Assessment Report on Naphthalene for
Developing Ambient Air Quality Objectives
2013 Update
December 16, 2015
Assessment Report on Naphthalene for Developing Ambient Air Quality Objectives
2013 Update
Although prepared with funding from Alberta Environment and Parks (AEP), the contents of this
report/document do not necessarily reflect the views or policies of AEP, 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
Alberta Environment and Parks
12th floor, Baker Centre
10025 – 106th Street
Edmonton, Alberta T5J 1G4
ISBN 978-1-4601-2582-3 (Print)
ISBN 978-1-4601-2583-0 (PDF)
© 2015 Government of Alberta
Dec 2015
Assessment Report on Naphthalene for Developing Ambient Air Quality Objectives
2013 Update
© 2015 Government of Alberta
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Assessment Report on Naphthalene
for
Developing Ambient Air Quality Objectives
2013 Update
Prepared by
ENVIRON International Corporation
for
Alberta Environment and Parks
October 2013
Dec 2015
Assessment Report on Naphthalene for Developing Ambient Air Quality Objectives
2013 Update
© 2015 Government of Alberta
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Acknowledgements
ENVIRON International Corporation would like to acknowledge the following individuals who
contributed to this report:
Debra A. Kaden, Ph.D.
Kerrie Canavan
Farah Chowdhury
Joshua Gambrell
Greg Yarwood, Ph.D.
Allison Glessner
Taylor Roumeliotis, Ph.D.
Mike Jammer
Ted Pollock, Ph.D., P. Eng.
Dec 2015
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2013 Update
© 2015 Government of Alberta
Page 4 of 87
Table of Contents
Acknowledgements ..................................................................................................................................... 4
Table of Contents ........................................................................................................................................ 5
List of Tables ............................................................................................................................................... 7
Acronyms and Abbreviations .................................................................................................................... 8
Summary.................................................................................................................................................... 10
1.0
Introduction .................................................................................................................................. 11
2.0
General Substance Information.................................................................................................. 12
2.1
Physical and Chemical Properties ..................................................................................... 12
2.2
Emission Sources and Ambient Levels............................................................................. 12
2.2.1 Natural Sources .................................................................................................... 12
2.2.2 Anthropogenic Sources ........................................................................................ 14
2.2.3 Ambient Concentrations of Naphthalene ............................................................. 15
3.0
Atmospheric Chemistry and Fate............................................................................................... 17
4.0
Effects on Humans and Animals ................................................................................................ 18
4.1
Overview of Chemical Metabolism and Disposition ........................................................ 18
4.1.1 Toxicokinetics...................................................................................................... 18
4.1.2 Absorption ........................................................................................................... 18
4.1.3 Distribution .......................................................................................................... 19
4.1.4 Metabolism .......................................................................................................... 19
4.1.5 Excretion .............................................................................................................. 20
4.2
Effects on Humans ............................................................................................................ 21
4.2.1 Acute and Sub-Acute Human Effects .................................................................. 21
4.2.2 Chronic Human Effects ....................................................................................... 21
4.2.3 Carcinogenicity .................................................................................................... 21
4.3
Effects on Animals............................................................................................................ 22
4.3.1 Acute and Sub-Acute Effects ............................................................................... 22
4.3.1.1 Respiratory Effects ................................................................................. 22
4.3.2 Chronic Effects .................................................................................................... 26
4.3.2.1 Respiratory and Carcinogenic Effects .................................................... 27
4.3.2.2 Other Effects ........................................................................................... 27
4.4
Genotoxicity...................................................................................................................... 28
4.5
Health Effects Summary ................................................................................................... 29
4.5.1 Metabolism and Disposition ................................................................................ 29
4.5.2 Genotoxicity ........................................................................................................ 30
4.5.3 Acute Health Effects ............................................................................................ 30
4.5.4 Chronic Health Effects......................................................................................... 30
4.5.5 Overall Summary ................................................................................................. 30
5.0
Effects on Vegetation ................................................................................................................... 32
5.1
Vegetation ......................................................................................................................... 32
6.0
Effects on Materials ..................................................................................................................... 35
7.0
Air Sampling and Analytical Methods ....................................................................................... 36
7.1
Reference Methods ........................................................................................................... 36
7.1.1 US EPA Compendium Method TO-13A ............................................................. 36
7.1.2 NIOSH Method 1501 ........................................................................................... 36
7.1.3 NIOSH Method 5506 ........................................................................................... 36
7.1.4 NIOSH Method 5515 ........................................................................................... 37
7.1.5 OSHA Method 35 ................................................................................................ 37
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2013 Update
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7.2
Alternative Emerging Technologies ................................................................................. 37
7.2.1 EC and AEP Naphthalene Monitoring................................................................. 38
7.2.2 Passive Samplers.................................................................................................. 38
7.2.3 Cold Fiber-Solid Phase Microextraction (CF-SPME) ......................................... 38
7.2.4 Annular Denuders and Quartz Fibre Filter Membrane ........................................ 39
8.0
Ambient Objectives in Other Jurisdictions ............................................................................... 40
8.1
Naphthalene Air Quality Objectives and Guidelines ........................................................ 40
8.1.1 Canada 40
8.1.2 United States ........................................................................................................ 40
8.1.3 International Agencies ......................................................................................... 41
9.0
References ..................................................................................................................................... 43
APPENDIX A ............................................................................................................................................ 54
APPENDIX B ............................................................................................................................................ 56
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2013 Update
© 2015 Government of Alberta
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List of Tables
Table 1
Identifying information for naphthalenea .......................................................................... 13
Table 2
Physical and chemical properties for naphthalenea ........................................................... 13
Table 3
Annual on-site releases of naphthalene reported to the NPRI for Canada and Alberta for
2002 to 2011 ..................................................................................................................... 15
Table 4
Average annual concentrations of naphthalene in Albertareported to NAPS for 2002 to
2011 .................................................................................................................................. 16
Table 5
Acute and sub-acute effects associated with naphthalene exposure ................................. 23
Table 6
Chronic and sub-chronic effects associated with naphthalene exposure .......................... 26
Table 7
Newly identified genotoxicity studies .............................................................................. 28
Table 8
Growth of trees exposed to PAH and statistically significant differences compared to
controls.............................................................................................................................. 34
Table 9
Summary of Air Quality Objectives and Guidelines for Naphthalene ............................. 42
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2013 Update
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Acronyms and Abbreviations
AAQC
ACGIH
AEP
ANR
AQMS
ATSDR
EF
CE
CEC
CEQ
CF-SPME
Cytochrome P-450
CYP
OSHA
DEM
DEP
DEQ
DES
DH
DHS
DNR
DOE
EC
ENR
EPEA
GAP
GCS
GC/FID
GC/MS
GSH
HEI
HPLC
LOAEL
LOD
LOQ
MDL
MOE
Dec 2015
Ambient Air Quality Criteria
American Conference of Governmental Industrial Hygienists
Alberta Environment and Parks
Agency of Natural Resources
Air Quality Management System
Agency for Toxic Substances and Disease Registry
Emission Factor
Capillary Electrophoresis
Capillary Electrochromatography
Council on Environmental Quality
Cold Fiber- Solid Phase Microextraction
A large and diverse group of enzymes that catalyze the oxidation of
organic substances (also abbreviated CYP)
Cytochrome P-450
Occupational Safety and Health
Department of Environmental Management
Department of Environmental Protection
Department of Environmental Quality
Department of Environmental Services
Department of Health
Department of Health Services
Department of Natural Resources
Department of Ecology
Environment Canada
Environment and Natural Resources
Environmental Protection and Enhancement Act
Gas-and-Particle samplers
glutamylcysteine synthetase
Gas Chromatography with Flame Ionization Detector
Gas chromatography with mass spectroscopy
Glutathione
Health Effects Institute
Higher-Performance Liquid Chromatography
Lowest observed adverse effect level
Limit of Detection
Limit of Quantification
Method detection limit
Ministry of the Environment
Assessment Report on Naphthalene for Developing Ambient Air Quality Objectives
2013 Update
© 2015 Government of Alberta
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NAICS
NAPS
NIOSH
NOAEL
NOEL
NPRI
NTP
OSHA
OVM
P-450
PAH
PEL
ppb
ppm
PUF
REL
RfC
RIVM
SFE
SPME
SUMMA
US EPA
VOCs
WHO
Dec 2015
North American Industry Classification System
National Air Pollution Surveillance
National Institute of Occupational Safety and Health
No observed adverse effect level
No observed effect level
National Pollutant Release Inventory
National Toxicology Program
Occupational Safety and Health
Organic Vapour Monitors
Cytochrome P-450
Polycyclic Aromatic Hydrocarbon
Permissible Exposure Limit
parts per billion
parts per million
Polyurethane filter
Recommended Exposure Limit
Reference concentration
The Netherlands National Institute of Public Health and the Environment
Supercritical Fluid Extraction
Solid Phase Microextraction
Evacuated, Stainless Steel Electropolished Canister
United States Environmental Protection Agency
Volatile Organic Compounds
Wold Health Organization
Assessment Report on Naphthalene for Developing Ambient Air Quality Objectives
2013 Update
© 2015 Government of Alberta
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Summary
Naphthalene is a bicyclic aromatic hydrocarbon, the lowest molecular weight of all polycyclic aromatic
hydrocarbons (PAHs). It is produced from distillation of either petroleum or coal tar, and its main use
includes serving as an intermediate in the production of phthalic anhydride, which is used in the
manufacture of plasticizers, resins, dyes, and insect repellents. Naphthalene is also used in the
manufacture of synthetic leather tanning agents and the insecticide carbaryl, and has historically been
used as a moth repellent and as a deodorizer for diaper pails and toilets. Naphthalene occurs naturally in
fossil fuels such as petroleum and coal, and is produced when organic matter such as fossil fuels or wood
are burned.
Air emissions of naphthalene account for 92% of all naphthalene releases to the environment.
Naphthalene is a natural component of crude oil, and is also emitted as a product of incomplete
combustion. It may therefore be released naturally from wildfires. Anthropogenic sources of naphthalene,
largely the result of domestic combustion of wood and fossil fuels, are a much larger source of exposure.
Naphthalene emissions from gasoline and diesel exhaust as well as gasoline evaporation represent a
major, if not the largest, source in urban areas. Major industrial sources of naphthalene include coal tar
and coke production, oil and gas extraction, petroleum refining, petrochemical manufacturing, wood
preserving operations (creosote impregnation), asphalt industries (paving and roofing), wastewater
treatment plants, and many other smaller sources.
Naphthalene emitted to the atmosphere will exist mainly in the gas-phase at ambient temperatures;
naphthalene in air is destroyed by reaction with hydroxyl radicals with a typical half-life of less than a
day. Due to this short time in the atmosphere, naphthalene has limited potential for long-range transport.
Naphthalene is metabolized to by the cytochrome P-450 family of enzymes, with significant differences
observed among different species. The rate of metabolism is faster in rats as compared to other rodents or
primates. Animal studies have shown that exposure to naphthalene caused damage to the respiratory tract,
especially the nasal region in rats. These effects include inflammation, metaplasia of the nasal olfactory
epithelium, and hyperplasia of the respiratory epithelium. In mice, naphthalene also causes damage to
ciliated and Clara cells of the bronchiolar epithelium, but rat lungs are somewhat resistant to this toxicity.
A differential toxicity among species is observed; these differences appear to be due, at least in part, to
differences in rates of metabolism.
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2013 Update
© 2015 Government of Alberta
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1.0
Introduction
Alberta Environment and Parks (AEP) develops ambient air quality objectives and guidelines under the
Alberta Environmental Protection and Enhancement Act (EPEA). Alberta’s Air Quality Management
System (AQMS) uses scientific, economic, and social information to achieve the objectives.
The purpose of this assessment report is to summarize recent scientific literature to support the
development of a new ambient air quality objective for naphthalene. This report is an update to a previous
assessment, “Review of Approaches for Setting an Objective for Mixtures in Ambient Air using
Polycyclic Aromatic Hydrocarbons (PAHs) as an Example – Naphthalene,” (Alberta Environment, 2004).
Naphthalene’s physical and chemical properties determine its behavior in the environment. Naphthalene’s
environmental presence is determined mainly due to emission sources and ambient concentrations.
Environment Canada’s National Pollutant Release Inventory (NPRI) provides anthropogenic emission of
naphthalene in Alberta and other jurisdictions provide emission information. This information is
reviewed in Section 2. Section 3 reviews the atmospheric chemistry and fate of naphthalene.
Scientific information on the effects of naphthalene on humans, animals, and materials is reported in
Section 4. Scientific literature was identified through literature searches of published scientific journals
and reports. Information includes toxicology, epidemiology, and ecology studies of effects due to
naphthalene exposure. To help put this information in context, Section 4 also reviews the metabolism and
disposition of naphthalene in animals and humans.
Sections 5 and 6 present information about the effects of naphthalene on vegetation and materials.
Methods currently used to measure volatile compounds in ambient air and alternative emerging
technologies for air sampling and analytical methods are reported in Section 7.
Ambient air guidelines for naphthalene are set in multiple jurisdictions. Guidelines are created on the
basis of occupational exposure and safety factors or non-cancer risk assessment procedures. Different
jurisdictional guidelines and approaches are analyzed and presented in Section 8 and Appendix B.
Fully analyzing the properties of naphthalene, effects on health and the environment, sampling methods,
and other jurisdictional guidelines will help the province of Alberta develop an ambient air objective for
naphthalene.
Dec 2015
Assessment Report on Naphthalene for Developing Ambient Air Quality Objectives
2013 Update
© 2015 Government of Alberta
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2.0
General Substance Information
Naphthalene is a bicyclic aromatic hydrocarbon, the lowest molecular weight of all polycyclic aromatic
hydrocarbons (PAHs). In its pure form, naphthalene is a white, water-insoluble solid at room temperature
but evaporates easily (United States Environmental Protection Agency (US EPA), 1998; Agency for
Toxic Substances and Disease Registry (ATSDR), 2005). Naphthalene has a strong, but not unpleasant
smell and vapors burn easily in air; the chemical can be detected by its odour at 440 μg m-3 (84 ppb) in air
and at 21 ppb in water (ATSDR, 2005).
Naphthalene is produced from distillation of either petroleum or coal tar. Its main uses include serving as
an intermediate in the production of phthalic anhydride, which is used in the manufacture of plasticizers,
resins, dyes, and insect repellents (EPA, 1998). Naphthalene is also used in the manufacture of synthetic
leather tanning agents and the insecticide carbaryl, and has historically been used as a moth repellent and
as a deodourizer for diaper pails and toilets (EPA, 1998).
Naphthalene occurs naturally in fossil fuels such as petroleum and coal, and is produced when organic
matter such as fossil fuels or wood are burned. Due to its ubiquitous nature in fuels and organic matter as
well as its use as an intermediate in the production of plasticizers, resins, and insecticides, naphthalene is
commonly found in industrial and automobile emissions and is present in water and air in the ambient
environment. Older style moth repellants were primarily comprised of naphthalene (ATSDR, 2005).
Table 1 provides information on naphthalene’s chemical structure and formula as well as a list of
identification numbers and common synonyms.
2.1
Physical and Chemical Properties
Physical and chemical properties of naphthalene are summarized in Table 2.
2.2
Emission Sources and Ambient Levels
Air emissions of naphthalene account for 92% of all naphthalene releases to the environment (ATSDR,
2003). Data collected over the past ten years from the NPRI (Environment Canada (EC), 2013b) suggests
that between 96.3% to greater than 99.9% of industrial facility’s on-site naphthalene releases were
emitted directly to air.
2.2.1
Natural Sources
Naphthalene is a natural component of crude oil and may evaporate or sublimate from this natural source.
Naphthalene is also emitted as a product of incomplete combustion and thus, may also be released
naturally from wildfires (Alberta Environment, 2004; HSDB, 2004; Jia and Batterman, 2010). Published
studies on naphthalene emission factors (EFs) for wood combustion were summarized by Jia and
Batterman (2010). These EFs generally range from less than 10 to 75 mg naphthalene per kg wood and
depend heavily on the type of wood.
Dec 2015
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2013 Update
© 2015 Government of Alberta
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Table 1
Identifying information for naphthalenea
Property
Chemical Formula
Chemical Structure
C10H8
CAS Registry Number
US EPA Chem. Sub. Inventory Number
US RCRA Waste Number
91-20-3
72931-45-4
U165
RTECS Number
UN Number
EU Inventory of Existing Commercial Chemical
Substance Number
Common Synonyms and Trade Names:
Albocarbon
Mighty 150 (RTECS)
Camphor tar
Mighty RD1 (RTECS)
Caswell No. 587
Moth balls
Dezodorator
Moth flakes
EPA Pesticide Chemical
Naftalen
Code 055801
Naftalen [Polish]
QJ0525000
UN1334; UN2304
EINECS 202-049-5
Naphtalene
Naphtalene [French]
Naphtalinum
Naphthalene
Naphthalin
Naphthaline
Naphthalinum
Naphthene
Tar camphor
White tar
a
Source: National Institute of Health, Department of Health and Human Services, United States National Library
of Medicine. ChemIDplus Advanced
Table 2
a
Physical and chemical properties for naphthalenea
Property
Molecular weight (g mol)
Physical state
Value
128.171
White flakes or powder
Melting point (°C)
Boiling point (°C)
Density (g cm-3)
Vapor pressure
Vapor density
Solubility in water (% mass)
80.26
217.9 (sublimes)
1.0253 (at T=20°C)
0.011 kPa (at T=25°C)
4.42
0.00316 (at T=25°C); insoluble in water
Solubility in other solvents
soluble in ethanol; very soluble in diethyl ether,
acetone, benzene and carbon disulfide
Henry’s Law Constant (kPa.m-3/mol)
Octanol water partition coefficient (log Kow)
Organic carbon partition coefficient (log Koc)
Bioconcentration factor (log BCF)
Odour
Odour threshold in air (mg m-3)
Flash point (°C)
0.043
3.34
2.60 to 3
1.6 to 3.0 (fish)
strong (tar or mothballs)
0.44
79 (open cup)
Flammability Limits
Autoignition temperature (°C)
Conversion factors for vapor (at 25 °C and 101.3 kPa)
0.09 to 5.9%
526
1 ppm = 5.24 mg m-3; 1 ppb = 5.24 μg m-3
1 mg m-3 = 0.191 ppm; 1 μg m-3 = 0.191 ppb
Source: Alberta Environment, 2004
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2013 Update
© 2015 Government of Alberta
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2.2.2
Anthropogenic Sources
Anthropogenic sources of naphthalene are much larger source of exposure than natural sources (Jia and
Batterman, 2010). Anthropogenic releases of naphthalene to the air are largely the result of domestic
combustion of wood and fossil fuels and the off-gassing of naphthalene-containing moth repellents
(Alberta Environment, 2004; ATSDR, 2005). Naphthalene emissions from gasoline and diesel exhaust as
well as gasoline evaporation represent a significant, if not the most significant, source in urban areas (Lu
et al., 2005; Jia and Batterman, 2010). Major industrial sources of naphthalene include coal tar and coke
production, oil and gas extraction, petroleum refining, petrochemical manufacturing, wood preserving
operations (creosote impregnation), asphalt industries (paving and roofing), wastewater treatment plants,
and many other smaller sources (ATSDR, 2005; Alberta Environment, 2004; CAREX Canada, 2012; EC,
2013a; Jia and Batterman, 2010). Tobacco smoke contains naphthalene and represents a major exposure
route of exposure to naphthalene (CAREX Canada, 2012). Open burning of agricultural residues can also
be a significant source in certain areas (Jia and Batterman, 2010), and open burning of scrap rubber tires,
unvented kerosene space heaters, oil spills, and leaking underground storage tanks have also been
identified as naphthalene emission sources (Alberta Environment, 2004).
Environment Canada’s NPRI database contains information on industrial releases of naphthalene,
providing insight into Canada and Alberta’s inventory of naphthalene sources. Table 3 summarizes the
on-site naphthalene releases, reported to the NPRI, for Canada and Alberta for 2002 to 2011 (EC, 2013a).
More detailed air emissions data for Alberta are presented in Appendix A, Table A1 for 2011 (EC,
2013a). Note that in 2011, no on-site releases of naphthalene to land or water were reported by any
facility in Alberta.
According to the NPRI, Canada-wide naphthalene releases over the past decade (2002-2011) were lowest
in the three most recent years. Prior to 2011, the largest industrial emitters of naphthalene in Canada were,
generally, coal tar/coke and paper mill industries and were located in Ontario and Quebec. In 2011, the
largest industrial emitter was in the non-conventional oil and gas extraction industry located in Alberta.
This finding is discussed in more detail below.
In Alberta, naphthalene emissions from industrial sources were lowest in 2009 and highest in the most
recent year due to increasing emissions from a few industrial facilities that represent a large portion the
total emissions. This increasing trend does not follow the national trend. A single industrial facility with
North American Industry Classification System (NAICS) 3-digit code 325 (Chemical Manufacturing) was
responsible for 52% to 83% of the total industrial emissions from 2002 to 2008 emitting between 5.3 and
11.3 tonnes per year. Other industrial sectors with significant on-site releases over these years include
petroleum refineries (10% to 39%), petrochemical manufacturing (2% to 10%), and conventional and
non-conventional oil and gas extraction (0% to 18%). In 2010 and 2011, two non-conventional oil and
gas extraction facilities in Alberta began reporting naphthalene emissions to the NPRI. These facilities
accounted for 90% and 95% of the total industrial emissions in Alberta in 2010 and 2011, respectively.
One of these facilities was the largest industrial emitter in Canada for 2011. Other sectors in Alberta have
reduced their total naphthalene releases in recent years.
In 2011, most naphthalene releases reported to the NPRI in Alberta were categorized as fugitive, storage,
and handling releases to air (see Appendix Table A1). These tend to be near or at ground-level releases
with poor dispersion characteristics in relation to stacks and vents.
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2013 Update
© 2015 Government of Alberta
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Table 3
Annual on-site releases of naphthalene reported to the NPRI for Canada and
Alberta for 2002 to 2011
Canada - Naphthalene Emissions
2.2.3
Alberta - Naphthalene Emissions
Year
Total Releases
(tonnes)
No. of Reporting
Facilities
Total Releases
(tonnes)
No. of Reporting
Facilities
2011
75.94
72
22.25
13
2010
67.04
69
7.94
9
2009
69.79
55
0.92
8
2008
120.60
67
7.25
9
2007
111.78
65
7.15
8
2006
99.31
68
12.96
11
2005
121.37
67
21.54
11
2004
114.12
81
15.05
12
2003
88.91
73
17.22
16
2002
103.51
78
13.34
17
Ambient Concentrations of Naphthalene
Naphthalene concentrations in outdoor ambient air are highest in areas with several local emission
sources (Alberta Environment, 2004). Naphthalene concentrations in urban areas are typically less than 1
µg m-3 (0.19 ppb) (Health Effects Institute (HEI), 2007) but some studies have reported average
concentrations over 3.0 µg m-3 (0.57 ppb) (Propper, cited in ATSDR, 2005).
Under certain circumstances, indoor air concentrations of naphthalene may be higher than in those in
ambient outdoor air (ATSDR, 2005). For example, mean indoor air concentrations can vary significantly
from as low as 1.2 µg m-3 (0.23 ppb) up to 350 µg m-3 (66.9 ppb) in a freshly lacquer-painted room
(Preuss et al., 2003; ATSDR, 2005). Although indoor air concentrations of naphthalene were often
reported to be 5-10-fold higher than outdoor air concentrations in the past (Preuss, cited in Alberta
Environment, 2004), the decreased use of naphthalene in moth repellants and pesticides has likely led to
decreased indoor air concentrations in recent years (Preuss, cited in HEI, 2007).
Ambient naphthalene concentrations were monitored at six National Air Pollutant Surveillance (NAPS)
monitoring stations in Alberta over the past decade (2002 to 2011); the annual average ambient
concentrations are reported in Table 4. Note that samples reported as below the method detection limit
(MDL) for naphthalene, or less than 0.1 µg m-3 (0.019 ppb) were calculated as half the MDL.
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2013 Update
© 2015 Government of Alberta
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Table 4
Average annual concentrations of naphthalene in Alberta reported to NAPS for
2002 to 2011
Average Naphthalene Concentration (µg m-3)a
Year
Calgary
Central
(ID 90227/8)
Edmonton
Central
(ID 90130)
Edmonton
East
(ID 90121)
Syncrude
UE1
(ID 90806)
Hightower
Ridge
(ID 91201)
Elk Island
(ID 91101)
2002
0.735
0.640
0.561
-
-
-
2003
0.236
0.205
0.127
-
below MDL
-
2004
0.218
0.214
0.124
-
below MDL
below MDL
2005
0.179
0.127
0.111
-
-
below MDL
2006
0.165
0.135
0.147
-
-
below MDL
2007
0.171
0.151
0.114
-
-
below MDL
2008
0.115
0.131
0.109
below MDL
-
-
2009
below MDL
0.107
0.089
below MDL
-
-
2010
below MDL
0.127
0.071
below MDL
-
-
2011
below MDL
below MDL
0.077
0.127
-
-
a "below MDL"
is reported for years with more than 50% of samples below method detection limit (MDL).
Average naphthalene concentrations in Calgary and Edmonton appear to be steadily decreasing over the
past decade and are approaching the detection limit of the analytical method. Average naphthalene
concentrations at stations in undeveloped areas (Hightower Ridge and Elk Island) were consistently
below the MDL. The Syncrude UE1 station, a monitor in an industrial area, reported more than 50% of
samples below MDL until 2011, where 46% of samples were below the MDL and the average
concentration was 0.127 µg m-3 (0.024 ppb). Overall, concentrations at these stations were consistent
with published findings in other areas, which suggested that concentrations in urban areas are typically
less than 1.0 µg m-3 (0.19 ppb).
Note that the NAPS network uses a speciated volatile organic carbon gas phase evacuated canister
sampler with subsequent gas chromatograph/mass spectrometer (GS/MS) analysis to measure VOC
concentrations, including naphthalene. Note that this method has not been fully validated for naphthalene
measurements as will be discussed in more detail in Chapter 7.0.
Dec 2015
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2013 Update
© 2015 Government of Alberta
Page 16 of 87
3.0
Atmospheric Chemistry and Fate
Naphthalene emitted to the atmosphere will exist mainly in the gas-phase because it is volatile at ambient
temperatures and has little affinity for water (see Table 2). Naphthalene in air is destroyed by reaction
with hydroxyl radicals with a typical half-life of less than a day (Atkinson, 1986; Atkinson, cited in
ATSDR, 2003). Other atmospheric reactions of naphthalene occur slowly with half-lives of longer than
one month for reactions with ozone (O3) (Atkinson and Aschmann, 1986), and dinitrogen pentoxide
(N2O5) ( Atkinson and Aschmann, 1988). Naphthalene is not destroyed in the lower atmosphere by
photolysis because it does not absorb light at the wavelengths present (λ > 300 nm). Because naphthalene
has low affinity for water, removal by deposition to surfaces and in precipitation will be slow and it has
been estimated that approximately 2-3% of the naphthalene emitted to the air is removed via partitioning,
mainly through dry deposition (US EPA, cited in ATSDR, 2003). Thus, the atmospheric lifetime and fate
of naphthalene will be controlled by its reaction with hydroxyl radicals over timescales of a day or less.
Its atmospheric lifetime will tend to be shorter in summer than in winter and shorter during daylight than
at night, due to the abundance of hydroxyl radicals produced primarily by sunlight. Naphthalene has
limited potential for long-range transport because of its short atmospheric lifetime ranging from a few
hours to a day.
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4.0
Effects on Humans and Animals
This assessment focuses on naphthalene exposure through inhalation and its subsequent adverse health
effects in humans and animals. Adverse effects due to oral and dermal exposure have been examined in
lesser detail. This assessment is an update of an earlier assessment, “Review of Approaches for Setting an
Objective for Mixtures in Ambient Air using Polycyclic Aromatic Hydrocarbons (PAHs) as an Example –
Naphthalene” (Alberta Environment, 2004). To update this assessment, we conducted a review and
synthesis of the peer-reviewed, published epidemiological and toxicological literature addressing
potential adverse health effects resulting from naphthalene exposure in humans and animals. Studies were
identified using PubMed, the US National Library of Medicine’s research tool that indexes health and
medical peer-reviewed journals since 1966. Searches were performed using the following key words in
various combinations: “naphthalene,” “animal,” “human,” “exposure,” “epidemiology,” “toxicology,”
“toxicity,” “toxicokinetics,” “health,” “outcome,” “carcinogen,” “cancer,” “case control,” “cohort,”
“inhalation,” “respiratory,” “air,” “dermal,” “skin,” “oral,” and “ingestion.” Past literature not included or
extensively discussed in the 2004 report were also included. In addition, several consensus documents
prepared by the United States Environmental Protection Agency (1998), the Agency for Toxic Substances
and Disease Registry (2005), and the Health Effects Institute (2007) provided additional information
regarding adverse health effects.
4.1
Overview of Chemical Metabolism and Disposition
4.1.1
Toxicokinetics
Toxicokinetics describes the rate a chemical enters and is absorbed, distributed, metabolized and
eliminated from the body to determine the relationship between exposure and toxicity. The toxicokinetics
of naphthalene have been reviewed by several consensus documents (US EPA, 1998; HEI, 2007;
ATSDR, 2005). The main route of exposure reviewed in this document is the inhalation route, although
other routes of exposure were considered.
4.1.2
Absorption
The respiratory tract, gastrointestinal tract, and skin are expected routes of exposure to naphthalene (U.S.
EPA, ATSDR, cited in US EPA, 1998). Few available studies provide information related to the rate and
extent of naphthalene absorption. Following inhalation in humans, naphthalene passively diffuses across
the alveolar membrane through the lipophilic matrix to enter the bloodstream. No literature documenting
naphthalene absorption in animals after inhalation exposure was identified, though localized effects have
been observed to congregate in the lungs and nasal passages (Abdo et al., NTP, cited in ATSDR, 2005).
Ingestion of naphthalene may lead to absorption in quantities sufficient to elicit toxic effects. Absorption
occurs in the intestinal membrane by passive diffusion through the lipophilic matrix. Based on case report
data from patients who ingested naphthalene-containing mothballs, gastric contents following ingestion
suggest that dissolved naphthalene is transported slowly into the intestines. Additionally, ocular effects in
rabbits and rats have been observed following oral exposures to naphthalene (Kojima, Murano et al.,
Yamauchi et al. Srivastava and Nath, Rossa and Pau, Van Heyningen and Pirie, cited in ATSDR, 2005).
A number of studies indicated that naphthalene can be absorbed through the skin, causing hemolytic
anemia; however, some cases included use of naphthalene-exposed diapers on neonates, and absorption
may have been aided by presence of oil applied to babies’ skin (ATSDR 2005).
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4.1.3
Distribution
Absorbed naphthalene is expected to be distributed throughout the body via the bloodstream to other parts
of the body (US EPA, 1998; US EPA, cited in ATSDR, 2005). The National Human Adipose Tissue
Survey concluded that 40% of adipose tissue samples contained naphthalene and trace amounts were also
detected in human milk samples (US EPA, cited in ATSDR, 2005).
No studies were identified to have examined naphthalene distribution following inhalation exposure.
Following oral exposure, naphthalene may cross the human placenta, potentially leading to anemia in
infants. In pigs, adipose tissue contained the highest concentration of label 24 hours after a single oral
exposure to 14C-labelled naphthalene; the kidneys, liver, and lungs had the next highest concentrations,
respectively. While concentrations of label in adipose tissues dropped 72 hours following exposure,
concentrations in other tissue levels remained constant (Eisele, cited in ATSDR, 2005). Subsequent
distribution after repeated oral exposure in pigs found the highest concentrations in the lungs, followed by
the liver, heart and adipose tissues (Eisele, cited in ATSDR, 2005). Single and repeated oral exposures
for 31 days to 14C-labelled naphthalene, in one dairy cow, resulted in label concentrations mainly in milk
and milk fat (Eiseke, cited in ATSDR, 2005). This pattern of distribution was also seen among other
species by the US EPA (1998).
No human studies were identified reporting on naphthalene distribution following dermal exposure. In
rats, dermal exposure to naphthalene resulted in distribution of the chemical to the ileum and duodenum
segments of the small intestine, and the kidney, with highest concentrations at the site of application
(Turkall, cited in ATSDR, 2005).
4.1.4
Metabolism
Numerous studies have examined naphthalene metabolism in mammalian systems. The initial step in
metabolism of naphthalene is believed to be oxidation by members of the cytochrome P-450 family of
enzymes (also referred to as CYP). Mammalian tissues in the liver typically have the greatest cytochrome
P-450 activity, but metabolism has also been demonstrated in nasal and lung tissues (Baldwin, Buckpitt,
cited in US EPA, 2004).
The initial step in naphthalene metabolism is believed to be oxidation by a cytochrome P-450 enzyme to
form the naphthalene 1,2-oxide intermediate. Many members of the P-450 enzyme (CYP 1A1, 1A2, 1B1,
3A7, 3A5, 2B4, 2E1, and 2F) family have been shown to catalyze this step (Juchau, Van Winkle, Wilson,
Buckpitt, cited in US EPA, 2004). Reactive epoxide intermediates such as naphthalene 1,2-oxide can
spontaneously rearrange to form naphthols (predominately 1-naphthol) and subsequently conjugate with
glucuronic acid or sulfate which are then excreted in urine. Naphthols may also be enzymatically
hydrated, forming naphthalene-1,2-dihydrol (Warren, West, cited in US EPA, 2004). Catechol reductase
transforms the dihydrol into 1,2-naphthalenediol, which is subsequently oxidized into 1,2-naphthaquinone
or 1,4-naphthaquinone. Naphthalene 1,2-oxide, 1,2-naphthoquinone, 1,4-naphthoquinone, and 1,2dihydroxy-3,4-epoxy-1,2,3,4-tetrahydronaphthalene are hypothesized to be reactive metabolites that may
contribute to naphthalene toxicity (ATSDR, 2005; HEI, 2007).
Naphthalene metabolism rates differ among species, with substantially faster rates observed in mouse as
compared to hamster, rat, non-human primates or human airways. Humans and nonhuman primates are
the least efficient (Buckpitt, 1995; HEI, 2007). Naphthalene metabolism in dissected mouse airways was
twice as rapid as metabolism in dissected hamster airways and 3-5-times faster than metabolism in
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dissected rat airways prepared in a similar manner (Buckpitt, 1995). Naphthalene metabolism was also
examined in the lung and liver microsomes from mice and rats (O’Brien, 1985) and humans (HEI, 2007).
Metabolism of naphthalene in human lung microsomes occurred at rates 10-100 times slower than that of
mice, suggesting that the human respiratory tract may be much less sensitive to inhaled naphthalene (HEI,
2007). Species-specific metabolism differences can be observed in the isomers that are formed; 1,2dihydrol is the major metabolite produced by human liver microsomes, while 1-naphthol is preferred by
mouse liver microsomes (ATSDR, 2005). In humans, the cytochrome P-450 enzyme CYP1A2 appears to
be the primary isozyme involved in producing 1-naphthol, while the cytochrome P-450 enzyme CYP3A4
appears most involved in producing 2-naphthol (Cho, 2005). There is minimal expression of the
cytochrome P-450 isozyme CYP2F in rats (Baldwin, 2004). Metabolism in the nasal olfactory and
epithelial cells is more complex and less understood than that of the lung (ATSDR, 2005). Metabolic
differences between species are also shown in the stereo-specific metabolites produced, especially with
higher rates of a specific enantiomeric epoxide in lung microsomes: 1R,2S-naphthalene oxide is present
in mice lungs, while 1S,2R-naphthalene is preferentially formed in rats, hamster, and monkey lungs, as
well as human lymphoblastic microsomes (ATSDR, 2005).
4.1.5
Excretion
Excretion of naphthalene follows the conjugation of various forms of metabolites with glucuronic acid via
glucuronyl transferase. These naphthalene-glutathione conjugates are further metabolized to
premercapturic and mercapturic acids and then excreted in the urine or bile, with small quantities excreted
in the feces (US EPA, 2004). These pathways appear to be more active in rats and mice, and less active in
non-human primates (Stillwell, Chen ,Summer, Rozman, cited in US EPA, 1998). Observed differences
in glutathione conjugate formation may relate to decreased rates of epoxide formation in primates
compared to rodents or increased dihydrol formation (US EPA, 1998).
A single study was identified describing naphthalene excretion following inhalation exposures in people.
Naphthalene distillation workers and coke plant employees established peak 1-naphthol concentrations in
urinary samples 1 hour after shift completion, with a half-life of 4 hours (Bieniek, cited in ATSDR,
2005).
Few human studies examining naphthalene excretion following ingestion exposures were identified.
Reports from case studies in naphthalene-exposed humans suggest that urinary excretion may be
prolonged following exposure due to a delayed dissolution and absorption in the gastrointestinal tract.
Unabsorbed naphthalene can also be found in feces following ingestion exposure in humans (ATSDR,
2005).
In rhesus monkeys (Rozman et. al., cited in ATSDR, 2005) and chimpanzees (Summer et. al., cited in
ATSDR, 2005), naphthalene thioethers are not found, suggesting glutathione conjugation does not readily
occur in nonhuman primates. Instead, glucuronic acid and sulfate conjugates are found, suggesting a
different naphthalene excretion pathway in nonhuman primates. In contrast, rats exhibit dose-dependent
urinary thioethers following oral gavage dosage (Summer et. al., cited in ATSDR, 2005).
No studies related to naphthalene excretion following dermal exposure in humans were found. In rats, the
major excretory pathway following dermal exposure appears to be excretion in urine, with smaller
amounts excreted through feces and exhaled air (Turkall et. al., cited in ATSDR, 2005).
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4.2
Effects on Humans
The earlier assessment of naphthalene toxicity (Alberta Environment, 2004) indicated that the primary
endpoints of acute toxicity associated with inhalation exposure to naphthalene are hemolytic anemia
(fatigue, lack of appetite, restlessness, and a pale skin appearance), cataracts, and respiratory toxicity.
Humans were reported to be more sensitive than animals to the hemolytic effects of naphthalene, and both
neonates and individuals with a genetic defect in the enzyme glucose-6-phosphate dehydrogenase were
especially sensitive. However, this assessment concluded that concentrations of naphthalene in ambient
air in urban cities and indoor air were not sufficient to cause such effects (Figure 8-1, presented in Alberta
Environment, 2004). This report updates the scientific literature related to naphthalene toxicity, and
should be viewed as a supplement to the earlier assessment (Alberta Environment, 2004).
4.2.1
Acute and Sub-Acute Human Effects
Acute effects usually occur rapidly as a result of short-term exposures, and are of short duration –
generally for exposures less than 24 hours. Sub-acute effects usually occur as a result of exposures that
are of an intermediate duration – generally for exposures lasting a few days to no greater than one month
(Eaton and Klaasson cited in Alberta Environment, 2004).
One case study related to naphthalene inhalation was identified in the updated literature search. Fumes
from naphthalene-containing moth flakes were spilled into a heating vent one week prior to a pregnant
woman’s delivery, which resulted in reversible hemolytic anemia and methemoglobinemia in both the
mother and neonate (Molloy, 2004). The occurrence of hemolytic anemia following inhalation to high
concentrations of naphthalene is consistent with the studies reviewed in the earlier assessment (Alberta
Environment, 2004) and other reviews (ATSDR, 2005). Hemolytic anemia is the most common
manifestation of acute naphthalene exposure. Cataracts are also reported after human ingestion or
inhalation of naphthalene at high concentrations (ATSDR, 2005; US EPA, 1998). The details of exposure
are not available for most case studies (Alberta Environment, 2004).
4.2.2
Chronic Human Effects
Sub-chronic or intermediate exposures are generally one to three months; chronic effects occur as a result
of long-term exposures and are of longer duration – generally as repeated exposures for more than 3
months (Eaton and Klaassen cited in Alberta Environment, 2004).
No new studies specifically related to the health effects of naphthalene following chronic inhalation
exposure were identified.
4.2.3
Carcinogenicity
Human data regarding the carcinogenic potential of naphthalene is predominantly in the form of case
reports (Lewis, 2012), which are considered “inadequate” for providing evidence of naphthalene’s
carcinogenicity in humans (NTP, 2011; US EPA, 1998; WHO, 2002). Two human studies related to the
potential carcinogenicity of naphthalene were identified by the updated literature search that were not
discussed in the 2004 Alberta Environment report – an epidemiology study and a case study. Griego et
al., (2008) summarized three German studies at a naphthalene purification plant which identified four
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laryngeal cancer cases among workers who were also smokers. In addition, a Nigerian study identified 23
patients with colorectal carcinoma after taking a local indigenous treatment containing naphthalene
(WHO, 1992).
4.3
Effects on Animals
4.3.1
Acute and Sub-Acute Effects
Table 5 summarizes recent literature concerning respiratory effects of naphthalene in animals following
acute and sub-acute inhalation exposures to naphthalene or by exposure through intraperitoneal injection.
4.3.1.1
Respiratory Effects
Nasal olfactory and respiratory epithelial necrosis and lesions were examined in two rat species (Dodd et
al., 2010). Six hours of acute, whole-body inhalation induced dose-dependent nasal olfactory epithelial
necrosis with a lowest observed adverse effect level (LOAEL) of 5.24 mg m-3 (1 ppm) in F-344 rats and a
LOAEL of 0.52 mg m-3 (0.1 ppm) in Sprague-Dawley rats. Sub-acute exposure of 6 hours per day for 5
days followed by a 14 day recovery period of non-exposure elicited dose-dependent nasal olfactory
lesions with a 0.52 mg m-3 (0.1 ppm) LOAEL in female Sprague-Dawley rats. Similarly, a 4-hour
inhalation exposure to concentrations as low as 17.8 mg m-3 (3.4 ppm) naphthalene or systematic
exposure through a single intraperitoneal injection of as low as 100 mg/kg (but not 50 mg/kg)
naphthalene resulted in nasal mucosa injury in Sprague-Dawley rats (Lee et al., 2005). While the systemic
exposure resulted in more widespread injury in the olfactory mucosa, exposure through inhalation
generated region-specific injury along the medial meatus and ethmoturbinates (specific regions of the
nasal cavity). Overall, nasal injury occurred exclusively in the olfactory region after exposure by either
route of exposure, indicating those areas are capable of metabolism. Authors suggested that human nasal
tissue is the target organ for naphthalene exposure due to P-450 activity in the nasal mucosa (Lee et al.,
2005).
Clara cells appear to be a major target for naphthalene toxicity. Development of tolerance in rat and
mouse Clara cells were examined in a series of experiments where the animals were exposed to
naphthalene in vivo, followed by in vitro exposures to naphthalene in isolated Clara cells. In Swiss
Webster mice, an initial daily intraperitoneally injection of 200 mg/kg naphthalene for 7 days in vivo
followed by 2 hours in vitro exposure of Clara cells to naphthalene concentrations ranging from 0.003838 μg ml demonstrated a resistance of the Clara cells to further injury. Similarly, groups of mice exposed
to naphthalene by inhalation for 4 hours daily for 7 days showed subsequent resistance of isolated Clara
cells later exposed in vitro. Authors concluded that Clara cells became tolerant after repeated exposures,
and further experiments supported the theory that exposure to naphthalene increases the concentrations of
the protective protein glutathione in Clara cells through the induction of ϒ-glutamylcysteine synthetase,
the rate-limiting enzyme in glutathione synthesis. (West et al., 2003)
Inhalation exposures of NIH Swiss mice to 7.9 mg m-3 (1.5 ppm) naphthalene resulted in moderate
glutathione depletion and toxicity to the nasal olfactory epithelium (Phimister et al., 2004). When Clara
cells were isolated and treated with a chemical shown to deplete glutathione levels before exposure to
naphthalene, a decrease in the formation of naphthalene metabolites was seen following naphthalene
exposure. However, naphthalene-protein adducts were observed in these animals.
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To determine the importance of nasal cytochrome P-450 in metabolizing naphthalene, upper respiratory
tract uptake of naphthalene and nasal cavity toxicity were examined in a series of studies in rats and mice.
When Fischer 344 rats were first treated with an inhibitor of P-450 enzymes to reduce metabolism by
80% and subsequently exposed to naphthalene, upper respiratory tract uptake was reduced compared to
untreated controls. The degree of reduction was dose-dependent, with a greater reduction seen at lower
exposure concentrations of naphthalene (Morris and Buckpitt, 2009). A subsequent study examining the
dosimetry of inhaled naphthalene in the nasal region of mice reported that upper respiratory tract uptake
efficiency is dose-dependent, and confirmed a similar reduction in toxicity when metabolism was
inhibited (Morris, 2013). Authors conclude that inhaled naphthalene is metabolized in the mouse nose,
becoming saturated at higher concentrations, and speculated that nasal metabolism may serve to reduce
pulmonary exposures by removing the naphthalene.
Gender-specific differences in the development of tolerance to naphthalene were seen in NIH Swiss mice
exposed to naphthalene repeatedly for 7 days. Female mice developed dense populations of ciliated
epithelial cells and fewer Clara cells following daily intraperitoneal injections of 200 mg kg-1
naphthalene, while males appeared unaffected. When mice were subsequently exposed to a 300 mg kg-1
challenge dose of naphthalene, cytotoxicity was greater in female mice compared to males. Expression of
the cytochrome P-450 enzyme CYP2F2, as well as the enzyme involved in glutathione synthesis,
glutamate-cysteine ligase, was decreased in female mice. The authors concluded that while female mice
develop tolerance to repeated exposure to naphthalene, gender differences exist in the tolerant state by
airway level, and females remain more susceptible than males to repeated exposure (Sutherland et al.,
2012).
Species differences to naphthalene-induced toxicity were also examined in Swiss T.O. mice and Wistarderived rats exposed to naphthalene by intraperitoneal injection. Selective damage to non-ciliated
bronchiolar epithelial cells was observed in mice at exposures as low as 200 mg kg-1, with the epithelial
cells being unaffected. In contrast, exposures to naphthalene at doses up to 1,200 mg kg-1 induced no
adverse effects to the lung, liver, or kidney in the rat (O’Brien et al., 1985).
Table 5
Acute and sub-acute effects associated with naphthalene exposure
Effects Reported
Nasal olfactory epithelial necrosis
Exposure
Period
6 hrs
(inhalation)
LOAEL
NOAEL
NOAEL
5.24 (1)
1.57 (0.3)
0.524 (0.1)
Nasal respiratory epithelium
necrosis
LOAEL
NOAEL
LOAEL
NOAEL
Nasal olfactory epithelial lesions
Dec 2015
Concentration
mg m-3 (ppm)*
Strain/Species
Reference
Dodd et al., 2010
Fischer-344 rats
Sprague-Dawley
rats
6 hrs
(inhalation)
Dodd et al., 2010
52.4 (10)
5.24 (1)
5.24 (1)
Fischer-344 rats
Sprague-Dawley
rats
1.57 (0.3)
6 hrs/d,
5 days
(inhalation)
Female SpragueDawley rats
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Exposure
Period
Effects Reported
LOAEL
Recovery
Exposure
plus 14 d
recovery
Concentration
mg m-3 (ppm)*
0.524 (0.1)
Observed toxicity
in 52.4 (10)
exposure group
showed
considerable
recovery with
subsequent
exposure to clean
air for 14 days
Nasal mucosa injury
LOAEL
4 hrs
(inhalation)
Single IP
Injection
LOAEL
NOAEL
Lung and nasal glutathione
depletion
Reference
Male SpragueDawley rats
Lee et al., 2005
NIH Swiss Mice
Phimister et al.,
2004
NIH Swiss Mice
Sutherland et al.,
2012
Swiss Webster
mice
West et al., 2003
17.8 (3.4)
100 mg kg-1
50 mg kg-1
2 hr single
exposure
(inhalation)
LOAEL
7.86 (1.5)
Epithelial cell damage.
Daily IP
injection,
7d
LOAEL
Dense populations of ciliated cells
and fewer Clara cells in females, but
not males.
200 mg kg-1
Tolerance:
Toxicity of the challenge dose was
greater in females as compared to
males. Females also had decreased
expression of CYP2F2
Clara cell tolerance
Challenge dose of
300 mg/kg one
week after end
week of IP
injections
Clara cells in explants from tolerant
mice remained tolerant to injury in
culture.
Clara cells at all airway levels
became tolerant
GCS, the rate-limiting enzyme in
glutathione synthesis, is induced in
tolerant Clara cells
Dec 2015
Strain/Species
IP injection
(ex vivo)
daily, 7 d
followed
by 2 hr
treatment
in culture
(in vitro)
4 hrs/d, 7 d
(inhalation)
4 hrs/d, 7 d
(inhalation)
200 mg kg-1 (IP);
0.0038-38 μg ml
(in vitro)
78.6 (15)
78.6 (15)
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Effects Reported
Buthionine sulfoximine, a GCS
inhibitor, able to eliminate the
resistance of tolerant Clara cells
Upper respiratory tract uptake
In vitro metabolism of naphthalene
similar in nasal tissues from both
genders; 80% reduced by inhibitor
with effect being greater at lower
concentrations
Nasal dosimetry
Naphthalene uptake diminished by
5-phenyl-1-pentyne, indicating
inhaled naphthalene extensively
metabolized in the nose with
saturation of metabolism occurring
at higher concentrations
Metabolism
Exposure
Period
4 hrs/d, 7 d
(inhalation)
Concentration
mg m-3 (ppm)*
78.6 (15)
1 hr
(inhalation)
5.24, 20.96, 52.4,
157 mg m-3 (1, 4,
10, 30 ppm)
1 hr
(inhalation)
Strain/Species
F-344 rats
Morris et al., 2009
B6C3F1 mice
Morris, 2013
Male CFW mice
Buckpitt et al.,
1995
5.24, 20.96, 52.4,
157 mg m-3 (1, 4,
10, 30 ppm)
In vitro
0.5 mM
Metabolism in mouse at higher rates
than hamster or rat airways.
Male SpragueDawley mice
Rates of substrate turnover in mice 2
times greater than hamsters and 3-5
times greater than in rats.
Metabolism
Male Syrian
Golden
Hamsters
Recombinant
CYP2F from
Sprague-Dawley
rat tissue
Minimal pulmonary CYP2F1 and
CYP2F2 expression in rats,
although rates of metabolism similar
to mice. Suggests that low
expression levels of CYP2F protein
are sufficient to account for the
insensitivity of rats to naphthaleneinduced cytotoxicity.
Lung, liver, kidney, spleen tissue
damage, depletion of non-protein
sulfydryls
LOAEL
NOAEL
Reference
In vitro
Not applicable
Single IP
injection,
killed 24
hrs after
exposure
Baldwin et al.,
2004
O’Brien et al., 1985
200 mg kg-1
(selective damage
to non-ciliated
bronchiolar
epithelial cells)
1,200 mg kg-1
Swiss T.O. Mice
Wistar-derived
rats
* Naphthalene concentration in air unless otherwise indicated
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4.3.2
Chronic Effects
Table 6 summarizes the toxicological literature examining the relationship between chronic or subchronic naphthalene exposure and subsequent effects in animals, with an emphasis on inhalation
exposures.
Table 6
Chronic and sub-chronic effects associated with naphthalene exposure
Exposure
Period
Concentration
Microscopic features of
lesions and carcinomas
observed in original
publication (Abdo, 2001)
LOAEL
6 hrs plus
T90/day
5 d/wk, 105 wks
(inhalation)
52.4, 157 or 314 (10, 30,
or 60)
Nasal and pulmonary
lesions
6 hrs plus T90/d
5 d/wk, 105 wks
(inhalation)
Effects Reported
mg m-3 (ppm)*
Strain/Species
Reference
F344/N rats
Long et al., 2008
52.4, 157 or 314 (10, 30,
or 60)
F 344/N rats
Abdo et al., 2001
Nasal olfactory epithelium
neuroblastoma
LOAEL
LOAEL
52.4 (10)
157 (30)
Females
Males
Nasal respiratory
epithelum adenomas
LOAEL
LOAEL
157 (30)
52.4 (10)
Females
Males
Nasal non-neoplastic
lesions
LOAEL
52.4 (10)
Males and females
52.4 (10)
Males and females
52.4, or 157 (10, or 30)
B6CF1 mice
157 (30)
157 (30)
Females
Males
52.4 (10)
Males and females
52.4 (10)
Lung non-neoplastic
lesions
LOAEL
Alveolar/bronchiolar
adenomas and/or
carcinomas
LOAEL
NOAEL
6 hrs/d 5 d/wk
104 wks
(inhalation)
Non-neoplastic lung
and/or nasal lesions
LOAEL
Pulmonary adenoma
NOAEL
6 hrs/d, 5 d/wk
6 months
(inhalation)
NTP, 1992
Adkins et al., 1986
52.4 (10)
Strain A/J mice
* Naphthalene concentration in air unless otherwise indicated
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4.3.2.1
Respiratory and Carcinogenic Effects
One study regarding the health effects of chronic naphthalene exposure in animals was identified in the
updated literature search. The following National Toxicology Program (NTP) study by Long et al. (2003)
observed microscopic features of lesions. In the earlier assessment (Alberta Environment, 2004), two
NTP studies important to understanding naphthalene’s potential carcinogenicity and effects on the
respiratory system were summarized. These studies also investigated additional endpoints that are not
discussed in detail here. The NTP (1992) study in mice is important, as it is the study upon which the US
EPA bases their reference concentration (RfC) for naphthalene (US EPA, 1998). Additionally, both NTP
studies served as the basis of the ATSDR MRL calculation (ATSDR, 2005). The ATSDR notes that mice
appear to be “much more sensitive” to naphthalene-induced non-neoplastic lung damage than rats, and
that this difference may be explained by species differences in naphthalene metabolism (ATSDR, 2005).
The results of the NTP study are described in further detail below.
In the first study, male and female B6C3F1 mice were exposed to 0, 52.4, or 157 mg m-3 (0, 10, or 30
ppm) naphthalene by inhalation for approximately 6 hours per day, 5 days per week, 104 weeks (NTP,
1992). Female, but not male mice exposed to naphthalene concentrations of 157 mg m-3 (30 ppm) had a
statistically significant increased incidence of alveolar/bronchiolar adenomas or carcinomas. This tumor
type is considered benign in mice and the US EPA has therefore not developed a cancer potency value
based upon it (US EPA, 1998). Both naphthalene exposure concentrations were associated with increased
lymphocyte infiltration, inflammation, and granulomatous inflammation in both genders (NTP, 1992).
Metaplasia of the olfactory epithelium, hyperplasia of the respiratory epithelium, and nasal inflammation
were observed in most of the male and female mice exposed to naphthalene at concentrations of 52.4 or
157 mg m-3 (10 or 30 ppm) (NTP, 1992).
The second NTP study (NTP, 2000, Abdo et al., 2001) was designed similarly to the first study (NTP
1992), except that it investigated male and female rats exposed to naphthalene by inhalation at
concentrations of 0, 52.4, 157 or 314 mg m-3 (0, 10, 30, or 60 ppm). Olfactory epithelium neuroblastomas
and respiratory epithelium adenomas of the nose were significantly elevated among female F344 rats
exposed to naphthalene concentrations of 314 mg m-3 (60 ppm). Further, a positive dose-response
relationship was apparent in male rats for the development of respiratory epithelium adenomas. Nearly
all rats exposed to naphthalene (52.4, 157 or 314 mg m-3; 10, 30, or 60 ppm) displayed evidence of
hyperplasia, atrophy, chronic inflammation, and hyaline degeneration of the olfactory epithelium, and
hyperplasia, squamous metaplasia, and hyaline degeneration of the respiratory epithelium. Both male and
female rats exposed to naphthalene at concentrations of 52.4 (10 ppm) and 157 mg m-3 (30 ppm) showed
evidence of increased alveolar epithelial hyperplasia, while no significant differences were seen in the
highest (314 mg m-3; 60 ppm) exposure group (Abdo et al., 2001). Male rats exposed to naphthalene at
concentrations of 314 mg m-3 (60 ppm) developed increased incidence of chronic inflammation of the
lung. No neoplastic lesions of the lung were identified in this study (Abdo et al., 2001).
The olfactory neuroblastomas and respiratory epithelial adenomas in the NTP (1992) study were
considered carcinogenic effects related to naphthalene exposure based on their relatively high incidence
in exposed rats, their absence in concurrent control rats and historical controls from other NPT studies,
and their rare spontaneous occurrence in rats of any strain. Histological details of these lesions are
described in more detail in a recent publication which described the NTP study (Long, 2003).
4.3.2.2
Other Effects
No new studies were identified describing other health effects resulting from chronic exposure to
naphthalene in animals.
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4.4
Genotoxicity
A genotoxic agent damages the genetic information within an organism’s cells and may result in
mutations or chromosomal aberrations, which have the potential to lead to the development of cancer.
The genotoxicity of naphthalene has been reviewed previously (ATSDR, 2005). The following
discussion provides a brief overview of the genotoxicity of naphthalene, with some discussion of newer
studies.
Table 7 summarizes the newly identified studies investigating naphthalene’s potential genotoxicity. In
vivo genotoxicity studies involve exposure of animals or people to a substance (either intentionally or as a
result of occupational or environmental exposures) to understand the substance’s potential for causing
mutation, chromosomal damage, or other genetic effects. Of the 10 in vivo studies cited in the 2005
ATSDR report, 5 showed no effect of naphthalene on micronuclei induction, alkaline elution,
unscheduled DNA synthesis, and neoplastic transformation in mice or rats (ATSDR, 2005). The
remaining studies showed some association of exposure to naphthalene with somatic mutation and
recombination in Drosophila melanogaster, micronuclei induction in salamander larvae, and DNA
fragmentation in liver or brain tissue of mice or rats (ATSDR, 2005). One new in vivo study (Meng et al.,
2011) was identified; in which 25 male and 24 female rats were exposed to naphthalene by inhalation at
concentrations of 0, 0.524, 5.24, 52.4 and 157 mg m-3 (0, 0.1, 1.0, 10, and 30 ppm) naphthalene vapor for
6 hours a day, 5 days a week, over 13 weeks. Exposures to naphthalene did not result in significant
increases in mutation as measured as a p53 codon 271 CGT → CAT mutation. Significant losses of this
mutation were observed in respiratory and olfactory epithelia of male (but not female) rats exposed to 157
mg m-3. However, authors suggest that this decrease in mutation was due to cell toxicity rather than
genotoxic effects (Meng et al., 2011).
In some studies, detection of covalent adducts of a chemical or its metabolite with protein or DNA may
indicate that substance is chemically reactive, and has the potential to cause genetic damage. Protein
adducts, and in particular adducts with the blood proteins hemoglobin and albumin, are often used as such
an indicator. Male F344 rats exposed to naphthalene at concentrations ranging from 100 to 800 mg per kg
body weight using oral gavage, were examined 24 hours after exposure to determine the occurrence of
naphthalene-related hemoglobin and albumin adducts. These adducts were analyzed using mass
spectroscopy to determine which metabolite was reacting with the blood proteins. The authors reported
the detection of both types of adducts associated with different metabolites of naphthalene (Waidyanatha
et al., 2002). Such adducts have the potential to lead to mutation, although mutation is not demonstrated
directly. Another study (Saeed et al., 2007) found evidence of both depurinating and stable adducts when
DNA was exposed to metabolites of naphthalene.
Table 7
Newly identified genotoxicity studies
Effects Reported
Micronuclei
NOEL: point of
departure
LOAEL
NOAEL with 5mM
Dec 2015
Exposure
Period
In vitro
Naphthalene
Concentration, if
applicable
Strain/Species
Reference
Human TK6 cells,
with addition of rat
liver S9 fraction
metabolism system
Recio et al., 2011
Between 2.5 and 10 μM
10-500 μM
500 μM
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Effects Reported
glutathione
p53 Mutation
LOAEL
NOAEL
NOAEL
Protein adducts:
hemoglobin and
albumin
LOAEL
DNA damage:
N7Guanine and
N3Adenine adducts,
as well as
unidentified adducts
Exposure
Period
Naphthalene
Concentration, if
applicable
In vivo
Inhalation
exposure, 13
weeks
In vivo
Single oral
dose
In vitro
157 mg m-3 (30 ppm)
52.4 mg m-3 (10 ppm)
157 mg m-3 (30 ppm)
Cysteinyl adducts of
both proteins with NPO,
and 1,2- and 1,4-NPQ
were produced in a dosedependent manner.
100 mg/kg
Exposure to metabolites
1,2-Naphthoquinone
(1,2-NQ) and
enzymatically activated
1,2dihydroxynaphthalene
(1,2-DHN))
Strain/Species
Reference
F344 rats
Meng et al., 2011
Males
Males
Females
F344 rats
Deoxyguanosine
and DNA
Waidyanatha et
al., 2002
Saeed et al., 2007
In vitro studies are conducted using the components of interest independently from the intact,
living organism. Examples of in vitro studies include bacteria or mammalian cells grown in
culture, or purified substances such as DNA or protein. In a review of 22 bacterial gene
mutation, cytogenic, and DNA damage assays utilizing Salmonella typhimurium, Escherichia
coli, or Vibrio fischeri strains, all but one study failed to demonstrate the potential genotoxicity
of naphthalene (ATSDR, 2005). Additionally, among 12 eukaryotic gene mutation assays, all but
three studies did not demonstrate evidence for the genotoxicity of naphthalene. These three
studies with some evidence involve chromosomal aberrations or sister chromatid exchange in
Chinese hamster ovary cells, preimplantation whole mouse embryos, and human mononuclear
leukocytes. The study utilizing Chinese hamster ovary cells required an external metabolism
system derived from rat livers to observe evidence of genotoxicity. Increased micronuclei
induction in cultured human TK6 lymphoblast cells was observed at naphthalene concentrations
above a range of 2.5 to 10 μM in a recent study (Recio et al., 2011). However, in the presence of
glutathione, no induction of micronuclei or cytoxicity was apparent at naphthalene
concentrations up to 500 μM.
4.5
Health Effects Summary
4.5.1
Metabolism and Disposition
Naphthalene is metabolized to naphthalene 1,2-epoxide, a reactive intermediate, by the cytochrome P-450
family of enzymes. Both the 1S,2R- and the 1R,2S-stereoisomers are produced. Formation of the 1,2epoxide is the first and obligate step in the metabolism of naphthalene. Species differences in metabolism
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are observed, with the 1R,2S-stereoisomer formed preferentially in mice while the 1S,2R stereoisomer is
formed preferentially in rats, hamsters, and monkey lungs. In addition, the rate of metabolism of
naphthalene is 10-100-fold greater in mouse lung microsomes as compared to microsomes from rats,
monkeys, hamster, and humans. This suggests that rats are able to activate naphthalene to a chemicallyreactive metabolite, the 1,2-epoxide, at a faster rate in rats as compared to other rodents or primates.
4.5.2
Genotoxicity
Despite the identification of a few additional studies suggesting that naphthalene or its metabolites have
some genotoxicity properties, the overall body of evidence, as cited by ATSDR (2005), indicate that
naphthalene is not genotoxic.
4.5.3
Acute Health Effects
As summarized in the earlier assessment (Alberta Environment, 2004), the acute health effects resulting
from naphthalene exposure are generally limited to hemolytic anemia and respiratory toxicity. New
human data is limited to one case report of reversible hemolytic anemia and methemoglobinemia in a
pregnant woman and her neonate, while newer animal studies verify observations previously reported. In
mice, nasal cell toxicity dominates. Toxicity is observed in the nasal epithelium and in the Clara cells of
the lung. Repeated exposures to naphthalene appear to reduce Clara cell toxicity from subsequent acute
exposures, indicating that Clara cells may become tolerant to the toxicity of naphthalene.
4.5.4
Chronic Health Effects
One new study identified in the update search describes the microscopic features of lesions observed in a
NTP (2000) study in rats (Long et al., 2003). As summarized in the earlier assessment (Alberta
Environment, 2004), both of the NTP studies suggest the development of non-neoplastic lesions of the
olfactory and respiratory epithelia after naphthalene exposures, but only the rat study found evidence of
neoplastic lesions: adenomas of the respiratory epithelium of the nose and neuroblastomas of the olfactory
epithelium . The development of neoplasms following naphthalene exposure differs by animal species and
gender, with rats appearing to be more sensitive than mice, and female rats developing neuroblastomas of
the nose at lower concentrations than male rats.
4.5.5
Overall Summary
Animal studies have shown that exposure to naphthalene caused damage to the respiratory tract,
especially the nasal region in rats. These effects include inflammation, metaplasia of the nasal olfactory
epithelium, hyperplasia of the respiratory epithelium, and cancer. In mice, naphthalene also causes
damage to ciliated and Clara cells of the bronchiolar epithelium, but rat lungs are somewhat resistant to
this toxicity. Only a few new studies in humans were identified; one for non-cancer effects (hemolytic
anemia following inhalation to high concentrations of naphthalene), and two related to cancer (a case
study and a single epidemiology study with confounding exposures). Naphthalene is metabolized in to
reactive intermediates by the cytochrome P-450 family of enzymes. Metabolism profiles parallel many of
the toxicity effects. Metabolism appears to be concentrated in the nasal region in rats and in Clara cells in
mice, where much of the toxicity occurs. The activity of these enzymes is higher in mice as compared to
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rats or humans, although the same enzymes are present in all three species. The differential toxicity
appears to be due, at least in part, to the major differences in the expression of these enzymes, which
affects the overall rates of metabolism. The higher rate of metabolism in rat nasal cells has been suggested
as a mechanism of higher toxicity in the rat nasal region, with subsequently less naphthalene reaching
(and damaging) the lung regions. Naphthalene is correspondingly more cytotoxic in the respiratory tract
of mice than rats. The gender differences in metabolism also seem to correlate with toxicity differences.
Although the evidence for genotoxicity of naphthalene appears to be weak, the cytotoxicity and
inflammation may lead to increased cell proliferation.
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5.0
Effects on Vegetation
A handful of additional studies looking at the effects of naphthalene on vegetation were identified, adding
to the literature previously identified in the initial assessment (Alberta Environment, 2004). This section
references information contained in the initial assessment and incorporates the new information related to
the effects of naphthalene on vegetation and materials.
5.1
Vegetation
As discussed in the initial assessment (Alberta Environment, 2004), PAHs are primarily taken up by
plants via roots and leaves and subsequently translocated to other plant tissues. However, the uptake rate
is dependent on a number of factors such as PAH concentration, plant species, environmental factors (e.g.
light, temperature, and water), growth medium, PAH solubility, PAH phase (e.g. vapor or particulate),
and PAH molecular weight (Edwards, 1983). Only a limited number of studies have focused specifically
on naphthalene and its effects on vegetation.
Multiple studies have shown that plant species is an important factor in determining PAH uptake. In
addition to the study demonstrating that alfalfa roots had approximately twice the affinity for naphthalene
compared to fall fescue (Schwab et al., 1998), variable concentrations of naphthalene were found in inner
vegetable tissues (Kipopoulou et al., 1999). To assess the relationship between PAHs in inner vegetable
tissues and PAH concentrations in the growing environment, Kipopoulou and colleagues collected tissue
samples from five vegetables grown in an industrial area in northern Greece. Vegetable samples were
washed in the laboratory to remove surface dust, homogenized, ground using a food processor, and
freeze-dried prior to chemical extraction for the recovery of PAHs. Soil samples and total suspended
particulates were also collected. Atmospheric concentrations of naphthalene in two nearby residential
areas ranged from 2-179 ng m-3, with median values of 17 ng m-3 and 30 ng m-3. Median naphthalene
concentrations observed in various vegetable found the highest concentrations were present in lettuce
tissues (42 µg kg-1 dry weight), followed by endive (29 µg kg-1 dry weight), carrot (21 µg kg-1 dry
weight), leek (18 µg kg-1 dry weight), and cabbage (5 µg kg-1 dry weight). This difference may be due to
differences in the amount of exposed surface area-to-volume ratio of each crop. Leafy vegetables, such as
lettuce and endive, had higher naphthalene concentrations than the other vegetables, highlighting the
importance of atmospheric inputs of PAHs (Kipopoulou et al., 1999). Despite the variation in
naphthalene concentrations among different vegetables, naphthalene was consistently one of the most
abundant PAHs in all vegetables.
A laboratory study conducted to assess the effect of plant architecture and leaf hairs on PAH uptake,
using three Plantago species grown from seed in a greenhouse was conducted by Bakker and colleagues
(1999). After 15 weeks the plants were moved to an open greenhouse (missing the lower half of the
walls) in an urban area of Utrecht, The Netherlands. Plants were placed in close proximity to each other to
limit environmental variation. Leaf samples were collected on the last day in the greenhouse, and on days
6, 13, and 20. Leaves were not washed prior to extraction for PAHs. Leaves were also analyzed for leaf
wax, surface area, and fresh weight. Results of the laboratory exposure study showed that concentrations
of low molecular weight PAHs (such as naphthalene), which are largely present in the atmosphere as
gases, were significantly higher in freestanding, upright Plantago species compared with a lower, groundspreading species. The authors suggested that factors such as canopy surface roughness, density of leaf
hairs, and leaf overlap were responsible for the difference in PAH uptake. Plants with rougher canopy
surfaces, a lower density of leaf hairs, and lower overlap of leaves will have a higher foliar uptake of
gaseous contaminants.
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Numerous studies have shown that naphthalene can negatively affect plant growth and production (Slaski
et al.; Hulzebos et al.; Huang et al.; Soto et al.; Soto et al.; Soto et al.; Soto et al.; Ren et al.; cited in
Alberta Environment, 2004). The effect of PAHs on plant germination was reported following the
incubation of seeds of maize, lupin, barley, fescue, colza, rye grass, alfalfa, and red clover in closed petri
dishes with saturated aqueous solutions of pure PAHs (Henner et al., 1999). Initially, naphthalene delayed
the germination of all seeds. However, after five days germination was the same between PAHcontaminated and non-contaminated petri dishes. The authors also tested seed germination using PAHcontaminated industrial soils, agricultural soil spiked with liquid tar, and gaswork soil leaches. All
experiments indicated that volatile, water-soluble aromatic hydrocarbons were the main source of
toxicity. Naphthalene was identified as a main volatile compound using gas chromatography/mass
spectrometry.
The effect of PAHs in sludge from a wastewater treatment plant on the growth of willow trees was
examined using tests of willow trees in hydroponic solution and PAH-contaminated soil (Thygesen and
Trapp, 2002). The study involved cutting branches from willow trees into 40 cm pieces and pre-rooting
for several weeks indoors under natural light. Following root and leaf development, the plants were
transferred to Erlenmeyer flasks filled with standard nutrient solution and put under artificial light in a
climate chamber. After two days, the nutrient solution was exchanged for PAH solution or PAHcontaminated soils (except for controls). In order to get a constant concentration of PAH in the
hydroponic solutions, PAHs were added in concentrations above water solubility. Naphthalene
concentration was 325 mg L-1, phenanthrene was 5 mg L-1, and benzo(a)pyrene was 0.55 mg L-1. Five
tests were carried out using the hydroponic solution; in tests 1a-1d, over-saturated solutions were used,
while nominal concentrations below water saturation were used in test 1e. As shown in Table 8, below,
willows showed a dose-dependent response to naphthalene in hydroponic solution: compared to controls:
growth and transpiration of trees were significantly reduced at high naphthalene concentrations and
significantly higher than controls using low concentrations of naphthalene. Using the contaminated soils;
however, growth of willows was not correlated to the PAH content.
When exposed to ultraviolet radiation, PAHs can absorb light energy to reach photo-excited states. The
photo-excited PAH molecules can then react with molecular oxygen and produce reactive oxygen species
and other reactive intermediates that can disrupt cell membranes and produce phototoxic effects. This
phenomenon, known as PAH phototoxicity, has been demonstrated in a number of studies (Arfsten et al.;
Mallakin et al.; Ren et al.; McConkey et al.; Huang et al.; and Huang et al.; cited in Alberta
Environment, 2004). The vast majority of studies examining the effects of PAH phototoxicity have been
conducted in a controlled laboratory setting. However, McDonald and Chapman (2002) argue that these
laboratory-based characterize the phototoxicity dose-response relationship. However, the use of organic
solvents artificially elevate water concentrations and bioaccumulation rates. In addition, the laboratory
based experiments tend not to replicate conditions found in nature (e.g. angle of the sun, presence of other
constituents, oxygenation, and environmental fate of PAHs). These authors suggest that more appropriate
field studies involving ecologically relevant exposure scenarios should be conducted to determine
whether PAH phototoxicity is of significant concern to ecosystems.
-
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Table 8
Growth of trees exposed to PAH and statistically significant differences compared to
controls
Test
Test ID
# of Trees
Mean
growth
(g)
1a
Controls
5
0.136
0.28
0.12
1a
Naphthalene
4
-3.5
-10.31
7.69
smaller
1a
Phenanthrene
4
0.72
2.33
4.71
none
1a
Benzo(a)pyrene
4
0.40
0.99
0.71
larger
1a
Mixture
4
-6.72
-18.44
4.07
smaller
1b
Controls
5
2.05
5.14
3.03
1b
Naphthalene
4
-3.19
-8.08
5.89
smaller
1b
Phenanthrene
4
1.50
3.37
4.80
none
1b
Benzo(a)pyrene
4
1.50
3.56
2.15
none
1b
Mixture
4
-7.01
-14.8
3.78
smaller
1c
Controls
4
4.04
7.14
5.11
1c
Naphthalene
4
1.59
1.90
5.30
none
1c
Phenanthrene
4
2.19
4.24
2.12
none
1c
Benzo(a)pyrene
4
3.39
6.48
3.19
none
1d
Controls
4
2.19
4.61
3.56
1d
Naphthalene
4
-5.32
-9.09
3.83
smaller
1d
Phenanthrene
4
2.58
4.77
1.95
none
1d
Benzo(a)pyrene
4
3.42
5.93
1.67
none
1e
Controls
4
0.93
1.30
0.61
1e
Naphthalene 32
4
1.51
1.93
1.32
none
1e
Naphthalene 16
3
1.86
2.35
0.54
larger
1e
Phenanthrene 1
Phenanthrene
0.5
4
1.12
1.50
0.37
none
3
0.32
0.47
0.50
none
1e
Growth %
S%
Difference
Source: Thygesen and Trapp, 2002
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6.0
Effects on Materials
No studies were identified in the scientific literature to indicate naphthalene could significantly damage
material surfaces.
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7.0
Air Sampling and Analytical Methods
7.1
Reference Methods
The reference methods for naphthalene used in practice by established regulatory agencies are, for the
most part, well documented in the earlier assessment (Alberta Environment, 2004). Since the earlier
assessment, no new reference methods for naphthalene were identified which have been adopted by North
American agencies. The cited reference methods include those reported by the US EPA, the National
Institute of Occupational Safety and Health (NIOSH), and the Occupational Safety and Health (OSHA).
NIOSH/OSHA methods were developed for sampling related to occupational health and safety personal
sampling whereas the US EPA method is intended to be used for ambient air sampling and potentially has
much lower detection limits. These methods frequently use a sampling pump connected to a filter for
trapping particles and an adsorbent for collecting substances in the vapor phase (Alberta Environment,
2004; Jia and Batterman, 2010). More details and a summary table of the advantages and disadvantages
for each method can be found in the earlier assessment report (Alberta Environment, 2004). Each method
is described briefly below.
7.1.1
US EPA Compendium Method TO-13A
As discussed in the earlier assessment report (Alberta Environment, 2004), the US EPA Compendium
Method TO-13A describes the collection of PAHs (including naphthalene) in ambient air using a highvolume pump to draw air through a glass-fibre filter and either a polyurethane (PUF) or XAD-2 adsorbent
cartridge. PUF has demonstrated a lower recovery efficiency and storage capability for naphthalene than
XAD-2 so XAD-2 must be used for naphthalene sampling (US EPA, 1999a). After sampling, the filter
and cartridges are extracted, concentrated and then, analyzed using gas chromatography/mass
spectrometry (GC/MS) (Alberta Environment, 2004). The detection limit for the overall procedure is 0.5
to 500 ng m-3 (Alberta Environment, 2004).
7.1.2
NIOSH Method 1501
The NIOSH Method 1501 (Hydrocarbons, Aromatic) is primarily used to sample for aromatic
hydrocarbon that are not PAHs but can be used when naphthalene concentrations approach exposure
limits. The method uses a personal sampling pump connected to a coconut shell charcoal solid sorbent
tube (NIOSH, 2003). After sampling, a carbon disulphide reagent is used to desorb the PAHs and the
solution is analyzed by gas chromatography with flame ionization detection (GC/FID). Naphthalene was
originally validated for NIOSH Method 1501 but subsequently failed to meet the acceptable desorption
efficiency recovery in the 48.8 µg to 976 µg range and storage stability criteria in 2003 (NIOSH, 2003).
However, acceptable recovery criteria is achieved at naphthalene concentrations approaching the
REL/PEL (NIOSH, 2003). The level of detection for concentrations of naphthalene using this method is
0.01 mg/sample (Alberta Environment, 2004).
7.1.3
NIOSH Method 5506
The NIOSH Method 5506 (Polynuclear Aromatic Hydrocarbons by HPLC) describes the collection of
PAHs using a personal sampling pump connected to a Polytetrafluoroethylene (PTFE) filter and XAD-2
resion sorbent tube (NIOSH, 1998). After sampling, acetonitrile is used as a solvent to extract/desorb the
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polynuclear aromatic hydrocarbons from the filter and sorbent tube. The extract is analyzed by highperformance liquid chromatography (HPLC). The level of detection for concentrations of naphthalene
using this method is 0.8 µg/sample (Alberta Environment, 2004).
7.1.4
NIOSH Method 5515
The NIOSH Method 5515 (Polynuclear aromatic hydrocarbons by GC) uses the same sampling
equipment as the NIOSH Method 5506; however the extract is analyzed by capillary column GC/FID
instead of HPLC. The filter extraction solution can be a number of appropriate solvents including
acetonitrile, benzene, cyclohexane, methylene chloride, and others (NIOSH, 1994). The level of detection
for concentrations of naphthalene using this method is 0.5 µg /sample (Alberta Environment, 2004).
7.1.5
OSHA Method 35
The OSHA Method 35 (Naphthalene) is comparable to the NIOSH Method 1501 but is designed strictly
for naphthalene. Like NIOSH Method 1501, samples are collected using a personal sampling pump
connected to a solid sorbent tube and samples are subsequently analyzed using GC/FID. However, instead
of a charcoal tube, the OSHA Method’s solid sorbent tube is a Chromosorb 106 tube, which has a 100%
desorption efficiency over the range of 0.004 mg to 1.02 mg loading, when desorbed with carbon
disulfide, and samples were stable over a 17-day storage time (OSHA, 1982). This effectively eliminates
the issues with naphthalene sampling discussed by NIOSH (2003). The detection limit of the overall
procedure is 0.08 ppmv or 0.4 mg m-3 for a 10-L air sample (Alberta Environment, 2004).
7.2
Alternative Emerging Technologies
Naphthalene is considered a semi-VOC because its’ vapor pressure is just below the cut-off to be
classified as a VOC but it is also the most volatile PAH (Jia and Batterman, 2010). Since naphthalene’s
vapor pressure is very close to the VOC range, methods largely developed for non-PAH hydrocarbons,
such as NIOSH 1501, have the potential to be used for naphthalene as well. Unlike the US EPA,
naphthalene has been included by Environment Canada (EC) and AEP in the ambient volatile organic
compounds (VOCs) monitoring programs, instead of their PAH monitoring programs (EC, 2013; CASA,
2013). VOC monitoring in these programs is conducted using whole-air canister sampling that follows the
US EPA Compendium Method TO-15 for VOCs (US EPA, 1999). More details are discussed below.
Several alternative technologies were discussed in the earlier assessment (Alberta Environment, 2004),
including capillary electrophoresis (CE), capillary electrochromatography (CEC), supercritical fluid
extraction (SFE), and gas-and-particle (GAP) samplers. These methods were developed by research
groups or companies but still have not been adopted as reference methods by regulatory agencies and, for
the most part, have not had significant advancements since the earlier assessment report. Therefore, they
were not reiterated in this report. Additional reports, journal articles, conference proceedings and other
sources known to contain information on ambient measurement methods for PAHs and VOCs since the
earlier assessment report (Alberta Environment, 2004) were reviewed and three additional emerging
technologies were identified. These are discussed below.
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7.2.1
EC and AEP Naphthalene Monitoring
Naphthalene is monitored as a VOC by EC and AEP. VOC monitoring in the EC and AEP programs is
conducted using whole-air canister sampling that follows the US EPA Compendium Method TO-15 for
VOCs (US EPA, 1999).
In this method, air samples are collected by drawing air into an evacuated, stainless steel electropolished
(SUMMA) canister (AEP, 2013). The sampling apparatus (Xontech Incorporated VOC Sampler) is used
to maintain a constant the flow rate into the canister (10 to 15 mL min-1) for the 24-hour sample period
(EC, 2013; AEP, 2013). The Analysis and Air Quality Section at Environment Canada in Ottawa receives
these 24-hour integrated air samples and analyzes them by GC/FID and GC/MS systems using a
cryogenic pre-concentration technique to measure over 150 hydrocarbon species, including naphthalene
(EC, 2013; AEP, 2013). The SUMMA canisters are evacuated and cleaned prior to installation at the
monitoring sites by the Environment Canada Environmental Technology Centre in Ottawa (AEP, 2013).
This method has a nominal detection limit of 0.10 µg m-3 for naphthalene (EC 2013).
The US EPA does not use this method for naphthalene, instead the US EPA Compendium Method TO13A is used for PAHs, described above, to monitor naphthalene. Additionally, Jia and Batterman (2010)
note that canister methods for naphthalene measurements have not been fully validated. This method was
not initially intended for naphthalene sampling due to the potential of carryover in the GC analysis from
the previous canister sample (Hayes and Benton, 2007) but some independent studies have shown that
this canister method can perform well for naphthalene measurements especially if canisters are heated or
other sample conditioning techniques are used at the time of sample recovery (Hayes and Benton, 2007;
Robinson and Cardin, 2010).
It is worth noting that most monitoring stations measuring naphthalene in Alberta reported more than
50% of samples at below the detection limit cited by EC (2013) in recent years (See Section 2).
7.2.2
Passive Samplers
Some passive adsorbent samplers have become commercially available for sampling naphthalene,
specifically Organic Vapour Monitors (OVM) and Radiello® Passive Samplers (Smith et al., 2009;
Schultz, 2013). Passive samplers typically consist of a single charcoal sorbent wafer, axial/planar badge,
or, in the case of Radiello, a radial design. These devices rely on passive diffusion onto the charcoal
surface. Passive sampling devices, such as Radiello, have been deployed in numerous studies in the US
for sampling vapor intrusion compounds because of their low maintenance, ease of use, and low detection
limits (Schultz, 2013). OVM passive samplers have also been validated in several studies under
controlled, ambient and exposure conditions in urban areas (Smith et al., 2009; Mukerjee et al., 2004;
Chung et al., 1999). However, for outdoor air measurements with sub-microgram per cubic meter
naphthalene concentrations, sampling can take several weeks to obtain detectable measurements (Schultz,
2013).
7.2.3
Cold Fiber-Solid Phase Microextraction (CF-SPME)
Solid Phase Microextraction (SPME) is a method that combines sampling with a pre-concentration step
and it does not require the use of solvents for extraction by desorption directly into the injector of the
chromatographic system (Menezes and Cardeal, 2011).
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As described by Menezes and Cardeal (2013), a Cold Fiber-Solid Phase Microextraction (CF-SPME)
system is a passive air sampling method that exposes 100 µm polydimethylsiloxane fiber in a copper tube
to ambient air. The copper tube also connects the SPME device to a Dewer flask containing liquid
nitrogen. Another copper tube is used as a valve to control the nitrogen pressure and thus, the rate of
nitrogen evaporation. Nitrogen is passed through the tube and fiber at a constant rate, absorbing heat from
the manual SPME device and the fiber. When the nitrogen flow stopped, the cooling process in the tube
was terminated. This apparatus is connected to a sampling bulb through a silicone septum to perform the
extraction by direct thermal desorption.
For the extraction, the cooled fiber was immersed in the sample bulb. The air sampling extraction time
was 15 minutes. The sampling bulb is connected directly to a GC/MS system equipped with an ion trap
mass spectrometer, such that the desorbed PAHs will enter at the GC/MS injector (Menezes and Cardeal,
2013). The limit of detection (LOD) and quantification (LOQ) for naphthalene in a 15 minute sample
were 0.33 ± 0.01 µg m-3 and 0.55 ± 0.01 µg m-3, respectively. The CF-SPME method is considered to be
simple, fast, and inexpensive (Menezes and Cardeal, 2013).
7.2.4
Annular Denuders and Quartz Fibre Filter Membrane
Annular denuders in combination with filters can be used to determine the partitioning of PAHs between
the solid/liquid phase and gas phase. Appropriately coated annular denuder will collect gaseous phase
PAHs while allowing aerosols to pass relatively uncollected. The aerosols will collect on the downstream
filter. Temime-Roussel and colleagues (2004a, 2004b) as well as Possanzini and colleagues (2004) have
examined the collection efficiency of this system for PAHs with a focus on naphthalene. Both studies
used XAD-4 coated denuder(s) to adsorb volatile organic compounds, such as naphthalene. Possanzini
and colleagues (2004) used an upstream polyethylene cyclone with an aerodynamic cut-off of 5 µm to
pre-condition the air stream. A polyethylene filter holder containing a 47-mm, high-purity binderless
quartz fibre filter membrane was installed at the downstream end of the denuders. Both studies extracted
the denuders using cyclohexane and subsequent sonication but Possanzini et al. (2004) analyzed the
extract using GC/MS while Temime-Roussel and colleagues (2004a) analyzed the extract using HPLC.
Both studies demonstrated excellent collection efficiencies for naphthalene (90 to 97%) under a range of
environment conditions. No detection limits for naphthalene were provided in the studies.
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8.0
Ambient Objectives in Other Jurisdictions
Current and recommended or proposed ambient guidelines of other jurisdictions in Canada, as well as in
the United States and other countries were reviewed for naphthalene. Details for each jurisdiction
reviewed are presented in tabular format in Appendix B. Jurisdictions have many common uses for their
guidelines. These uses may include, but are not limited to:
•
•
•
8.1
Evaluation of 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; and
Determining whether to implement temporary emission control actions under persistent adverse
air quality conditions of a short-term nature.
Naphthalene Air Quality Objectives and Guidelines
Air quality objectives and guidelines for naphthalene are summarized in Table 9. Many agencies
developed their guidelines either based on occupational exposure levels (for example, from the American
Conference of Governmental Industrial Hygienists (ACGIH) 8-hour time weighted average occupational
exposure level, NIOSH relative exposure level or OSHA 8-hour Permissible Exposure Limit. Other
agencies started with the reference concentration (RfC) that the US EPA has derived for noncancer
effects, or developed an odour-based standard.
Guideline values are summarized in Table 9, with averaging times ranging from 1 hour to over a lifetime.
The sections below summarize these guidelines by country.
8.1.1
Canada
The Ontario Ministry of the Environment adopted two Ambient Air Quality Criterion (AAQC) for
naphthalene – a one hour AAQC of 50 μg m-3 (9.6 ppb) and a 24-hour AAQC of 22.5 μg m-3 (4.29 ppb).
These criterion are based on odour (1 hour AAQC) and health (24 hour AAQC). The Ontario Ministry of
the Environment uses a maximum Point of Impingement guideline of 36 μg m-3 (6.9 ppb) based on odour.
The Quebec Ministère du Développement durable, de l’Environnement, de la Faune et des Parcs has
established an annual clean air regulation of 3 μg m-3 (0.57 ppb).
8.1.2
United States
Several US Federal and State agencies have developed guidelines for naphthalene. The US EPA has
established a chronic Reference Concentration of 3 μg m-3 (0.57 ppb); the ATSDR has established a
chronic Minimal Risk Level of 3.7 μg m-3 (0.7 ppb). Both guidelines are based on a human-equivalent
LOAEL using rodent LOAELs related to hyperplasia and metaplasia in respiratory and olfactory
epithelium in lifetime exposure rodent studies.
Sixteen State agencies have established guidelines related to naphthalene exposure. Guidelines for short
term exposure timeframes of less than or equal to 1 hour (Arizona, Minnesota, Texas, and Wisconsin)
range from 200-75,000 μg m-3 (38-14,300 ppb) based on eye irritation, nasal and respiratory changes, and
odour. Guidelines for 8 or 24 hour exposures (Idaho, Indiana, Louisiana, Massachusetts, Michigan,
Minnesota, New Hampshire, New Jersey, Oklahoma, Oregon, Rhode Island, and Wisconsin) range from 3
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to 50,000 μg m-3 (0.57-9,540 ppb) based on various Federal air quality and occupational standards for
both shorter term and longer term exposures. These guidelines are based on a mixture of health endpoints
and odour. Several of the guidelines are meant to be protective for daily exposures over a lifetime, so
although the averaging time is 24 hours, they are meant to be protective for chronic exposures.
Guidelines for annual averages (Arizona, California, Massachusetts, Michigan, New Hampshire, Rhode
Island, Texas, Vermont, and Washington State) range from 0.0294-50 μg m-3 (0.0056 – 9.5 ppb) based
largely on the US Environmental Protection Agency and Agency for Toxic Substances and Disease
Registry guidelines.
8.1.3
International Agencies
No air guidelines for naphthalene exposure were found outside of North America.
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2013 Update
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Table 9
Summary of Air Quality Objectives and Guidelines for Naphthalene
Objective Value (µg m-3)
Averaging Time
Agency
Objective Title
Ambient air quality criterion
Maximum point of impingement
(POI) Guideline (30-min.
averaging time*)
Clean Air Regulation
Ontario MOE
Quebec
Chronic Minimum Risk Level
Reference Concentration
Ambient Air Quality Guideline
Short Term Exposure Limit
Chronic Reference Exposure
Level
Acceptable Ambient
Concentration
Occupational Exposure Level
Reference Concentration
Ambient air standard
Allowable Ambient Limit
Threshold Effects Exposure Limit
Initial threshold screening level
Initial risk screening level
Secondary risk screening level
US ATSDR
US EPA
Arizona DEQ
California EPA
Idaho DEQ
Indiana DEM
Louisiana DEQ
Massachusetts DEP
Michigan DEQ
Oregon DEQ
Rhode Island DEM
Texas CEQ
Vermont ANR
Acute Health Based Value
Chronic Health Based Value
Ambient air limit
Reference Concentration
Maximum acceptable ambient
concentration
Ambient Benchmark
Acceptable Ambient Levels
Effects screening level
Hazardous ambient air standard
Washington DOE
Wisconsin DNR
Acceptable source impact level
Acceptable ambient concentration
Minnesota DH
New Hampshire DES
New Jersey DEP
Oklahoma DEQ
Dec 2015
1-hour
50 (10 min)
36
8-hour
24-hour
22.5
Annual
3
3.7
3
0.0558
75,000
9
2,500
50,000
3
1,190
14.25
14.25
3
0.08
0.8
200
9
186
3
1,000
0.03
3
200
3
0.03
50
0.03
0.0294
52,000
Assessment Report on Naphthalene for Developing Ambient Air Quality Objectives
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1,258
Page 42 of 87
9.0
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Ontario Ministry of the Environment. Ontario’s Ambient Air Quality Criteria. Standards Development
Branch, Ontario Ministry of the Environment, Toronto, ON. April 2012, 15 pp.
Ontario Ministry of the Environment. Summary of Standards and Guidelines to support Ontario
Regulation 419/05 – Air Pollution – Local Air Quality (Sorted by Contaminant Name). Standards
Development Branch, Ontario Ministry of the Environment, Toronto, ON. April 2012, 29 pp.
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July 2013).
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2013 Update
© 2015 Government of Alberta
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Epithelial Cells in Response to Naphthalene or Diethyl Maleate. American Journal of Respiratory
Cell and Molecular Biology 43(3): 316.
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Office of Air Resources. (2008) Air Pollution Control Regulation No. 22. Air Toxics. Last
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Amendments to the Regulations Adopted Through: September 2011. Air Pollution Control
Division. Department of Environmental Conservation Agency of Natural Resources. Waterbury,
VT.
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Hemoglobin and Hematocrit in White, Black, and Hispanic Adults: Results from the 2003-2004
National Health and Nutrition Examination Survey. Journal of Medical Toxicology 9: 133-138.
Sutherland KM, Edwards PC, Combs TJ, Van Winkle LS (2012) Sex Differences in the Development of
Airway Epithelial Tolerance to Naphthalene. American Journal of Physiology-Lung Cellular and
Molecular Physiology 302(1): L68-L81.
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Pharmacokinetic Model for Naphthalene and Naphthalene Oxide in Mice and Rats. Annals of
Biomedical Engineering 24, 305–320.
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for Atmospheric PAH Partitioning Studies – 1: Evaluation of the Trapping Efficiency of Gaseous
PAHs. Atmospheric Environment 38: 1913–1924.
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© 2015 Government of Alberta
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Temime-Roussel B, Monod A, Massiani C, Wortham H (2004b) Evaluation of an Annular Denuder
Tubes for Atmospheric PAH Partitioning Studies – 2: Evaluation of Mass and Number Particle
Losses. Atmospheric Environment 38: 1925–1932.
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of Air Permitting Data. http://www.tceq.texas.gov/toxicology/esl/list_main.html#esl_1.
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some human-toxicological Maximum Permissible Risk levels earlier evaluated in the period
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Journal of Soils and Sediments 2(2): 77-82.
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In Support of Summary Information on the Integrated Risk Information System (IRIS). Available
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(GC/MS). Center for Environmental Research Information. EPA/625/R-96/010b
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Administration of Naphthalene to F344 rats. Chemico-Biological Interactions 141, 189–210.
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Exposures to the Bioactivated Cytotoxicant Naphthalene (NA) Produce Airway-specific Clara
cell Tolerance in Mice. Toxicological Sciences 75(1): 161-168.
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2013 Update
© 2015 Government of Alberta
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Willems BAT, Melnick RL, Kohn MC, Portier CJ (2001) A Physiologically Based Pharmacokinetic
Model for Inhalation and Intravenous Administration of Naphthalene in Rats and Mice.
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Hazardous Pollutants. Wisconsin Department of Natural Resources. Madison WI.
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[translated from German by the UK HSE]. Translation date: May, 1995, HSE translation. No.:
15329(A). Zeitschrift fur die gesamte Hygiene und ihre Grenzgebiete. 24: 737–739.
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Regional Publications, European Series, No. 91. WHO Regional Office for Europe, Copenhagen.
273 pp.
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to Humans: Some Traditional Herbal Medicines, Some Myotoxins, Naphthalene and Styrene.
Volume 82.
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2013 Update
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APPENDIX A
NPRI Releases of Naphthalene to Air in Alberta
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2013 Update
© 2015 Government of Alberta
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Table A1. Naphthalene Emissions to Air in Alberta According to the 2011 NPRI Database (ordered by highest to lowest total emissions).
NPRI
ID
City
Company Name
2230
Fort
McMurray
Suncor Energy Oil
Sands Limited
Partnership
3707
Fort
McMurray
Edmonton
5243
Edmonton
1779
Red Deer
2994
Calgary
5304
Calgary
23560
Grande Cache
2274
2960
6572
10218
280
5351
Fort
Saskatchewan
Fort
McMurray
Edmonton
Fort
Saskatchewan
Calgary
Dec 2015
Syncrude Canada Ltd.
Imperial Oil
Lehigh Hanson
Materials Ltd.
NOVA Chemicals
Corporation
Nufarm Agriculture
Champion
Technologies Ltd.
Grande Cache Coal
Corporation
Shell Canada Products
Syncrude Canada Ltd.
Imperial Oil
Dow Chemical Canada
ULC
Baker Hughes Canada
Facility Name
NAICS
Code
Naphthalene Emissions to Air (tonnes)
Other
Stacks/ Storage/
Fugitives NonVents
Handling
Point
Suncor Energy Inc.
Oil Sands
211114
0.3171
Mildred Lake Plant
Site
Strathcona Refinery
Edmonton Plant
NOVA Chemicals
Corporation (Joffre)
Calgary Plant
Calgary Plant
Grande Cache Coal
Corporation
Shell Scotford
Refinery
Aurora North Mine
Site
Edmonton Terminal
Western Canada
Operations
Baker Petrolite
Corporation Eastfield
0.0905
20.0537
Total
20.461
211114
324110
Total OnSite
Releases
(tonnes)
20.4613
0.666
0.02
0.3
0.1
0.007
0.427
0.427
327310
0.2776
325110
0.123
115110
0.1
418410
0.0137
212114
0.044
324110
0.0058
0.0237
0.0193
0.0576
0.011
0.095
0.095
0.044
0.044
0.0361
0.0361
211114
0.01
412110
0.0047
325190
0.002
213118
Assessment Report on Naphthalene for Developing Ambient Air Quality Objectives
2013 Update
© 2015 Government of Alberta
0.002
0.002
0.001
Page 55 of 87
APPENDIX B
Air Quality Objectives and Guidelines
Dec 2015
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2013 Update
© 2015 Government of Alberta
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Agency:
Alberta Environment and Parks (AEP)
Air Quality Guideline:
Alberta AEP does not have an air quality guideline for this chemical.
Averaging Time to Which Guideline Applies:
n/a
Basis for Development:
n/a
Date Guideline Developed:
n/a
How Guideline is Used in Practice:
n/a
Additional Comments:
n/a
Reference and Supporting Documentation:
Alberta Environment and Sustainable Resource Development. Ambient Air Quality Objectives and
Guidelines. January 31, 2013.
Dec 2015
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2013 Update
© 2015 Government of Alberta
Page 57 of 87
Agency:
British Columbia Environmental Protection Division, Ministry of Environment
Air Quality Guideline:
British Columbia Environmental Protection Division does not have an air quality guideline for this
chemical.
Averaging Time to Which Guideline Applies:
n/a
Basis for Development:
n/a
Date Guideline Developed:
n/a
How Guideline is Used in Practice:
n/a
Additional Comments:
n/a
Reference and Supporting Documentation:
British Columbia Environmental Protection Division, Ministry of Environment, Air Quality Objectives
and Standards. 2009.
Dec 2015
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2013 Update
© 2015 Government of Alberta
Page 58 of 87
Agency:
Ontario Ministry of the Environment (Ontario MOE)
Air Quality Guideline:
24-hour Ambient Air Quality Criterion (AAQC) = 22.5 μg m-3(4.29 ppb)
10-minute AAQC = 50 μg m-3 (9.6 ppb)
30-minute averaging time : Maximum point of impingement (POI) Standard = 36 μg m-3
(6.9 ppb)
Averaging Time to Which Guideline Applies:
See above.
Basis for Development:
Limiting effect based on health (24-hour) and odour (10-minute and 30 minute).
Date Guideline Developed:
Unknown.
How Guideline is Used in Practice:
AAQCs are used by Ontario MOE to represent human health or environmental effect-based values not
expected to cause adverse effects based on continuous exposure. The POI is used by Ontario MOE to
review permit applications for stationary sources that emit naphthalene to the atmosphere.
Additional Comments:
AAQC is not used by Ontario MOE to permit stationary sources that emit naphthalene to the atmosphere.
A “point of impingement” standard is used to for permitting situations.
Reference and Supporting Documentation:
Ontario Ministry of the Environment. Ontario’s Ambient Air Quality Criteria. Standards Development
Branch, Ontario Ministry of the Environment, Toronto, ON. April 2012, 15 pp.
Ontario Ministry of the Environment. Summary of Standards and Guidelines to support Ontario
Regulation 419/05 – Air Pollution – Local Air Quality (Sorted by Contaminant Name). Standards
Development Branch, Ontario Ministry of the Environment, Toronto, ON. April 2012, 29 pp.
Dec 2015
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2013 Update
© 2015 Government of Alberta
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Agency:
Quebec Ministère du Développement durable, de l’Environnement, de la Faune et des Parcs
Air Quality Guideline:
Clean Air Regulations
3 µg m-3 limit (0.6 ppb)
Averaging Time to Which Guideline Applies:
1 year
Basis for Development:
n/a
Date Guideline Developed:
n/a
How Guideline is Used in Practice:
The object of this Regulation is to establish particle and gas emission standards, emission opacity
standards, air quality standards and monitoring measures to prevent, eliminate, or reduce the emission of
contaminants into the atmosphere. This Regulation applies to every source of atmospheric contamination
(subject to specific cases)
Additional Comments:
n/a
Reference and Supporting Documentation:
Quebec Ministère du Développement durable, de l’Environnement, de la Faune et des Parcs. Clean Air
Regulation. Environmental Quality Act. Updated July, 2013.
Dec 2015
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2013 Update
© 2015 Government of Alberta
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Agency:
US Agency for Toxic Substances and Disease Registry (US ATSDR)
Air Quality Guideline:
Chronic inhalation minimum risk level (MRL) = 0.0037 mg m-3 (0.0007 ppm)
Averaging Time to Which Guideline Applies:
365 days and longer (i.e. continuous exposure over a lifetime).
Basis for Development:
A human equivalent LOAEL (lowest-observed-adverse-effects-level) concentration of 10 ppm was
identified based on non-neoplastic lesions in the nasal olfactory epithelium (metaplasia, hyperplasia,
atrophy, and chronic inflammation) and respiratory epithelium (hyperplasia, metaplasia, hyaline
degeneration, or gland hyperplasia) in mouse and rat studies.
Date Guideline Developed:
August 2005
How Guideline is Used in Practice:
MRLs are intended to serve as a screening tool to help public health professionals decide where to look
more closely. Inhalation MRLs are exposure concentrations that, based on current information, might
cause adverse health effects in the people most sensitive to such substance-induced effects for 365 days,
and longer, exposure durations.
Additional Comments:
Inhalation MRLs provide a basis for comparison with levels that people might encounter in air.
If a person is exposed to naphthalene at an amount below the MRL, it is not expected that harmful (noncancer) health effects will occur. Because these levels are based only on information currently available,
some uncertainty is always associated with them. Also, because the method for deriving MRLs does not
use any information about cancer, an MRL does not imply anything about the presence, absence, or level
of risk for cancer.
Reference and Supporting Documentation:
Agency for Toxic Substances and Disease Registry (ATSDR). 2005. Toxicological Profile for
Naphthalene, 1-Methylnaphthalene, and 2-Methylnaphthalene. ATSDR, Public Health Service, US
Department of Health and Human Services. Atlanta, GA. August 2005. 347 pp. Available at
http://www.atsdr.cdc.gov/toxprofiles/tp67.pdf (Accessed 9 July 2013).
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2013 Update
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Agency:
US Environmental Protection Agency (US EPA)
Air Quality Guideline:
Reference Concentration (RfC) = 3 µg m-3 (6 ppb)
Averaging Time to Which Guideline Applies:
Continuous exposure (daily exposure over a lifetime).
Basis for Development:
Based on nasal effects (hyperplasia in respiratory epithelium and metaplasia in olfactory epithelium)
observed in a chronic mouse inhalation study. An adjusted human equivalent concentration (HEC)
LOAEL of 9.3 mg m-3 was adjusted with a total uncertainty factor of 3,000 and a value of 3x10--3 mg m-3
was derived.
Date Guideline Developed:
September 1998
How Guideline is Used in Practice:
The Reference concentration (RfC) is intended for use by US EPA staff in risk assessments, decisionmaking and regulatory activities.
Additional Comments:
The Integrated Risk Information System (IRIS) is prepared and maintained by the US EPA.
IRIS is an electronic database containing information on human health effects that may result from
exposure to various chemicals in the environment.
Reference and Supporting Documentation:
US Environmental Protection Agency. 2004. Integrated Risk Information System. Available at:
http://www.epa.gov/iris/ (accessed 9 July 2013).
Dec 2015
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2013 Update
© 2015 Government of Alberta
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Agency:
Arizona Department of Environmental Quality (DEQ)
Air Quality Guideline:
Acute Ambient Air Concentration (AAC): 75 mg m-3 (14.3ppm)
Chronic AAC: 0.0558 µg m-3 (0.011 ppb)
Averaging Time to Which Guideline Applies:
The Arizona DEQ defines “Acute Ambient Air Concentration (AAAC)” as the “concentration of a
hazardous air pollutant, in the ambient air, above which the general population, including susceptible
populations, could experience acute adverse effects to human health.” The “Chronic Ambient Air
Concentration (CAAC)” is defined as the “concentration of a hazardous air pollutant, in the ambient air,
above which the general population, including susceptible populations, could experience chronic adverse
effects to human health.”
Basis for Development:
The acute AAC is equivalent to the National Institute for Occupational Safety and Health (NIOSH) shortterm relative exposure level (REL) of 75 mg m-3. According to the methods outlined in Appendix 12 of
the Arizona Administrative Code, the chronic AAC is derived from the US Environmental Protection
Agency reference concentrations (RfCs) and cancer unity risk factors, as presented in the Integrative Risk
Information System (IRIS), Preliminary Remediation Goals (PRGs) developed by Region 9 of US EPA,
Risk-Based Concentrations (RBCs) developed by Region 3 of the US EPA, or the US ARSDR MRL.
RfCs and MRLs are corrected by adjusting to reflect an assumed exposure of 350, rather than 365 days
per year.
Date Guideline Developed:
Unknown.
How Guideline is Used in Practice:
Acute and chronic ACC are used for permitting for new and modified sources.
Additional Comments:
n/a
Reference and Supporting Documentation:
Arizona Department of State. 2012. Title 18, Article 2: Ambient Air Quality Standards; Area
Designations; Classifications. Office of the Secretary of State, Arizona Department of State. Available at
http://www.azsos.gov/public_services/Title_18/18-02.htm#Article_2 (Accessed 12 July 2013).
Dec 2015
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2013 Update
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Agency:
California Environmental Protection Agency (Cal EPA).
Air Quality Guideline:
Chronic Reference Exposure Level (REL) = 9 μg m-3 (1.7 ppb)
Averaging Time to Which Guideline Applies:
Continuous (daily) exposure over a lifetime.
Basis for Development:
Based on nasal effects (nasal inflammation, olfactory epithelial metaplasia, and respiratory epithelial
hyperplasia) observed in a chronic mouse inhalation study. An average experimental concentration of
1,800 ppb was established from a LOAEL of 10,000 ppb x 6/24 x 5/7. A cumulative safety factor of
1,000 was used (10 for use of a LOAEL, 10 for interspecies uncertainty, and 10 for intraspecies
uncertainty) to derive the chronic REL of 2 ppb (9 μg m-3) after rounding.
Date Guideline Developed:
April 2000.
How Guideline is Used in Practice:
Chronic RELs are for use in facility health risk assessments conducted for the AB 2588 Air
Toxics “Hot Spots” Program.
Additional Comments:
n/a
Reference and Supporting Documentation:
California Environmental Protection Agency (Cal EPA). 2000. Air Toxics Hot Spots Program
Risk Assessment Guidelines, Part III, Technical Support Document for the Determination of
Noncancer Chronic Reference Exposure Levels. Office of Environmental Health Hazard
Assessment, Air Toxicology and Epidemiology Section, Cal EPA. Oakland, CA. April 2000.
California Office of Environmental Health Hazard Assessment (OEHHA)/Air Resources Board
(ARB). 2003. OEHHA Acute, 8-hour and Chronic Reference Exposure Level (REL) Summary. (last
updated 12 February 2012). Available at: http://oehha.ca.gov/air/allrels.html (accessed 9 July 2013).
Dec 2015
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2013 Update
© 2015 Government of Alberta
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Agency:
Colorado Department of Public Health and Environment
Air Quality Guideline:
Colorado does not have an air quality guideline for this chemical.
Averaging Time to Which Guideline Applies:
n/a
Basis for Development:
n/a
Date Guideline Developed:
n/a
How Guideline is Used in Practice:
n/a
Additional Comments:
n/a
Reference and Supporting Documentation:
Colorado Department of Public Health and Environment. Air Quality Control Commission Regulations.
Air Quality Standards, Designation and Emission Budgets. Adopted December 2012, effective February
2013.
Colorado Department of Public Health and Environment. Air Quality Control Commission Regulations.
Regulation Number 8, Control of Hazardous Air Pollutants. Adopted May 2013, effective July 2013.
Dec 2015
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2013 Update
© 2015 Government of Alberta
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Agency:
Idaho Department of Environmental Quality
Air Quality Guideline:
Occupational Exposure Level = 50 mg m-3 (9.6 ppm)
Emissions Screening Level = 3.33 lb/hr
Acceptable Ambient Concentration = 2.5 mg m-3 (0.48 ppm)
Averaging Time to Which Guideline Applies:
OEL = 8 hour time weighted average
EL = 1 hour
AAC = 24 hour averages
Basis for Development:
n/a
Date Guideline Developed:
n/a
How Guideline is Used in Practice:
AACs are the maximum concentration levels allowed in the outside air from a pollution source or sources
under construction or modification. Compliance is often verified by computer modeling or ambient air
sampling. AACs for non-carcinogens are 24-hour averages. ELs are stack-based emission levels based on
pounds of each pollutant emitted per hour. Compliance is often verified by engineering calculations,
computer modeling, or stack sampling.
Additional Comments:
n/a
Reference and Supporting Documentation:
Idaho Department of Environmental Quality. Toxic Air Pollutants. IDAPA 58, Title 01, Chapter 01 Rules
for the control of air pollution in Idaho.
Dec 2015
Assessment Report on Naphthalene for Developing Ambient Air Quality Objectives
2013 Update
© 2015 Government of Alberta
Page 66 of 87
Agency:
Indiana Department of Environmental Management (IDEM).
Air Quality Guideline:
Inhalation Unit Risk (IUR, based on cancer toxicity data) = 3.4 x 10-5 μg m-3 (6.5 x 10-6 ppb)
Reference Concentration (RfC) = 3 μg m-3 (0.57 ppb)
Averaging Time to Which Guideline Applies:
Continuous exposure (daily exposure over a lifetime).
Basis for Development:
IUR based on California EPA value, 2007
RfC based on US EPA value, 2004
Date Guideline Developed:
Unknown.
How Guideline is Used in Practice:
The guidelines listed were used to create toxicity parameters in a 2010 air toxics study that took place in
Southwest Indianapolis.
Additional Comments:
n/a
Reference and Supporting Documentation:
Indiana Department of Environmental Management. 2010. Southwest Indianapolis Air Toxics Study –
Final Technical Report. Available at: http://www.in.gov/idem/toxic/files/swindy_final_tech_report.pdf
(accessed 12 July 2013).
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2013 Update
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Agency:
Louisiana Department of Environmental Quality
Air Quality Guideline:
Ambient air standard (AAS) for toxic air pollutants = 1,190 μg m-3 (227 ppb).
Averaging Time to Which Guideline Applies:
8-hour averaging time.
Basis for Development:
The AAS is equivalent to the National Institute for Occupational Safety and Health (NIOSH) relative
exposure level (REL) of 50 mg m-3 divided by a factor of 42 and rounded. The factor of 42 is a common
adjustment representing a safety factor of 10 and 8/24 and 5/7 multipliers to convert 8-hour per 24-hour
day and 5-day per 7-day week occupational exposures to continuous exposures.
Date Guideline Developed:
Unknown
How Guideline is Used in Practice:
AASs are used by Louisiana DEQ to review permit applications for stationary sources that emit
naphthalene to the atmosphere.
Additional Comments:
n/a
Reference and Supporting Documentation:
Louisiana Administrative Code (LAC). Title 33 Environmental Quality, Part III Air, Chapter 51.
Comprehensive Toxic Air Pollutant Emission Control Program. Louisiana Department of
Environmental Quality. Baton Rouge, LA.
National Institute for Occupational Safety and Health (NIOSH). 2010. NIOSH Pocket Guide to
Chemical Hazards (NPG) Online. NIOSH, Department of Health and Human Services, Centers
for Disease Control and Prevention, Atlanta, GA. Available at:
http://www.cdc.gov/niosh/npg/npgd0439.html (accessed 9 July 2013).
Dec 2015
Assessment Report on Naphthalene for Developing Ambient Air Quality Objectives
2013 Update
© 2015 Government of Alberta
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Agency:
Massachusetts Department of Environmental Protection (MA DEP).
Air Quality Guideline:
Allowable Ambient Limit (AAL) (Annual Average) = 14.25 μg m-3 (2.72 ppb)
Threshold Effects Exposure Limit (TEL) (24-hr Average) = 14.25 μg m-3 (2.72 ppb)
Averaging Time to Which Guideline Applies:
See above.
Basis for Development:
Unknown.
Date Guideline Developed:
Unknown.
How Guideline is Used in Practice:
Information could not be obtained to identify how the guideline is used in practice, but it is expected that
the guideline is used in some manner to meet state level permitting.
Additional Comments:
n/a
Reference and Supporting Documentation:
Massachusetts Department of Environmental Protection (DEP). 1995. Ambient Air Toxics Guidelines.
Massachusetts DEP, Boston, MA. January 2012. Available at:
http://www.mass.gov/eea/agencies/massdep/toxics/sources/air-guideline-values.html (accessed 9 July
2013).
Dec 2015
Assessment Report on Naphthalene for Developing Ambient Air Quality Objectives
2013 Update
© 2015 Government of Alberta
Page 69 of 87
Agency:
Michigan Department of Environmental Quality (MI DEQ).
Air Quality Guideline:
Initial threshold screening level (ITSL) = 3 μg m-3 (0.57 ppb) [24-hour averaging time]
Initial risk screening level (IRSL) = 0.08 μg m-3 (0.015 ppb) [annual averaging time]
Secondary risk screening level (SRSL) = 0.8 μg m-3 (0.15 ppb) [annual averaging time]
Averaging Time to Which Guideline Applies:
See above.
Basis for Development:
The ITSL is based on the US EPA reference concentration of 3 μg m-3 listed in this report.
The IRSL and SRSL are intended to be based on an inhalation unit risk factor and lifetime cancer risks of
one in one million (10-6) and 1 in 100,000 (10-5), respectively. However, it is unknown what inhalation
unit risk factor is used in establishing the IRSL and SRSL.
Date Guideline Developed:
ITSL: 1998.
IRSL: Unknown.
SRSL: Unknown.
How Guideline is Used in Practice:
There are two basic requirements of Michigan air toxic rules. First, each source must apply the best
available control technology for toxics (T-BACT). After the application of T-BACT, the emissions of the
toxic air contaminant cannot result in a maximum ambient concentration that exceeds the applicable
health based screening level for non-carcinogenic effects (ITSL).
Application of an ITSL is required for any new or modified emission source or sources for which a
permit to install is requested and which emits a toxic air contaminant.
Additional Comments:
The applicable air quality screening level for chemical treated as non-carcinogens by Michigan
DEQ is the ITSL. There are two health based screening levels for chemical treated as
carcinogens by Michigan DEQ: the initial risk screening level (IRSL) – based on an increased cancer risk
of one in one million, and the secondary risk screening level (SRSL) – based on as an increased cancer
risk of 1 in 100,000.
Reference and Supporting Documentation:
Michigan Department of Environmental Quality. Table 2. List of Screening Levels (ITSL, IRSL, and
SRSL) in Alphabetical Order. Air Quality Division, Lansing, MI. Available at:
http://www.michigan.gov/documents/deq/deq-aqd-toxics-ITSLALPH_244167_7.pdf (accessed 11 July
2013).
Dec 2015
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2013 Update
© 2015 Government of Alberta
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Agency:
Minnesota Department of Health
Air Quality Guideline:
Acute Health-Based Value (HBV), one hour exposure: 200 μg m-3 (38 ppb)
Chronic HBV, continuous exposure (24 hr/day, 7 days/week): 9 μg m-3 (1.7 ppb)
Averaging Time to Which Guideline Applies:
See above. Acute HBV: 1 hr
Chronic HBV: 24 hr, 7 days/week continuous exposure
Basis for Development:
The acute air quality guideline is based on a rat study that reported respiratory changes (cell swelling and
sloughing) following four hours of exposure to naphthalene; in this study, the NOAEL was 240 mg m-3.
Applying an uncertainty factor of 1,000 (10 for intraspecies variability, 10 for interspecies variability, and
10 for database deficiencies) yielded the acute HBV. The chronic air quality guideline is based on two
NTP studies in mice and rats. The studies yielded a LOAEL of 10 ppm, to which an uncertainty factor of
1,000 (10 for intraspecies variability, 10 for interspecies variability, and 10 for the use of a LOAEL rather
than a NOAEL) was applied. Adverse endpoints included marked respiratory and nasal impacts.
Date Guideline Developed:
Unknown.
How Guideline is Used in Practice:
As described by the Minnesota Department of Health, “HRVs are used by the Minnesota Department of
Health and other state agencies, such as the Minnesota Pollution Control Agency (MPCA), to assist in the
assessment of potential health risks from exposures to chemicals in ambient air. HRVs can be used for
assessing risks in the environmental review process, issuing air permits, risk assessments and other sitespecific assessments.”
Additional Comments:
Developed by the Minnesota Department of Health, at the request of the Minnesota Pollution Control
Agency
Reference and Supporting Documentation:
Minnesota Department of Health. 2004. Naphthalene: Acute and Chronic Health-Based Values (last
updated 6 July 2004). Available at:
http://www.health.state.mn.us/divs/eh/risk/guidance/air/naphthalene.html (accessed 11 July 2013).
Minnesota Department of Health. Frequently Asked Questions about MDH Air Guidance. Available at:
http://www.health.state.mn.us/divs/eh/risk/rules/air/hrvfaqs.html (accessed 11 July 2013).
Dec 2015
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2013 Update
© 2015 Government of Alberta
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Agency:
New Hampshire Department of Environmental Services (NH DES).
Air Quality Guideline:
24-hour ambient air limit (AAL) = 186 μg m-3 (35.5 ppb)
Annual AAL = 3 μg m-3 (0.57 ppb)
Averaging Time to Which Guideline Applies:
See above.
Basis for Development:
The AALs were developed in the following manner:
24-hour Ambient Air Limit – The American Conference of Governmental Industrial Hygienists (ACGIH)
8-hour time weighted average occupational exposure limit (OEL) of 10 ppm (52 mg m-3) is divided by a
safety factor (SF of 100 and a time adjustment factor (TAF) of 2.8.
Annual Ambient Air Limit – Based on the US EPA reference concentration (RfC)
Date Guideline Developed:
Unknown.
How Guideline is Used in Practice:
AALs are used by New Hampshire DES to review permit applications for sources that emit naphthalene
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:
n/a
Reference and Supporting Documentation:
New Hampshire Administrative Rule. Chapter Env-A 1400. Regulated Toxic Air Pollutants. New
Hampshire Department of Environmental Services. Concord, NH.
American Conference of Governmental Industrial Hygienists (ACGIH). 2013. 2013 TLVs and
BEIs. Publication #0103. ISBN: 978-1-607260-59-2. ACGIH, Cincinnati, OH. 242 pp.
Dec 2015
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2013 Update
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Agency:
New Jersey Department of Environmental Protection (DEP).
Air Quality Guideline:
Reporting threshold = 2,000 lbs/yr
SOTA Threshold = 10,000 lbs/yr
Within NJDEP, the Bureau of Technical Services compiles the inhalation information available from
IRIS and other appropriate sources into lists of URFs and RfCs. In the case of naphthalene, US EPA has a
Reference Concentration (RfC) of 3 μg m-3 listed in this report.
Averaging Time to Which Guideline Applies:
Continuous exposure (daily exposure over a lifetime).
Basis for Development:
n/a
Date Guideline Developed:
n/a
How Guideline is Used in Practice:
n/a
Additional Comments:
n/a
Reference and Supporting Documentation:
New Jersey Administrative Code (NJAC). 2011. Title 7, Chapter 27, Subchapter 8. Permits and
Certificates for Minor Facilities (and Major Facilities without an Operating Permit). New Jersey
Department of Environmental Protection. Trenton, NJ.
New Jersey Department of Environmental Protection. 2009. Technical Manual 1003. Guidance
on Preparing a Risk Assessment for Air Contaminant Emissions. Air Quality Permitting
Program, Bureau of Air Quality Evaluation, New Jersey Department of Environmental
Protection. Trenton, NJ. Revised November 2009.
Dec 2015
Assessment Report on Naphthalene for Developing Ambient Air Quality Objectives
2013 Update
© 2015 Government of Alberta
Page 73 of 87
Agency:
North Carolina Department of Environment and Natural Resources (NC ENR).
Air Quality Guideline:
North Carolina ENR does not have an air quality guideline for this chemical.
Averaging Time to Which Guideline Applies:
n/a
Basis for Development:
n/a
Date Guideline Developed:
n/a
How Guideline is Used in Practice:
n/a
Additional Comments:
n/a
Reference and Supporting Documentation:
North Carolina Administrative Code (NCAC). North Carolina Air Quality Rules 15A NCAC 02D .1104
TOXIC AIR POLLUTANT GUIDELINES –North Carolina Department of Environment and Natural
Resources. Raleigh, NC.
Dec 2015
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2013 Update
© 2015 Government of Alberta
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Agency:
Ohio Environmental Protection Agency (OH EPA).
Air Quality Guideline:
Ohio EPA does not have an air quality guideline for this chemical.
Averaging Time to Which Guideline Applies:
n/a
Basis for Development:
n/a
Date Guideline Developed:
n/a
How Guideline is Used in Practice:
n/a
Additional Comments:
Ohio measured naphthalene in each county and is on the list of 188 Hazardous Air Pollutants, but there is
no guideline set.
Reference and Supporting Documentation:
Ohio Environmental Protection Agency (EPA). 2006. Review of New Sources of Toxic
Emissions. Air Toxics Unit, Division of Air Pollution Control, Ohio EPA. Columbus, OH.
Dec 2015
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2013 Update
© 2015 Government of Alberta
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Agency:
Oklahoma Department of Environmental Quality (DEQ)
Air Quality Guideline:
Maximum acceptable ambient concentration (MAAC) = 1,000 μg m-3 (200 ppb)
Averaging Time to Which Guideline Applies:
24-hour
Basis for Development:
The American Conference of Governmental Industrial Hygienist (ACGIH) TLV – 8-hour time
weighted average occupational exposure limit (OEL) of 10 mg m-3 is divided by a safety factor of 50.
Date Guideline Developed:
Not stated.
How Guideline is Used in Practice:
MAACs are used by Oklahoma DEQ to review permit applications for sources that emit
naphthalene to the atmosphere.
Additional Comments:
Air Toxics Partial list is for historical/archival purposes.
Reference and Supporting Documentation:
Oklahoma Department of Environmental Quality (DEQ). 2005. Total Air Toxics Partial Listing
[maximum acceptable ambient concentrations (MAAC) for air toxics]. Oklahoma City, OK.
http://www.deq.state.ok.us/aqdnew/toxics/listings/AirToxicsPartialListing9.html
Dec 2015
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2013 Update
© 2015 Government of Alberta
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Agency:
Oregon Department of Environmental Quality
Air Quality Guideline:
Ambient benchmark: 0.03 μg m-3 (0.0057 ppb)
Averaging Time to Which Guideline Applies:
Continuous exposure (daily exposure over a lifetime).
Basis for Development:
As described by the Oregon Department of Environmental Quality: “The ambient benchmark
concentrations for 52 air toxics of concern in Oregon are based on consensus recommendations from the
Air Toxics Scientific Advisory Committee, a panel of experts that provides advice on the state air toxics
program that is scientifically and technically sound, independent and balanced.” The naphthalene
Ambient Benchmark Concentration for is based on a cancer endpoint.
Date Guideline Developed:
Unknown.
How Guideline is Used in Practice:
As described by the Oregon Department of Environmental Quality: “Ambient benchmarks are not
regulatory standards, but reference values by which air toxics problems can be identified, addressed and
evaluated. The Department will use ambient benchmarks as indicated in these rules, to implement the
Geographic, Source Category, and Safety Net Programs.”
Additional Comments:
n/a
Reference and Supporting Documentation:
Oregon Department of Environmental Quality. Oregon Air Toxics Benchmarks. Air Quality Division,
Portland, OR. Available at: http://www.deq.state.or.us/aq/toxics/benchmark.htm
Oregon Department of Environmental Quality. Ambient Benchmarks for Air Toxics. Air Quality
Division, Portland, OR. Available at: http://www.deq.state.or.us/aq/toxics/docs/abcRuleFinal.pdf
Dec 2015
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2013 Update
© 2015 Government of Alberta
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Agency:
Rhode Island Department of Environmental Management (DEM).
Air Quality Guideline:
Acceptable Ambient Levels (AALs):
24 hour = 3 µg m-3 (0.57 ppb)
Annual = 0.03 µg m-3 (0.0057 ppb)
Averaging Time to Which Guideline Applies:
See above.
Basis for Development:
Not stated.
Date Guideline Developed:
Unknown
How Guideline is Used in Practice:
"Acceptable Ambient Level" is the maximum ambient air concentration of a listed toxic air contaminant
that may be contributed by a stationary source, at or beyond that facility's property line. The purpose of
this regulation is to limit emissions of toxic air contaminants from stationary sources.
Additional Comments:
n/a
Reference and Supporting Documentation:
State Department of Rhode Island and Providence Plantations Department of Environmental Management
Office of Air Resources. Air Pollution Control Regulation No. 22. Air Toxics. 2008. Last Amended 9
October 2008.
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2013 Update
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Agency:
Texas Commission on Environmental Quality (TCEQ)
Air Quality Guideline:
Short-term effects screening level (ESL) = 200 μg m-3 (38 ppb)
Long-term effects screening level (ESL) = 50 μg m-3 (9.6 ppb)
Averaging Time to Which Guideline Applies:
Short-term =1-hour
Long-term = annual
Basis for Development:
Short-term ESL is based on odour and long-term is based on health
Date Guideline Developed:
10/29/2012
How Guideline is Used in Practice:
Effects Screening Levels (ESLs) are currently used by the TCEQ Toxicology Division for air permitting
Additional Comments:
Naphthalene ESL’s are interim values indicating that the ESL is current and will be reviewed by the
Toxicology Division at a later date. Also, interim ESLs can be updated pending the release of updated
toxicity information or odour data.
Reference and Supporting Documentation:
Texas Commission on environmental Quality. Effects Screening Levels (ESL) Lists Used in the Review
of Air Permitting Data. http://www.tceq.texas.gov/toxicology/esl/list_main.html#esl_1.
Dec 2015
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2013 Update
© 2015 Government of Alberta
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Agency:
Vermont Agency of Natural Resources (VT ANR).
Air Quality Guideline:
Hazardous Ambient Air Standard And Stationary Source Hazardous Air Impact Standard:
0.3 µg m-3 (0.057 ppb) (action level: 0.02 lbs/8hrs)
Averaging Time to Which Guideline Applies:
Annual Average
Basis for Development:
An ambient standard was originally derived for each Hazardous Air Contaminant by dividing its
work place (occupational) air standard, called a Threshold Limit Value or TLV, by 100 to account for
some model uncertainties and then by a time factor of 4.2 to extrapolate from a standard designed to
protect the average healthy worker from adverse health effects to an outdoor air standard designed to
protect the general public from adverse effects (i.e., to go from 8 hours per day, 5 days per week to
continuous exposures of 24 hours per day, 7 days per week).
Date Guideline Developed:
November 1981
How Guideline is Used in Practice:
"Hazardous Ambient Air Standard (HAAS)" means the highest acceptable concentration in the ambient
air of a hazardous air contaminant.
Additional Comments:
n/a
Reference and Supporting Documentation:
State of Vermont Agency of Natural Resources. 2011. Air Pollution Control Regulations Including
Amendments to the Regulations Adopted Through: September 2011. Air Pollution Control Division.
Department of Environmental Conservation Agency of Natural Resources. Waterbury, VT.
State of Vermont Agency of Natural Resources.1988. Air toxics Report. Chapters 2-7. Department of
Environmental Conservation Agency of Natural Resources. Waterbury, VT.
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2013 Update
© 2015 Government of Alberta
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Agency:
Washington State Department of Ecology (WA DOE).
Air Quality Guideline:
Acceptable source impact level (ASIL) = 0.0294 µg m-3 (0.0056 ppb)
Averaging Time to Which Guideline Applies:
year
Basis for Development:
Acceptable source impact level (ASIL) means a screening concentration of a toxic air pollutant in the
ambient air.
Date Guideline Developed:
Unknown.
How Guideline is Used in Practice:
To establish the systematic control of new or modified sources emitting toxic air pollutants (TAPs) in
order to prevent air pollution, reduce emissions to the extent reasonably possible, and maintain such
levels of air quality as will protect human health and safety.
Additional Comments:
n/a
Reference and Supporting Documentation:
Washington Administrative Code (WAC). Chapter 173-460-150 WAC. Controls For New Sources Of
Toxic Air Pollutants. Table of ASIL, SQER and de minimis emission values. Washington State
Department of Ecology. Olympia, WA.
Dec 2015
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2013 Update
© 2015 Government of Alberta
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Agency:
Wisconsin Department of Natural Resources (WI DNR).
Air Quality Guideline:
Acceptable ambient concentration (AAC):
= 1,258 μg m-3 (240 ppb) 24-hour averaging time.
= 52 mg m-3 (10 ppm) 1-hour averaging time.
Averaging Time to Which Guideline Applies:
See above
Basis for Development:
The 24-hour AAC represents two and four tenths percent of the American Conference of
Governmental Industrial Hygienists (ACGIH) 8-hour time weighted average occupational
exposure limit (OEL) of 50 mg m-3.
The 1-hour AAC represents 10 percent of the ACGIH 8-hour OEL of 50 mg m-3.
Date Guideline Developed:
Unknown
How Guideline is Used in Practice:
Used by Wisconsin DNR to control hazardous air pollutants.
Additional Comments:
n/a
Reference and Supporting Documentation:
Wisconsin Administrative Code (WAC). Air Pollution Control Rules. Chapter NR 445. Control of
Hazardous Pollutants. Wisconsin Department of Natural Resources. Madison WI.
American Conference of Governmental Industrial Hygienists (ACGIH). 2013. Guide to Occupational
Exposure Values. ISBN: 978-1-607260-60-8. ACGIH, Cincinnati, OH.
Dec 2015
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2013 Update
© 2015 Government of Alberta
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Agency:
Australia Department of Sustainability, Environment, Water, Population and Communities
Air Quality Guideline:
Australia does not have an air quality guideline for this chemical.
Averaging Time to Which Guideline Applies:
n/a
Basis for Development:
n/a
Date Guideline Developed:
n/a
How Guideline is Used in Practice:
n/a
Additional Comments:
n/a
Reference and Supporting Documentation:
Australia Department of Sustainability, Environment, Water, Population and Communities. National
standards for criteria air pollutants in Australia.
http://www.environment.gov.au/atmosphere/airquality/publications/standards.html#fn1
Dec 2015
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2013 Update
© 2015 Government of Alberta
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Agency:
European Commission
Air Quality Guideline:
The EC does not have an air quality guideline for this chemical.
Averaging Time to Which Guideline Applies:
n/a
Basis for Development:
n/a
Date Guideline Developed:
n/a
How Guideline is Used in Practice:
n/a
Additional Comments:
n/a
Reference and Supporting Documentation:
European Commission Environment Air Quality Standards
http://ec.europa.eu/environment/air/quality/standards.htm (accessed August 28, 2013)
Dec 2015
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2013 Update
© 2015 Government of Alberta
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Agency:
The Netherlands National Institute of Public Health and the Environment (RIVM)
Air Quality Guideline:
RIVM does not have an air quality guideline for this chemical.
Averaging Time to Which Guideline Applies:
n/a
Basis for Development:
n/a
Date Guideline Developed:
n/a
How Guideline is Used in Practice:
n/a
Additional Comments:
n/a
Reference and Supporting Documentation:
The Netherlands National Institute of Public Health and the Environment (RIVM). 2009. Re-evaluation
of some human-toxicological Maximum Permissible Risk levels earlier evaluated in the period 19912001. Report 711701092. RIVN, Bilthoven, The Netherlands.
Dec 2015
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2013 Update
© 2015 Government of Alberta
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Agency:
New Zealand Ministry for the Environment (MOE) and New Zealand Ministry of Health
(MOH)
Air Quality Guideline:
New Zealand MOE and MOH do not have an air quality guideline for this chemical.
Averaging Time to Which Guideline Applies:
n/a
Basis for Development:
n/a
Date Guideline Developed:
n/a
How Guideline is Used in Practice:
n/a
Additional Comments:
n/a
Reference and Supporting Documentation:
New Zealand Ministry for the Environment and Ministry of Health (New Zealand). 2002. Ambient Air
Quality Guidelines. May 2002.
New Zealand Ministry for the Environment and Ministry of Health (New Zealand). 2009. Proposed
Amendments to the National Environmental Standards for Air Quality. Discussion Document. June 2009.
Dec 2015
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2013 Update
© 2015 Government of Alberta
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Agency:
World Health Organization (WHO)
Air Quality Guideline:
WHO does not have an air quality guideline for this chemical.
Averaging Time to Which Guideline Applies:
n/a
Basis for Development:
n/a
Date Guideline Developed:
n/a
How Guideline is Used in Practice:
n/a
Additional Comments:
n/a
Reference and Supporting Documentation:
World Health Organization (WHO). 2000. Air Quality Guidelines for Europe, 2nd Edition. WHO
Regional Publications, European Series, No. 91. WHO Regional Office for Europe, Copenhagen. 273 pp.
Dec 2015
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2013 Update
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