vvEPA
United States
Environmental Protection
Agency
Office of Water
Regulations and Standards
Criteria and Standards Division
Washington DC 20460
EPA 440/5-80-049
October 1980
Ambient
Water Quality
Criteria for
Fluoranthene
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AMBIENT WATER QUALITY CRITERIA FOR
FLUORANTHENE
Prepared By
U.S. ENVIRONMENTAL PROTECTION AGENCY
Office of Water Regulations and Standards
Criteria and Standards Division
Washington, D.C.
Office of Research and Development
Environmental Criteria and Assessment Office
Cincinnati, Ohio
Carcinogen Assessment Group
Washington, D.C.
Environmental Research Laboratories
Corvalis, Oregon
Duluth, Minnesota
Gulf Breeze, Florida
Narragansett, Rhode Island
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DISCLAIMER
This report has been reviewed by the Environmental Criteria and
Assessment Office, U.S. Environmental Protection Agency, and approved
for publication. Mention of trade names or commercial products does not
constitute endorsement or recommendation for use.
AVAILABILITY NOTICE
This document is available to the public through the National
Technical Information Service, (NTIS), Springfield, Virginia 22161.
11
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FOREWORD
Section 304 (a)(l) of the Clean Water Act of 1977 (P 1_ 95-217)
requires the Administrator of the Environmental Protection Agency to
publish criteria for water quality accurately reflecting the latest
scientific knowledge on the kind and extent of all identifiable effects
on health and welfare which may be expected from the presence of
pollutants in any body of water, including ground water. Proposed water
quality criteria for the 65 toxic pollutants listed under section 307
(d -i u?,. the C ean Water Act were developed and a notice of their
?raoJa ty was Published for public comment on March 15, 1979 (44 FR
15926), July 25, 1979 (44 FR 43660), and October 1, 1979 (44 FR 56628)
This document is a revision of those proposed criteria based upon a
consideration of comments received from other Federal Agencies State
agencies, special interest groups, and individual scientists' The
criteria contained in this document replace any previously published EPA
criteria for the 65 pollutants. This criterion document is also
published in satisfaction of paragraph 11 of the Settlement Agreement
]n Natural .Resources Defense Council, et. al . vs Train 8 ERC 21?n
(D.D.C. 1976), modified, 12 ERC 1833 (D.D.C. 19/9).'
The term "water quality criteria" is used in two sections of the
Clean Water Act, section 304 (a)(l) and section 303 (c)(2). The term has
a different program impact in each section. In section 304 the term
represents a non-regulatory, scientific assessment of ecological ef-
!!"!: The critcer\? Panted in this publication are such scientific
assessments. Such water quality criteria associated with specific
stream uses when adopted as State water quality standards under section
303 become enforceable maximum acceptable levels of a pollutant in
ambient waters The water quality criteria adopted in the State water
quality standards could have the same numerical limits as the criteria
developed under section 304. However, in many situations States may want
to adjust water quality criteria developed under section 304 to reflect
local environmental conditions and human exposure patterns before
incorporation into water quality standards. It is not until their
the state water quality standards that the Cr1teria
Guidelines to assist the States in the modification of criteria
presented in this document, in the development of water quality
b EP'A" ^ Water-related Pr°9rams of thi* Agency, are being
STEVEN SCHATZOW
Deputy Assistant Administrator
Office of Water Regulations and Standards
111
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ACKNOWLEDGEMENTS
Aquatic Life Toxicology:
William A. Brungs, ERL-Narragansett
U.S. Environmental Protection Agency
John H. Gentile, ERL-Narragansett
U.S. Environmental Protection Agency
Mammalian Toxicology and Human Health Effects:
Joseph Santodonato (author)
Syracuse Research Corporation
Debdas Mukerjee (doc. mgr.) ECAO-Cin
U.S. Environmental Protection Agency
Jerry F. Stara (doc. mgr.) ECAO-Cin
U.S. Environmental Protection Agency
Patrick Durkin
Syracuse Research Corporation
Rolf Hartung
University of Michigan
Si Duk Lee, ECAO-RTP
U.S. Environmental Protection Agency
Michael Pereira, HERL
U.S. Environmental Protection Agency
Alan B. Rubin
U.S. Environmental Protection Agency
Benjamin L. Van Duuren
New York Univ. Medical Center
Fred Passman
Energy Resources Company
Julian Andelman
University of Pittsburgh
Fred Boch
Roswell Memorial Institute
Herbert Cornish
University of Michigan
Alfred D. Garvin
University of Cincinnati
Edmond LaVoie
American Health Foundation
Steven D. Lutkenhoff, ECAO-Cin
U.S. Environmental Protection Agency
Quentin H. Pickering
Newtown Fish Toxicology Lab.
U.S. Environmental Protection Agency
William W..Sutton, EMSL-Las Vegas
U.S. Environmental Protection Agency
Jan Connery
Energy Resources Company.
Technical Support Services Staff: D.J. Reisman, M.A. Garlough, B.L. Zwayer,
P.A. Daunt, K.S. Edwards, T.A. Scandura, A.T. Pressley, C.A. Cooper,
M.M. Denessen.
Clerical Staff: C.A. Haynes, S.J. Faehr, L.A. Wade, D. Jones, B.J. Bordicks,
B.J. Quesnell, P. Gray, B. Gardiner.
IV
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TABLE OF CONTENTS
Introduction A-l
Aquatic Life Toxicology B-l
Introduction B-l
Effects B-l
Acute Tbxicity B-l
Chronic Toxicity B-l
Plant Effects B-2
Residues B-2
Summary B-2
Criteria B-2
References B-8
Mammalian Toxicology and Human Health Effects C-l
Exposure C-l
Ingestion from Water C-l
Ingestion from Food C-8
Inhalation C-17
Dermal C-19
Pharmacokinetics C-19
Absorption C-21
Distribution C-21
Metabolism C-22
Excretion C-23
Effects C-24
Acute, Subacute and Chronic Toxicity C-24
Synergism and/or Antagonism C-26
Teratogenicity C-27
Mutagenicity C-27
Carcinogenicity C-28
Criteria Formulation C-40
Existing Guidelines and Standards C-HO
Current Levels of Exposure C~4l
Special Groups at Risk C-^3
Basis and Derivation of Criteria C-43
References C-48
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CRITERIA DOCUMENT
FLUORANTHENE
CRITERIA
Aquatic Life
The available data for fluoranthene indicate that acute toxicity to
freshwater aauatic life occurs at concentrations as low as 3,980 ug/1 and
would occur at lower concentrations among species that are more sensitive
than those tested. No data are available concerning the chronic toxicity of
fluoranthene to sensitive freshwater aquatic life.
The available data for fluoranthene indicate that acute and chronic tox-
icity to saltwater aauatic life occur at concentrations as low as 40 and 16
ug/1, respectively, and would occur at lower concentrations among species
that are more sensitive than those tested.
Human Health
For the protection of human health from the toxic properties of fluoran-
thene ingested through water and contaminated aquatic organisms, the ambient
water criterion is determined to be 42 ug/1.
For the protection of human health from the toxic properties of fluoran-
thene ingested through contaminated aquatic organisms alone, the ambient
water criterion is determined to be 54 ug/1.
VI
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INTRODUCTION
Fluoranthene, a polynuclear aromatic hydrocarbon (PAH), is produced by
the pyrolysis of organic raw materials such as coal and petroleum at high
tempertures (Andelman and Snodgrass, 1974). It is also known to occur natu-
rally as a product of plant biosynthesis (Borneff, et al. 1968).
Fluoranthene (1,2-benzacenaphthene or Idryl) has the molecular formula
C16H10* I1" has a mo1ecular weight of 202, a melting point of 111°C, a
boiling point of approximately 375°C, and a vapor pressure of 0.01 mm Hg at
25°C. It is soluble in water to the extent of 265 yg/1 (Davis, et al. 1942;
Klevens, 1950).
Fluoranthene is ubiquitous in the environment and has been detected in
air in the U.S. (Searle, 1976), in foreign and domestic drinking waters
(Harrison, et al. 1975; Basu and Saxena, 1977, 1978; U.S. EPA, 1977), and in
foodstuffs (Howard, et al. 1966a,b,c).
A-l
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REFERENCES
Andelman, J.B. and J.E. Snodgrass. 1974. Incidence and significance of
polynuclear aromatic hydrocarbons in the water environment. CRC Critical
Reviews in Environmental Control. 4: 69.
Basu, O.K. and J. Saxena. 1977. Analysis of raw and drinking water samples
for polynuclear aromatic hydrocarbons. U.S. Environ. Prot. Agency, P.O.
No. Ca-7-2999-A, Exposure Evaluation Branch, HERL, Cincinnati, Ohio.
Basu, O.K. and J. Saxena. 1978. Polynuclear aromatic hydrocarbons in
selected U.S. drinking waters and their raw water sources. Environ. Sci.
Technol. 12: 795.
Borneff, J., et al. 1968. Experimental studies on the formation of poly-
cyclic aromatic hydrocarbons in plants. Environ. Res. 2: 22.
Davis, W.W., et al. 1942. Solubility of carcinogenic and related hydrocar-
bons in water. Jour. Amer. Chem. Soc. 64: 108.
Harrison, R.M., et al. 1975. Polynuclear aromatic hydrocarbons in raw,
potable and wastewaters. Water Res. 9: 311.
Howard, J.W., et al. 1966a. Extraction and estimation of polycyclic aro-
matic hydrocarbons in vegetable oils. Jour. Assoc. Off. Anal. Chem.
49: 1236.
A-2
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Howard, J.W., et al. 1966b. Extraction and estimation of polycyclic aro-
matic hydrocarbons in smoked foods. II. Benzo(a)pyrene. Jour. Assoc. Off.
Anal. Chem. 49: 611.
Howard, J.W., et al. 1966c. Extraction and estimation of PAH in smoked
foods. Part I. General Method. Jour. Assoc. Off. Anal. Chem. 49: 595.
Kleven, H.B. 1950. Solubilization of polycyclic hydrocarbons. Jour. Phys.
Chem. 54: 283.
Searle, C.E. 1976. Chemical carcinogens, ACS Monograph 173. Amer. Chem.
Soc., Washington, D.C. p. 341.
U.S. EPA. 1977. National Organic Monitoring Survey (NOMS). Technical Sup-
port Division, Office of Water Supply, U.S. Environ. Prot. Agency, Cincin-
nati, Ohio.
A-3
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Aquatic Life Toxicology*
INTRODUCTION
Bluegill, Daphnia magna, and the alga, Selenastrum capricornutum, have
been studied using static test procedures and unmeasured concentrations.
The range of LC5Q and EC5Q values is 3,980 to 325,000 ug/l and the blue-
gill is most sensitive.
In contrast to the relationship between freshwater fish and inverte-
brate species, the mysid shrimp and a polychaete are much more sensitive to
fluoranthene than the sheepshead minnow. The numerical relationship between
acute and chronic effect concentrations of fluoranthene on the mysid shrimp
is small, with the acute-chronic ratio being 2.5.
EFFECTS
Acute Toxicity
Daphnia magna is more resistant than the bluegill (Table 1) with a
48-hour EC5Q value of 325,000 ug/l; the 96-hour LC5Q value for the blue-
gill is 3,980 wg/l (U.S. EPA, 1978).
The 96-hour LC5Q values for the mysid shrimp and a polychaete are 40
and 500 wg/l, respectively (Table 1). The sheepshead minnow was exposed to
concentrations of fluoranthene as high as 560,000 wg/l with no observed
LC5Q value (Table 4).
Chronic Toxicity
The chronic value for the mysid shrimp is 16 wg/l (Table 2) and when
this concentration is divided by the acute value a ratio of 2.5 is obtained.
*The reader is referred to the Guidelines for Deriving Water Oualitv
Criteria for the Protection of Aquatic Life and Its Uses Border to better
understand the following discussion and recommendation. The following
J It K0rllain *he aPPr°Priate dat* that were found in the literature and
at the_ bottom of each table are calculations for deriving various measures
of toxicity as described in the Guidelines. measures
B-l
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Plant Effects
The freshwater alga, Selenastrum capricornutum, has been exposed to
fluoranthene and the 96-hour ECgo values for cell numbers and chlorophyll
a_ are 54,400 and 54,600 ug/1, respectively (Table 3).
The 96-hour EC5Q values for chlorophyll £ and cell numbers of the
saltwater alga, Skeletonema costatum, are 45,000 and 45,600 ug/1, respec-
tively.
Residues
No measured, steady-state bioconcentration factors are available for
freshwater or saltwater organisms and fluoranthene.
Summary
The bluegill (96-hour LC5Q = 3,980 ug/l) is much more sensitive to
fluoranthene than the cladoceran, Daphnia magna (48-hour EC™ = 325,000
ug/1). No chronic data are available for freshwater organisms. The 96-hour
EC5Q values for the alga, Selenastrum capricornutum, were 54,400 and
54,600 ug/1.
The saltwater mysid shrimp and a polychaete were much more sensitive
than the sheepshead minnow. The LC5Q values for the invertebrate species
were 40 and 500 ug/l; the 96-hour LC5Q value for the sheepshead minnow was
greater than 560,000 ug/1. The chronic value and acute-chronic ratio for
the mysid shrimp were 16 yg/l and 2.5, respectively. The EC^ values for
DU
the saltwater alga were 45,000 and 45,600 ug/1.
CRITERIA
The available data for fluoranthene indicate that acute toxicity to
freshwater aauatic life occurs at concentrations as low as 3,980 ug/1 and
would occur at lower concentrations among species that are more sensitive
B-2
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than those tested. No data are available concerning the chronic toxicity of
fluoranthene to sensitive freshwater aquatic life.
The available data for fluoranthene indicate that acute and chronic
toxicity to saltwater aquatic life occur at concentrations as low as 40 and
16 ug/1, respectively, and would occur at lower concentrations among species
that are more sensitive than those tested.
B-3
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Table 1. Acute values for fluoranthene
03
I
Spec 1 es
Cladoceran,
Daphnla magna
Blueglll,
Lepomls macrochlrus
Polychaete (Immature),
Neanthes arenaceodentata
Mysld shrimp (juvenile).
Mysldopsls bah la
LC50/EC50 Species Acute
Method* (ug/l) Value (ug/l) Reference
FRESHWATER SPECIES
S, U 325,000 325,000 U.S. EPA, 1978
S, U 3,980 3,980 U.S. EPA, 1978
SALTWATER SPECIES
S, u 500 500 Rossi 4 Neff, 1978
S, u 40 40 U.S. EPA, 1978
* S = static, U = unmeasured
No Final Acute Values are calculable since the minimum data base requirements are not met.
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Table 2. Chronic values for fluoranthene (U.S. EPA. 1978)
Chronic
Species u *,. -« Limits Value
P • Method* (Ufl/l) (ug/l)
Mysld shrimp.
Mysldopsls
SALTWATER SPECIE^
LC ]9 __
12'22
* LC = life cycle or partial life cycl
Acute-Chronic Ratio
Mysld shrimp,
Mysldopsls bah I a
Chronic
Value
,6
Acute
Ratlo
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Table 3. Plant values for fIuoranthene (U.S. EPA, 1978)
CO
I
:les
Effect
FRESHWATER SPECIES
Alga,
SeIenastrum caprIcornutum
Alga,
Selenastrum caprlcornutum
EC50 96-hr
ce11 numbers
EC50 96-hr
chlorophy 11 _a_
SALTWATER SPECIES
Alga,
Skeletonema costatum
Alga,
Skeletonema costatum
EC50 96-hr
ch lorophy 11 _a_
EC50 96-hr
eel I numbers
Result
(ug/l)
54,400
54,600
45,000
45,600
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Table 4. Other data for fluoranthene (U.S. EPA, 1978)
c , Result
sPecles Duration Effect (iig/l)
SALTWATER SPECIES
Sheepshead minnow (adult), 96 hrs LC50 >560 000
Cyprlnodon variegatus '
03
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REFERENCES
Rossi, S.S. and J.M. Neff. 1978. Toxicity of polynuclear aromatic hydro-
carbons to the polychaete, Neanthes arenaceodentata. Marine Pollution
Bull. 9: 220.
U.S. EPA. 1978. In-depth studies on health and environmental impacts of
selected water pollutants. U.S. Environ. Prot. Agency. Contract No.
68-01-4646.
B-8
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Mammalian Toxicology and Human Health Effects
EXPOSURE
Ingestion from Water
The sources of fluoranthene in aqueous environments are both
natural and man-made. The occurrence of fluoranthene in water sed-
iments, bacteria, algae, and plant materials in areas remote from
industry and human habitation suggest natural origin. Suess (1970)
h«s suggested that fluoranthene in surface waters arises from con-
ta .ation of estuaries and coastal waters by shipping and harbor
oil, industrial and municipal effluents, atmospheric fallout, pre-
cipitation, and road run-off.
The two most important properties influencing the concentra-
tions of fluoranthene in water are its stability and solubility.
Its relatively high molecular weight and relative nonpolarity make
fluoranthene very insoluble in water. Although the solubility of
fluoranthene in water at 25°C is only 265 ug/1 (Klevens, 1950), its
presence in environmental waters can be increased by detergents,
solvents and by adsorption on the surface of solid matter, both
biotic and abiotic.
Studies have shown that fluoranthene can be adsorbed and con-
centrated on a variety of particulate matter. Thus, the presence
of particulate matter in suspended and settled form in natural wa-
ters can be sources of relatively high concentrations of fluoran-
thene. Analyzing sediment samples from Buzzards Bay, Mass., Giger
and Blumer (1974) found the concentration of fluoranthene to be
from 110 ug/kg to 790 ug/kg of dry sediment. Similarly, the analy-
sis of recent sediments from a Swiss lake and river showed the
C-l
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fluoranthene content as 0.42 jug/g and 0.39 ug/g of dry material,
respectively (Giger and Schaffner, 1978). River particulate mat-
ter, on the other hand, was found to contain 5.7 jag/g of fluoran-
thene (Giger and Schaffner, 1978). The analysis of sediments from
an English valley showed fluoranthene concentrations of 0.6 to 13.8
ug/g of dry sediments (John and Nickless, 1977). There is evidence
of accumulation of fluoranthene in edible aquatic organisms. Thus,
it is considered necessary to monitor fluoranthene levels not only
in surface waters, but also in contaminated water since the use of
these waters for irrigation also can spread fluoranthene into other
foodstuffs (Shabad and Il'nitskii, 1970).
Industrial effluents from oil refineries, coke production,
plastic and dyestuff industries, and industries using high tempera-
ture furnaces are some of the primary sources of man-made fluoran-
thene (Harrison, et al. 1975). The fluorantihene concentration in
an industrial effluent was determined to be 2,198 ng/1 (Borneff and
Kunte, 1965). Except for pyrene, the amount of fluoranthene in
this industrial effluent was much higher than that of all other
individual polynuclear aromatic hydrocarbons (PAH) determined.
The fluoranthene concentration in municipal effluents was
determined by Borneff and Kunte (1965). The value in domestic
effluents was determined to be 273 to 352 ng/1. Although fluor-
anthene can be found in human urine and feces, the concentrations
found in domestic sewage are unlikely to originate exclusively
or primarily from this source (Harrison, et al. 1975). Other
possible contributing sources include the washing of clothing, in-
filtration from soil, washout from the atmosphere and road run-off
C-2
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(Harrison, et al. 1975). When the sewage contained a high percent-
age of industrial effluents, the fluoranthene level was found to be
high and varied from 2,660 ng/1 to 3,420 ng/1 (Borneff and Kunte,
1965).
Road run-off can be an important factor in increasing the
fluoranthene content of sewage. Fluoranthene in road run-off can
arise in a number of ways. Bituminous road surfaces (Borneff and
Kunte, 1965), car tire wear (Falk, et al. 1964), and vehicle ex-
hausts (McKee and McMahon, 1967; Commins, 1969) contribute to the
increased fluoranthene content in road run-off. Road run-off was
primarily responsible for the increase of fluoranthene levels in
sewage, from 352 ng/1 on a dry day to 16,350 ng/1 during a heavy
rain (Borneff and Kunte, 1965). This finding of Borneff and Kunte
has been confirmed by Acheson, et al. (1976) who found that highway
run-off samples contained higher levels of fluoranthene (0.49 ug/1
to 1.10 ug/1) than Thames River water (0.11 ug/1 to 0.27 ug/1).
The removal of fluoranthene from water by conventional sewage
treatment processes was investigated by Borneff and Kunte (1967).
Removal of fluoranthene during primary sedimentation was found to
be 62 to 66 percent (from an initial value of 3.23 - 43.5 ug/1 to
1.22 - 14.6 Aig/1) and the removal was 91 to 99 percent (final value
of 0.28 - 0.26 iig/1) after biological purification with activated
sludge processes.
The fluoranthene level in surface waters (lakes and rivers)
was determined by a number of authors. Borneff and Kunte (1964,
1965) found the concentration of fluoranthene in German rivers to
be in the range from 38.5 to 761 ng/1. Acheson, et al. (1976)
C-3
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determined the value for Thames River water in England to be from 140
to 360 ng/1. Analyzing fourteen water samples from the Winni-
pesaukee, Oyster and Cocheco rivers in New Hampshire, Keegan (1971)
detected fluoranthene in three samples, and the concentration
ranged from 320 to 1,000 ng/1.
One surface water supply used for drinking water in England
was analyzed for fluoranthene, and the concentration was found to
be 150 ng/1 (Harrison, et al. 1976). Surface waters in the U.S.
were analyzed by Basu and Saxena (1977,1978) and Basu, et al.
(1978). These investigators detected fluoranthene in four of the
seven surface waters sampled. The average fluoranthene concentra-
tion in the positive samples was 325.7 ng/1 with a range of 23.5
ng/1 to 408.3 ng/1. These authors also analyzed three ground water
samples and failed to detect any fluoranthene.
The fluoranthene levels in U.S. drinking waters were analyzed
by Basu and Saxena (1977,1978) and Basu, et al. (1978). Of the 16
water supplies monitored, four showed positive fluoranthene levels.
The concentrations of fluoranthene in the four positive samples
were 2.4, 4.3, 8.9, and 94.5 ng/1, with an average of 27.5 ng/1.
The analytical limit of detection for fluoranthene in these studies
was 2.3 ng/1. The U.S. EPA also conducted the National Organic
Monitoring Survey (U.S. EPA, 1977) to determine the frequency of
occurrence of fluoranthene in drinking water supplies. Seventeen
out of 110 samples analyzed showed the presence of fluoranthene
(limit of detection = 10 ng/1). The mean fluoranthene concentra-
tion in positive samples in this study was 20.0 ng/1, with a range
of concentrations varying from 10 ng/1 to 80 ng/1. The values for
C-4
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fluoranthene concentrations in various surface and drinking waters
are shown in Table 1.
The removal of fluoranthene during drinking water treatment
processes was studied by Harrison, et al. (1976). A fluoranthene
concentration in river intake water of 150 ng/1 was reduced to 140
ng/1 when stored in a reservoir, reduced to 81 ng/1 after filtra-
tion, and further reduced to 45 ng/1 after chlorination. Thus,
there was a 70 percent total reduction of fluoranthene concentra-
tion. The removal efficiency with a full water treatment process
involving flocculation, activated carbon treatment, filtration,
and chlorination was studied by Basu and Saxena (1977,1978) and
Basu, et al. (1978). They found an 87.5 to 100 percent reduction in
fluoranthene levels. The removal efficiency was 100 percent when
two stages of activated carbon purification were used. These remov-
al efficiencies are presented in Table 2.
There is no epidemiological evidence to prove that polynuclear
aromatic hydrocarbons (PAH) in general, and fluoranthene, in parti-
cular, found in drinking water are related to the development of
cancer (Andelman and Snodgrass, 1974). Also, Shabad and Il'nitskii
(1970) stated that the amount of carcinogenic PAH consumed by man
in water is typically only 0.1 percent of the amount consumed
from food. Nevertheless, accumulation of PAH in edible aquatic
organisms can greatly increase this amount (Andelman and Snodgrass,
1974). The use of contaminated water for irrigation also can
spread PAH into other foodstuffs (Shabad and Il'nitskii, 1970).
Therefore, in 1970, the World Health Organization (WHO, 1970) re-
commended that the concentration of six representative PAH (including
C-5
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TABLE 1
Fluoranthene Concentrations in Various Water Samples
Hastewater Containing:
Water
Source
Domestic
sewage
(dry day)
Concentration 2
(ng/1) 273-352
Reference
Borneff and
Kunte, 1965
Domestic Domestic and
sewage industrial
(heavy rain) sewage
16350 3040
(2660-3420)a
Borneff and Borneff and
Kunte, 1965 Kunte, 1965
Surface water
320-1000
140-360
38.5-761
Keegan, 1971;
Borneff and Kunte
(1964, 1965);
Acheson, et al.
1976
Surface water used
for drinking water Ground Water
325.7 N.D.b
(23.5-408.3)
150
Basu and Saxena, 1977; Basu and
Basu and Saxena, 1978; Saxena, 1978
Basu, et al. 1978
Drinking Water
27.5 (2.4-94.5)
20.0 (10-80)
Basu and Saxena,
1977; Basu and
Saxena, 1978;
Basu, et al. 1978;
U.S. EPA, 1977
Values in parentheses are concentration ranges
N.D.: not detected
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TABLE 2
Pluoranthene Removal Efficiencies as a
Result of Water Treatment3
Initial
Water Source cone., ng/1
Pittsburgh, Pa.
Huntington, Va.
Philadelphia, Pa.
Wheeling, W. Va.
408.
23.
114.
756.
3
5
3
5
Final
cone. , ng/1 % Reduction
N.D.b 100
2.4 89.7
8.9 92.2
94.5 87.5
a
Sources: Basu and Saxena, 1977, 1978;
Basu, et al. 1978.
N.D.: not detected.
C-7
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fluoranthene) in drinking water not exceed 0.2 jug/1, it furth-
er recommended that there should be at least one center in each
country capable of carrying out investigations of PAH in drinking
water. However, from the data given for fluoranthene (Table 1) and
the other PAH data available in the references provided, the PAH
level in U.S. drinking waters is well below the WHO recommended
level.
Ingestion from Food
PAH formed through both natural and man-made sources can enter
the food chain in a variety of ways. The absorption of PAH from the
soil by various plant roots and translocation to the shoots is well
documented (Lo and Sandi, 1978). Some plant waxes act as collect-
ors of PAH present in polluted air (Hetteche, 1971). It has been
shown that 10 percent of benzo(a)pyrene (BaP) in lettuce, kale,
spinach, leeks, and tomatoes can be removed by cold water washing,
an indication that it was originally deposited externally (Lo and
Sandi, 1978). Oysters and clams collected from moderately polluted
waters also concentrate PAH (Cahnmann and Kuratsune, 1957;
Guerrero, et al. 1976). Food additives and packages as well as
dairy waxes containing PAH increase PAH levels in processed foods.
Hexane, a commercial solvent used to extract edible vegetable oils,
is also a source of PAH contamination. PAH present in food-grade
carbon blacks used for food processing can be transported to the
food products. Curing smoke and other pyrolysis products used dur-
ing food cooking add to the level of PAH in food.
It has been demonstrated by Zitko (1975) that PAH are not bio-
accumulated along the food chain. However, Bjtfrseth (1978)
C-8
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concluded that both common and horse mussels bioaccumulated PAH, al-
though not to the same degree. Dunn and Stich (1976) have shown
that mussels cannot metabolize BaP upon their removal from water.
In water, mussels released 79 percent of naphthalene in three days,
with a half-life of 1.3 days. The BaP release from both clams and
mussels in water took place with a half-life of 2 to 5 weeks.
The fluoranthene levels in various foods are discussed indivi-
dually below.
Various European workers have reported the presence of PAH in
fruits and related products (International Agency for Research on
Cancer (IARC), 1973). However, fluoranthene concentrations were not
reported in this IARC study. No study from North America concern-
ing PAH levels in fruits and related products was reported.
Kuratsune and Hueper (1958, 1960) published PAH levels in coffee
soot and roasted coffee. The coffee soot was found to contain 340
to 1,000 ppb fluoranthene. The moderately dark and fully roasted
(darkest) coffees contained 1 to 7 ppb and 0 to 15 ppb fluoran-
thene, respectively. Grimmer and Hildebrandt (1967) determined the
fluoranthene content in coconut and reported values of 0.3 ppb, 3.9
ppb and 92.7 ppb for fresh, sun-dried, and smoke-dried coconut,
respectively.
Fluoranthene was also qualitatively detected from germinated
rye, wheat, and lentil seedlings, although none was detected in the
ungerminated products (Graf and Nowak, 1966). These authors also
demonstrated the uptake of fluoranthene in radishes from polluted
environments. According to Borneff (1977), the main human intake
of PAH comes from fruits, vegetables, and bread. He estimated that
C-9
-------
the total PAH intake from all of these sources amounted to 3-4
mg/pe rson/year.
The fluoranthene levels found in these products are shown in
Table 3. The relatively high levels of fluoranthene found indicate
that the heating of such oils might have led to a slight increase of
fluoranthene concentration (Lo and Sandi, 1978). In a total diet
study, Howard, et al. (1968) found only trace amounts (less than
0.5 ppb) of seven PAH (fluoranthene not studied) in the composite
sample containing the fats and oils. However, Borneff (1977) esti-
mated that the yearly human intake of PAH from these sources was
0.1 mg.
Raw meat does not normally contain fluoranthene, but smoked or
cooked meat may contain varying amounts of fluoranthene. The pyro-
lysis of fats, and incomplete combustion of the fuel contribute to
the fluoranthene content in meats. Casing around the meat changes
PAH levels in cooked meats. Cellulose casing is more effective as
a barrier to the passage of PAH than is gut casing (Simon, et al.
1969). Further investigations have shown that the amount of PAH in
broiled meats is directly proportional to the temperature of the
treatment (Lijinsky and Ross, 1967). The dependency of fluoran-
thene content in meat and meat products on all the above factors is
summarized in Tables 4 and 5.
Fish from unpolluted waters usually do not contain detectable
amounts of PAH. Smoked and cooked food, however, contain varying
levels of fluoranthene. The amount of fluoranthene depends on the
method of cooking, that is, the nature of the heat source, the tem-
perature of combustion, and the degree of smoking in the case of
C-10
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TABLE 3
Fluoranthene Levels in Vegetable Pats, Oils and Shortenings
Product
Concentration,
ppb
Reference
Linseed oil (unrefined)
Cocoa butter oil (unrefined)
Coconut oil (smoke-dried)
Coconut oil (hot-air dried)
Coconut oil (commercial)
Coconut oil (dried copra,
treated with slaked lime)
Cotton seed oil (unrefined)
Ground nut oil (unrefined)
Palm oil (unrefined)
Palm-kernel oil (unrefined)
Pumpkin seed oil
Rapeseed oil (unrefined)
Soybean oil (unrefined)
Soybean oil
Sunflower oil
Wesson oil
n-paraffin oil (acid-washed
for yeast fermentation)
n-paraffin oil (silica-gel
treated for yeast fermen-
tation)
Olive oil
Peanut oil
15.1
20.5
372.0
255.0
445.0
18.0
7.0
8.4
7.1
39.0
25.0
10.9
6-4a
1.3a
(0.6-2.6)
21.1
N.D.b
1.9
(1.0-3.0)
3.8
(0.5-7.3)
3.2
(2.2-4.4)
3.3
Grimmer & Hildebrandt,
Grimmer & Hildebrandt,
Grimmer & Hildebrandt,
Biernoth & Rost, 1967
Biernoth & Rost, 1967
Biernoth & Rost, 1967
Grimmer
G r imme r
Grimmer
Grimmer
Biernoth
Grimmer
G r imme r
Howard,
& Hildebrandt,
& Hildebrandt,
& Hildebrandt,
& Hildebrandt,
& Rost, 1967
& Hildebrandt,
& Hildebrandt,
et al. 1966c
1967
1967
1967
1967
1967
1967
1967
1967
1967
Grimmer & Hildebrandt, 1967
Lijinsky & Ross, 1967
McGinnis, 1975
McGinnis, 1975
Howard, et al. 1966c
Howard, et al. 1966c
Values in parenthesis are ranges in concentrations
N.D.: not detected.
C-ll
-------
TABLE 4
Fluoranthene Levels in Meat and Meat Products
Under a Variety of Conditions
Product
Concentration,
ppb
Reference
Charcoal broiled steak
(lab. preparation)
Charcoal broiled ribs
(commercial)
Charcoal broiled steak
(commercial)
Liquid smoke
Smoked ham
Smoked bacon
Smoked chipped beef
Smoked frankfurters
Smoked mutton (lab.)
Smoked mutton (commercial)
Smoked pork roll
Smoked barbecued beef
Smoked mutton sausage
(commercial)
Home-smoked mutton (close to
stove & with cover)
Home-smoked mutton (close to
stove & without cover)
Home-smoked mutton (distant
from stove & with cover)
Home- smoked lamb
Cold-smoked sausage (with
casing)
Cold-smoked sausage (without
casing)
Hot-smoked sausage (with
casing)
Hot-smoked sausage (without
casing)
Hot-smoked salami (without
• .
casing)
Hot-smoked mortadella
without casing)
20.0
49.0
43.0
10.0-16.0
14.0
0.6-2.9
4-156
8.0
35.0
0.6
6.4
4.6
18.0
3.1
2.0
6.0
35.0
303.0
47.0
158.0
40.0
7.2
35.2
13.0
5.6
22.0
Lijinsky & Shubik, 1965b
Lijinsky & Shubik, 1965b
Lijinsky & Shubik, 1965b
Lijinsky & Shubik, 1965a,b
Howard, et al. 1966a;
Malanoski, et al. 1968;
Lo & Sandi, 1978
Lijinsky & Shubik, 1965b
Lo & Sandi, 1978
Howard, et al. 1966a
Howard, et al. 1966a
Bailey & Dungal, 1958
Thorsteinsson, 1969
Howard, et al. 1966a
Malanoski, et al. 1968
Thorsteinsson, 1969
Thorsteinsson, 1969
Thorsteinsson, 1969
Thorsteinsson, 1969
Thorsteinsson, 1969
Lo & Sandi, 1978
Lo & Sandi, 1978
Lo & Sandi, 1978
Lo & Sandi, 1978
Lo & Sandi, 1978
Lo & Sandi, 1978
C-12
-------
TABLE 5
Effect of Fat Content and Temperature of Cooking
on Fluoranthene Levels in Cooked Meats
Product and Cooking Method Concentration, ppb
Charcoal broiled:
Hamburger, fat (hot)3 13-3
Hamburger, fat (cold)3 6-4
Hamburger, lean (hot) °-3
Hamburger, lean (cold) 1-3
Hamburger (no drip pan) °-2
Hamburger frozen (hot) 4-9
pork Chop (hot) 22-5
Chicken (hot) 1-1
Sirloin steak (hot) 12-6
T-Bone steak (hot) L9-8
Flame broiled:
T-Bone steak (hot) 19-°
*Source: Lijinsky and Ross, 1967
acold: 25 cm from heat source; hot: 7 cm from heat source;
fat: 21% fat; lean: 7% fat
C-13
-------
smoked fish, in a study sponsored by the U.S. Food and Drug Admin-
istration, PAH levels in unsmoked and smoked fish were compared
(Howard, et al. 1966a,b). In addition to fish, various other mar-
ine foods were investigated and found to contain fluoranthene
(Table 6). According to a recent estimate by Borneff (1977), the
total human intake of PAH from smoked meat, smoked fish and drink-
ing water sources amounts to 0.05 mg/person/year. The fluoranthene
levels detected in a variety of dairy and bakery products are list-
ed in Table 7.
A bioconcentration factor (BCF) relates the concentration of a
chemical in aquatic animals to the concentration in the water in
which they live. The steady-state BCFs for a lipid-soluble com-
pound in the tissues of various aquatic animals seem to be propor-
tional to the percent lipid in the tissue. Thus the per capita
ingestion of a lipid-soluble chemical can be estimated from the per
capita consumption of fish and shellfish, the weighted average per-
cent lipids of consumed fish and shellfish, and a steady-state BCF
for the chemical.
Data from a recent survey on fish and shellfish consumption in
the United States were analyzed by SRI International (U.S. EPA,
1980). These data were used to estimate that the per capita con-
sumption of freshwater and estuarine fish and shellfish in the
United states is 6.5 g/day (Stephan, 1980). in addition, these
data were used with data on the fat content of the edible portion of
the same species to estimate that the weighted average percent
C-14
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TABLE 6
Fluoranthene Levels in Fishes and Other Sea Foods
Product
Concentration,
ppb
Reference
Unsmoked haddock
Unsraoked herring (salted)
Unsmoked salmon (canned)
Smoked Cod
Smoked haddock
Smoked herring
Smoked herring (dried)
Smoked Red fish
Smoked salmon
Smoked sturgeon
Smoked trout
Smoked white fish
Smoked eel
Smoked lump fish
Horse mackerel (gas broiled)
Horse mackerel (electric
broiled)
Kale
Algae, Chlorella vulgar is
Algae, Scenedesmus acutus
1.6
0.8
1.8
0.5
1.1
3.0
1.8
4.0
6.0
3.2
2.4
N.D.
12.0
4.6
4.0
2.0
3.6-7.0
0.2-5.2
82-6760
650
44
Howard, et al. 1966a
Howard, et al. 1966a
Howard, et al. 1966a
Dungal, 1961
Lijinsky & Shubik, I965a
Howard, et al. 1966a
Howard, et al. 1966a
Dungal, 1961
Lijinsky & Shubik, 1965b
Howard, et al. 1966a
Howard, et al. 1966a
Howard, et al. 1966a
Thorsteinsson, 1969
Baily & Dungal, 1958
Thorsteinsson, 1969
Thorsteinsson, 1969
Lo & Sandi, 1978
Lo & Sandi; 1978
Hetteche, 1971
Borneff, et al. 1968
Payer, et al. 1975
N.D.: not detected
C-15
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TABLE 7
Fluoranthene Concentrations Determined in
Yeast and Cheese
o
i
M
cr>
Product
Concentra-
tion, ppb
French
Baking Yeast
German
Scottish
Russian
"least"
Smoked Gouda
cheese
Cheddar
cheese
Reference
Grimmer, 1974
Grimmer,
1974
Howard, et
al. 1966a
Howard,
et al.
1966a
-------
lipids for consumed freshwater and estuarine fish and shellfish is
3.0 percent.
No measured steady-state bioconcentration factor (BCF) is
available for fluoranthene, but the equation "Log BCF = (0.85
Log P) - 0.70" can be used (Veith, et al. 1979) to estimate the BCF
for aquatic organisms that contain about 7.6 percent lipids (Veith,
1980) from the octanol/water partition coefficient (P). Since no
measured log P value could be found, a log P value of 4.90 was cal-
culated for fluoranthene using the method described in Hansch and
Leo (1979). Thus, the steady-state bioconcentration factor is
estimated to be 2,900. An adjustment factor of 3.0/7.6 = 0.395 can
be used to adjust the estimated BCF from the 7.6 percent lipids on
which the equation is based to the 3.0 percent lipids that is the
weighted average for consumed fish and shellfish. Thus, the
weighted average bioconcentration factor for fluoranthene and the
edible portion of all freshwater and estuarine aquatic organisms
consumed by Americans is calculated to be 2,900 x 0.395 = 1,150.
Inhalation
A variety of PAH, including fluoranthene, have been detected
in ambient air. Because of its carcinogenic properties, BaP has
been most extensively monitored and has frequently been used as an
indicator of ambient PAH. However, the relative amount of indivi-
dual PAH in ambient air is dependent on the location. This has been
demonstrated by Stocks, et al. (1961) by studying ambient rural,
suburban, and urban air in England. The exact amount of fluoran-
thene intake by inhalation is difficult to determine because of the
different sources of exposure, such as, tobacco smoke inhalation,
C-17
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occupational exposure, and exposure to ambient air. The fluoran-
thene exposure due only to inhalation of ambient air will be dis-
cussed in this section.
Concentrations of fluoranthene are different in various cities
and at different times of the year. The concentrations are usually
highest during the winter months, probably from heating sources
(Sawicki, 1962). However, there may be some exceptions to this
High winter - low summer concentration pattern. It has been sug-
gested that in areas with significant industrial emissions of PAH
the fluoranthene level may remain uniform throughout the year (U.S.
EPA, 1974). In other areas such as Los Angeles, which do not re-
quire heating during winter, automobile and industrial emissions
control the PAH pattern in the ambient air (Gordon, 1976). The
fluoranthene concentration in Los Angeles ambient air during four
quarterly periods of 1974-1975, May-July, Aug.-Oct., Nov.-Jan., and
Feb.-Apr. were 0.38 ppb, 0.15 ppb, 0.24 ppb, and 0.68 ppb, respec-
tively (Gordon, 1976).
The declining trend of fluoranthene concentration in U.S. am-
bient air from the 1960's to 1970's may be from the decreased use of
coal for power generation. Also contributing to this decline is
the improved disposal of solid wastes and restrictions on open
burning (U.S. EPA, 1974).
The possibility of long distance transport of PAH which might
result in PAH contamination in areas downwind from large emission
sources has been studied by Lunde and Bjjzfrseth (1977). They deter-
mined that samples with trajectories from Western Europe contained
about 20 times more fluoranthene than samples with trajectories
C-18
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from northern Norway. This proves that some PAH, including fluor-
anthene, are stable enough to be transported from distant industri-
al sources to the suburban and rural areas.
Fluoranthene levels determined in various locations and at
different times are presented in Table 8.
Various factors, particularly smoking, can alter the concen-
tration of fluoranthene in indoor environments. Under standard
smoking conditions the smoke of a cigarette generated between puffs
(sidestream-smoke) contains 1,255 ng of fluoranthene per cigarette
compared to the smoke which is inhaled (mainstream-smoke) which
contains 272 ng of fluoranthene per cigarette (Grimmer, et al.
1977). In a 36 m room with ventilation equal to a single air
change per hour, the smoke from 5 cigarettes per hour from 2 smok-
ers produced an average level of 99 ng/m3 of fluoranthene in air
samples collected over a period of 8 hours from an average of two
tests (Grimmer, et al. 1977).
Dermal
No direct information is available on the importance of dermal
absorption in total human exposure to fluoranthene. Fluoranthene
can be absorbed through the skin by animals (see Absorption). For
those humans exposed to only background levels of fluoranthene,
dermal absorption is not likely to be a significant route of entry.
PHARMACOKINETIC S
There are no data available concerning the pharmacokinetics of
fluoranthene in humans. Moreover, animal studies have not been
conducted for the specific purpose of supplying pharmacokinetic
data on fluoranthene. Nevertheless, it is possible to make limited
C-19
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TABLE 8
Ambient Fluoranthene Levels at Different Locations
Location
Concentration,
jjg/1,000 m3
Reference
Average U.S. Urban air,
1963a
Birmingham, AL, 1964-65
Detroit, MI, 1965
Los Angeles, CA, 1973
College Park, MD, 1976
Baltimore Harbor Tunnel, MD,
1976
Los Angeles, CA,1976
Providence, RI, 1977
England, Urban, 1961
Summer
Winter
England, Bus Depot, 1961
Summer
Winter
England, Bus Garage, 1961
Summer
Winter
England Tunnel, 1961
Summer
Winter
England Suburban, 1961
Summer
Winter
England, Rural, 1961
Summer
Winter
Rome, 1966
Rome, 1972
Budapest, 1975
Sidney, 1965
Ontario, 1966
Ontario, 1962 inversion
per iod
Norway, 1977
Switzerland, 1978
Ohmuta, Japan, 1978
4.0
5.5
0.19-15.0
0.1-3.4
4.1
93.0
0.31
0.16-1.5
6.5
44.9
5.0
40.0
5.0
83.0
24.0
54.5
4.6
26.6
4.5
10.5
2.1-4.5
1.0-18.0
10.4
0.06-2.6
0.3-10.6
0.6-41.0
0.17-0.32
12.9
5.75
Hoffman & Wynder, 1968
U.S. EPA, 1975
Hoffman & Wynder, 1968
Hoffman & Wynder, 1977
Fox & Staley, 1976
Fox & Staley, 1976
Gordon, 1976
Krstulovic, et al. 1977
Stocks, et al. 1961
Stocks, et al. 1961
Stocks, et al. 1961
Stocks, et al. 1961
Stocks, et al. 1961
Stocks, et al. 1961
Hoffman & Wynder, 1977
Hoffman & Wynder, 1977
Kertesz-Saringer &
Morlin, 1975
Hoffman & Wynder, 1977
Hoffman & Wynder, 1977
Hoffman & Wynder, 1977
Lunde & Bjjrfrseth, 1977
Giger & Schaffner, 1978
Tokiwa, et al. 1977
Values from a composite sample of downtown areas in approximately
100 cities.
C-20
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assumptions based on the results of animal studies conducted with
other PAH that are structurally similar to fluoranthene.
Absorption
The demonstrated toxicity of fluoranthene by oral and dermal
administration indicates that it can pass across epithelial mem-
branes (Smyth, et al. 1962). The high lipid solubility of fluoran-
thene supports this observation. Animal studies with structurally
related PAH, such as benzo(a)pyrene, chrysene, 7,12-dimethylbenz-
(a)anthracene, benz(a)anthracene, and 3-methylcholanthrene, con-
firmed that intestinal transport readily occurs, primarily by pas-
sive diffusion (Rees, et al. 1971). In addition, there is ample
evidence to indicate that benzo(a)pyrene (and presumably other PAH)
is easily absorbed through the lungs (Kotin, et al. 1959; Vainio,
et al. 1976).
Distribution
The tissue distribution and accumulation of fluoranthene has
not been studied. It is known, however, that other PAH (e.g.,
benzo(a)pyrene, 7,12-dimethylbenz(a)anthracene, 3-methylcholan-
threne, phenanthrene) were found in a wide variety of body tissues
following their absorption in experimental rodents (Kotin, et al.
1959; Bock and Dao, 1961; Flesher, 1967). Relative to other tis-
sues, PAH such as fluoranthene can be expected to localize primari-
ly in body fat and fatty tissues.
The potential for transplacental passage of fluoranthene can-
not be predicted. With other PAH, passage into the fetus following
intragastric or intravenous administration to pregnant rats has
been variable (Shendrikova and Aleksandrov, 1974).
C-21
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Metabolism
Experimental studies have not been conducted on the metabolism
of fluoranthene. However, it is well established that the metabo-
lism of PAH is accomplished by the microsomal enzyme complex of
mixed-function oxidases, often termed aryl hydrocarbon hydroxyl-
ase. This enzyme system has been studied extensively and is the
subject of numerous reviews (Conney, 1967; Gelboin, 1967; Mar-
quardt, 1977). These microsomal oxidases, while most abundant in
the liver, have been found in most mammalian tissues. This enzyme
complex is responsible for the metabolic detoxification of PAH, but
also activates PAH to toxic and carcinogenic metabolites.
As a group, PAH are metabolized to substances that have been
arbitrarily divided into two groups on the basis of solubility. In
one group are metabolites that can be extracted from an aqueous in-
cubation mixture by an organic solvent. This group consists of
ring-hydroxylated products such as phenols and dihydrodiols. Nu-
merous studies indicate that epoxide intermediates are involved in
the formation of phenolic metabolites for the expression of toxic
and carcinogenic effects (Sims and Grover, 1974; Sims, 1976; Jerina
and Daly, 1974; Jerina, et al. 1977).
In the second group of metabolites are water-soluble products
that remain after extraction with an organic solvent. It is gener-
ally agreed that most of these PAH derivatives are formed by conju-
gation of the hydroxylated products with glutathione, glucuronic
acid, or sulfate. This process would render the derivatives more
hydrophilic and presumably less toxic.
C-22
-------
It is reasonable to assume that fluoranthene is metabolized in
a manner which is consistent with the general biochemical scheme
for biotransformation of PAH. However, the exact chemical struc-
ture of fluoranthene metabolites or their chemical and biological
reactivity is not presently known.
Excretion
There is no direct information available concerning the excre-
tion of fluoranthene in experimental animals or man. Limited in-
ferences can be drawn from animal studies with related PAH, how-
ever.
In 1936 it was recognized that various PAH were excreted pri-
marily through the hepatobiliary system and the feces (Peacock,
1936; Chalmers and Kirby, 1940). However, the rate of disappear-
ance of various PAH from the body and the principal routes of ex-
cretion are influenced both by structure of the parent compound and
the route of administration (Heidelberger and Weiss, 1951; Aitio,
1974). Moreover, it has been shown that the rate of disappearance
of benzo(a)pyrene from body tissues can be markedly stimulated by
prior treatment with inducers of microsomal enzymes (e.g.,
benzo(a)pyrene, 7,12-dimethylbenz(a)anthracene, 3-methylcholan-
threne, chrysene) (Schlede, et al. 1970a,b; Welch, et al. 1972).
From the available evidence concerning excretion of PAH in animals,
it is apparent that extensive bioaccumulation is not likely to
occur.
C-23
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EFFECTS
Acute, Subacute, and Chronic Toxicity
Smyth and coworkers (1962) determined the acute toxicity of
fluoranthene following oral and inhalation exposures in rats and
dermal administration to rabbits. The acute oral LD5Q for fluoran-
thene, determined using groups of five male Carworth-Wistar rats,
was 2.00 g/kg (range from 1.27 to 3.13 g/kg). The dermal LD5Q in
rabbits resulting from 24-hour contact with fluoranthene was 3.18
g/kg (range from 2.35 to 4.29 g/kg). Exposure of six male or female
albino rats to concentrated vapors of fluoranthene for eight hours
produced no mortality. Taken together, these results from animal
studies indicate that fluoranthene has a relatively low acute toxi-
city. Where deaths occurred, no information was reported concern-
ing target organs or specific cause of death.
In earlier studies, Haddow and coworkers (1937) examined the
effect of various PAHs, including fluoranthene, on body growth in
hooded rats of the Lister strain. A single intraperitoneal injec-
tion of 30 mg fluoranthene dissolved in sesame oil had no adverse
effect on body weight gain over a 24-day observation period. By
comparison, certain carcinogenic PAH (10 mg of benzo(a)pyrene or
dibenz(a,h)anthracene) caused an initial weight reduction followed
by resumption of growth at a reduced rate.
Only limited data are available concerning the toxic effects
of fluoranthene produced by repeated administration. These are
limited to reports of mortality produced in mice by repeated dermal
application or subcutaneous injection. Pertinent data from these
studies are summarized in Table 9.
C-24
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TABLE 9
Toxicity of Fluocanthene by Repeated Administration to Mice
O
I
to
Species
Mouse
(Strain A)
Mouse
Mouse
Mouse
(Ha/ICR/Mil
Preparation
No- Sex and Dose
14 M&F 10 mg crystalline
fluoranthene in
glycerol, repeated
4 tiroes
10 ? 0.3 % solution of
fluoranthene in
benzene applied
twice weekly
10 ? 0.3 % solution of
fluoranthene in
benzene applied
twice weekly
20 F 50 nl of 1.0% fluor-
anthene solution
Route of
Administration
subcutaneous in-
jection in the
left flank
dermal applica-
tion to inter-
scapular region
dermal applica-
tion to inter-
scapular region
dermal applica-
tion
Effect
6 mice survived
for 18 months;
experiment ter-
minated at 19
months
3 of 10 alive
after 6 months;
3 of 10 alive
after 1 year; last
mouse died after
501 days
4 of 10 alive
after 6 months;
1 of 10 alive
after 1 year; last
mouse died after
379 days
No mortality
after 15 months
Reference
Shear, 1938
Barry, et al.
1935
Barry, et al.
1935
Hoffman, et
al. 1972
Swiss Albino)
in acetone applied
3 times weekly
for 12 months
-------
Synerqism and/or Antagonism
Because fluoranthene is normally encountered in the environ-
ment as part of a complex mixture of PAH, concern has often been
expressed over its interactive toxic effects. in this regard,
Pfeiffer (1973,1977) tested ten noncarcinogenic PAH found in auto-
mobile exhaust in combination with benzo(a)pyrene (3-100 pg) and
dibenz(a,h)anthracene (2-75 pg) by subcutaneous injection in groups
of female NMRI mice. The ten noncarcinogens tested were:
benzo(e)pyrene (2-70 ug); benz(a)anthracene (3-100 ug); phenan-
threne (125-4,000 ug); anthracene (31-1,000 pg); pyrene (62-2,100
ug); chrysene (3-100 ug); perylene (0.2-7.0 ug); benzo(g,h,i)pery-
lene (12.8 - 410 ug); coronene (3-100 ug); and fluoranthene (28-900
pg). The tumor incidence resulting from all 12 compounds being ad-
ministered together could be attributed to the presence of dibenz-
(a,h)anthracene, with little influence from benzo(a)pyrene or the
other ten chemicals. No inhibitory effect of the ten noncarcino-
gens was evident; moreover, an increased tumor yield resulted from
injection of mixtures containing increasing amounts of the compo-
nents. This effect, however, was less dramatic than if benzo(a)py-
rene were administered alone, and paralleled the dose-response
curve of dibenz(a,h)anthracene acting alone.
Similar experiments were conducted by Schmahl and coworkers
(1977) involving the dermal application of mixtures containing car-
cinogenic and noncarcinogenic PAH to mice. They concluded that the
tumorigenic response obtained with PAH mixtures that included
fluoranthene could be attributed almost entirely to the presence of
C-26
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the carcinogenic PAH (benzo(a)pyrene, dibenz(a,h)anthracene, benz-
(a)anthracene, benzo(b)fluoranthene) in the mixture.
There is evidence that fluoranthene may considerably enhance
the tumorigenic response produced by benzo(a)pyrene. These studies
are discussed in the Carcinogenicity section of this report.
Teratogenicity
There is no information available concerning the possible
teratogenic effects of fluoranthene in animals or man. Further-
more, only limited data are available regarding the teratogenic ef-
fects of other PAH in experimental animals.
Benzo(a)pyrene had little effect on fertility or embryonic
development in several mammalian and nonmammalian species (Rigdon
and Rennels, 1964; Rigdon and Neal, 1965). On the other hand,
7,12-dimethylbenz(a)anthracene and its hydroxymethyl derivatives
apparently possess considerable teratogenic potency in the rat
(Currie, et al. 1970; Bird, et al. 1970).
Mutagenicity
The concept that carcinogenesis is an expression of an altera-
tion in the genetic material of a cell (i.e., somatic mutation) im-
plies that a formal relationship exists between mutagenesis and
carcinogenesis (Nery, 1976; Miller, 1978). The results obtained
with several ijn vitro mutagenesis test systems, particularly the
Ames Salmonella typhimurium assay, support the belief that most
carcinogenic chemicals are mutagenic as well. For PAH, the Ames
assay has been very effective in detecting parent structures and
their biotransformation products that possess carcinogenic activ-
ity (McCann, et al. 1975; Teranishi, et al. 1975; McCann and Ames,
C-27
-------
1976; Sugimura, et al. 1976; Wislocki, et al. 1976; Wood, et al.
1976).
Tokiwa and coworkers (1977) employed the Ames assay to search
for mutagenic activity in a series of PAH, including fluoranthene,
which were detected in the particulate fraction of urban air pol-
lutants. Salmonella strain TA 98 in the presence of rat liver S-9
fraction (to provide bioactivation) was employed. Under these test
conditions, fluoranthene displayed no mutagenic activity.
In a comparative study of the mutagenic activity, tumor initi-
ating activity, and complete carcinogenicity of several PAH, fluor-
anthene was also found to be inactive towards both tester strains
TA 98 and TA 100 in the presence of Araclor 1254-induced rat liver
homogenate (LaVoie, et al. 1978).
No reports are available regarding the potential mutagenicity
of fluoranthene in other test systems, either _in vitro or j._n vivo.
Carcinogenicity
Among the unsubstituted polycyclic hydrocarbons containing a
nonaromatic ring, a number of active carcinogens are known. The
most prominent examples of this type of compound are: cholanthrene;
11,12-ace-benz(a)anthracene; 6,7-ace-benz(a)anthracene; 8,9-cyclo-
pentabenz(a)anthracene; acenaphthanthracene; 1,2,5,6-te trahydro-
benzo(j)cyclopenta(f,g)aceanthrylene, and "angular" stearanthrene
(Arcos and Argus, 1974). In addition, alkyl substitution of par-
tially and fully aromatic condensed ring systems may also add con-
siderable carcinogenic activity. The best examples of this type of
activation are 3-methylcholanthrene, a highly potent carcinogen, 2-
methylfluoranthene, and 5-methylchrysene.
C-28
-------
Fluoranthene was first tested for carcinogenic activity more
than four decades ago (Barry, et al. 1935). The results from that
investigation, and from several studies conducted since that time,
indicate that fluoranthene has virtually no activity as a complete
carcinogen. The conditions employed and results obtained in these
studies are summarized in Table 10. Both dermal application and
subcutaneous injection in mice have been employed for the bioassay
of fluoranthene.
Despite the fact that fluoranthene shows no activity as a com-
plete carcinogen in the mouse, a number of fluoranthene derivatives
are active carcinogens. These include 2-methylfluoranthene (Hoff-
mann, et al. 1972) and several benzofluoranthenes and dibenzofluor-
anthenes (IARC, 1973; Arcos and Argus, 1974).
Investigations in which polycyclic carcinogens were applied to
the skin of mice have shown the two-stage theory of skin carcino-
genesis (Van Duuren, 1976). The first stage, initiation, results
from the ability of a carcinogen to effect a permanent change with-
in a cell or cell population following a single application. The
measure of carcinogenic potency is often regarded as the capacity
for tumor initiation. However, some weak or inactive complete car-
cinogens can be active as tumor initiators (e.g., dibenz(a,c)an-
thracene, 1-methylchrysene, benz(a)anthracene). The second stage,
promotion, is a prolonged process which does not necessarily re-
quire the presence of a carcinogen, but nevertheless a chemical
stimulus must be supplied (e.g., by croton oil). A complete car-
cinogen is one that is capable of producing tumors when applied
alone in sufficient quantity.
C-29
-------
TABLE 10
Activity of Fluoranthene as a Complete Carcinogen in Mice
O
I
u>
o
Species
Mouse
Mouse
Mouse
(Strain A)
Mouse
(CAP,
Jackson)
Mouse
(Swiss,
Millerton)
Mouse
NO Sex Preparation
No- Sex and Dose
10 ? 0.3% solution of
fluoranthene in
benzene, applied
twice weekly
10 ? 0.3% solution of
fluoranthene in
benzene, applied
twice weekly
14 M&F 10 mg crystalline
fluoranthene in
glycerol, repeated
4 times
25- M&F 10% solution of
50 fluoranthene in
acetone 3 times
weekly
25- M&F 10% solution of
50 fluoranthene in
acetone applied
3 times weekly
20 M&F not specified
Route of
Administration
dermal applica-
tion to inter-
scapular region
dermal applica-
tion to inter-
scapular region
subcutaneous
injection in
the left flank
dermal applica-
tion to the
back
dermal applica-
tion to the
back
subcutaneous
injection
Results
70% mortality
after 6 months;
no tumors by
1 year
60% mortality
after 6 months;
no tumors by
1 year
6 mice survived
for 18 months;
no tumors by
19 months
No papillomas or
carcinomas found
by 13 months
No papillomas or
carcinomas found
by 13 months
No sarcomas
produced
Reference
Barry, et al.
1935
Barry, et al.
1935
Shear, 1938
Suntzeff, et
al. 1957
Suntzeff, et
al. 1957
Buu-hoi, 1964
-------
TABLE 10 (Continued)
O
I
u>
Species No.
Mouse 20
(Ha/ICR/Mil
Swiss Albino)
Mouse 15
(C3H)
Mouse 15
(C3H)
Sex Preparation
and Dose
F 50 pi of 1.0%
fluoranthene
solution In
acetone applied
3 times weekly
for 12 months
M 50 mg fluoranthene
as an 0.5% solution
in decalin applied
2 times each week
for 82 weeks
M 50 mg fluoranthene
as an 0.5% solution
in 50:50 decalin-
n-dodecane applied
2 times each week
for 82 weeks
Route of
Administration Results
dermal appllca- No tumors observed
tion after 15 months;
no mortality
encountered
dermal applica- No skin tumors
tion observed; 13 of
15 mice were
alive at 52
weeks
dermal applica- No skin tumors
tion observed; 12 of
15 mice were
alive at 52
weeks
Reference
Hoffmann, et
al. 1972
Horton and
Christian, 1974
Horton and
Christian, 1974
Mouse
(ICR/Ha
Swiss)
50
40 pg fluoranthene
in acetone applied
3 times weekly *
for 440 days
dermal applica-
tion
No skin tumors
observed
Van Duuren and
Goldschmidt,
1976
-------
It has been established for many years that fluoranthene is
inactive as a complete carcinogen. In recent years fluoranthene
has also been tested for tumor initiating and promoting activity
(Hoffmann, et al. 1972; Van Duuren and Goldschmidt, 1976).
Fluoranthene was applied repeatedly to the shaved backs of
mice and followed by application of croton oil (a known tumor pro-
moter) to test for initiating activity (Hoffmann, et al. 1972). As
indicated in Table 11, fluoranthene displayed no significant capa-
city for tumor initiation.
In related studies conducted by Van Duuren and Goldschmidt
(1976) fluoranthene was tested as a tumor promoter in a two-stage
carcinogenesis test system. Their results were equivocal and indi-
cated that, at best, fluoranthene was only a very weak tumor pro-
moter in comparison to the action of classical tumor promoting
chemicals such as phorbol myristate acetate (PMA) (the active com-
ponent of croton oil) (Table 12).
The most remarkable aspect of the biological activity of
fluoranthene is its potency as a cocarcinogen. The designation of
a cocarcinogen is here intended to denote a compound that on re-
peated application to mouse skin together with low doses of a com-
plete carcinogen such as benzo(a)pyrene, produces a considerable
enhancement in carcinogenic effect (Van Duuren, 1976). It should
be noted that, by this definition, a cocarcinogen need not neces-
sarily possess either tumor initiating or tumor promoting activity
in the two-stage carcinogenesis system.
It was first recognized by Hoffmann and Wynder (1963) in stud-
ies on the components of gasoline engine exhaust that fluoranthene
C-32
-------
TABLE 11
Tumor Initiating Activity of Fluoranthene3'
Species
No.
Sex
Dose and
Preparation
Tumors After
20 weeks
Mouse 30
(Swiss-Albino
Ha/ICR/Mil)
Mouse
30
0.1 mg fluoranthene
in 50 yul acetone
applied every 2nd
day for 10 applications
10 applications at
5 ug benzo(a)-pyrene
Ib(l)c29d
19(67)29
aTen days after last application of fluoranthene, the tumor promoter
2.5% croton oil in acetone, average dose 3.8 mg, was applied for
20 weeks
Tumor-bearing mice
°Number in parenthesis = total number of tumors
Surviving mice
ePositive control
*Source: Hoffmann, et al. 1972
033
-------
TABLE 12
Two-stage Carcinogenesis: Tumor-Promoting Activity of
Cocarcinogens and Inactive Analogues '
Secondaryb
treatment
(dose)
to Mice with
Days of Survival first papillomas/toctal
testing time in days papilloma papillomas
Pyrene (40 ug)
Fluor anthene (40 ug )
Catechol (2 mg)
Resorcinol (10 mg)
Hydroquinone (5 mg)
Pyrogallol (5 mg)
PMA (2.5 ug )
Anthralin (80 ug )
Acetone
No treatment
PMA alone (2.5 ug)
448
448
448
449
409
449
449
434
450
443
368
448
448
448
449
409
449
357
434
450
427
•p
414
401
328
54
85
174
1/1
1/1
1/1
43/155
9/14
5/5
(1)
(1)
0
0
0
(0)
(18)
(2)
0
0
(0)
Swiss mice per group, except for the anthralin
experiment in which 20 mice were used.
b!50 ug B(a)P/0.1 ml acetone applied to dorsal skin once by micropi-
pette. For the anthralin experiment, the initiating dose was
100 ug B(a)P. For the duration of the test, the promoters were
applied to the dorsal skin 3 times weekly in 0.1 ml acetone beginning
14 days after initiator. For data on the application of promoting
compounds, see Table 2.
cNumbers in parentheses are numbers of mice with squamous carcinoma.
100 mice.
*Source: Van Duuren and Goldschmidt, 1976
C-34
-------
could enhance the yield of benzo(a)pyrene-induced skin carcinomas
in mice. These results are depicted in Figures 1 and 2. Although
the details of their experimental protocol were not reported, the
authors concluded that the potential interaction of components in
complex environmental mixtures dictates the need for caution in
interpretation of results. In particular, the extrapolation of re-
sults from animal bioassays with single chemicals may not provide a
realistic estimate of human risk resulting from exposure to these
chemicals in combination.
A more detailed investigation of the cocarcinogenic activity
of fluoranthene was undertaken by Van Duuren and Goldschmidt
(1976). In that study, fluoranthene not only increased the total
number of papillomas and carcinomas produced by benzo(a)pyrene on
mouse skin, but also decreased the number of days to the appearance
of the first tumor as compared to mice treated with benzo(a)pyrene
only (Table 13). Among all the cocarcinogens tested in this study,
only fluoranthene caused a marked decrease in the tumor latency
period. These results led the authors to conclude that fluoran-
thene possesses potent cocarcinogenic activity.
The mechanism of action for cocarcinogenic compounds is not
understood. Since both aliphatic and aromatic compounds have dis-
played cocarcinogenic activity, the elucidation of structure-acti-
vity relationships is difficult. Van Duuren and coworkers (1978)
have proposed a number of possibilities to explain the effects of
cocarcinogens. These include: (a) ability to alter the rate of
absorption and disappearance of the carcinogen, (b) ability to
alter metabolic pathways for the carcinogen, and (c) metal-chelating
C-35
-------
90
80
a 70
§ 60
2 50
8
40 —I
30 —
.2
<5
I
II
111
IV
Banzo ( a ) pyrena 0.005%
Benzo ( a ) pyrena 0.005% +0.1% Pyrene
Benzo ( a ) pyrene 0.005% + 0.1% Fiuoranthene
Banzo ( a ) pyrena 0.005% + 0.1%
Phenanthrena
Banzo ( a ) pyrena 0.005% +• 0.015%
Benz ( a ) anthracene
I ' I ' I ' | ' I ' ! ' | ' |
7 8 9 10 11 12 13 14
Months
FIGURE 1
Effect of Pluoranthene on Production of Skin Carcinomas in Mice
Source: Hoffmann and Wynder, 1963
C-36
-------
w
n
i
u>
g,
(D
U)
0)
O
O
rn
C
O
Source
••
Hoffmann
01
3
a
•««
nthene
o
3
Product!
o
3
o
n\
FIGURE 2
03
O
^
01
Ul
00
I
g. «>
Cumulative Percent of Tumor Bearing MUe
—4
Ci CJ ^3 ^3 ^^ C3 O C^ ^5 ^i
.1.1.1.1. 1,1 . I . I , I I I
o
-------
TABLE 13
a
Cocarcinogenesis: Bioassay in Mouse Skin '
Carcinogen
Days to Mice with
Cocarcinogen Days of first papillomas/toctal
(dose) testing papilloma papillomas
Benzo(a)pyrene
none
Benzo(a)pyrene
none
none
Fluoranthene
(40 ug)
Fluoranthene
(40 ug)
Acetone
Acetone
none
440 99
440
440 210
440
440
39/126 (37)
0
16/26 (12)
0
0
a50 female iCR/Ha Swiss mice used per group.
bBenzo(a)pyrene was applied in the same solution as the cocarcinogen
(5 ug/0.1 ml acetone) three times weekly to the dorsal skin.
GNumbers in parentheses are numbers of mice with squamous carcinoma.
d!00 mice, as stated by the source.
*Source: Van Duuren and Goldschmidt, 1976
C-38
-------
ability. However, none of these possibilities is considered
acceptable as a general mechanism of action for all compounds dis-
playing cocarcinogenic activity. Furthermore, there is not enough
information available to determine the importance of the cocarcino-
genic activity of fluoranthene to human health.
There is no information available concerning the carcinogeni-
city of fluoranthene to humans.
C-39
-------
CRITERION FORMULATION
Existing Guidelines and Standards
There have been no standards developed for fluoranthene in
air, water, food, or the workplace. The only existing standard
that takes fluoranthene into consideration is a drinking water
standard for PAH. The 1970 World Health Organization European
Standards for Drinking Water recommends a concentration of PAH not
exceeding 0.2 ug/1. This recommended standard is based upon the
analysis of the following six PAH in drinking water:
Fluoranthene
Benzo(a)pyrene
Benzo(g,h,i)perylene
Benzo(b)fluoranthene
Benzo(k)fluoranthene
Indeno(l,2,3-cd)pyrene
The designation of the above six PAH for analytical monitoring
of drinking water was not made on the basis of potential health
effects or bioassay data on these compounds (Borneff and Kunte,
1969). It should not be assumed that these six compounds have spe-
cial significance in determining the likelihood of adverse health
effects resulting from absorption of any particular PAH. They are
considered to be a useful indicator for the presence of PAH pollut-
ants. Borneff and Kunte (1969) found that PAH were present in
ground water at concentrations as high as 50 ng/1, and in drinking
water at concentrations as high as 100 ng/1. Based on these data
they suggested that water containing more than 200 ng/1 should be
rejected. However, as data from a number of U.S. cities indicate
(see Ingestion from water section), levels of PAH in raw and fin-
ished waters are typically less than the 0.2 jug/1 criterion recom-
mended by WHO (1970).
C-40
-------
Current Levels of Exposure
Quantitative estimates of human exposure to fluoranthene re-
quire numerous assumptions concerning routes of exposure, extent of
absorption, lifestyle, and variables relating to specifics of geo-
graphy, sex, and age. Nevertheless, working with estimates devel-
oped for PAH as a class, certain extrapolations are possible to
arrive at a crude estimate of fluoranthene exposure.
An estimate of fluoranthene intake from drinking water may be
derived from data obtained in a survey of 16 U.S. cities (Basu and
Saxena, 1977; Basu and Saxena, 1978). By arbitrarily assigning the
lower limit of detectability for fluoranthene to those samples
where none was detected, and using the measured values of fluoran-
thene in the four positive samples found, the estimated average
fluoranthene level in drinking water would be 8.6 ng/1. Thus the
daily intake of fluoranthene in drinking water may be calculated:
8.6 ng/1 x 2 liters/day =17.2 ng/day
Borneff (1977) estimates that the daily dietary intake of PAH
is about 8-11 ug/day. As a check on this estimate, fluoranthene
intake may be calculated based upon reported concentrations of
fluoranthene in various foods (see Distribution section of the doc-
ument), and the per capita estimates of food consumption by the
International Commission on Radiological Protection (1974). Taking
a range from 1 to 10 ppb as a typical concentration for fluoran-
thene in various foods, and 1,600 g/day as the total daily food
consumption by man from all types of foods (i.e., fruits, vegeta-
bles, cereals, dairy products, etc.), the intake of fluoranthene
from the diet would be in the range of 1.6-16 ug/day.
C-41
-------
It has recently been reported that fluoranthene concentrations
in ambient air average about 4 jig/1,000 m (Santodonato, et al.
1978). If it is assumed that 100 percent of the fluoranthene which
is inhaled is absorbed, and that the average amount of air inhaled
by a human each day is about 10-20 m3, then fluoranthene intake via
the air would be in the range of 40-80 ng/day. However, in certain
indoor environments, particularly in the presence of sidestream
tobacco smoke, PAH exposure from inhaled air may be considerably
higher (Grimmer, et al. 1977).
In summary, a crude estimate of total daily exposure to fluor-
anthene would be as follows:
Source Estimated Exposure
Water 0.017 ug/day
Food 1.6 - 16 ug/day
Air 0.040 - 0.080 jag/day
The above cited figures show that foods are the greatest source of
fluoranthene to humans. Accordingly, the present levels of fluor-
anthene in drinking water would be expected to contribute little to
the total human intake.
It should be noted that two factors in the above estimates are
not taken into account. First, it is known that tobacco smoking
can contribute greatly to fluoranthene exposure in man. It is es-
timated that smoking one cigarette will increase exposure to fluor-
anthene via the lungs by about 0.26 yg (Hoffmann, et al. 1972). The
sum of methylfluoranthene in the smoke of a nonfiltered cigarette
is about 0.18 ng (Hoffmann, et al. 1972). Second, it is assumed
that dermal absorption of fluoranthene contributes only a negligi-
ble amount to the total exposure. It is expected that only in
C-42
-------
certain occupational situations would dermal exposure be a quan-
titatively important route of exposure.
Special Groups at Risk
Individuals living in areas which are heavily industrialized,
and in which large amounts of fossil fuels are burned, would be ex-
pected to have greatest exposure from ambient sources of fluoran-
thene. In addition, certain occupations (e.g., coke oven workers,
steelworkers, roofers, automobile mechanics) would also be expected
to have greater exposure than the general population.
Exposure to fluoranthene will be considerably increased among
tobacco smokers or those who are exposed to smokers in closed envi-
ronments (i.e., indoors).
Basis and Derivation of Criteria
The attempt to develop a valid drinking water criterion for
fluoranthene is hindered by several gaps in the scientific data
base:
(1) There have been no chronic dose-response stud-
ies conducted with fluoranthene in animals.
(2) There are no chronic animal toxicity studies
involving oral exposure to fluoranthene.
(3) There are no human data concerning the effects
of exposure to fluoranthene.
From a survey of PAH in U.S. drinking waters using the same
criteria for analysis as recommended by the World Health Organiza-
tion, it is possible to calculate the amount of fluoranthene rela-
tive to other PAH in the same sample (Saxena, et al. 1977; Basu and
Saxena, 1977,1978). These data indicate that in drinking water
samples where fluoranthene was detected, it represented about 58.9
percent of the total PAH. Therefore, the drinking water standard
C-43
-------
recommended by WHO (1970) for PAH of 0.2 ug/1 would be equivalent
to a drinking water standard for fluoranthene of:
0.2 jig/1 x 0.589 = 0.12 ug/1
Attempts to develop a water quality criterion based upon ani-
mal toxicity data are seriously hindered by an inadequate data
base. The only study available which shows a no-effect level for
fluoranthene (in terms of chronic mortality) was reported by Hoff-
mann, et al. (1972). This study involved dermal administration of
fluoranthene to mice, and necessitates the assumption that 100 per-
cent of the applied dose was absorbed. Their data can be used to
develop a water quality criterion based on the method employed by
the U.S. EPA in formulating national interim primary drinking water
regulations (Saxena, et al. 1977).
Calculation of the criterion is summarized in Table 14. The
approach took into consideration the contribution of dietary and
airborne sources of fluoranthene. Once these factors are accounted
for, this procedure leads to the conclusion that 42 jig/1 of fluor-
anthene in drinking water would represent an acceptable level of
exposure. It must be emphasized, however, that the criterion is
based on chronic toxicity data with mortality being the endpoint,
and applies only to situations where exposure occurred to fluoran-
thene alone.
Because of the limitations in the data base concerning fluor-
anthene toxicity, it is considered necessary to apply an uncertain-
ty factor of 1,000 in the calculation of an exposure criterion.
The animal study upon which the criterion is derived involved only
20 mice, which received dermal applications of fluoranthene at one
C-44
-------
TABLE 14
Derivation of Criterion for Fluoranthene in Water
0
1
>tx
01
Species
Mouse
(lla/ICR/Mil
Swiss Albino
Assume weiah
Chronic No-effect rag/kg body
,u ff Level weight/day3
(Hoffman, et al. 1972)
50 ul of 1.0% fluor- 6.12
anthene in acetone
applied 3 times weekly
for 12 months
Calculated Maximum
Safe Levels
Safety mg/kg/ rag/man/
Factor (x) day day°
1/1000 0.006 0.420
Intake
Diet
nig/man/
day
0.016
Maximum
Permissible
from: Intake from
Air Water
ing/man/
day mg/day
0.0001 0.400
Recommended
Limit
"9/1
42.0
^Assume average weight of human adult = 70 kg
Calculated as described
Assume average daily intake of water for man
Calculated as follows:
0.400 mg
" °-042
2 liters.
42-°
-------
dose level three times weekly for 12 months. Thus, the use of these
data for calculation of a criterion relating to ingestion of fluor-
anthene in humans will admittedly be imprecise. To justify the use
of an uncertainty factor of less than 1,000, however, valid results
of long-term feeding studies in one or more species of experimental
animal would be required. In environmental situations, it is well
established that fluoranthene is found in the presence of numerous
PAH; a situation having important implications for potential toxic
interactions.
Several studies have clearly shown that fluoranthene possesses
no carcinogenic activity, and is neither a tumor initiator nor a
tumor promoter (see Carcinogenicity section). However, two care-
fully conducted studies have shown that fluoranthene, when applied
to mouse skin together with much smaller quantities of benzo(a)py-
rene, could act as a cocarcinogen to increase tumorigenic response.
These data do not permit a quantitative estimation of health risks
incurred by this type of biological phenomenon. Nevertheless, be-
cause fluoranthene is present in environmental mixtures together
with other PAH (including several carcinogens) it may pose an ad-
ditional risk to the population exposed. In view of the cocarcino-
genic and anticarcinogenic properties of several environmental PAH,
the degree of added risk, if one exists, cannot be easily deter-
mined on the basis of our present scientific knowledge. At least
one study (Pfeiffer, 1977) has demonstrated that when fluoranthene
was administered together with 11 other PAH (carcinogenic and non-
carcinogenic) by cutaneous injection to mice, it had no enhanc-
ing effect on tumor incidence. However, because of the close
C-46
-------
association between fluoranthene and the other PAH, some of which
are known carcinogens, it would seem prudent to temporarily limit
the level of fluoranthene in drinking water to no more than the
acceptable concentration of all non-fluoranthene PAH. In any
event, the adoption of the recommended water quality criterion for
PAH as a class would undoubtedly result in levels of fluoranthene
in water which are below the 42 jug/1 criterion derived in Table 14.
Inadequacies in the current scientific data base prevent the
formulation of a water quality criterion for fluoranthene based on
potential cocarcinogenicity. In addition, since environmental
exposures to fluoranthene will almost certainly involve concomitant
exposure to carcinogenic PAH, their potential interaction should be
considered in future research and health criteria development.
In summary, based on the use of chronic mouse toxicological
data and an uncertainty factor of 1,000, the criterion level of
fluoranthene corresponding to an acceptable daily intake of 0.4 mg,
is 42 jug/1. Drinking water contributes 21 percent of the assumed
exposure while eating contaminated fish products accounts of 79
percent. The criterion level can similarly be expressed as 54 ;ug/l
if exposure is assumed to be from the consumption of fish and
shellfish products alone.
C-47
-------
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Andelman, J.B. and J.E. Snodgrass. 1974. Incidence and signifi-
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