EPA-540/1-86-014
Environmental Protection
Agency
Office of Emergency and
Remedial Response
Washington DC 20460
Off'ce of Research and Development
Office of Health and Environmental
Assessment
Environmental Criteria and
Assessment Office
Cincinnati OH 45268
Superfund
&EPA
HEALTH EFFECTS ASSESSMENT
FOR NAPHTHALENE
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EPA/540/1-86-014
September 1984
HEALTH EFFECTS ASSESSMENT
FOR NAPHTHALENE
U.S. Environmental Protection Agency
Office of Research and Development
Office of Health and Environmental Assessment
Environmental Criteria and Assessment Office
Cincinnati, OH 45268
U.S. Environmental Protection Agency
Office of Emergency and Remedial Response
Office of Solid Waste and Emergency Response
Washington, DC 20460
U.S. Environmental Protection Ag«ney
Region V, Library
230 South Dearborn Ctrcet
Chicago, Illinois 60604
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DISCLAIMER
This report has been funded wholly or In part by the United States
Environmental Protection Agency under Contract No. 68-03-3112 to Syracuse
Research Corporation. It has been subject to the Agency's peer and adminis-
trative review, and 1t has been approved for publication as an EPA document.
Mention of trade names or commercial products does not constitute endorse-
ment or recommendation for use.
Environmental Protection A'geffcy
11
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PREFACE
This report summarizes and evaluates Information relevant to a prelimi-
nary Interim assessment of adverse health effects associated with
naphthalene. All estimates of acceptable Intakes and carcinogenic potency
presented 1n this document should be considered as preliminary and reflect
limited resources allocated to this project. Pertinent toxlcologlc and
environmental data were located through on-Hne literature searches of the
Chemical Abstracts, TOXLINE, CANCERLINE and the CHEMFATE/OATALOG data
bases. The basic literature searched supporting this document 1s current up
to September, 1984. Secondary sources of Information have also been relied
upon 1n the preparation of this report and represent large-scale health
assessment efforts that entail extensive peer and Agency review. The
following Office of Health and Environmental Assessment (OHEA) source have
been extensively utilized:
U.S. EPA. 1980a. Ambient Hater Quality Criteria for Naphthalene.
Environmental Criteria and Assessment Office, Cincinnati, OH.
EPA-440/5-80-059. NTIS PB 81-117707.
U.S. EPA. 1982. Revision and Update of Hazard Profile on Naphtha-
lene. Prepared by the Environmental Criteria and Assessment
Office, Cincinnati, OH, OHEA for the Office of Solid Haste and
Emergency Response, Washington, DC.
The Intent 1n these assessments 1s to suggest acceptable exposure levels
whenever sufficient data were available. Values were not derived or larger
uncertainty factors were employed when the variable data were limited In
scope tending to generate conservative (I.e., protective) estimates. Never-
theless, the Interim values presented reflect the relative degree of hazard
associated with exposure or risk to the chemlcal(s) addressed.
Hhenever possible, two categories of values have been estimated for sys-
temic toxicants (toxicants for which cancer Is not the endpolnt of concern).
The first, the AIS or acceptable Intake subchronlc. Is an estimate of an
exposure level that would not be expected to cause adverse effects when
exposure occurs during a limited time Interval (I.e., for an Interval that
does not constitute a significant portion of the Hfespan). This type of
exposure estimate has not been extensively used or rigorously defined, as
previous risk assessment efforts have been primarily directed towards
exposures from toxicants 1n ambient air or water where lifetime exposure 1s
assumed. Animal data used for AIS estimates generally Include exposures
with durations of 30-90 days. Subchronlc human data are rarely available.
Reported exposures are usually from chronic occupational exposure situations
or from reports of acute accidental exposure.
111
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The AIC, acceptable Intake chronic, 1s similar 1n concept to the ADI
(acceptable dally Intake). It 1s an estimate of an exposure level that
would not be expected to cause adverse effects when exposure occurs for a
significant portion of the Hfespan [see U.S. EPA (1980b) for a discussion
of this concept]. The AIC 1s route specific and estimates acceptable
exposure for a given route with the Implicit assumption that exposure by
other routes 1s Insignificant.
Composite scores (CSs) for noncardnogens have also been calculated
where data permitted. These values are used for ranking reportable quanti-
ties; the methodology for their development 1s explained 1n U.S. EPA (1983b).
For compounds for which there 1s sufficient evidence of carc1nogen1dty,
AIS and AIC values are not derived. For a discussion of risk assessment
methodology for carcinogens refer to U.S. EPA (1980b). Since cancer 1s a
process that 1s not characterized by a threshold, any exposure contributes
an Increment of risk. Consequently, derivation of AIS and AIC values would
be Inappropriate. For carcinogens, q-]*s have been computed based on oral
and Inhalation data 1f available.
1v
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ABSTRACT
In order to place the risk assessment 1n proper context, the reader 1s
referred to the preface of this document. The preface outlines limitations
applicable to all documents of this series, as well as the appropriate
Interpretation and use of the quantitative estimates.
The absence of adequate toxlcologlcal data on naphthalene precludes
estimation of acceptable Intakes for any route.
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ACKNOWLEDGEMENTS
The Initial draft of this report was prepared by Syracuse Research
Corporation under Contract No. 68-03-3112 for EPA's Environmental Criteria
and Assessment Office, Cincinnati, OH. Dr. Christopher DeRosa and Karen
Blackburn were the Technical Project Monitors and Helen Ball was^the Project
Officer. The final documents 1n this series were prepared for the Office of
Emergency and Remedial Response, Washington, DC.
Scientists from the following U.S. EPA offices provided review comments
for this document series:
Environmental Criteria and Assessment Office, Cincinnati, OH
Carcinogen Assessment Group
Office of Air Quality Planning and Standards
Office of Solid Waste
Office of Toxic Substances
Office of Drinking Water
Editorial review for the document series was provided by:
Judith Olsen and Erma Durden
Environmental Criteria and Assessment Office
Cincinnati, OH
Technical support services for the document series was provided by:
Bette Zwayer, Pat Daunt, Karen Mann and Jacky Bohanon
Environmental Criteria and Assessment Office
Cincinnati, OH
v1
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TABLE OF CONTENTS
1.
2.
3.
4.
5.
ENVIRONMENTAL CHEMISTRY AND FATE
ABSORPTION FACTORS IN HUMANS AND EXPERIMENTAL ANIMALS . . .
2.1.
2.2,
ORAL
INHALATION
TOXICITY IN HUMANS AND EXPERIMENTAL ANIMALS
3.1,
3.2.
3.3.
3.4.
SUBCHRONIC
3.1.1. Oral
3.1.2. Inhalation
CHRONIC
3.2.1. Oral
3.2.2. Inhalation
TERATOGENICITY AND OTHER REPRODUCTIVE EFFECTS. . . .
3.3.1. Oral
3.3.2. Inhalation
TOXICANT INTERACTIONS
CARCINOGENICITY
4.1.
4.2.
4.3.
4.4.
HUMAN DATA
4.1.1. Oral
4.1.2. Inhalation
BIOASSAYS
4.2.1. Oral
4.2.2. Inhalation
OTHER RELEVANT DATA
WEIGHT OF EVIDENCE
REGULATORY STANDARDS AND CRITERIA
Page
... 1
... 2
... 2
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... 3
. . . 3
. . . 3
. . . 3
... 4
... 4
... 4
... 4
... 4
... 4
... 4
... 5
... 5
... 5
... 5
... 5
. . . 5
... 5
... 6
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V11
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TABLE OF CONTENTS (cont.)
Page
6. RISK ASSESSMENT 8
6.1. ACCEPTABLE INTAKE SUBCHRONIC (AIS) 8
6.1.1. Oral 8
6.1.2. Inhalation 8
6.2. ACCEPTABLE INTAKE CHRONIC (AIC),
6.2.1. Oral 8
6.2.2. Inhalation 8
6.3. CARCINOGENIC POTENCY
6.3.1. Oral 9
6.3.2. Inhalation 9
7. REFERENCES 10
APPENDIX: Summary Table for Naphthalene 16
V111
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LIST OF ABBREVIATIONS
ADI Acceptable dally Intake
AIC Acceptable Intake chronic
AIS Acceptable Intake subchronlc
CAS Chemical Abstract Service
CS Composite score
ppm Parts per million
RQ Reportable quantity
STEL Short-term exposure limit
TLV Threshold limit value
TWA Time-weighted average
1x
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1. ENVIRONMENTAL CHEMISTRY AND FATE
The relevant physical and chemical properties and environmental fate of
naphthalene (CAS No. 91-20-3) are as follows:
Chemical class:
Molecular weight:
Vapor pressure at 25°C:
Water solubility at 25°C:
Log octanol/water partition
coefficient:
B1oconcentrat1on factor:
Half-life 1n air:
Half-life 1n water:
Half-life 1n soil:
polycycllc aromatic hydrocarbon
128.19 (Callahan et al., 1979)
0.082 mm Hg (MacKay et al., 1982)
31.7 mg/a (MacKay et al., 1980)
3.37 (MacKay et al.. 1980)
146 (estimated from the equation
of Velth et al., 1979)
0.7 (Atkinson et al., 1984)
~1 day (Callahan et al., 1979)
2.3 days (Zoeteman et al., 1980)
<1 day (estimated)
The half-life for naphthalene 1n aquatic media caused by blodegradatlon
can be estimated to be -14 hours from the estimated blotransformatlon rate
constant (lxlO~7 ma cell"1 hr"1) reported by Mabey et al. (1981) and
the concentration of microorganisms at 5x10* cell ma."1 (Burns et al.,
1982).
Pertinent data regarding the Teachability of this compound 1n soils
could not be located 1n the available literature. Considering the soil
sorptlon coefficient (Kenaga and Goring, 1980) and the water solubility,
this compound 1s expected to have higher mobility 1n soils compared with
most other polycycllc aromatic hydrocarbons. The b1odegradabH1ty of this
compound 1n soils, however, 1s such that significant leaching Into
groundwater 1s not likely.
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2. ABSORPTION
2.1. ORAL
Information regarding the absorption of naphthalene 1n humans and
animals 1s limited. When Ingested as a solid, naphthalene 1s sufficiently
absorbed to cause toxldty 1n man (Chusld and Fried, 1955; Zuelzer and Apt,
1949; Nash, 1903; Gross et al., 1958; Haggerty, 1956). Furthermore,
naphthalene seems to be more toxic when dissolved 1n oil before 1ngest1on
(Talakln, 1966). Sanborn and Mallns (1977) suggested that naphthalene may
be absorbed to a greater extent when Ingested 1n water than 1n food.
2.2. INHALATION
Data regarding the absorption of Inhaled naphthalene are limited;
however, Valaes et al. (1963) reported toxldty and death 1n newborn Infants
exposed to naphthalene vapors from clothes or blankets that had been stored
In or near the Infants' rooms.
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3. TOXICITY IN HUMANS AND EXPERIMENTAL ANIMALS
3.1. SUBCHRONIC
3.1.1. Oral. Data regarding subchronlc oral exposure to naphthalene are
limited. Several Investigators (Anz1ulew1cz et al., 1959; Zlnkham and
Chllds, 1958) reported the occurrence of hemolytlc anemia 1n Infants born to
mothers who had "sniffed" and Ingested unspecified quantities of naphthalene
(1n the form of mothballs) during pregnancy. The mothers themselves were
also anemic, but to a lesser extent than were the Infants.
Several animal studies focused upon ocular effects of naphthalene, but
failed to mention whether any other signs of toxldty were measured or
observed. Fltzhugh and Buschke (1949) observed slight cataracts 1n weanling
rats exposed to 254 naphthalene 1n the diet for 60 days. Assuming a rat
consumes food equivalent to 5% of Us body weight/day, this dietary level 1s
equivalent to a dose of 1 g/kg bw/day.
In two separate studies, rabbits exposed to 1 g naphthalene/kg bw/day by
gavage (either 1n light paraffin or an unspecified vehicle) for ~46 days
developed cataracts (Ghettl and Mar1an1, 1956; Van Heynlngen and P1r1e,
1976) and degeneration of the retina (Van Heynlngen and P1r1e, 1976) within
the first few days of treatment.
3.1.2. Inhalation. Subchronlc data regarding the Inhalation of naphtha-
lene are limited to two studies of occupational exposure. Van der Hoeve
(1906) reported that one man who worked with powdered naphthalene developed
cataracts and retinal hemorrhage, while another man exposed similarly had
Chor1oret1n1t1s. Ghettl and Mar1an1 (1956) reported that 8/21 workers
exposed to unspecified "high" concentrations of naphthalene 1n a dye-manu-
facturing process developed cataracts. Since these men were <50 years of
age, 1t Is unlikely that they would have developed cataracts spontaneously.
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3.2. CHRONIC
3.2.1. Oral. Pertinent data regarding the chronic toxldty of orally
administered naphthalene could not be located 1n the available literature.
3.2.2. Inhalation. Pertinent data regarding chronic toxldty of Inhaled
naphthalene could not be located 1n the available literature.
3.3. TERATOGENICITY AND OTHER REPRODUCTIVE EFFECTS
3.3.1. Oral. Pertinent data regarding the teratogenldty of Ingested
naphthalene could not be located 1n the available literature; however,
naphthalene or Us metabolites are known to cross the placenta 1n sufficient
quantities to cause fetotoxlc effects (Anzlulewlcz et al., 1959; Van der
Hoeve, 1913). These effects Included hemolytlc anemia 1n humans and
cataracts and retinal damage 1n rabbits. Doses either were not estimated or
were not reported 1n the secondary sources.
3.3.2. Inhalation. Pertinent data regarding the teratogenldty of
Inhaled naphthalene could not be located In the available literature.
3.4. TOXICANT INTERACTIONS
A woman exposed for 3 weeks to a combination of naphthalene and paradl-
chlorobenzene (while mothproofing clothing) developed aplastlc anemia 1
month after exposure (Harden and Baetjer, 1978). No other cases of aplastlc
anemia associated with exposure to either napthalene or paradlchlorobenzene
alone have been reported 1n the literature.
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4. CARCINOGENICITY
4.1. HUMAN DATA
4.1.1. Oral. Pertinent data regarding the cardnogenldty of Ingested
naphthalene could not be located In the available literature.
4.1.2. Inhalation. Pertinent data regarding the cardnogenldty of
Inhaled naphthalene could not be located 1n the available literature;
however. Wolf (1976) reported that 6/15 workers exposed to vapors of both
naphthalene and coal tar developed laryngeal carcinomas (4) or neoplasms of
the pylorus and cecum (2). There was no control group. Schmeltz et al.
(1978), however, showed that the d1-, tr1- and tetramethyl naphthalene
contaminants of coal tar were carcinogenic when applied to mouse skin but
that naphthalene alone was not.
4.2. BIOASSAYS
4.2.1. Oral. In a study designed to Investigate the carcinogenic effects
of anthracene delivered by a naphthalene vehicle, the cardnogenldty of
naphthalene alone was tested (Druckrey and Schmahl, 1955). A group of 28 BD
I and BD III strain rats were exposed orally to 10 g naphthalene/rat for an
unspecified amount of time and monitored for >1000 days. A second group of
10 rats were exposed subcutaneously to 0.82 g naphthalene/rat for a similar
period of time. No tumors were observed 1n either group. No other studies
pertaining to the cardnogenldty of orally administered naphthalene were
located 1n the available literature.
4.2.2. Inhalation. Pertinent data regarding the cardnogenldty of
Inhaled naphthalene could not be located 1n the available literature.
-5-
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4.3. OTHER RELEVANT DATA
The genotoxlc activity of naphthalene has been tested 1n two Ui vitro
systems. Cell transformation was not seen 1n rodent embryo cells pretreated
with leukemia virus and exposed to concentrations of naphthalene up to 100
mg/8, of culture medium {Freeman et al., 1973; Rh1m et al., 1974). Simi-
larly, cell transformations were not seen 1n a murlne mammary gland organ
culture system at naphthalene concentrations up to 1000 mg/i of culture
medium (TonelH et al., 1979).
Naphthalene was not found to be mutagenlc 1n a number of bacter1al/m1-
crosomal assay systems (McCann et al., 1975; Kraemer et al., 1974).
4.4. WEIGHT Of EVIDENCE
IARC has not evaluated the risk to humans associated with oral or Inha-
lation exposure to naphthalene. Applying the criteria for evaluating the
overall weight of evidence for carc1nogen1dty proposed by the Carcinogen
Assessment Group of the U.S. EPA (Federal Register, 1984), the evidence for
cardnogenldty of naphthalene 1n humans and animals 1s Inadequate and the
chemical 1s most appropriately designated a Group D-Not Classified chemical.
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5. REGULATORY STANDARDS AND CRITERIA'
The ACGIH (1983) has recommended a TLV-TWA of 50 mg/m3 (10 ppm) and an
STEL of 75 mg/m3 for occupational exposure to naphthalene. Since eye
Irritation was seen at 15 ppm, this criterion was chosen "to prevent ocular
effects but possibly not blood changes 1n hypersusceptlbles." The OSHA
standard for exposure to naphthalene 1n the workplace 1s a TWA of 50 mg/m3
(Code of Federal Regulations, 1981).
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6. RISK ASSESSMENT
6.1. ACCEPTABLE INTAKE SUBCHRONIC (AIS)
6.1.1. Oral. The only studies that defined exposure levels (Ghet£1 and
Mar1an1, 1956; Van Heynlngen and P1r1e, 1976) failed to mention whether end-
points other than ocular effects were monitored. Since other effects such
as hemolytlc anemia have been associated with exposure to naphthalene, H
would not be prudent to calculate an AIS on the basis of these studies.
6.1.2. Inhalation. The lack of pertinent, quantitative data precludes
assessment of risk caused by Inhalation of naphthalene.
6.2. ACCEPTABLE INTAKE CHRONIC (AIC)
6.2.1. Oral. Data regarding chronic oral exposure to naphthalene were
not located 1n the available literature. For reasons given 1n Section
6.1.1., an AIC cannot be derived from the subchronlc data, data from which
a CS for oral exposure to naphthalene can be calculated have not been
located 1n the available literature (U.S. EPA, 1983a).
6.2.2. Inhalation. Data regarding chronic exposure to naphthalene by
Inhalation could not be located 1n the available literature. Furthermore,
H would be Imprudent to use the TLV established by the ACGIH (1983) to
calculate an AIC, since this value was established essentially on the basis
of eye Irritation and with the hypothesis that chronic exposure might cause
more severe effects. Data from which a CS for Inhalation exposure to
naphthalene can be calculated have not been located 1n the available
literature (U.S. EPA, 1983a).
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6.3. CARCINOGENIC POTENCY (q.,*)
6.3.1. Oral. Naphthalene was not carcinogenic 1n strain BO I and BO III
rats (Druckrey and Schmahl, 1955). Furthermore, mutagenlcHy and In vitro
bloassays that tested only naphthalene yielded negative results. It 1s
therefore not possible to derive a q * for oral exposure to naphthalene.
6.3.2. Inhalation. The lack of pertinent data regarding the cardnoge-
nlcHy of Inhaled naphthalene precludes assessment of carcinogenic potency.
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8. REFERENCES
ACGIH (American Conference of Governmental Industrial Hyg1en1sts). 1983.
Threshold Limit Values for Chemical Substances and Physical Agents 1n the
Workroom Environment with Intended Changes for 1983-84. Cincinnati, OH.
p. 26.
Anz1ulew1cz, 3.A., H.J. Dick and E.E. Ch1arull1. 1959. Transplacental
naphthalene poisoning. Am. J. Obstet. Gynecol. 78: 519-521. (Cited In
U.S. EPA, 1983a)
Atkinson, R., S.M. Aschmann and J.N. PUts, Jr. 1984. Kinetics of the
reactions of naphthalene and blphenyl with OH radicals and with 0- at
294ilK. Environ. Sd. Techno!. 18: 110-113.
Burns, L.A., D.A. CUne and R.R. LassHer. 1982. Exposure Analysis
Modeling System (EXAMS). User Manual and System Documentation.
Environmental Research Laboratory, ORD, U.S. EPA, Athens, GA. EPA
600/3-82-023.
Callahan, M.A., M.W. SUmak, N.W. Gabel, et al. 1979. Water-Related
Environmental Fate of 129 Priority Pollutants. Vol. II. Office of Water
Planning and Standards, Office of Water and Waste Management. U.S. EPA,
Washington, DC. EPA 440/4-79-029b.
Chusld, E. and C.T. Fried. 1955. Acute hemolytlc anemia due to naphthalene
1ngest1on. Am. J. D1s. Child. 89: 612-614. (Cited In U.S. EPA, 1980a)
-10-
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Code of Federal Regulations. 1981. OSHA Safety and Health Standards 29 CFR
1910.1000.
Druckrey, H. and D. Schmahl. 1955. Cancerogene wlrkung von anthracen. Die
Naturwissenschaften. 42: 159. (Ger.) (Cited 1n U.S. EPA, 1982)
Federal Register. 1984. Environmental Protection Agency. Proposed
guidelines for carcinogenic risk assessment. 49 FR 46294-46299.
FHzhugh, 0.6. and W.H. Buschke. 1949. Production of cataract 1n rats by
betatetralol and other derivatives of naphthalene. Arch. Opthal.
41: 572-582. (Cited 1n U.S. EPA, 1983a)
Freeman, A.E., et al. 1973. Transformation of cell cultures as an
Indication of the carcinogenic potential of chemicals. 3. Natl. Cancer
Inst. 51: 799-807. (Cited 1n U.S. EPA, 1980a; 1982)
Ghettl, G. and L. Mar1an1. 1956. Eye changes due to naphthalene. Med.
Lav. 47: 533-538. (Cited 1n U.S. EPA, 1980a; 1983a)
Gross, R.T., et al. 1958. An hereditary enzymatic defect 1n erythrocyte
metabolism: glucose-6-phosphate dehydrogenase deficiency. J. Clln.
Invest. 37: 1176-1184. (Cited 1n U.S. EPA, 1980a)
Haggerty, R.J. 1956. Toxic hazards: naphthalene poisoning. New England
J. Med. 255: 919-920. (Cited 1n U.S. EPA, 1980a)
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Harden, R.A. and A.M. Baetjer. 1978. Aplastlc anemia following exposure to
paradlchlorobenzene and naphthalene. J. Occup. Med. 20: 820-822. (Cited
In U.S. EPA, 1980a)
Kenaga, E.E. and C.A. I. Goring. 1980. Relationships between water
solubility, soil sorptlon, octanol-water partitioning and concentration of
chemicals 1n biota. In: Aquatic Toxicology, ASTM STP 707, J.G. Eaton, P.R.
ParMsh and A.C. Hendrlcks, Ed., ASTM, Philadelphia, PA.
Kraemer, M., et al. 1974. S. typhlmuMum and £.. coll to detect chemical
mutagens. Arch. Pharmacol. 284: R46. (Cited 1n U.S. EPA, 1980a; 1982)
Mabey, W.R., J.H. Smith, R.T. Podoll, et al. 1981. Aquatic Fate Process
Data for Organic Priority Pollutants. Monitoring and Data Support Dlv.,
Office of Water Regulations and Standards, Washington, DC. EPA 440/4-81-014.
MacKay, D., A. Bobra, W.Y. Shin and S.H. Yalkowsky. 1980. Relationships
between aqueous solubility and octanol-water partition coefficients.
Chemosphere. 9: 701-711.
MacKay, D., A. Bobra, D.W. Chan and W.Y. Shin. 1982. Vapor pressure
correlations of low-volatility environmental chemicals. Environ. Sd.
Technol. 16: 645-649.
McCann, J., et al. 1975. Detection of carcinogens as mutagens 1n the
Salmonella/mlcrosome test. Assay of 300 chemicals. Proc. Natl. Acad. Sd.
72: 5135-5139. (Cited 1n U.S. EPA, 1980a; 1982a)
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Nash, L.F. 1903. Naphthalene poisoning. Br. Med. J. 1: 251. (Cited 1n
U.S. EPA, 1980a)
Rh1m, J.S., et al.* 1974. Evaluation of an in vitro assay system for
carcinogens based on prior Infection of rodent cells with nontransformlng
RNA tumor virus. J. Natl. Cancer Inst. 52: 1167-1173. (Cited 1n U.S. EPA,
1982)
Sanborn, H.R. and D.C. Mallns. 1977. Toxldty and metabolism of
naphthalene: a study with marine larval Invertebrates. Proc. Soc. Exp.
B1ol. Med. 154: 151-155. (Cited 1n U.S. EPA, 1980a)
Schmeltz, I., et al.* 1978. Bloassays of Naphthalene and Alkyl
Naphthalenes for Co-Carcinogenic Activity. Relation to Tobacco
Cardnogenesls. In: Cardnogenesls,. Vol. 3: Polynuclear Aromatic
Hydrocarbons, P. Jones and I. Freudenthal, Ed. Raven Press, NY. p. 47-60.
(Cited 1n U.S. EPA, 1980a)
Talakln, Yu. N. 1966. Sanltary-toxlcologlcal characteristics of
o-naphthoqu1none. Vop. Kommunal. G1g. 6: 37-43. (Cited 1n U.S. EPA,
1980a)
TonelH, Q., et al. 1979. Transformation of cultured mouse mammary glands
by aromatic amines and amides and their derivatives. Cancer Res.
39: 1784-1792. (Cited 1n U.S. EPA, 1980a; 1982)
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U.S. EPA. 1980a. Ambient Water Quality Criteria for Naphthalene. U.S.
EPA, Environmental Criteria and Assessment Office, Cincinnati, OH.
EPA-440/5-80-059. NTIS PB 81-117707.
U.S. EPA. 1980b. Guidelines and Methodology Used 1n the Preparation of
Health Effects Assessment Chapters of the Consent Decree Water Quality
Criteria. Federal Register. 45:79347-79357.
U.S. EPA. 1982. Revision and Update of Hazard Profile on Naphthalene.
Prepared by the Environmental Criteria and Assessment Office, Cincinnati,
OH, OHEA for the Office of Solid Waste and Emergency Response, Washington,
DC.
U.S. EPA. 1983a. Reportable Quantity for Naphthalene. Prepared by the
Environmental Criteria and Assessment Office, Cincinnati, OH, OHEA for the
Office of Solid Waste and Emergency Response, Washington, DC.
U.S. EPA. 1983b. Methodology and Guidelines for Reportable Quantity
Determinations Based on Chronic Tox1c1ty Data. Prepared by the Environ-
mental Criteria and Assessment Office, Cincinnati, OH, OHEA for the Office
of Solid Waste and Emergency Response, Washington, DC.
Valaes, T., et al. 1963. Acute hemolysls due to naphthalene Inhalation.
J. Ped. 63: 904-915. (Cited 1n U.S. EPA, 1980a)
Van der Hoeve, J. 1906. Choreoret1n1t1s belm menschen durch die e1nw1rk1ng
von naphthalln. Arch. Augenhellk. 56: 259. (Ger.) (Cited 1n U.S. EPA,
1980a; 1983a)
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Van der Hoeve, J. 1913. Wlrkung von naphthol auf die ^yen von menschen,
tleren, und auf fatale augen. Graele Arch. Ophthal. 85: 305. (CHed 1n
U.S. EPA, 1980a)
Van Heynlngen, R. and A. P1r1e. 1976. Naphthalene cataract 1n plgmented
and albino rabbits. Exp. Eye Res. 22: 393-394. (Cited 1n U.S. EPA, 1983a)
Velth, 6.D., D.L. Defoe and B.V. Bergstedt. 1979. Measuring and estimating
the bloconcentratlon factor of chemicals 1n fish. J. F1sh Res. Board Can.
36: 1040-1048.
Wolf, 0. 1976. Cancer diseases In chemical workers 1n a former naphthalene
cleaning plant. Deutche Gesundheltwesen. 31: 996-999. (Cited In U.S. EPA,
1980a)
Zlnkham, W.J. and B. ChUds. 1958. A defect of glutathlone metabolism 1n
erythrocytes from patients with a naphthalene-Induced hemolytlc anemia.
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U.S. Environmental Protection Agency
Region V, Library
230 South Dearborn Gtrest _15_
Chicago, Illinois 60604
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APPENDIX
Summary Table for Naphthalene
Experimental
Species Dose/Exposure Effect
Inhalation
AIS
AIC
Carcinogenic
potency
Oral
AIS
AIC
Carcinogenic
potency
Acceptable
Intake
(AIS or AIC) Reference
NO
ND
NO
ND
ND
ND
ND = Not derived
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