in a decrease in
net photosynthesis (US EPA, 1993).
A large number of studies have been conducted on the effects of NO2 exposure on plant growth
and yield (Table 9); and no clear pattern has emerged, but certain trends can be generalized
(EPA, 1993). Pasture grasses demonstrated reduced growth following exposure to relatively low
levels of NO2 (0.1 ppm (188 µg m-3) (Ashenden and Williams; Whitemore and Mansfield; cited
in CAL/EPA, 2007). Reduced growth was reported for white ash, sweet gum and loblolly pine
(Kress and Skelly, cited in CAL/EPA, 2007). Negative effects of yield and growth rate are
observed with exposures of NO2 greater than 0.2 ppm (376 µg m-3). For example, Sinn and Peel
(1984) exposed potato plants to 0.2 ppm (376 µg m-3) NO2 for 5 hour/day for 2 days/week for
period of 12-16 weeks. Plants developed NO2 induced lesions and a decrease of 43 and 51% in
tuber yield was observed.
Assessment Report on Nitrogen Dioxide for Developing Ambient Air Quality Objectives
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Table 9
Effects Following Plant Exposure to NO2
Species
Air
Concentration
ppm (µ
µg m-3)
Exposure
Period
Effects Reported
Reference
Green bean
12-day-old seedlings
0.02 (37.6)
5 days
Increase in plant height, decrease in mass and area of leaf Srivastava and Ormrod,
depended on level of nitrate supplied
1984
Green bean
23-day-old seedlings
0.02( 37.6)
6 h/day
14 days
Decrease in mass of shoot and root and increase in the
number of nodules depended on level of nitrate
Srivastava and Ormrod,
1986
Perennial ryegrass
0.024 (45.1)
to 215 day
Significantly increased mass of shoots after 156, but not
after 207 days of exposure, decreased number of
flowering shoots after 207 days
Lane and Bell, 1984b
Common timothy
Significantly increased mass of shoot after 97, but not
215 days of exposure
Bean plants
57-day-old
0.025 (47)
7 h/day, 5
days/week
3 weeks
Significantly increased the mass of seeds
Sandhu and Gupta,
1989
Sitka spruce
6-mo-old seedlings
0.03 (56.4)
8 weeks
Did not significantly affect mass of plant, but advanced
bud-break exposed during dormancy
Freer-Smith and
Mansfield, 1987
European white birch
rooted cuttings
0.04 (75.2)
9 weeks
Significantly increased mass and height of stem, mass of
leaves, and internode length (depending on photoperiod
and light intensity)
Freer-Smith, 1985
Green bean
57-day-old
0.05 (94)
7 h/day, 5
days/week
3 weeks
Significantly increased mass of shoot, roots and seeds
Sandhu and Gupta,
1989
Eastern white pine
2-year-old ramets
0.05 (94)
4 h/day
35 days
No significant effect on length of needles
Yang et al. 1983b
European white birch
1-month-old seedlings
0.05 (94)
4 weeks
No significant effect of shoot, roots or leaves
Freer-Smith, 1985
Soybean
7-week-old
0.1 (188)
3 h every 2 days
4 weeks
No effect on mass of leaves, stem, roots, or nodules or on Klarer et al. 1984
the number of nodules
Soybean
5-weel-old
0.1 (188)
7 h/day
5 days
No effect on relative growth rate
Sabaratnam and Gupta,
1988
Green bean
0.1 (188)
7 h/day, 5
Significantly increased mass of shoot and roots, number
Sandhu and Gupta,
Assessment Report on Nitrogen Dioxide for Developing Ambient Air Quality Objectives
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Species
Air
Concentration
ppm (µ
µg m-3)
Exposure
Period
Effects Reported
Reference
days/week
3 weeks
of pods and seeds, and mass of seeds
1989
Green bean
23-day-old seedlings
0.1 (188)
6 h/day
14 days
Significantly decreased mass of shoot and roots, but
increased number of nodules, depending on level of
nitrate
Srivastava and Ormrod,
1986
Eastern white pine
2-year-old ramets
0.1(188)
4 h/day
35 days
Significantly reduced length and mass of needles,
depending on the clone
Yang et al. 1983b
Green bean
12-day-old seedlings
0.1(188)
5 days
Significantly increased plant height, but decreased mass
and area of leaf, depending upon level of nitrate
Srivastava and Ormrod,
1986
Green beans or common
sunflower
0.1 (188)
10 days
No effect on growth
Totsuka et al. 1978
Garden pea, green bean,
potato, tobacco
0.1 (188)
15 days
No effect on mass of plant
Strand et al., 1996 a
Maize seedlings
Increased mass of plant and leaf area
Tomato
0.1 (188)
19 days
No effect on leaf area, mass of leaves, shoot, or roots
Capron and Mansfield,
1985
Barley seedlings
0.1 (188)
20 days.
No effect on number of tillers or leaves, leaf area, or
mass of leaves or roots
Pande and Mansfield,
1985
Kentucky bluegrass
seedlings
0.1 (188)
104 h/week
8 weeks
Significantly reduced mass of plant (but not numbers of
leaves or tillers), depending upon cultivar
Whitmore and
Mansfield, 1983;
Whitmore et al, 1982
Kentucky bluegrass
seedlings
0.1 (188)
104 h/week
21 weeks
No effect on mass - exposed from emergence
Whitmore and
Mansfield, 1983;
Whitmore et al, 1982
Black poplar, downy
birch, or common apple
second-year cuttings
0.1 (188)
104 h/week
22 weeks
No significant effect on stem height, leaf area, or mass of Freer-Smith, 1984;
shoot
Whitmore and FreerSmith, 1982
European white birch and
white alder
Increased stem height
Small-leaved European
linden
Increased leaf area and mass of shoot
Assessment Report on Nitrogen Dioxide for Developing Ambient Air Quality Objectives
40
Species
Air
Concentration
ppm (µ
µg m-3)
Exposure
Period
Effects Reported
Reference
Common timothy,
perennial ryegrass,
Kentucky bluegrass
0.1 (188)
104 h/week
28 weeks
No effect on orchard grass; significant decreased mass of Whitmore and
shoot – depending upon cultivar and stage of
Mansfield, 1983;
development
Whitmore et al, 1982
Kentucky bluegrass
0.1 (188)
104 h/week
33 weeks
Significantly reduced mass of shoot and number of culms Whitmore and
Mansfield, 1983;
Whitmore et al, 1982
Black poplar, downy
birch, common apple,
small leaved European
linden
second-year cuttings
0.1 (188)
104 h/week
60 weeks
No significant effect on stem height or mass of shoot
European white birch
Increased mass of shoot
White alder
Increased stem height and mass of shoot
Freer-Smith, 1984;
Whitmore and FreerSmith, 1982
Radish
0.2 (376)
3 or 6 h
No effect on mass of leaves or roots
Reinert and Gray, 1981
Soybean
5-week-old
0.2 (376)
7 h/day, 5days
No effect on relative growth rate
Sabaratnam and Gupta,
1988
Soybean
7-week-old
0.2 (376)
3 h/day, once/2
days, 4 weeks
No effect on mass of leaves, stem, roots or nodules or
number of nodules
Klarer et al. 1984
Sunflower
28-day-old
0.2 (376)
14 days
Significantly decreased leaf area, but did not affect mass
of leaves, stem, or roots in plants
Okano et al. 1985a
Maize
No effect
Sunflower
0.2 (376)
38 days
No effect on leaf area
Natori and Totsuka,
1980
Tomato, cucumber
0.2 (376)
60-67 days
No effect on leaf area
Natori and Totsuka,
1980
Two populations of
perennial ryegrass
0.2 (376)
11 weeks
Significantly increased mass of roots and shoots and
number of tillers
Taylor and Bell, 1988
Potato
0.2 (376)
5 h/day, 2
days/week
12-16 weeks
Significantly decreased number and mass of tubers and
accelerated senescence and abscission of foliage
Sinn and Pell, 1984
Assessment Report on Nitrogen Dioxide for Developing Ambient Air Quality Objectives
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Species
Air
Concentration
ppm (µ
µg m-3)
Exposure
Period
Effects Reported
Reference
Soybean
5-week-old
0.3 (564)
7 h/day, 5 days
No effect on relative growth rate
Sabaratnam and Gupta,
1988
Maize
0.3 (564)
10 h/day
14 days
Significantly decreased leaf area and mass of leaf sheath
Yoneyama et al. 1980c
Tomato or Swiss chard
Had no effect on leaf area or mass of leaf, stem, or roots
Cucumber
Significantly increased leaf area, mass of leaves, stem,
and roots
Sunflower
Significantly increased leaf area and mass of leaves and
stem
Green bean
Significantly increased leaf area and masses of stem and
roots
Radish
25-day-old plants
0.4 (752)
3 or 6 h
No effect on mass of leaves or roots
Reinert and Gray, 1981
Soybean
0.4 (752)
2.9 h event
10 events
No effect on yield of plants grown in field plots
Irving et al. 1982
Black poplar
rooted cuttings
0.5 (940)
1h
No effect on height or number of leaves, but significantly Eastman and Ormrod,
increased leaf area, mass of leaves and mass of stem
1986
Carolina poplar
Significantly increased leaf area
Soybean
0.5 (940)
7 h/day, 5 days
Significantly decreased number of pods and seeds and
mass of seeds
Sabaratnam and Gupta,
1988
Soybean
5- week-ol
0.5 (940)
7 h/day, 5 days
Significantly decreased relative growth rate
Sabaratnam and Gupta,
1988
Green bean
23-day-old seedlings
0.5 (940)
6 h/day
Significantly decreased mass of shoot and root, but
increased or decreased number of nodules, depending on
level of nitrate
Srivastava and Ormrod,
1986
Black poplar
1.0 (940)
1h
Significantly decreased mass of stem
Eastman and Ormrod,
1986
Carolina poplar
Decreased height
Assessment Report on Nitrogen Dioxide for Developing Ambient Air Quality Objectives
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6.0
EFFECTS ON MATERIALS
A review was undertaken to identify effects of ambient NO2 on materials. The result indicates
that no major direct effects exist due, in part, to the fact that once released into the atmosphere
NO2 usually reacts quickly with other chemicals to form secondary pollutants. For instance, it is
the precursor for nitric acid which is a large contributor to acid deposition (wet and dry). Hence,
NO2 indirectly impacts most materials to some degree (US EPA, 2007a). This includes impacts
to structures, metals, paints and coatings, and everyday items such as leather and paper.
Structural damage to underground pipes, cables and foundations submerged in acid waters can
occur, in addition to damage to buildings and bridges above ground. Limestone, marble and
sandstone are particularly vulnerable, while granite-based rocks are more resistant to acidity. All
types of metals that are left exposed to acid rain are affected very noticeably in the form of
corrosion, tarnishing, cracking, and loss of thickness. These effects significantly reduce the
societal value of buildings, bridges, and cultural objects (such as statues, monuments, and
tombstones). Dry deposition of acidic compounds can also dirty buildings and other structures,
leading to increased maintenance costs.
Paints and organic coatings may experience simple discoloration or even corrosion if exposed to
large amounts of acid deposition. One of the objects most widely affected are automobiles which
consist of metal frames coated in paints of different colors. First, the acid deposition may
discolour the paint on an automobile and eventually eat the paint away. Once the paint has been
eroded, the acid deposition will start to work on the metal and will eventually tarnish the frame.
On a smaller scale, ordinary things such as paper and the leather are also affected by acid
deposition. Paper exposed to acid deposition over a long period of time will be discoloured,
becoming a yellowish color. Photographic paper is also similarly affected, but taking not nearly
as much time for a similar result. Contact with acid deposition can immediately cause micro
blemishes on photographs and unused film. Acid deposition components such as nitrogen oxides
also adversely affect common leather which, when exposed to acid rain, will develop a powdery
surface and can actually be weakened. Rubber in shoes and other objects will experience
cracking and brittleness when in contact with acid deposition.
Assessment Report on Nitrogen Dioxide for Developing Ambient Air Quality Objectives
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7.0
AIR SAMPLING AND ANALYTICAL METHODS
Several techniques are available to measure NO2 concentrations in the atmosphere. The
chemiluminescent analyzer is widely used for continuous monitoring of NO2 concentrations
throughout the World. It is the reference method of choice for many regulatory agencies and
jurisdictions, including Alberta and Canada, and for many researchers. Other methods of
measurement, such as passive samplers, colourimetric methods, electrochemical sensors, thick
film sensors, various spectroscopic methods, and FTIR analyzers are also available, and can
provide useful data in many circumstances and for different applications. Refer to Table 9 for a
description of individual method advantages and disadvantages.
7.1
Chemiluminescence Methods
7.1.1
Gas-Phase Chemiluminescence
The gas-phase chemiluminescence method for NO2 is based on reduction to NO by a heated
catalytic converter, measurement of NO and NOx and calculation of the concentration of NO2 as
the difference between NOx and NO. The US EPA has designated several analyzers based on this
method as reference methods for monitoring airborne NO2 (US EPA, 2007b). In addition, both
AENV and EC make use of these monitors as part of their monitoring program (AENV, 2007;
EC, 2007f). Not only are the chemiluminescent analyzers continuous but detection limits of
around 1 µg m-3 and short time resolutions make them more than adequate for ambient
measurements. Potential interferences include photochemically produced compounds such as
nitric acid, peroxyacetyl nitrate and ammonia which are oxidized to NO on the converter
(Grosjean and Harrison, 1985). In addition, these analyzers need compressed air to operate, are
expensive and require significant maintenance.
It is important to note that chemiluminescent analyzers do not directly measure concentrations of
NO2. Within some analyzer types, measurement is achieved by having a dual-chamber
configuration that measures NOx and NO simultaneously in individual reaction chambers. Some
dual-chamber instruments have dual detectors and some have only a single detector. NO is
measured by mixing O3 into the NO sample flow path. In the mixing chamber, all NO is oxidized
to NO2, resulting in temporarily excited NO2 molecules. As the excited NO2 molecules release
photons of energy, a photomultiplier tube measures the emitted light. NOx is measured by
diverting a separate sample flow through a thermal converter prior to the addition of O3, as
mentioned above. In the thermal converter, NO2 is reduced to NO. Analysis is performed using
the same photomultiplier tube with the aid of a sample flow splitter. In recent years, many
manufacturers have moved to the production of single-chamber instruments, mainly to save on
the costs of plumbing and electronics. In this case, the measurements of NOx and NO must be
made sequentially.
Assessment Report on Nitrogen Dioxide for Developing Ambient Air Quality Objectives
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7.1.2
Liquid-Phase Chemiluminescence
Another method for the direct chemiluminescence determination of NO2 was developed by
Maeda et al. (1980) and is based on the chemiluminescence reaction of NO2 with a surface
wetted with an alkaline solution of luminol (5-amino-2,3-dihydro-1,4-phthalazinedione). The
light emission is strong at wavelengths between 380 and 520 nm. The intensity of the light is
proportional to the NO2 concentration in the sampled air, and the NO2 concentration can be
determined by calibration of the instrument with air of known NO2 concentration. Since the
introduction of the luminol method, improvements have been made to develop an instrument
suitable for use in the field (Wendel et al., 1983).
This method has been automated for continuous sampling and analysis and easily achieves
excellent detection limits of 5 to 30 pptv with a response time of seconds without high additional
costs (Schiff et al., 1986; Wendel et al., 1983). However, the technique is still poorly
characterized and initial problems with O3 interference, low-end non-linearity, and luminol
solution instability have not been fully addressed (Kelly et al. 1990; Drummond, et al. 1988).
Furthermore, since this monitor works with a liquid phase reaction, it needs more regular service
than the ordinary chemiluminescence instruments. Nevertheless, it is a direct NO2 measurement
method with lower costs than other chemiluminescent analyzers and continues to be used.
7.2
Passive Samplers
Passive techniques using diffusion tubes, badges and plates have been developed and employed
successfully over many years for the measurement of ambient NO2 concentrations. These passive
techniques take samples of NO2 from the atmosphere at a rate controlled by the natural diffusion
of the gas across a membrane but which does not involve active movement of air through the
sampler. The sample is then analyzed by an appropriate analytical method. The advantages of
these samplers are that they are cheap, simple to use, have no moving parts to break down,
regular flow calibration is unnecessary, able to provide high spatial resolution, do not require
power supplies, can be used to assess long-term concentrations and are well-suited for remote
area measurements. However, only when high contaminant concentrations are present can
shorter sampling periods more reflective of exposure be employed.
Diffusion tube samplers widely used are based on the design introduced by Palmes et al. (1976)
and are comprised of an acrylic tube that can be sealed at both ends. One end of the tube contains
stainless steel grids coated with triethanolamine (TEA) that adsorbs NO2 to produce a nitrite salt
that produces an intensely-coloured solution. The intensity of the colour is measured by a
spectrometer and is proportional to the concentration of the NO2 over the time of exposure in the
sampled air. The method gives values for average air quality over periods requiring at least
several days sampling.
Analysis by ion chromatography has also been used (Krochmal and Kalina, 1997; Gair et al.,
1991) to improve the detection limit for monitoring in remote rural areas (i.e., 0.02 ppbv).
Additional improvements have recently been made by modifying the traditional Palmes tube by
fitting a membrane at the open end to avoid the effect of turbulence due to wind speed (Gerboles
Assessment Report on Nitrogen Dioxide for Developing Ambient Air Quality Objectives
45
et al., 2005). Some studies have indicated that diffusion tube samplers may overestimate
concentrations by up to 30% (Heal et al., 1999), whereas others have shown an underestimation
(Bush et al., 2001). In practice there are circumstances when overestimation or underestimation
can occur depending on a number of factors (the laboratory doing the preparation and analysis,
the exposure interval, the time of year, the location and setting, etc.).
The passive badge method is based on the work of Yanagisawa and Nishimura (1982) and has
been further refined by De Santis et al. (1997). A fibre filter paper impregnated with TEA,
mounted behind a diffusion barrier, is exposed to the air. The NO2 is passively absorbed on the
filter and after exposure is analysed in a similar manner to the diffusion tube method above. As
the area of filter is relatively large and the contact with air is greater than with the tube, the
device is able to provide averages of NO2 concentration over sampling periods of several hours
and upwards. Data provided using this badge method, using several hours averaging time, can be
compared against 1-hour levels but will result in conservative comparisons.
Another type of passive NO2 sampler for ambient application is the nitration plate. It is
essentially an open Petri-dish containing TEA-impregnated filter paper (Mulik and Williams,
1987). The device employs a TEA-coated cellulose filter paper, two 200-mesh stainless steel
diffusion screens and two stainless steel perforated plates on each side of the coated filter to act
as diffusion barriers and permit NO2 collection on both faces of the filter paper. After sampling,
the paper is removed from the sampler, extracted in water, and analyzed for NO2 by ion
chromatography. Comparison of nitration plate results with chemiluminescence determinations
of NO2 in laboratory tests at concentrations between 10 and 250 ppbv showed high correlation
(Mulik and Williams, 1987).
7.3
Colourimetric Samplers
Colourimetric samples are based upon the reaction of NO2 with solutions of organic dyes to form
coloured species. Optical absorbence of the coloured complex in solution, measured
spectrophotometrically, is linearly proportional to the concentration of the coloured species
according to Beer’s Law. This method is sensitive and more selective than the
chemiluminescence method, but the colour to be measured spectrophotometrically is developed
during sampling, and the measurement has to be performed immediately after sampling due to
instability. This makes the method unsuitable if the exposed absorbing solution has to be
transported to a chemical laboratory far from the sampling site. The US EPA, NIOSH, and
OSHA have designated several analyzers based on this method as reference methods for
monitoring airborne NO2 (US EPA, 2007b; NIOSH, 1994; OSHA, 1991). Many variations of
this method exist, including both manual and automated versions. These include the GriessSaltzman method, the continuous Saltzman method, the alkaline guiacol method, the sodium
arsenite method (manual or continuous), the triethanolamine-guaiacol-sulfite (TGS) method and
the TEA method. While a number of wet chemical methods based on colourimetry have been
developed, these are no longer widely used, and have been almost entirely replaced by the other
techniques described.
Assessment Report on Nitrogen Dioxide for Developing Ambient Air Quality Objectives
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7.4
Electrochemical Sensors
There are a number of portable samplers available based on the use of electrochemical cells
(Currie et al., 1999). These devices can offer some of the highest selectivity, long lifetimes, low
drift and low costs of all NO2 samplers. The principal of operation depends on the
electrochemical reduction of NO2 between two electrodes immersed in an electrolyte reservoir.
NO2 present in the sample air passes through a capillary diffusion barrier into the reaction cell
where it is reduced at the electrode. The migration of electrons produced by the reaction results
in a net current flow which is proportional to the NO2 concentration. The instrument gives direct
readings which can be used to provide continuous or hourly average values. These types of
samplers continue to be widely used for the assessment of occupational exposures and as part of
urban traffic control systems but their application to ambient monitoring are limited due to the
high limit of detection of around 200 µg m-3. In addition, there is evidence that some or all
varieties of electrochemical cell intended to measure NO2 actually measure a combination of
NO2 and O3. This may make interpretation of the data difficult. Recent developments using
carbon-fluorocarbon membranes have greatly increased the sensitivity of these devices for NO2
detection (Mizutani et al., 2005).
7.5
Thick Film Sensors
The development of solid-state thick film gas sensors based on semi-conducting oxides has
provided a new range of samplers for environmental monitoring (Su et al., 2003; Carotta et al.,
2000). These sensors are constructed from nano-structured semi-conducting metal oxides, which
are maintained at an operating temperature of between 250 and 400°C. As current is passed
through the sensor, an electrical response is produced in proportion to a specific gas
concentration. Currently, these thick film sensors have been produced for a range of common
pollutants including NOx and commercial instruments are becoming available that have
demonstrated reasonable comparison with a co-located chemiluminescent analyzer (Viricelle et
al., 2006). It not envisaged that these samplers will replace the chemiluminescent method but
they do offer a number of potential benefits, such as use in screening surveys in urban locations,
the identification of pollution hot spots, and mobile monitoring in automobiles.
7.6
Spectroscopic Methods
Many spectroscopic methods have been used to measure airborne NO2. These method all vary
slightly but generally they are based on the interaction between light and matter. NO2 has been
spectroscoptically measured by differential optical absorption spectrometry (DOAS) (Cheng and
Chan, 2004; Kim and Kim, 2001), fibre-optic spectrometry (Morales and Walsh, 2005),
differential absorption lidar (DIAL) (Alden et al., 1982; Menyuk et al., 1980), laser induced
fluorescence (Matsumoto and Kajii, 2003; Simeonsson et al., 1999), photoionization
(Simeonsson et al., 1999), pulsed laser photoacoustic detection (Roman et al., 1998), surface
acoustic wave devices (Muller et al., 2000), and TDLAS (Li et al., 2004; Sauer et al., 2003;
Kormann et al., 2002). These methods offer good detection limits (1 µg m-3) and specificity and
can be used for real-time measurement of a wide range of air pollution species. They may be
Assessment Report on Nitrogen Dioxide for Developing Ambient Air Quality Objectives
47
useful if path-integrated measurements are required or in near source situations. However, the
techniques are relatively complex and considerably more expensive than the other NO2
measurement methods discussed. Unfavourable weather conditions such as fog, snow or rain can
affect instrument performance. Particularly careful attention to calibration and quality control is
required if meaningful measurements are to be made.
Differential optical absorption spectrometry is perhaps the spectroscopic method which has seen
the most recent widespread use. In the usual configuration, light from a light source passes
through a fixed path in the atmosphere, typically 100 to 1000 m in length. At the end of this path,
the light received is analysed and the amount of a specific gaseous substance in the atmosphere is
determined by Beer’s Law. In commercial analyzers, sophisticated signal processing is
undertaken to account for interfering species and variability in atmospheric optical transmission
conditions. Many species can be measured by the DOAS technique, but the most common
configuration for ambient air monitoring is to measure NO2, SO2, O3 and benzene. A number of
commercial DOAS instruments have been designated US EPA Reference Methods for the
measurement of NO2 provided certain operational and calibration requirements are followed (US
EPA, 2007b). Many intercomparison studies have demonstrated that DOAS can provide
comparable NO2 data to chemiluminescent analyzers, within the constraint that the DOAS
analyzer is averaging concentration measurements along the path length of measurement, rather
than measuring at a single point (Kim and Kim, 2001).
7.7
Fourier Transform Infrared Spectrometry
Fourier transform infrared spectrometry (FTIR) analyzers with path lengths of 1 km or more
have been designed to monitor a wide range of pollutants in ambient air including NO2 along
with CO, NO, SO2 and O3. This method is based on absorption of incident electro-magnetic
radiation at characteristic infrared wavelengths by NO2 across long distances. By monitoring the
magnitude of infrared light absorption by NO2 over the path length, NO2 can be detected at low
ppb levels. Computerized Fourier transformations of the absorption signals are used to separate
the NO2 signals from the instrumental noise by superimposing repetitive infrared scans until an
absorption peak is resolved. A Michelson interferometer modulates the absorption frequency
range so it can be measured. The application of infrared absorption to the monitoring of NO2 in
ambient air has not yet gained wide acceptance as a routine monitoring method and its use has, to
date, largely been restricted to the laboratory and to emissions testing.
Assessment Report on Nitrogen Dioxide for Developing Ambient Air Quality Objectives
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Table 10
Advantages and Disadvantages of Sampling and Analytical Methods
Method
Advantages
Disadvantages
Gas-Phase Chemiluminescent Reference method of choice
Analyzers
Low detection limit
Provides real-time data with
short time resolution
Easy to operate
Relatively expensive
High operating costs
Potential interferences
Liquid-Phase
Chemiluminescent Analyzers
Lower cost
Automated
Low detection limits
Needs reagent solution
Expensive
Ozone interferences
Passive Samplers
Low capital and operating costs
Possible to carry out surveys
over wide geographical areas
Require no power supply
Minimal training of site staff
Site calibrations are not required
Low detection limit
Only provide averaged concentrations
Accuracy and bias is dependent upon
preparation and analysis
Colourimetric Samplers
Sensitive and selective
Requires immediate analysis
Wet chemistry is involved
No longer widely used
Electrochemical Sensors
Portable samplers that can be
easily deployed in the field
Low cost
High selectivity
Direct readings
Higher detection limit makes them
unsuitable for ambient monitoring
Interferences
Thick Film Sensors
Portable samplers that can be
easily deployed in the field
Potential to measure a number of
pollutants simultaneously
Provides real-time data with
short time resolution
Low detection limit
At this time, not been commercially
released
Only measurements of NOx may
currently be carried out
Spectroscopic Methods
Gives an integrated concentration
that can be useful to assess
public exposure
Potential to measure a number of
pollutants simultaneously
Provides real-time data with
short time resolution
Low detection limit
Integrated measurement cannot be
directly compared with air quality
objectives
High capital cost
Unfavourable weather conditions can
affect the instrument performance
FTIR
Low detection limits
Very expensive
Untested
Assessment Report on Nitrogen Dioxide for Developing Ambient Air Quality Objectives
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8.0
AMBIENT OBJECTIVES IN OTHER JURISDICTIONS
Current and/or recommended and proposed ambient guidelines of jurisdictions in Canada, United
States and elsewhere were reviewed for nitrogen dioxide. Details about guidelines that exist for
each jurisdiction reviewed are presented in tabular format in this section. Most jurisdictions
have common uses for their guidelines. These uses may include:
• reviewing permit applications for sources that emit air pollutants to the atmosphere,
• investigating accidental releases or community complaints about adverse air quality for
the purpose of determining follow-up or enforcement activity,
• determining whether to implement temporary emission control actions under persistent
adverse air quality conditions of a short-term nature.
8.1
Canadian Nitrogen Dioxide Air Quality Guidelines and Objectives
The Federal-Provincial Working Group on Air Quality Objectives and Guidelines (WGAQOG,
1996) developed National Ambient Air Quality Objectives (NAAQOs) that identify benchmark
levels of protection for people and the environment. NAAQOs were developed to guide federal,
provincial, territorial and regional governments in making risk-management decisions, playing
an important role in air quality management (e.g. local source permitting, for air quality index
and as benchmarks for developing provincial objectives and standards). NAAQOs are viewed as
effects-based long-term air quality goals.
Some of the Canadian agencies that have air quality guidelines for nitrogen based on the
NAAQOs are Alberta Environment, British Columbia Ministry of Environment (MOE),
Manitoba Conservation, Ontario MOE, and Nova Scotia Environment and Labour. These limits
are shown in Table 10.
8.2
United States Nitrogen Dioxide Air Quality Guidelines and Objectives
The United States Clean Air Act (CAA) requires US Environmental Protection Agency to set
primary National Ambient Air Quality Standards (NAAQSs) for commonly occurring air
pollutants that pose public health threats. In addition, secondary NAAQSs are intended to
protect vegetation. The US Environmental Protection Agency permits states to adopt additional
or more protective air quality standards if needed. At a minimum, US states are required to use
the NAAQSs, or more stringent standards, for permit applications for nitrogen dioxide sources
and as criteria to monitor and investigate air quality.
All 18 US state agencies reviewed use the primary and secondary NAAQSs (100 µg m-3, annual
average) set by the US Environmental Protection Agency in their regulatory programs. In
addition, the CAL/EPA has added a 1-hour standard of 470 µg m-3.
Assessment Report on Nitrogen Dioxide for Developing Ambient Air Quality Objectives
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8.3
International Nitrogen Dioxide Air Quality Guidelines and Objectives
Five international jurisdictions and agencies were investigated. These included Australia
Environment Protection and Heritage Council (EPHC), New Zealand MOE, United Kingdom
(UK) Environment (including England, Scotland, Wales, and Northern Ireland), the European
Commission, and the World Health Organization (Table 10). All of these jurisdictions have
health-based guidelines in place ranging from 200 to 226 µg m-3 with a 1-hour averaging time
period. In addition, all of these jurisdictions except New Zealand MOE have health-based
guidelines in place ranging from 40 to 56 µg m-3 with an annual averaging time period. Two of
these jurisdictions – UK Environment and the European Commission – have a reduced annual
guideline of 30 µg m-3 in place to protect vegetation (UK Environment and the European
Commission) (Table 10).
Assessment Report on Nitrogen Dioxide for Developing Ambient Air Quality Objectives
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Table 11
Summary of Ambient Air Quality Objectives and Guidelines for Nitrogen
Dioxide
Agency
Canadian Government
Objective Title
Objective Value [µg m-3]
Averaging Time:
1-hour
24-hour
Annual
National ambient air quality objectives:
Maximum desirable level
60
Maximum tolerable level
400
200
Maximum acceptable level
1,000
300
400
200
200
Alberta Environment
Ambient air quality objectives (AAQOs):
British Columbia MOE
Uses Canadian government guidelines.
Manitoba Conservation
Uses Canadian government guidelines.
Ontario MOE
Ambient air quality criteria (AAQC):
400
Nova Scotia Environment
and Labour
Maximum permissible ground level
concentrations:
400
US EPA
National ambient air quality standard:
Primary standard:
Secondary standard:
Arizona DEQ
Adopted US EPA NAAQSs.
California EPA
State ambient air quality standard:
NAAQS Primary standard:
NAAQS Secondary standard:
Indiana DEM
100
60
100
100
100
470
100
100
Adopted US EPA NAAQSs.
Louisiana DEQ
Massachusetts DEP
Michigan DEQ
Minnesota DOH
New Hampshire DES
New Jersey
North Carolina ENR
Ohio EPA
Oklahoma DEQ
Pennsylvania DEP
Rhode Island DEM
Texas CEQ
Vermont ANR
Washington DOE
Wisconsin DNR
Australia EPHC
National air quality standards:
226
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52
Agency
Objective Title
Objective Value [µg m-3]
Averaging Time:
1-hour
24-hour
Annual
New Zealand MOE
Ambient air quality standard:
2001
UK Environment Agency
National air quality standard:
Local air quality objective:
Human health:
Vegetation:
200
European Commission
Limit values:
Human health:
Vegetation
World Health Organization Air quality guideline:
not to be exceeded more than 9 times per year
2
not to be exceeded more than 18 times per year
3
to be achieved by January 2010
2002
40
30
2002,3
403
30
200
40
1
Assessment Report on Nitrogen Dioxide for Developing Ambient Air Quality Objectives
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9.0
LITERATURE CITED
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Standards. Arizona DEQ, Air Quality Division, Phoenix, AZ.
http://www.azdeq.gov/environ/air/download/naaqs.pdf (accessed 10 July 2007).
Australia Environment Protection and Heritage Council (EPHC) (1998) National Standards for
Criteria Air Pollutants in Australia, Air quality fact sheet. Australia EPHC, Department
of the Environment and Heritage, Adelaide, Australia.
http://www.environment.gov.au/atmosphere/airquality/publications/standards.html
(accessed 10 July 2007).
British Columbia Ministry of Environment (MOE) (2007) Air Quality Objectives and Standards,
Air Quality Objectives for British Columbia and Canada. British Columbia MOE,
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Assessment Report on Nitrogen Dioxide for Developing Ambient Air Quality Objectives
63
APPENDIX A
North American and International
Air Quality Guidelines for Nitrogen Dioxide
Assessment Report on Nitrogen Dioxide for Developing Ambient Air Quality Objectives
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Assessment Report on Nitrogen Dioxide for Developing Ambient Air Quality Objectives
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Agency:
Canadian Government.
Air Quality Guideline:
National ambient air quality objectives (NAAQOs):
Maximum desirable level:
Annual AAAQG: 32 ppb (60 µg m-3)
Maximum tolerable level:
Annual AAAQG: 53 ppb (100 µg m-3)
24-hour AAAQG: 106 ppb (200 µg m-3)
1-hour AAAQG: 212 ppb (400 µg m-3)
Maximum acceptable level:
24-hour AAAQG: 160 ppb (300 µg m-3)
1-hour AAAQG: 532 ppb (1,000 µg m-3)
Averaging Time To Which Guideline Applies:
See above.
Basis for Development:
NAAQOs are primarily effects-based but reflective of technological, economic and societal
information.
Date Guideline Developed:
1999.
How Guideline is Used:
NAAQOs identify benchmark levels of protection for people and the environment in Canada and
guide federal/provincial/territorial and regional governments in making risk-management
decisions, playing an important role in air quality management (e.g., local source permitting, for
air quality index, and as benchmarks for developing provincial objectives and standards).
Additional Comments:
Up until 1998, Canada had a three-tiered system of NAAQOs (desireable, tolerable, and
acceptable levels). The current framework establishes a single level NAAQO, which is a
national goal for outdoor air quality that protects public health, the environment, or aesthetic
properties of the environment. It represents the air quality management goal for the protection of
the general public and the environment of Canada.
Reference and Supporting Documentation:
Federal-Provincial Working Group on Air Quality Objectives and Guidelines (WGAQOG).
1996. A protocol for the development of national ambient objectives, Part 1, Science assessment
document and derivation of the reference level(s). Catalogue #En42-17/5-1-1997E. Environment
Canada and Health Canada, Toronto and Ottawa, ON.
Health Canada. 2007. Regulations Related To Health And Air Quality. National Ambient Air
Quality Objectives (NAAQOs). Health Canada, Ottawa, ON. http://www.hc-sc.gc.ca/ewh­
semt/air/out-ext/reg_e.html (accessed 10 July 2007).
Assessment Report on Nitrogen Dioxide for Developing Ambient Air Quality Objectives
67
Agency:
Alberta Environment (AENV).
Air Quality Guideline:
Ambient air quality objectives (AAQOs):
Annual AAAQG: 32 ppb (60 µg m-3)
24-hour AAAQG: 106 ppb (200 µg m-3)
1-hour AAAQG: 212 ppb (400 µg m-3)
Averaging Time To Which Guideline Applies:
See above.
Basis for Development:
Alberta AAQOs are based on an evaluation of scientific, social, technical, and economic factors.
In the case of nitrogen dioxide, odour perception represented the endpoint driving its
development at the time.
Date Guideline Developed:
1975.
How Guideline is Used:
Used by Alberta Environment to establish approval conditions and can be used to assess
compliance and evaluate performance at industrial facilities.
Additional Comments:
Reference and Supporting Documentation:
Alberta Environment. 2005. Alberta Ambient Air Quality Objectives. Facts At Your Fingertips.
Alberta Environment, Environmental Policy Branch, Edmonton, AB. April 2005. 4 pp.
http://environment.gov.ab.ca/info/library/5726.pdf (accessed 10 July 2007).
Assessment Report on Nitrogen Dioxide for Developing Ambient Air Quality Objectives
68
Agency:
British Columbia Ministry of Environment (MOE).
Air Quality Guideline:
British Columbia MOE does not have an air quality guideline for this chemical. Canadian
NAAQOs are used.
Averaging Time To Which Guideline Applies:
Basis for Development:
Date Guideline Developed:
How Guideline is Used:
Additional Comments:
Reference and Supporting Documentation:
British Columbia Ministry of Environment (MOE). 2007. Air Quality Objectives and Standards,
Air Quality Objectives for British Columbia and Canada. British Columbia MOE, Victoria, BC.
http://www.env.gov.bc.ca/air/airquality/pdfs/aqotable.pdf (accessed 10 July 2007).
Assessment Report on Nitrogen Dioxide for Developing Ambient Air Quality Objectives
69
Agency:
Manitoba Conservation.
Air Quality Guideline:
Ambient air quality criteria (AAQC):
Maximum desirable level:
Annual AAAQG: 32 ppb (60 µg m-3)
Maximum tolerable level:
Annual AAAQG: 53 ppb (100 µg m-3)
24-hour AAAQG: 106 ppb (200 µg m-3)
1-hour AAAQG: 212 ppb (400 µg m-3)
Maximum acceptable level:
24-hour AAAQG: 160 ppb (300 µg m-3)
1-hour AAAQG: 532 ppb (1,000 µg m-3)
Averaging Time To Which Guideline Applies:
See above.
Basis for Development:
Canadian NAAQOs are used.
Date Guideline Developed:
Unknown.
How Guideline is Used:
Ambient air quality criteria are intended to serve as a guide by Manitoba Conservation for the
evaluation of air quality and for planning purposes
Additional Comments:
Reference and Supporting Documentation:
Manitoba Conservation. 2005. Objectives and Guidelines for Various Air Pollutants: Ambient
Air Quality Criteria (updated July, 2005). Manitoba Conservation, Air Quality Section,
Winnipeg, MB. http://www.gov.mb.ca/conservation/airquality/aq-criteria/ambientair_e.html
(accessed 10 July 2007).
Assessment Report on Nitrogen Dioxide for Developing Ambient Air Quality Objectives
70
Agency:
Ontario Ministry of the Environment (OME).
Air Quality Guideline:
Ambient air quality criteria (AAQC):
24-hour AAAQG: 200 µg m-3
1-hour AAAQG: 400 µg m-3
Averaging Time To Which Guideline Applies:
See above
Basis for Development:
Ontario developed their AAQC for nitrogen dioxide based on health endpoints.
Date Guideline Developed:
2005.
How Guidelines Used:
Used by OME to review permit applications for stationary sources that emit nitrogen dioxide to
the atmosphere.
Additional Comments:
Reference and Supporting Documentation:
Ontario Ministry of the Environment (OME). 2005. Summary of O. Reg. 419/05 Standards and
Point of Impingement Guidelines & Ambient Air Quality Criteria (AAQC). Standards
Development Branch, Ontario Ministry of the Environment, Toronto, ON. December 2005. 16
pp. http://www.ene.gov.on.ca/envision/gp/2424e04.pdf (accessed 10 July 2007).
Assessment Report on Nitrogen Dioxide for Developing Ambient Air Quality Objectives
71
Agency:
Nova Scotia Environment and Labour.
Air Quality Guideline:
Maximum permissible ground level concentrations:
Annual concentration: 100 µg m-3
1-hour concentration: 400 µg m-3
Averaging Time To Which Guideline Applies:
See above.
Basis for Development:
Not stated.
Date Guideline Developed:
February 2005.
How Guideline is Used:
Used by Nova Scotia Environment to establish approval conditions and to assess compliance and
evaluate performance at industrial facilities.
Additional Comments:
Reference and Supporting Documentation:
Nova Scotia Environment and Labour. 2005. Air Quality Regulations made under Section 112 of
the Environment Act. Nova Scotia Environment and Labour, Halifax, NS. February 2005.
http://www.gov.ns.ca/enla/air/ (accessed 10 July 2007).
Assessment Report on Nitrogen Dioxide for Developing Ambient Air Quality Objectives
72
Agency:
US Agency for Toxic Substances and Disease Registry (ATSDR).
Air Quality Guideline:
US ATSDR does not have an air quality guideline for this chemical.
Averaging Time To Which Guideline Applies:
Basis for Development:
Date Guideline Developed:
How Guideline is Used:
Additional Comments:
Reference and Supporting Documentation:
Agency for Toxic Substances and Disease Registry (ATSDR). 2007. Minimal Risk Levels
(MRLs) for Hazardous Substances. ATSDR, Public Health Service, US Department of Health
and Human Services. Atlanta, GA. http://www.atsdr.cdc.gov/mrls/index.html (accessed 10 July
2007).
Assessment Report on Nitrogen Dioxide for Developing Ambient Air Quality Objectives
73
Agency:
US Environmental Protection Agency (EPA).
Air Quality Guideline:
National ambient air quality standard (NAAQS):
Primary Standard: 100 µg m-3
Secondary Standard: 100 µg m-3
Averaging Time To Which Guideline Applies:
Annual average.
Basis for Development:
Primary standards set limits to protect public health, including the health of "sensitive"
populations such as asthmatics, children, and the elderly.
Secondary standards set limits to protect public welfare, including protection against visibility
impairment, damage to animals, crops, vegetation, and buildings.
Date Guideline Developed:
1993.
How Guideline is Used:
The United States Clean Air Act (CAA) requires US EPA to set primary National Ambient Air
Quality Standards (NAAQS) for commonly occurring air pollutants that pose public health
threats. US EPA permits states to adopt additional or more protective air quality standards if
needed At a minimum, US states are required to use these or more stringent standards for permit
applications for nitrogen dioxide sources and as criteria to monitor and investigate air quality.
Additional Comments:
Reference and Supporting Documentation:
US Environmental Protection Agency (EPA). 2007. National Ambient Air Quality Standards
(NAAQSs). US EPA Technology Transfer Network. US EPA, Washington, D.C.
http://www.epa.gov/ttn/naaqs/ (accessed 10 July 2007).
US Environmental Protection Agency (EPA). 1993. Air Quality Criteria for Oxides of Nitrogen:
Final Report. EPA/600/8-91/049aF-cF. US EPA, Washington, D.C.
http://cfpub.epa.gov/ncea/cfm/recordisplay.cfm?deid=40179 (accessed 10 July 2007).
Assessment Report on Nitrogen Dioxide for Developing Ambient Air Quality Objectives
74
Agency:
Arizona Department of Environmental Quality (DEQ).
Air Quality Guideline:
National ambient air quality standard (NAAQS):
Primary Standard: 100 µg m-3
Secondary Standard: 100 µg m-3
Averaging Time To Which Guideline Applies:
Annual average.
Basis for Development:
Arizona DEQ has adopted the US Environmental Protection Agency NAAQS as the state
ambient air quality standards.
Date Guideline Developed:
Unknown.
How Guideline is Used:
These standards are used by Arizona DEQ for regulating the emission of nitrogen dioxide from
industries and investigating complaints and violations of Arizona'
s air quality laws.
Additional Comments:
Reference and Supporting Documentation:
Arizona Department of Environmental Quality (DEQ). 2007. National Ambient Air Quality
Standards. Arizona DEQ, Air Quality Division, Phoenix, AZ.
http://www.azdeq.gov/environ/air/download/naaqs.pdf (accessed 10 July 2007).
Assessment Report on Nitrogen Dioxide for Developing Ambient Air Quality Objectives
75
Agency:
California Environmental Protection Agency (Cal EPA).
Air Quality Guideline:
California ambient air quality standard (CAAQS): 470 µg m-3 (1-hour)
National ambient air quality standard (NAAQS):
Primary Standard: 100 µg m-3
Secondary Standard: 100 µg m-3
Averaging Time To Which Guideline Applies:
CAAQS: 1 hour average.
NAAQS: annual average.
Basis for Development:
The California Air Resources Board (CARB) adopted the U.S. EPA ambient air quality
standards that define good air quality. These levels are the ambient air quality standards and
were established to protect human health and/or welfare. CARB has also set a 1-hour standard
for nitrogen dioxide that is not addressed by federal standards.
Date Guidelines Developed:
Unknown.
How Guideline is Used:
These standards are used by CARB for regulating the emission of nitrogen dioxide from
industries and investigating complaints and violations of state air quality laws.
Additional Comments:
Reference and Supporting Documentation:
California Air Resources Board (CARB). 2007. California Ambient Air Quality Standards
(CAAQS). CARB, Sacramento, CA. http://www.arb.ca.gov/research/aaqs/caaqs/caaqs.htm
(accessed July 10, 2007).
Assessment Report on Nitrogen Dioxide for Developing Ambient Air Quality Objectives
76
Agency:
Indiana Department of Environmental Management (IDEM).
Air Quality Guideline:
Ambient air quality standards (AAQSs):
Primary Standard: 100 µg m-3
Secondary Standard: 100 µg m-3
Averaging Time To Which Guideline Applies:
Annual average.
Basis for Development:
IDEM has adopted the US Environmental Protection Agency NAAQS as the state ambient air
quality standards.
Date Guideline Developed:
Unknown.
How Guideline is Used:
These standards are used by IDEM for regulating the emission of nitrogen dioxide from
industries and investigating complaints and violations of state air quality laws.
Additional Comments:
Reference and Supporting Documentation:
Indiana Department of Environmental Management (DEM). 2007. Ambient Air Quality
Standards, 326 IAC 1-3. Indiana DEM, Office of Air Quality, Indianapolis, IN.
http://www.in.gov/idem/rules/agency.html#air (accessed 10 July 2007).
Assessment Report on Nitrogen Dioxide for Developing Ambient Air Quality Objectives
77
Agency:
Louisiana Department of Environmental Quality (DEQ).
Air Quality Guideline:
Ambient air quality standards (AAQSs):
Primary Standard: 100 µg m-3
Secondary Standard: 100 µg m-3
Averaging Time To Which Guideline Applies:
Annual averaging time.
Basis for Development:
Louisiana DEQ has adopted the US Environmental Protection Agency NAAQS as the state
ambient air quality standards.
Date Guideline Developed:
Unknown.
How Guideline is Used:
Louisiana DEQ uses the standards to define the limits of air contamination, above which limits
the ambient air is declared to be unacceptable and requires air pollution control measures. These
standards are further used by Louisiana DEQ to review permit applications for stationary sources
that emit nitrogen dioxide to the atmosphere.
Additional Comments:
Reference and Supporting Documentation:
Louisiana Department of Environmental Quality (DEQ). 2003. Louisiana Administrative Code
(LAC). Title 33 Environmental Quality, Part III Air, Chapter 7. Ambient Air Quality. Louisiana
DEQ, Baton Rouge, LA. http://www.deq.louisiana.gov/portal/tabid/1674/Default.aspx#Title33
(accessed 10 July 2007).
Assessment Report on Nitrogen Dioxide for Developing Ambient Air Quality Objectives
78
Agency:
Massachusetts Department of Environmental Protection (DEP).
Air Quality Guideline:
Ambient air quality standards (AAQSs):
Primary Standard: 100 µg m-3
Secondary Standard: 100 µg m-3
Averaging Time To Which Guideline Applies:
Annual average.
Basis for Development:
Massachusetts DEP has adopted the US Environmental Protection Agency NAAQS as the state
ambient air quality standards.
Date Guideline Developed:
Unknown.
How Guideline is Used:
These standards are used by Massachusetts DEP for regulating the emission of nitrogen dioxide
from industries and investigating complaints and violations of state air quality laws.
Additional Comments:
Reference and Supporting Documentation:
Massachusetts Department of Environmental Protection (DEP). 2007. Ambient Air Quality
Standards for the Commonwealth of Massachusetts. 310 CMR 6.00. Massachusetts DEP,
Boston, MA. http://www.mass.gov/dep/air/laws/regulati.htm#ambient (accessed 10 July 2007).
Assessment Report on Nitrogen Dioxide for Developing Ambient Air Quality Objectives
79
Agency:
Michigan Department of Environmental Quality (DEQ).
Air Quality Guideline:
Ambient air quality standards (AAQSs):
Primary Standard: 100 µg m-3
Secondary Standard: 100 µg m-3
Averaging Time To Which Guideline Applies:
Annual average.
Basis for Development:
Michigan DEQ has adopted the US Environmental Protection Agency NAAQS as the state
ambient air quality standards.
Date Guideline Developed:
1994.
How Guideline is Used:
These standards are used by Michigan DEQ for regulating the emission of nitrogen dioxide from
industries and investigating complaints and violations of state air quality laws.
Additional Comments:
Reference and Supporting Documentation:
Michigan Department of Environmental Quality (DEQ). 1994. Natural Resources and
Environmental Protection Act 451 of 1994, Part 55 Air Pollution Control, Section 324.5512
Rules. Michigan DEQ, Air Quality Division, Lansing, MI.
http://www.michigan.gov/deq/0,1607,7-135-3310_4108-10415--,00.html (accessed 10 July
2007).
Assessment Report on Nitrogen Dioxide for Developing Ambient Air Quality Objectives
80
Agency:
Minnesota Pollution Control Agency (MCPA).
Air Quality Guideline:
State ambient air quality standards:
Primary Standard: 100 µg m-3
Secondary Standard: 100 µg m-3
Averaging Time To Which Guideline Applies:
Annual average.
Basis for Development:
MPCA has adopted the US Environmental Protection Agency NAAQS as the state ambient air
quality standards.
Date Guideline Developed:
Updated April 2000.
How Guideline is Used:
These standards are used by MCPA for regulating the emission of nitrogen dioxide from
industries and investigating complaints and violations of state air quality laws.
Additional Comments:
Reference and Supporting Documentation:
Minnesota Pollution Control Agency (MCPA). 2007. State Ambient Air Quality Standards.
Minnesota R. 7009.0080. MCPA, St. Paul, MN. http://www.revisor.leg.state.mn.us/arule/7009/
(accessed 10 July 2007).
Assessment Report on Nitrogen Dioxide for Developing Ambient Air Quality Objectives
81
Agency:
New Hampshire Department of Environmental Services (DES).
Air Quality Guideline:
State ambient air quality standards:
Primary Standard: 100 µg m-3
Secondary Standard: 100 µg m-3
Averaging Time To Which Guideline Applies:
Annual average.
Basis for Development:
New Hampshire DES has adopted the US Environmental Protection Agency NAAQS as the state
ambient air quality standards.
Date Guideline Developed:
April 1996.
How Guideline is Used:
These standards are used by New Hampshire DES to review permit applications for sources that
emit nitrogen dioxide to the atmosphere. Sources are regulated through a statewide air
permitting system and include any new, modified or existing stationary source, area source or
device.
Additional Comments:
Reference and Supporting Documentation:
New Hampshire Department of Environmental Services (DES). 2007. New Hampshire
Administrative Rule. Chapter Env-A 300. Ambient Air Quality Standards. New Hampshire DES,
Concord, NH. http://www.des.state.nh.us/Rules/air.htm (accessed 10 July 2007).
Assessment Report on Nitrogen Dioxide for Developing Ambient Air Quality Objectives
82
Agency:
New Jersey Department of Environmental Protection (NJDEP).
Air Quality Guideline:
State ambient air quality standards:
Primary Standard: 100 µg m-3
Secondary Standard: 100 µg m-3
Averaging Time To Which Guideline Applies:
Annual average.
Basis for Development:
NJDEP has adopted the US Environmental Protection Agency NAAQS as the state ambient air
quality standards.
Date Guideline Developed:
Updated in 1991.
How Guideline is Used:
These standards are used by NJDEP for regulating the emission of nitrogen dioxide from
industries and investigating complaints and violations of state air quality laws.
Additional Comments:
Reference and Supporting Documentation:
New Jersey Department of Environmental Protection (NJDEP). 2007. Ambient Air Quality
Standards. N.J.A.C. 7:27-13. NJDEP, Trenton, NJ. http://www.state.nj.us/dep/aqm/rules.html
(accessed 10 July 2007).
Assessment Report on Nitrogen Dioxide for Developing Ambient Air Quality Objectives
83
Agency:
North Carolina Department of Environment and Natural Resources (ENR).
Air Quality Guideline:
State ambient air quality standards:
Primary Standard: 100 µg m-3
Secondary Standard: 100 µg m-3
Averaging Time To Which Guideline Applies:
Annual average.
Basis for Development:
North Carolina ENR has adopted the US Environmental Protection Agency NAAQS as the state
ambient air quality standards.
Date Guideline Developed:
Last updated October 1989.
How Guideline is Used:
These standards are used by North Carolina ENR for regulating the emission of nitrogen dioxide
from industries and investigating complaints and violations of state air quality laws.
Additional Comments:
Reference and Supporting Documentation:
North Carolina Department of Environment and Natural Resources (ENR). 2007. North Carolina
Administrative Code (NCAC), North Carolina Air Quality Rules 15A NCAC 02D .0407 –
Nitrogen Dioxide. North Carolina ENR, Raleigh, NC. http://reports.oah.state.nc.us/ncac.asp
(accessed 10 July 2007).
Assessment Report on Nitrogen Dioxide for Developing Ambient Air Quality Objectives
84
Agency:
Ohio Environmental Protection Agency (EPA).
Air Quality Guideline:
State ambient air quality standards:
Primary Standard: 100 µg m-3
Secondary Standard: 100 µg m-3
Averaging Time To Which Guideline Applies:
Annual average.
Basis for Development:
Ohio EPA has adopted the US Environmental Protection Agency NAAQS as the state ambient
air quality standards.
Date Guideline Developed:
Unknown.
How Guideline is Used:
These standards are used by Ohio EPA for regulating the emission of nitrogen dioxide from
industries and investigating complaints and violations of state air quality laws.
Additional Comments:
Reference and Supporting Documentation:
Ohio Environmental Protection Agency (EPA). 2007. Nitrogen Oxide Standards, Ohio
Administrative Code (OAC) 3745-23. Ohio EPA, Division of Air Pollution Control, Columbus,
OH. http://www.epa.state.oh.us/dapc/regs/regs.html (accessed 10 July 2007).
Assessment Report on Nitrogen Dioxide for Developing Ambient Air Quality Objectives
85
Agency:
Oklahoma Department of Environmental Quality (DEQ).
Air Quality Guideline:
State ambient air quality standards:
Primary Standard: 100 µg m-3
Secondary Standard: 100 µg m-3
Averaging Time To Which Guideline Applies:
Annual average.
Basis for Development:
Oklahoma DEQ has adopted the US Environmental Protection Agency NAAQS as the state
ambient air quality standards.
Date Guideline Developed:
Updated 1/14/1994.
How Guideline is Used:
These standards are used by Oklahoma DEQ for regulating the emission of nitrogen dioxide
from industries and investigating complaints and violations of state air quality laws.
Additional Comments:
Reference and Supporting Documentation:
Oklahoma Department of Environmental Quality (DEQ). 2007. Oklahoma Administrative Code
(OAC). Title 252. Chapter 100. Air Pollution Control. Primary Standards 100:100-3-2 and
Secondary Standards 100-3-3. Oklahoma DEQ, Oklahoma City, OK.
http://www.sos.state.ok.us/oar/oar_welcome.htm (accessed 10 July 2007).
Assessment Report on Nitrogen Dioxide for Developing Ambient Air Quality Objectives
86
Agency:
Pennsylvania Department of Environmental Protection (DEP).
Air Quality Guideline:
State ambient air quality standards:
Primary Standard: 100 µg m-3
Secondary Standard: 100 µg m-3
Averaging Time To Which Guideline Applies:
Annual average.
Basis for Development:
Pennsylvania DEP has adopted the US Environmental Protection Agency NAAQS as the state
ambient air quality standards.
Date Guideline Developed:
September 1971.
How Guideline is Used:
These standards are used by Pennsylvania DEP for regulating the emission of nitrogen dioxide
from industries and investigating complaints and violations of state air quality laws.
Additional Comments:
Reference and Supporting Documentation:
Pennsylvania Department of Environmental Protection (DEP). 2007. Pennsylvania State Code,
Title 25 Environmental Protection, Article III Air Resources, Section 131.1 Ambient Air Quality
Standards. Pennsylvania DEP, Bureau of Air Quality, Harrisburg, PA.
http://www.pacode.com/secure/data/025/chapter131/chap131toc.html (accessed 10 July 2007).
Assessment Report on Nitrogen Dioxide for Developing Ambient Air Quality Objectives
87
Agency:
Rhode Island Department of Environmental Management (DEM).
Air Quality Guideline:
State ambient air quality standards:
Primary Standard: 100 µg m-3
Secondary Standard: 100 µg m-3
Averaging Time To Which Guideline Applies:
Annual average.
Basis for Development:
Rhode Island DEM has adopted the US Environmental Protection Agency NAAQS as the state
ambient air quality standards.
Date Guideline Developed:
Last updated March 1993.
How Guideline is Used:
These standards are used by Rhode Island DEM for regulating the emission of nitrogen dioxide
from industries and investigating complaints and violations of state air quality laws.
Additional Comments:
Reference and Supporting Documentation:
Rhode Island Department of Environmental Management (DEM). 2007. Air Pollution Control
Regulation #7, Emission of Air Contaminants Detrimental to Person or Property. Division of Air
and Hazardous Materials, Rhode Island DEM, Providence, RI.
http://www.dem.ri.gov/pubs/regs/index.htm#Air (accessed 10 July 2007).
Assessment Report on Nitrogen Dioxide for Developing Ambient Air Quality Objectives
88
Agency:
Texas Commission on Environmental Quality (CEQ) – formerly Texas Natural Resource
Conservation Commission (TRNCC).
Air Quality Guideline:
State ambient air quality standards:
Primary Standard: 100 µg m-3
Secondary Standard: 100 µg m-3
Averaging Time To Which Guideline Applies:
Annual average.
Basis for Development:
Texas CEQ has adopted the US Environmental Protection Agency NAAQS as the state ambient
air quality standards.
Date Guideline Developed:
Unknown.
How Guideline is Used:
These standards are used by Texas CEQ for regulating the emission of nitrogen dioxide from
industries and investigating complaints and violations of state air quality laws.
Additional Comments:
Reference and Supporting Documentation:
Texas Commission on Environmental Quality (CEQ). 2007. The National Ambient Air Quality
Standards. Texas CEQ, Austin, TX.
http://www.tceq.state.tx.us/compliance/monitoring/air/monops/naaqs.html (accessed 10 July
2007).
Assessment Report on Nitrogen Dioxide for Developing Ambient Air Quality Objectives
89
Agency:
Vermont Agency of Natural Resources (ANR).
Air Quality Guideline:
State ambient air quality standards:
Primary Standard: 100 µg m-3
Secondary Standard: 100 µg m-3
Averaging Time To Which Guideline Applies:
Annual average.
Basis for Development:
Vermont ANR has adopted the US Environmental Protection Agency NAAQS as the state
ambient air quality standards.
Date Guideline Developed:
Last updated December 2003.
How Guideline is Used:
These standards are used by Vermont ANR for regulating the emission of nitrogen dioxide from
industries and investigating complaints and violations of state air quality laws.
Additional Comments:
Reference and Supporting Documentation:
Vermont Agency of Natural Resources (ANR). 2003. Air Pollution Control Regulations.
Subchapter III Ambient Air Quality Standards, 5-309 Nitrogen Dioxide, Primary and Secondary
Ambient Air Quality Standards. State of Vermont ANR, Air Pollution Control Division,
Waterbury, VT. http://www.anr.state.vt.us/air/docs/apcregs.pdf (accessed 10 July 2007).
Assessment Report on Nitrogen Dioxide for Developing Ambient Air Quality Objectives
90
Agency:
Washington State Department of Ecology (DOE).
Air Quality Guideline:
State ambient air quality standards:
Primary Standard: 100 µg m-3
Secondary Standard: 100 µg m-3
Averaging Time To Which Guideline Applies:
Annual average.
Basis for Development:
Washington DOE has adopted the US Environmental Protection Agency NAAQS as the state
ambient air quality standards.
Date Guideline Developed:
Unknown.
How Guideline is Used:
These standards are used by Washington DOE for regulating the emission of nitrogen dioxide
from industries and investigating complaints and violations of state air quality laws.
Additional Comments:
Reference and Supporting Documentation:
Washington State Department of Ecology (DOE). 2007. Chapter 173-475 WAC. Ambient Air
Quality Standards for Carbon Monoxide, Ozone, and Nitrogen Dioxide. Washington State DOE,
Olympia, WA. http://apps.leg.wa.gov/wac/default.aspx?cite=173 (accessed 10 July 2007).
Assessment Report on Nitrogen Dioxide for Developing Ambient Air Quality Objectives
91
Agency:
Wisconsin Department of Natural Resources (DNR).
Air Quality Guideline:
State ambient air quality standards:
Primary Standard: 100 µg m-3
Secondary Standard: 100 µg m-3
Averaging Time To Which Guideline Applies:
Annual average.
Basis for Development:
Wisconsin DNR has adopted the US Environmental Protection Agency NAAQS as the state
ambient air quality standards.
Date Guideline Developed:
Unknown
How Guideline is Used:
These standards are used by Wisconsin DNR for regulating the emission of nitrogen dioxide
from industries and investigating complaints and violations of state air quality laws.
Additional Comments:
Reference and Supporting Documentation:
Wisconsin Department of Natural Resources (DNR). 2007. Wisconsin Administrative Code
(WAC). Air Pollution Control Rules. Chapter NR 404. Ambient Air Quality. Wisconsin DNR,
Madison WI. http://www.legis.state.wi.us/rsb/code/nr/nr404.pdf (accessed 10 July 2007).
Assessment Report on Nitrogen Dioxide for Developing Ambient Air Quality Objectives
92
Agency:
Australia Environment Protection and Heritage Council (EPHC).
Air Quality Guideline:
National Air Quality Standards:
Annual AAAQG: 30 ppb (56 µg m-3)
1-hour AAAQG: 120 ppb (226 µg m-3)
Averaging Time To Which Guideline Applies:
See above.
Basis for Development:
The standards were developed on the basis of scientific studies of air quality and human health
from all over the world, as well as the standards set by other organizations, such as the World
Health Organization. Australian conditions, e.g., climate, geography, and demographics, were
taken into account in estimating exposure of Australians to this air pollutant. The air quality
standard for each pollutant has two elements: the maximum acceptable concentration and the
period of time period over which the concentration is averaged.
Date Guideline Developed:
1998.
How Guideline is Used:
The standards are legally binding on each level of Government in Australia, and must be met by
the year 2008. The National Environment Protection Measure for Ambient Air Quality (Air
NEPM) requires Australian jurisdictions to monitor air quality and the standard helps to identify
potential air quality problems. All jurisdictions commenced formal reporting against Air NEPM
standards in 2002.
Additional Comments:
Reference and Supporting Documentation:
Australia Environment Protection and Heritage Council (EPHC). 1998. National Standards for
Criteria Air Pollutants in Australia, Air quality fact sheet. Australia EPHC, Department of the
Environment and Heritage, Adelaide, Australia.
http://www.environment.gov.au/atmosphere/airquality/publications/standards.html (accessed 10
July 2007).
Assessment Report on Nitrogen Dioxide for Developing Ambient Air Quality Objectives
93
Agency:
New Zealand Ministry for the Environment (MOE) and New Zealand Ministry of Health
(MOH).
Air Quality Guideline:
Ambient air quality standard: 200 µg m-3 (9 exceedances are allowed per year).
Averaging Time To Which Guideline Applies:
1-hour average.
Basis for Development:
The guideline was developed following a comprehensive review of international and national
research, and are widely accepted amongst New Zealand practitioners.
Date Guideline Developed:
2005.
How Guideline is Used:
The ambient standard is the minimum requirements that outdoor air quality should meet in order
to guarantee a set level of protection for human health and the environment. The regulations
place a requirement on New Zealand regional councils to monitor air quality and to report
exceedances to the public.
Additional Comments:
Reference and Supporting Documentation:
New Zealand Ministry for the Environment. 2004. National Environmental Standards for Air
Quality. New Zealand Ministry for the Environment, Wellington, New Zealand.
http://www.mfe.govt.nz/laws/standards/air-quality-standards.html (accessed 10 July 2007).
Assessment Report on Nitrogen Dioxide for Developing Ambient Air Quality Objectives
94
Agency:
UK Environment Agency.
Air Quality Guideline:
National air quality standard: 105 ppb (200 µg m-3) (1-hour average).
Local air quality objectives:
Annual average for protection of human health: 21 ppb (40 µg m-3)
Annual average for protection of vegetation: 16 ppb (30 µg m-3)
1-hour average:1 105 ppb (200 µg m-3)
1
not to be exceeded more than 18 times per year
Averaging Time To Which Guideline Applies:
1-hour average.
Basis for Development:
Unknown.
Date Guideline Developed:
2000.
How Guideline is Used:
The UK Government’s Air Quality Strategy for England, Scotland, Wales, and Northern Ireland
set national air quality standards to protect human health and vegetation.
Additional Comments:
Reference and Supporting Documentation:
UK Environment Agency. 2007. Air Quality Standards – An Overview. UK Environment
Agency, http://www.environment-agency.gov.uk/ (accessed 10 July 2007).
UK Department for the Environment, Food and Rural Affairs in partnership with the Scottish
Executive, The National Assembly for Wales, and the Department of the Environment for
Northern Ireland. 2000. The Air Quality Strategy for England, Scotland, Wales and Northern
Ireland. http://www.environment-agency.gov.uk/yourenv/eff/1190084/air/1158715/1159519/
(accessed 10 July 2007).
Assessment Report on Nitrogen Dioxide for Developing Ambient Air Quality Objectives
95
Agency:
European Commission.
Air Quality Guideline:
Limit Values:
Annual limit:1 40 µg m-3
Annual limit:2 30 µg m-3
1-hour limit:1,3 200 µg m-3
1
for protection of human health (to be achieved by January 2010)
for protection of vegetation (in effect since July 2001)
3
not to be exceeded more than 18 times a calendar year
2
Averaging Time To Which Guideline Applies:
See above.
Basis for Development:
Policy choice.
Date Guideline Developed:
1999.
How Guideline is Used:
Established numerical criteria relating to the assessment and management of nitrogen dioxide in
air in European Commission member countries.
Additional Comments:
European legislation on air quality is built on certain principles. The first of these is that member
countries divide their territory into a number of zones and agglomerations. In these zones and
agglomerations, the member countries are supposed to undertake assessments of air pollution
levels using measurements and modeling and other empirical techniques. Where levels are
elevated, member countries are supposed to prepare an air quality plan to ensure compliance
with the limit value before the date when the limit value formally enters into force. In addition,
information on air quality is supposed to be disseminated to the public.
Reference and Supporting Documentation:
Commission of the European Communities. 1999. Council Directive 1999/30/EC of 22 April
1999 relating to limit values for sulphur dioxide, nitrogen dioxide and oxides of nitrogen,
particulate matter and lead in ambient air. Official Journal of the European Communities. pp.
L163/41 to L163/60. European Commission, Brussels, Belgium.
http://europa.eu/scadplus/leg/en/lvb/l28031a.htm (accessed 10 July 2007).
Assessment Report on Nitrogen Dioxide for Developing Ambient Air Quality Objectives
96
Agency:
World Health Organization (WHO).
Air Quality Guideline:
Annual limit: 40 µg m-3
1-hour limit: 200 µg m-3
Averaging Time To Which Guideline Applies:
See above.
Basis for Development:
Based on review of more-recent animal and human experimental studies and epidemiological
studies.
Date Guideline Developed:
2005.
How Guideline is Used:
WHO air quality guidelines are designed to offer guidance in reducing the health impacts of air
pollution. These guidelines are intended to inform policy-makers and to provide appropriate
targets for a broad range of policy options for air quality management in different parts of the
world.
Additional Comments:
Reference and Supporting Documentation:
World Health Organization (WHO). 2006. WHO Air Quality Guidelines for Particulate Matter,
Ozone, Nitrogen Dioxide and Sulfur Dioxide, Global Update 2005, Summary of Risk
Assessment. WHO Press, World Health Organization, Geneva, Switzerland. 20 pp.
http://www.euro.who.int/Document/E87950.pdf (accessed 10 July 2007).
Assessment Report on Nitrogen Dioxide for Developing Ambient Air Quality Objectives
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