CHLORINATED NAPHTHALENES
Ambient Water Quality Criteria
Criteria and Standards Division
Office of Water Planning and Standards
U.S. Environmental Protection Agency
Washington, D.C.
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CRITERIA DOCUMENT
CHLORINATED NAPHTHALENES
Criteria
Aquatic Life
^For 1-chloronaphthalene, the criterion to protect fresh-
water aquatic life] as derived using procedures other than
the GuidelinesrQs 29 fig/1 as a 24-hour average andT\the
concentration ^should never exceed 67 ^ug/l| at any time.
For 1-chloronaphthalene,£the criterion to protect salt-
water aquatic life^ as derived using the Guidelines,("Ts
2.8 ^jg/1 as a 24-hour average and^ the concentration [should
never exceed 6.4 ^jg/l| at any time.
Human Health
For the protection of human health from the toxic proper
ties of chlorinated naphthalenes ingested through water
and through contaminated aquatic organisms, the ambient
water criteria for the various classes of chlorinated naphtha
lenes are:
Criterion Level Qug/1)
Trichloronaphthalenes 3.9
Tetrachloronaphthalenes 1.5
Pentachloronaphthalenes 0.39
Hexachloronaphthalenes 0.15
Octachloronaphthalene 0.08
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Introduction
Chlorinated naphthalenes consist of two fused six carbon-
membered aromatic rings where any or all of the eight hydro-
gen atoms can be replaced with chlorine. Theoretically,
76 individual isomers are possible and may exist. The commer-
cial products are usually mixtures with various degrees
of chlorination, and are presently manufactured and marketed
in the United States under the trade name, Halowaxes .
Mixtures of tri- and tetrachloronaphthalenes (solids)
comprise the bulk of market use as the paper impregnant
in automobile capacitors. Less use is made of mixtures
of the mono- and dichloronaphthalenes as oil additivies
for engine cleaning, and in fabric dyeing. In 1956, the
total United States production of chlorinated naphthalenes
was approximately 3,175 metric tons (Hardie, 1964).
Possible impurities of these products are chlorinated
derivatives, corresponding to the impurities in coal tar,
or petroleum-derived naphthalene feedstocks which may include
biphenyls, fluorenes, pyrenes, anthracenes, and dibenzofurans.
The potential for environmental exposure may be signifi-
cant when these compounds are used as oil additives, in
the electroplating industry, and in the fabric dyeing industry.
The extent of leaching of chlorinated naphthalenes from
discarded capacitors and old cable insulation (manufactured
prior to curtailment of the chemical's use in such products)
has not been determined.
Chlorinated naphthalenes have been detected as a contami-
nant in foreign commercial PCB formulations (Phenoclor,
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Clophen, and Kanechlor) along with chlorinated dibenzofurans,
and are present in domestic PCBs (Aroclors) but at lower
levels than in foreign formulations (Vos, et al. 1970; Bowes,
et al. 1975; Roach and Pomerantz, 1974).
The synthesis of chlorinated naphthalenes generally
involves the chlorination of naphthalene by chlorine in
the presence of catalytic amounts of ferric or antimony
chloride. This production process yields mixtures of highly
chlorinated naphthalenes in varying quantities by further
chlorination of the lesser substituted products. Only 1-
chloronaphthalene and octachloronaphthalene are readily
isolated from the products of direct chlorination (Hardie,
1964). All of the possible two monochloro-, 10 dichloro-,
and 14 trichloronaphthalenes have been isolated and identi-
fied. However, not all of the tetra- and higher chloro-
isomers have been characterized.
Table 1 presents physical property data for all of
the chlorinated naphthalenes which have been isolated and
identified. The physical properties of the chlorinated
naphthalenes are generally dependent on the degree of chlori-
nation. Melting points of the pure compounds range from
17 degrees C for 1-chloronaphthalene to 198 degrees C for
1,2,3,4-tetrachloronaphthalene (Hardie, 1964). Also, as
the degree of chlorination increases, the specific gravity,
boiling point, fire and flash points all increase, while
the vapor pressure and water solubility decrease (Hardie,
1964). Mixtures of the mono- and dichloronaphthalenes are
generally liquid at room temperature, whereas mixtures of
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the more highly chlorinated naphthalenes tend to be waxy
solids (Howard and Durkin, 1973).
Chlorinated naphthalenes, like PCBs, exhibit a high
degree of chemical and thermal stability as indicated by
their resistance to most acids and alkalies and to dehydro-
chlorination (Kover, 1975).
Limited data exist on the toxicity of chlorinated naph-
thalenes toward aquatic organisms. Only two pure isomers,
1-chloronaphthalene and 1,2,3,4,5,6,7,8-octachloronaphthalene,
have been tested in freshwater aquatic organisms. Results
from bioassays on these compounds show that the monochloro-
isomer is more acutely toxic than the octachloro-isomer
for a freshwater plant, a freshwater invertebrate species,
and a freshwater vertebrate species.
The same trend in acute toxicity for the mono- and octa-
chloro-isomers exists in saltwater organisms. An embryo-
larval chronic toxicity test conducted on a saltwater verte-
brate species for 1-chloronaphthalene demonstrated chronic
toxic effects. No other chronic data exist for any other
chlorinated naphthalene for any other freshwater or saltwater
species.
A considerable amount of acute toxicity data on chlori-
nated naphthalene mixtures (Halowaxes) for saltwater organisms
has been compiled. Reported acute 96 hr. LC50 values for
invertebrate species do not suggest a trend in toxicity
versus degree of mixture chlorination. Other toxicity data
for saltwater organisms also do not suggest a consistent
trend in toxicity with an increased degree of mixture chlori-
nation.
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TABLE 1
Physical properties of chloronaphthalenes (Hardie, 1964)
Isomer
1-chloronaphthalene
2-chloronaphthalene
1.2-dichloronaphthalene
1.3-dichloronaphthalene
1.4-dichloronaphthalene
1.5-dichloronaphthalene
1.6-dichloronaphthalene
1/7-dichloronaphthalene
1/8-dichloronaphthalene
2,3-dichloronaphthalene
2.6-dichloronaphthalene
2.7-dichloronaphthalene
1,2,3-trichloronaphthalene
1,2, 4-trichloronaphthalene
1.2.5-trichloronaphthalene
1.2.6-tr ichloronaphthalene
1.2.7-trichloronaphthalene
1.2.8-trichloronaphthalene
1.3.5-trichloronaphthalene
1.3.6-trichloronaphthalene
1.3.7-trichloronaphthalene
Mp degrees C Bp degrees C densitytemPJ(
Ca.17
61
35
61.5
67.5
106.5
48.5
63.5
88.5
135
120
114
81
92
78
92.5
88
83
94
80.5
113
259.3
265
291
(755 mm Hg)
287
285.5
285
1.1938
20
1.265616
1.314748*5
1.2997
75.9
1.261199 *5
1.292499'8
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1,3,8-trichloronaphthalene 89.5
1.4.5-trichloronaphthalene 133
1.4.6-trichloronaphthalene 65
2.3.5-trichloronaphthalene 109.5
2.3.6-trichloronaphthalene 90.5
1,2,3,4-tetrachloronaphthalene 198
1,3,5,8-tetrachloronaphthalene 131
1,4,6,7-tetrachloronaphthalene 139
1,2,3,4,5-pentachloronaphthalene 168.5
1,2,3,4,5,6,8-heptachloronaphthalene 194
1,2,3,4,5,6,7,8-octachloronaphthalene 192
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Halowaxes bioconcentrate in saltwater algal and salt-
water invertebrate species 25 to 2,300 fold with no consistent
trend for the raagntude of the bioconcentration with respect
to degree of mixture chlorination (Walsh, et al. 1977; U.S.
EPA, 1976).
Chlorinated naphthalenes demonstrate acute and chronic
toxic effects for a large variety of non-human mammais includ-
ing rats (Bennett, et al. 1938), rabbits (Hambrick, 1957),
pigs (Link, et al. 1958), cattle (Olson, 1969), and sheep
(Brock, et al. 1957). Generally the mono- and dichloro-isomers
are only slightly toxic, the tri-, tetra-, penta- and hexa-
isomers are the most toxic and the octachloro-isomer generally
the least toxic in these studies. Prevalent pathological
symptoms include hyperkeratosis and damage to the liver
and kidney of each species. Toxicity is caused either by
ingestion, inhalation, or dermal application of the toxicant.
A similar situation for chlorinated naphthalene toxicity
in humans has been demonstrated (Hambrick, 1957; McLetchie
and Robertson, 1942; Kleinfeld, et al. 1972; Cotter, 1944;
Greenburg, et al. 1939). Toxicity can be caused by dermal
contact, inhalation, and presumably ingestion. The prevalent
pathological symptoms are liver injury, changes in serum
enzyme levels, and dermal manifestations such as chloracne.
The primary hepatotoxic isomers for man seem to be penta-
and hexachloronaphthalene (Am. Ind. Hyg. Assoc. 1966).
The higher chlorinated naphthalenes appear to be the most
toxic for dermal exposure.
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In several mammalian species, the chlorinated naphtha-
lenes are metabolized to some extent to chlorinated naphthols,
and to some extent are excreted unchanged (Cornish and Block,
1958; Ruzo, et al. 1976a,b). These studies indicate that
as the degree of isomer chlorination increases, the extent
of isomer metabolism to chlorinated naphthols decreases
with no metabolism of pentachloro- and higher chlorinated
isomers apparent (Cornish and Block, 1958; Ruzo, et al.
1976a). Howard and Durkin (1973) report that the available
data on metabolism coupled with the chemical and physical
similarities to polychlorinated biphenyls indicate that
the higher chlorinated naphthalenes are relatively stable
and are likely to persist when released to the environment.
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REFERENCES
American Industrial Hygiene Association. 1966.
Chloronaphthalenes. Hyg. Guide Ser. Jan-Feb.
Bennett, G.A., et al. 1938. Morphological changes in the
liver of rats resulting from exposure to certain chlorinated
hydrocarbons. Jour. Ind. Hyg. Toxicol. 20: 97.
Bowes, G.W., et al. 1975. Identification of chlorinated
dibenzofurans in American polychlorinated biphenyls. Nature
256: 305.
Brock, W.E., et al. 1957. Chlorinated naphthalene intoxica-
tion in sheep. Am. Jour. Vet. Res. 18: 625.
Cornish, H.H., and W.D. Block. 1958. Metabolism of chlori-
nated naphthalenes. Jour. Biol. Chem. 231: 583.
Cotter, L.H. 1944. Pentachlorinated naphthalenes in industry.
Jour. Am. Med. Assoc. 125: 373.
Greenburg, L., et al. 1939. The systemic effects resulting
from exposures to certain chlorinated hydrocarbons. Jour.
Ind. Hyg. Toxicol. 21: 29.
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Hambrick, G.W. 1957. The effect of substituted naphthalenes
on the pilosebaceous apparatus of rabbit and man. Jour.
Invest. Dermat. 28: 89.
Hardief D.W.F. .1964. Chlorocarbons and chlorohydrocarbons:
chlorinated naphthalenes. Pages 297-303 jji Kirk-Othmer ency-
clopedia of chemical technology. 2nd ed. John Wiley and
Sons. Inc., New York.
Howard, P.H., and P.R. Durkin. 1973. Preliminary environmental
hazard assessment of chlorinated napthalenes, silicones,
fluorocarbons, benzenepolycarboxylates, and chlorophenols.
EPA Publ. No. 560/2-74-001. U.S. Environ. Prot. Agency.
Washington, D.C.
Kleinfeld, M., et al. 1972. Clinical effects of chlorinated
naphthalene exposure. Jour. Occup. Med. 14: 377.
Kover, F.D. 1975. Environmental hazard assessment report:
chlorinated naphthalenes. EPA Publ. No. 560/8-75-001.
U.S. Environ. Prot. Agency. Washington, D.C.
Link, R.R., et al. 1958. Toxic effect of chlorinated naph-
thalenes in pigs. Jour. Am. Vet. Med. Assoc. 133: 83.
McLetchie, N.G.R., and D. Robertson. 1942. Chlorinated
naphthalene poisoning. Br. Med. Jour. 1: 691.
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Olson, C. 1969. Bovine hyperkeratosis (X-disease, highly
chlorinated naphthalene poisoning). Historical review
in C.A. Bradley and C.E. Cornelius, eds. Advances in vet-
erinary science and comparative medicine. Academic Press,
New York.
Roach, J.A.G. and I.H. Pomerantz. 1974. The finding of
chlorinated dibenzofurans in a Japanese polychlorinated
biphenyl sample. Bull. Environ. Contam. Toxicol. 12: 338.
Ruzo, L., et al. 1976a. Metabolism of chlorinated naphtha-
lenes. Jour. Agric. Food Chem. 24: 581.
Ruzo, L., et al. 1976b. Uptake and distribution of chloro-
naphthalenes and their metabolites in pigs. Bull. Environ.
Contam. Toxicol. 16: 233.
U.S. EPA. 1976. Semi-annual report, Environ. Res. Lab.,
Gulf Breeze, Fla. April-September, 1976. U.S. Environ.
Prot. Agency.
Vos, J.G., et al. 1970. Identification and toxicological
evaluation of chlorinated dibenzofurans and chlorinated
naphthalenes in two commercial polychlorinated biphenyls.
Food Cosmet. Toxicol. 8: 625.
Walsh, G.E., et al. 1977. Effects and uptake of chlorinated
naphthalenes in marine unicellular algae. Bull. Environ.
Contam. Toxicol. 18: 297.
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AQUATIC LIFE TOXICOLOGY*
FRESHWATER ORGANISMS
Introduction
The only chlorinated naphthalenes for which data are
available for freshwater organisms are 1-chloronaphthalene
and octachloronaphthalene. The available LC50 and EC50
values for the bluegill, Daphnia magna, and an alga indicate
similar sensitivity of these groups.
Acute Toxicity
The 96-hour LC50 for the bluegill and 1-chloronaphthalene
is 2,270 yug/1 (Table 1). After adjustment for testing method-
ology and species sensitivity according to the Guidelines,
the Final Fish Acute Value is 320 yug/1. A single test with
Daphnia magna and. the- same chemical (U.S. EPA, 1978) provides
a 48-hour EC50 of 1,600 pg/1 (Table 2) and a Final Invertebrate
Acute Value of 67 jug/1. The latter becomes the Final Acute
Value.
Chronic Toxicity
No embryo-larval or life-cycle tests have been conducted
with freshwater fish or invertebrate species and any chlori-
nated naphthalene.
*The reader is referred to the Guidelines for Deriving Water
Quality Criteria for the Protection of Aquatic Life (43
FR 21506 (May 18, 1978) and 43 FR 29028 (July 5, 1978))
and the Methodology Document in order to better understand
the following discussion and recommendation. The following
tables contain the appropriate data that were found in the
literature, and at the bottom of each table are the calcula-
tions for deriving various measures of toxicity as described
in the Guidelines.
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Plant Effects
The alga, Selenastrum capricornutum, has been exposed
to 1-chloronaphthalene and the 96-hour EC50 values for chloro-
phyll a and cell numbers are 1,030 and 1,000 pg/1, respectively
(Table 3).
Miscellaneous
A variety of acute tests of the effects of octachloro-
naphthalene have been conducted with the bluegill, Daphnia
magna, and an alga (U.S. EPA, 1978). No adverse effects
were observed at concentrations as high as 500,000 to 600,000
jjg/1 (Table 4) .
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CRITERION FORMULATION
Freshwater - Aquatic Life
Summary of Available Data
The concentrations below have been rounded to two signi-
ficant figures.
1-chloronaphthalene
Final Fish Acute Value = 320 jug/1
Final Invertebrate Acute Value = 67 jug/1
Final Acute Value = 67 yug/1
Final Fish Chronic Value = not available
Final Invertebrate Chronic Value = not available
Final Plant Value = 1,000 pg/1
Residue Limited Toxicant Concentration = not available
Final Chronic Value = 1,000 jug/1
0.44 x Final Acute Value = 29 fig/1
No freshwater criterion can be derived for any chlori-
nated naphthalene using the Guidelines because no Final
Chronic Value for either fish or invertebrate species or
a good substitute for either value is available.
Data for 1-chloronaphthalene and saltwater organisms
can be used to estimate a criterion.
For 1-chloronaphthalene and saltwater organisms, 0.44
times the Final Acute Value is less than the Final Chronic
Value derived from results of an embryo-larval test with
the sheepshead minnow. Therefore, a reasonable estimate
of a criterion for 1-chloronaphthalene and freshwater organisms
would be 0.44 times the Final Acute Value.
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The maximum concentration for 1-chloronaphthalene is
the Final Acute Value of 67 jug/1 and the 24-hour average
concentration is 0.44 times the Final Acute Value. No impor-
tant adverse effects on freshwater aquatic organisms have
been reported to be caused by concentrations lower than
the 24-hour average concentration.
CRITERION: For 1-chloronaphthalene the criterion to
protect freshwater aquatic life as derived using procedures
other than the Guidelines is 29 /ig/1 as a 24-hour average
and the concentration should not exceed 67 pg/1 at any time.
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Table 1. Freshwater fish acute values for chlorinated naphthalenes (U.S. EPA, 1978)
Adjusted
Bioacsay Test Chemical Time LCiO LCbli
Organism Metnod Cone.** Description (hrsl (mi/11 fug/ii
Blueglll, S U 1-chloro- 96 2,270 1,240
Lepomla nmcrochlrus naphthalene
* S » static
«* u = unmeasured
Geometric mean of adjusted values t 1-chloronaphthalene » 1,240 pg/1 ^$^9" •» 320 ng/1
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Table 2. Freshwater invertebrate acute values for chlorinated naphthalenes (U.S. EPA, 1978)
Ornanism
Biaaseay Teat Chemical Time LOU
Method* Cone.** Description thre)- (ug/i>
Adjusted
LCbu
iaaiU
Cladoceran,
Daphnla maftna
1-chloro-
naphthalene
48
1.600
1,400
* S » static
** I) » unmeasured
1,400
Geometric mean of adjusted values; 1-chloronaphthalene - l,400.wg/l —^— - 67 Mg/1
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Tabla 3. Freshwater plant effecCB for chlorinated naphthalenes (U.S. EPA, 1978)
Organism
E££ect
Concentration
mq/it
Alga,
Selenaatrum
capricornutum
Alga,
Selenaatrum
capricornutum
1-chloronaphthalene
1,030
ECSO 96- hr
chloropyll a
EC50 96-hr
cell numbers
1,000
Lowest plant value; 1-chloronaphthalene = 1,000 pg/1
ta
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Table 4. Other freshwater data for chlorinated naphthalenes (U.S. EPA, 1978)
Orgdiii am
Test
Bumlen IUM
Result
CO
I
cx>
Alga,
Selenastrum
capricornutum
Alga,
Selenastrum
capricornutum
Cladoceran,
Daphnla magna
Blueglll,
Lepomis macrochirus
Octachloronaphthalene
96 hrs EC50 chlorophyll a >500,000
96 hrs EC50 cell numbers >500,000
48 hrs LC50 >530,000
96 hrs LC50 >600,000
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SALTWATER ORGANISMS
Introduction
Most of the data concerning the effects of chlorinated
naphthalenes on saltwater organisms are for commercial mix-
tures of mono- through hexachloronaphthalenes in different
proportions. These results do not appear to be useful in
the derivation of criteria for specific chlorinated naphtha-
lenes, and the data for these mixtures are included in the
tables for information purposes. Most of the remaining
data are for 1-chloronaphthalene. These results are very
similar to those freshwater data for a fish, an invertebrate,
and an alga using comparable test procedures (U.S. EPA,
1978).
Acute Toxicity
The sheepshead minnow has been exposed to 1-chloronaph-
thalene (U.S. EPA, 1978) and the 96-hour LC50, after adjust-
ment using the appropriate Guidelines factors, is 1,290
jjg/l (Table 5) . Adjustment for species sensitivity results
in a Final Fish Acute Value of 350 jig/1. Of the saltwater
invertebrate species, only the mysid shrimp has been tested
with 1-chloronaphthalene. The adjusted 96-hour LC50 is
313 /jg/1 (Table 6) , which indicates a greater sensitivity
than the sheepshead minnow. After this result is divided
by the sensitivity factor of 49, the Final Invertebrate
Acute Value is 6.4 jig/1. This concentration also becomes
the Final Acute Value since this invertebrate species value
is lower than the equivalent value for fish.
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Chronic Toxicity
An embryo-larval test has been conducted with the sheeps-
head minnow and 1-chloronaphthalene (U.S. EPA, 1978). The
chronic value is 329 pg/1 and this results in a Final Fish
Chronic Value of 49 pg/1 after division by the sensitivity
factor (Table 7). No other chronic data are available so
49 pg/1 also becomes the Final Chronic Value for 1-chloronaph-
thalene.
Plant Effects
The 96-hour EC50 values for chlorophyll a and cell
numbers of the alga, Skeletonema costatum are 1,130 and
1,300 pg/1, respectively for 1-chloronaphthalene (Table 8).
Residues
The only available equilibrium residue datum (Table
9) for chlorinated naphthalenes is for Halowax 1014, a mixture
for tetra-, penta-, and hexachloronaphthalene (U.S. EPA,
1976). The bioconcentration factor for this mixture is
2,300 which indicates a need for comparable data on individual
chlorinated naphthalenes.
Miscellaneous
As with the freshwater species, the acute toxicity
results for the sheepshead minnow, mysid shrimp, and an
alga (U.S. EPA, 1978) were all greater than 500,000 ^ig/1
for octachloronaphthalene (Table 10). A great variety of
other data is available for various mixtures of chlorinated
naphthalenes and bioconcentration, inhibition of algal growth,
intermolt time for crabs, and other effects (Table 10).
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CRITERION FORMULATION
Saltwater - Aquatic Life
Summary of Available Data
The concentrations below have been rounded to two signi-
ficant figures.
1-chloronaphthalene
Final Fish Acute Value = 350 pg/1
Final Invertebrate Acute Value = 6.4 ^ig/1
Final Acute Value = 6.4 pg/1
Final Fish Chronic Value = 49 /ig/1
Final Invertebrate Chronic Value = not available
Final Plant Value = 1,100 pg/1
Residue Limited Toxicant Concentration = not available
Final Chronic Value = 49 /ig/1
0.44 x Final Acute Value = 2.8 /ag/1
The commercial mixtures of chlorinated naphthalenes
are not considered in the development of a criterion since
the toxicity of each chlorinated naphthalene in the mixtures
may be different, and different proportions of these individ-
ual chemicals would have different toxicity.
The maximum concentration of 1-chloronaphthalene is
the Final Acute Value of 6.4 ;ug/l and the 24-hour average
concentration is 0.44 times the Final Acute Value. No impor-
tant adverse effects on saltwater aquatic organisms have
been reported to be caused by concentrations lower than
the 24-hour average concentration.
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CRITERION: For 1-chloronaphthalene the criterion to
protect saltwater aquatic life as derived using the Guidelines
is 2.8 fig/1 as a 24-hour average and the concentration should
not exceed 6.4 pg/1 at any time.
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Table 5. Marine fish acute values for chlorinated naphthalenes (U.S. EPA, 1978)
Adjusted
Bioi6say Test Chemical Time LC5U Lcbo
Or danism Mfctftod* Cone .** Description Ihrs) (ug/it )i>g/XI
Sheepshead minnow, S U 1-chloro- 96 2,360 1,290
Cyprinodon varie^atus naphthalene
* S " static
** u a unmeasured
1 290
Geometric mean of adjusted value » 1,290 pg/1 " y~j - 350 iig/1
ttJ
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H-*
U)
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Table 6. Marine invertebrate acute values for chlorinated naphthalenes
Organism
Bioassay
Method*
Test
Cone.**
Chemical
Description
Time
ilULS)
LCbU
(ucj/l)
AdJus ted
LC!>U
luq/ll
Reference
Mysid shrimp,
Mysidopsis bahia
S
U
1-chloro-
naphthalene
96
370
313
U.S. EPA, 1978
Brown shrimp,
Penaeus aztecus
FT
M
llalowax
1014***
96
7.5
7.5
U.S. EPA, 1976
Grass shrimp,
Palaemonetes pugio
FT
M
llalowax
1014***
96
248
248
U.S. EPA, 1976
Grass shrimp (post-larva), R
Palaemonetes pugio
M
Halowax
1000****
96
440
484
Green & Neff,
1977
Grass shrimp (adult),
Palaemonetes pugio
R
M
Halowax
1000****
96
325
358
Green & Neff,
1977
Grass shrimp (post-larva), R
Palaemonetes pugio
M
Halowax
1013*****
96
74
81
Green & Neff,
1977
Grass shrimp (post-larva), R
Palaemonetes pugio
M
Halowax
1099******
96
69
76
Green & Neff,
1977
Grass shrimp (adult),
Palaemonetes pugio
R
M
Halowax
1099******
96
90
99
Green & Neff,
1977
S = static; FT «¦ flow-through; R ¦» renewal
** M =« measured; U ¦» unmeasured
*** llalowax 1014: 20% tetrachloronaphthalene, 40% pentachloronaphthalene, 40% hexachloronaphthalene
**** Halowax'* 1000: 60% monochloronaphthalene, 40% dichloronaphthalene
***** Halowax®* 1013; 10% trichloronaphthalene, 50% tetrachloronaphthalene, 40% pentachloronaphthalene
****** Halowax®* 1099: 40% trichloronaphthalene, 60% tetrachloronaphthalene
Geometric mean of adjusted values for 1-chloronaphthalene = 313 wg/1 = 6.4 Mg/1
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Table 7. Marine flah chronic values for chlorinated naphthalenes (U.S. EPA, 1978)
Chronic
Limits Value
Organism Test* .lug/11 fug/1)
1-chloronaphthalene
Sheepshead minnow, E-L 460-940 329
Cyprinodon varlegacus
*E-L « embryo-larval
Geometric mean of chronic value » 329 wg/1 " 49 ug/1 1-chloronaphthalene
Lowest chronic value ¦ 329 Mg/1
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Table 8. Marine plant effects for chlorinated naphthalenes (U.S. EPA, 1978)
Concentration
Organism Ettect (ug/11
1-chloronaphthalene
Alga, Chlorophyll a 1,130
Skeletonema costatura EC50 after 95 hr
Alga, Cell numbers 1,300
Skeletonema costatum KC50 after 96 hr
Lowest plant value — 1,130 ug/1
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Table 9. Marine residues for chlorinated naphthalenes (U.S. EPA, 1976)
Time
Organlam Bloconcentration Factor (days)
Halowax 1014*
Brown shrimp, 2,300 4
Penaeus aztecus
*llalowax '1014: 20% tetrachloronaphthalene, 40% pentachloronaphthalene, 40% hexachloronpahthalene
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Table 10.
Test
Organism Duration
Alga, 24 hra
Chlorococcum sp.
Alga, 24 hrs
Chlorococcum sp.
Alga, 24 hra
Chlorococcum sp.
Alga, 7 days
Chlorococcum sp.
Alga, 7 days
Chlorococcum sp.
Alga, 7 days
Dunallella tertiolecta
Alga, 7 days
Dunallella tertlolecta
Alga, 7 days
Dunallella tertlolecta
Alga, 7 days
Nltzschla sp.
Alga, 7 days
Nltzschla sp.
Alga, 7 days
Nltzschla sp.
Alga, 7 days
Nltzschla sp.
Alga, 96 hrs
Skeletonema costaturn
Alga, 96 hrs
Skeletonema coataturn
Alga, 7 days
Thalassloslra pseudonana
r marine data for chlorinated naphthalenes
Bloconcentratlon
factor = 25-32*
Bloconcentratlon
factor «=> 60-120**
Bloconcentratlon
factor - 110-140***
11.7% Inhibition
of growth*
45.8% inhibition
of growth*
11% inhibition of
growth*
18.6% inhibition
of growth*
43% inhibition
of growth*
17.1% inhibition
of growth*
42.37. inhibition
of growth*
13.2% inhib11 ion
of growth**
16.6% inhibition
of growth**
Chlorophyll a
EC50*****
Cell numbers
EC50*****
21.3% inhibition
of growth*
Reference
Walsh, et al. 1977
Walsh, et al. 1977
Walsh, et al. 1977
Walsh, et al. 1977
Walsh, et al. 1977
Walsh, et al. 1977
Walsh, et al. 1977
Walsh, et al. 1977
Walsh, et al. 1977
Walsh, et al. 1977
Walsh, et al. 1977
Walsh, et al. 1977
U.S. EPA, 1978
U.S. EPA, 1978
Walsh, et al. 1977
Result
500
1,000
100
500
1,000
500
1,000
500
1,000
>500,000
>500,000
500
-------
Table 10. (Continued)
Organ!am
Test
Duration
CO
t—1
Alga, 7 days
Thftlassiosira pseudonana
Alga, 7 days
Thalassioslra paeudonana
Horseshoe crab, 27 days
Llmulua polyphemus
Horseshoe crab,
Limulus polyphemus
Horseshoe crab,
Limulus polyphemus
Horseshoe crab,
Limulus polyphemus
Horseshoe crab,
Limulus polyphemus
Horseshoe crab,
Limulus polyphemus
Grass shrimp, 15 days
Palaemonetes pugio
Grass shrimp, 12 days
Palaemonetes puaio
Grass shrimp, 5 days
Palaemonetes pugio
Mysid shrimp, 96 hrs
Myaldopaia bahia
Result
Etfect. Om/U
48.4% inhibition 1,000
of growth*
7.17. inhibition 1,000
of growth**
Time required for 50% 80
mortality (LT50) of Ti
stage larvae****
Average length of time of 40
intermolt between and
T<> stages reduced by
3.4 days****
Average length of time 20
of intermolt between To
and T, stages reduced
by 14.8 days****
Average length of time 20
of intermolt between To
and Ta stages reduced By
16.8 days****
Average length of time 80
of intermolt between To
and stages reduced
by 18.4 days****
Increased rates of respira- 20
tion of T^ and T2Stages**** and
Bioconcentration
factor «* 63*
Bioconcentration
factor = 18?**
Bioconcentration
factor = 257****
LCSO*****
>500,000
ReteretiCfa
Walsh, et al. 1977
Walsh, et al. 1977
Neff & Giam, 1977
Neff & Giam, 1977
Neff & Giam. 1977
Heff & Giam, 1977
Neff & Giam, 1977
Neff & Giam, 1977
Green & Neff, 1977
Green & Neff, 1977
Green & Neff, 1977
U.S. EPA, 1978
-------
Table 10. (Continued)
Organ! sni
Test
Duration
tc
M
O
Mud crab, 13 days
Rhlthropanopeua harrlsl
Mud crab, 27 days
Rhlthi-opanopeus harrlsl
Mud crab,
Rhlthropanopeua harrlsl
Mud crab,
Rhlthropanopeua harrlsl
Mud crab,'
Rhlthropanopeus harrlsl
Mub crab,
Rhlthropanopeus harrlsl
Mud crab,
Rhlthropanopeus harrlsl
Sheepshead minnow, 96 hra
Cyprlnodon variegatus
Sheepshead minnow, 96 hrs
Cyprlnodon variegatus
Striped mullet 96 hrs
(Juvenile)
Mug11 cephalus
Result
Etfect lim/xt
Slightly lowered 300
survival of larvae
to megalopa*
15% survival of larvae 100
to megalopa****
Length of intermolt time 300
from 4th zoeal molt to
megalopa stage extended
to 2.9 days*
Length of intermolt time 100
from 4th zoeal molt to
megalopa stage extended
by 4.9 days****
Supernumerary zoeae 100
(a fifth zoeal stage)****
Deformed megalopa 300
(eyestalks and appendages
malformed)*
Deformed megalopa 100
(eyestalks and appendages
malformed)****
LC50*** >343
LC5Q*****
LC50***
>560,000
>263
Neff. et al. 1977
Neff, et al. 1977
Neff. et al. 1977
Neff, et al. 1977
Neff, et al. 1977
Neff, et al. 1977
Neff, et al. 1977
U.S. EPA, 1976
U.S. EPA, 1978
U.S. EPA, 1976
* Halowax 1000: 60% monochloronaphthalene, 40% dichloronaphthalene
** llalowax 1013: 10% trichloronaphthalene, 50% tetrachloronaphthalene, 40% pentachloronaphthalene
*** Halowax 1014: 20% tetrachloronaphthalene, 40% pentachloronaphthlene, 40% hexachloronaphthalene
**** llalowax 1099: 40% trichloronaphthalene, 60% tetrachloronaphthalene
***** Octachloronaphthalene
-------
REFERENCES
Green, F.A., Jr., and J.M. Neff. 1977. Toxicity, accumula-
tion, and release of three polychlorinated napthalenes
(Halowax 1000, 1013, and 1099) in postlarval and adult grass
shrimp, Palaemonetes pugio. Bull. Environ. Contam. Toxicol.
14: 399.
Neff, J.M., and C.S. Giam. 1977. Effects of Aroclor 1016
and Halowax 1099 on juvenile horseshoe crabs, Limulus poly-
phemus. Pages 21-36 jLn F.J. Vernberg, et al.,eds. Physio-
logical responses of marine biota to pollutants. Academic
Press, N.Y.
Neff, J.M., et al. 1977. Effects of polychlorinated biphenyls,
polychlorinated naphthalenes and phthalate esters on larval
development of the mud crab, Rhithropanopeus harrisii.
Pages 95-110 ui C.S. Giam, ed. Pollutant effects on marine
organisms. Lexington Books, D.C. Heath and Co., Lexington,
Mass.
U. S. EPA. 1976. Semi-annual report, Environ. Res. Lab.,
Gulf Breeze, Fla. April - September, 1976. U. S. Environ.
Prot. Agency.
B-21
-------
U. S. EPA. 1978. In-depth studies on health and environ-
mental impacts of selected water pollutants. Contract No.
68-01-4646. U.S. Environ. Prot. Agency. Washington, D.C.
Walsh, G.E., et al. 1977. Effects and uptake of chlorinated
naphthalenes in marine unicellular algae. Bull. Environ.
Contam. Toxicol. 18: 297.
B-22
-------
Mammalian Toxicology and Human Health Effects
Introduction
Polychlorinated naphthalenes have been used in various
industrial processes since the turn of the century. Peak
use of these compounds occurred during World War I in Germany
where they were used in place of rubber, and in the United
States during World War II where they were used to a large
extent in heat-resistant electrical insulation. Since then
many uses of polychlorinated naphthalenes have been replaced
by a growing variety of plastics. In 1956 production and
utilization of polycholorinated naphthalenes in the United
States had decreased to approximately 3,200 metric tons
per year. By 1972 production had decreased further to approx-
imately 2,300 metric tons per year. At the present, Halochem,
Inc. in Boonton, N.J., is the only manufacturer of polychlori-
nated naphthalenes in the United States. Amounts of chlori-
nated naphthalenes processed in 1978 were less than 22 metric
tons for monochloronaphthalene, less than 45 metric tons
total for di-, tri-, and tetrachloronaphthalene, less than
1 metric ton for pentachloronaphthalene, and virtually zero
for the more highly chlorinated naphthalenes (R. Cuozzo,
1978, President, Halochem, Inc., personal communication).
Projected production for 1979 totals less than 270 metric
tons with 20 percent of this total expected to be monochloro-
naphthalene, less than 5 percent pentachloronaphthalene,
and none the more highly chlorinated naphthalenes. Although
C-l
-------
several foreign companies manufacture polychlorinated naphtha-
lenes, there are no known imports of these compounds. Because
of their chemical and thermal stability, dielectric properties,
and low viscosity in a liquid state, polychlorinated naphtha-
lenes are still used as engine oil additives, cutting oil
additives, capacitor dielectrics, and electroplating stopoff
compounds. They are also used to some extent in the production
of fabric dyes. In the past, polychlorinated naphthalenes
have been used as pesticides, waterproofing and flame retardent
compounds, and cable-covering materials.
During World Wars I and II, the industrial use of poly-
chlorinated naphthalenes was implicated in many cases of
chloracne and, to a lesser extent, liver disease. The pur-
pose of this report is to summarize information on the occur-
rence, pharmacokinetic properties, and health effects of
polychlorinated naphthalenes in an effort to set a criterion
for acceptable levels of polychlorinated naphthalenes in
water.
EXPOSURE
Polychlorinated naphthalenes do not occur naturally
in the environment. Potential environmental accumulation
can occur around points of manufacture of polychlorinated
naphthalenes or products containing them, near sites of
disposal of polychlorinated naphthalene-containing wastes,
and, since polychlorinated biphenyls (PCBs) are to some
extent contaminated by polychlorinated naphthalenes (Vos,
et al. 1970; Bowes, et al. 1975), near sites of'heavy poly-
chlorinated biphenyl contamination. Because polychlorinated
C-2
-------
naphthalenes are relatively insoluble in water, they would
not be expected to migrate far from their point of disposition.
Currently available industrially produced polychlori-
nated naphthalenes occur as mixtures of various isomers
as noted in Table 1 (Brinkman and Reymer, 1976). These
mixtures are marketed by Koppers, Inc. under the trade name
HaIowax
Approximate Compositions (WT.-%) of Halowaxes (PCN's) (Brinkman and Reymer, 1976)
Halowax Type of
PCN Mono- Di- Tri- Tetra- Penta- Hexa- Hepta- Octa-
TABLE 1
1031
1000
1001
1099
1013
1014
1051
95
60
5
40
10
10
40
40
10
40
40
50
20
10
10
40
40
40
10
90
-------
Ingestion from Water and Food
To date polychlorinated naphthalenes have not been
identified in either drinking water or market basket foods.
Polychlorinated naphthalenes have been found in waters or
sediments adjacent to point sources or areas of heavy poly-
chlorinated biphenyl contamination (Table 2).
Polychlorinated naphthalene-contaminated sediments
occur less frequently than polychlorinated biphenyl-contami-
nated sediments. Law and Goerlitz (1974) found polychlori-
nated naphthalenes in only 1 of 39 sediment samples from
streams emptying into San Francisco Bay. In contrast, 97
percent of the samples contained measurable levels of poly-
chlorinated biphenyls.
Polychlorinated naphthalenes do appear to be biomagnified
in the aquatic ecosystem. As noted in Table 2, Crump-Wiesner,
et al. (1973) found that concentrations of polychlorinated
naphthalenes in sediments were 220- to 877-fold greater than
in the water overlying these sediments. Erickson, et al.
(1978), however, found a polychlorinated naphthalene level
in contaminated sediments near a capacitor factory that
was only six-fold greater than the level in the overlying
water. Algae definitely accumulate polychlorinated naphtha-
lenes. Walsh, et al. (1977) have found polychlorinated
naphthalene levels in algae that were 24 to 140-fold higher
than in the surrounding water. The degree of biomagnification
was greater for the more highly chlorinated polychlorinated
naphthalene mixtures. Biomagnification of polychlorinated
naphthalenes also occurs in shrimp. Grass shrimp concentrate
C-4
-------
TABLE 2
Water and Sediment Polychlorinated Naphthalene Levels
Industry
Type of Sample
Level Reference
(pg/kg or ^g/i)
Airplane engine Sediment
overhaul
Airplane engine Water
overhaul
None identified Sediment
Reprocessing oil Sediment
Polychlorinated Naph-
thalene manufacturer Water
Capacitor manufac-
turer A Water
Capacitor manufac-
turer B Water
Capacitor manufac-
turer B Sediment
Capacitor dumps (2) Water
1250-5000
5-7
55
trace
n.da.-1.4
n. d.
n.d.-0.6
1.8-2.6
n.d.
Crump-Wiesner,
et al. 1973
Crump-Wiesner,
et al. 1973
Law and Goerlitz, 1974
Minagawa, 1976
Erickson, et al. 1978
Erickson, et al. 1978
Erickson, et al. 1978
Erickson, et al. 1978
Erickson, et al. 1978
n.d. means not detectable with a sensitivity threshold of 0.2 jjg/1
for water and 0.5 pg/kg for soil and sediment.
C-5
-------
various mixtures of polychlorinated naphthalenes by a factor
ranging from 63 to 257 compared to the surrounding water
(Green and Neff, 1977). As with algae there is greater
biomagnification with the more highly chlorinated naphtha-
lenes. A bioconcentration factor (BCF) relates the concentra-
tion of two chemicals in water to the concentration in aquatic
organisms, but BCF's are not available for the edible portions
of all four major groups of aquatic organisms consumed in
the United States. Since data indicate that the BCF for
lipid-soluble compounds is proportional to percent lipids,
BCF's can be adjusted to edible portions using data on percent
lipids and the amounts of various species consumed by Americans.
A recent survey on fish and shellfish consumption in the
United States (Cordle, et al. 1978) found that the per
capita consumption is 18.7 g/day. From the data on the
19 major species identified in the survey and data on the
fat content of the edible portion of these species (Sidwell,
et al. 1974), the relative consumption of the four major
groups and the weighted average percent lipids for each
group can be calculated:
Group
Consumption Weighted Average
(Percent) Percent Lipids
Freshwater fishes
12
4.8
Saltwater fishes
61
2.3
Saltwater molluscs
9
1.2
Saltwater decapods
18
1.2
C-6
-------
Using the percentages for consumption and lipids for each
of these groups, the weighted average percent lipids is
2.3 for consumed fish and shellfish.
A measured bioconcentration factor of 2,300 was obtained
for Halowax 1014 using brown shrimp containing about 1.1
percent lipids (U.S. EPA, 1976). Since this test only lasted
4 days and the result was based on whole body, this BCF
is probably lower than the steady-state value. An adjustment
factor of 2.3/1.1 = 2.1 can be used to adjust the measured
BCF from the 1.1 percent lipids of the brown shrimp to the
2.3 percent lipids that is the weighted average for consumed
fish and shellfish. Thus, the weighted average bioconcen-
tration factor for Halowax 1014 and the edible portion of
all aquatic organisms consumed by Americans is calculated
to be 2,300 x 2.1 = 4,800.
Erickson, et al. (1978) also noted a higher level of
polychlorinated naphthalenes in a dead fish (39 /ig/kg) than
in the adjacent water (0.2 ;ig/l).
Erickson, et al. (1978) also noted a higher relative
biomagnification of the lowest chlorinated naphthalenes
by the fruit of apple trees grown on contaminated soil.
The soil was found to have a polychlorinated naphthalene
level of 190 jug/kg of which 1.6 pg/kg consisted of monochloro-
naphthalenes. While the apples grown on this soil had only
90 ^g/kg of polychlorinated naphthalenes, the level of mono-
chloronaphthalenes was 62 pg/kg.
C-7
-------
Inhalation
The American Conference of Governmental Industrial
Hygienists (ACGIH) (1971), in the documentation of threshold
limit values for polychlorinated naphthalenes, noted that
3
in industry air concentrations of 1,000 to 2,000 jig/m of
a penta- and hexachloronaphthalene mixture and concentrations
3
of 300 /jg/m of trichloronaphthalene (possibly with some
tetrachloronaphthalene present) had been associated with
adverse effects. Erickson, et al. (1978) found ambient
air concentrations of polychlorinated naphthalenes ranging
from 0.025 to 2.90 /ag/m near the Koppers' polychlor inated
naphthalene plant. Concentrations of trichloronaphthalene
3
were as high as 0.95 /ig/m while hexachloronaphthalene concen-
3
trations never exceeded 0.007 ^jg/m . Near one capacitor
factory, ambient air concentrations of polychlorinated naph-
3
thalenes ranged from non-detectable to 0.005 jig/m , while
at a second factory they ranged from 0.0098 to 0.033 pg/m .
Dermal
The likelihood of significant dermal absorption of
polychlorinated naphthalenes from an environmental source
is negligible. Link, et al. (1958) found no evidence of
systemic disease after spraying pigs with 1,386 to 1,704
mg/kg of hexachloronaphthalene over a period of 28 days,
while a total dose of only 41 mg/kg of hexachloronaphthalene
given orally over a period of 10 days was uniformly fatal.
C-8
-------
PHARMACOKINETICS
Absorption, Distribution, and Excretion
There is currently no information on the pharmacokinetic
mechanisms of absorption, distribution and excretion of
polychlorinated naphthalenes in man. Chu, et al. (1977a)
noted that in rats fed 1,2-dichloronaphthalene, the half-
life for loss of this compound from the blood after the
first day was 24 hours. This chemical and its metabolites
were found primarily in the intestine, kidney, and adipose
tissue (Table 3). Although initially more of this chemical
and its metabolites were found in the urine, a greater propor-
tion had been excreted in the feces by the end of 7 days.
A stool analysis disclosed only unchanged 1,2-dichloronaphtha-
lene. In contrast, only a glucoronide-bound dihydrodiol
metabolite of 1,2-dichloronaphthalene could be identified
in the urine. Sixty-two percent of the dose was excreted
in the bile in 24 hours compared to 18.9 percent lost in
the feces in 24 hours. This suggests that there is an appre-
ciable reabsorption and enterohepatic recirculation of this
particular compound.
C-9
-------
TABLE 3
Distribution and Excretion of 1,2-Dichloronaphthalene in Rats,
(as a percentage of dose) (Chu, et al. 1977a)
Adipose
Lung
Liver
Bladder
Intestine
Skin
Gastrointestinal
content
Fecal excretion
Urine excretion
At 24 hours
At 48 hours
0.1
0.04
0.7
0.01
0.45
0.07
18.3
18.9
26.4
0.15
0.03
0.07
0.01
3.6
0.08
17.9
30.8
32.6
At 7 days
0.04
0.01
0.04
42.0
35.2
In seagulls with environmental exposures to chlorinated
naphthalenes, analyses of fat, liver, and plumage resulted
in the detection of polychlorinated naphthalenes only in
liver samples, the highest value being 62,500 jig/kg calcu-
lated as octachloronaphthalene (Vannucchi, et al. 1978).
C-10
-------
Metabolism
There appears to be appreciable metabolism in mammals
of polychlorinated naphthalenes containing four chlorine
atoms or less. Cornish and Block (1958) investigated the
excretion of polychlorinated naphthalenes in rabbits. They
found that 79 percent of 1-chloronaphthalene, 93 percent
of dichloronaphthalene, and 45 percent of tetrachloronaph-
thalene were excreted in the urine as metabolites of the
parent compounds. There was no measurable urinary excretion
(either as metabolite's or the unchanged compound) of penta-,
hepta-, or octachloronaphthalene.
There have been detailed evaluations of the various
urinary metabolites of polychlorinated naphthalenes as noted
in Table 4. Thus, metabolism may involve hydroxylation
alone or hydroxylation in combination with dechlorination.
Ruzo, et al. (1976) investigated the 1,2 shift of a
chlorine atom during the metabolism of 1,4-dichloronaphthalene
by substituting a deuterium atom for the one-position chlorine.
The shift of the deuterium atom to the two-position suggested
an arene oxide intermediary metabolite in the conversion
of 1,4-dichloronaphthalene to 2,4-dichloro-l-naphthol. (See
Figure 1).
Figure 1. Conversion of 1,4-dichloronaphthalene to 2,4-
dichloro-l-naphthol via an arene oxide intermediary meta-
bolite. (Brinkman and Reymer, 1976).
a
OH
-------
TABLE 4
Polychlorinated Naphthalene Metabolites Found in Urine
Parent
Metabolite
Animal
Reference
1-chloronaphthalene 4-chloro-l-naphthol
2-chloronaphthalene 3-chloro-2-naphthol
1,2-dichloro-
naphthalene
1,4-dichloro-
naphthalene
2.6-dichloro-
naphthalene
2.7-dichloro-
naphthalene
1,2-dichloro-
naphthalene
1,2,3,4-tetrachloro-
naphthalene
1,2,3,4,5,6-hexa-
chloronaphthalene
frogs
pigs
pigs
3,4-dichloro-l-naphthol pigs
2,4-dichloro-l-naphthol pigs
frogs
6-chloro-2-naphthol rats
2,6-dichloronaphthol
7-chloro-2-naphthol rats
5,6-dichloro-l,2-dihy- rats
droxy-l,2-dihydronaphthalene
5,6,7,8-tetrachloro-1-
and -2-naphthol
none
pigs
pigs
Sundstrom,
et al. 1975
Ruzo, et al. 1976
Ruzo, et al. 1976
Ruzo, et al. 1976
Ruzo, et al. 1976
Sundstrom,
et al. 1975
Chu, et al. 1977b
Chu, et al. 1977b
Chu, et al. 1977b
Ruzo, et al. 1976
Ruzo, et al. 1976
C-12
-------
>1
EFFECTS
In man the first disease that was recognized as being
associated with exposure to polychlorinated naphthalenes
was halowax acne (a form of chloracne) also known as "cable
itch" or "cable rash." Occurrence of this disease was asso-
ciated with the manufacture or use of polychlorinated naph-
thalene-treated electrical cables. During World War II
chloracne was commonly found among shipyard electricians.
Individuals who stripped the polychlorinated naphthalene-
treated covering from cables would often contaminate their
clothes with dust or flakes from the covering. If they
wore their dirty work clothes home, their wives or children
could get a milder form of chloracne (Schwartz, 1943).
Chloracne has resulted both from skin contact and inhalation
of polychlorinated naphthalene fumes. Polychlorinated naph-
thalenes dissolve readily and concentrate in the sebum material
found in hair follicles (Jones, 1941). Initial symptoms
are loss of the sebaceous glands emptying into the follicle,
derangement of keratin formation, and plugging of the follicle
with resultant comedo. If exposure stops at this point,
the sebaceous glands can regenerate and the rash can clear
after several months. Continued exposure injures the follicle
walls causing an inflammatory reaction and formation of
a pustule. Later, the walls deteriorate and rupture with
loss of follicular material to the surrounding tissues.
This results in the formation of a cyst or sterile abcess.
C-13
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Not all polychlorinated naphthalenes are acneigenic.
Shelley and Kligman (1975) applied various polychlorinated
naphthalenes to human subjects. They found chloracne only
after treating their subjects with a suspension containing
a mixture of penta- and hexachlorinated naphthalenes. Simi-
larly, Hambrick (1957) noted chloracne only after treating
his subjects with a 3 percent solution of hexachloronaph-
thalene or a mixture of penta- and hexachlorinated naphtha-
lenes. These were the only two mixtures that produced hyper-
keratosis when applied to the ears of rabbits. Epidemiologic
studies confirm these clinical and experimental impressions.
Crow (1970) noted a continuing incidence of chloracne in
a capacitor plant that utilized both tri-/tetrachlorinated
and penta-/hexachlorinated naphthalene mixtures. As soon
as the use of the latter mixture was stopped, chloracne
ceased to be found at this factory. Kleinfeld, et al. (1972)
noted that an electric coil manufacturing plant had no problems
with chloracne while using a mono- and dichloronaphthalene
mixture. When a tetra-/pentachlorinated naphthalene mixture
was unwittingly substituted for the original mixture, 56
of the 59 potentially exposed workers developed chloracne
within a short time. They also complained of puritis, eye
irritation, headaches, fatigue, vertigo, nausea, loss of
appetite, and weight loss. Liver function studies in five
of the affected individuals were normal. Kimbrough and
Chamblee (1972) give a general review of chloracne in indus-
trially exposed populations.
C-14
-------
Individuals with high-level exposures to the fumes
of polychlorinated naphthalenes can develop acute or sub-
acute liver disease with or without an associated chloracne.
With a rapidly progressive course there is jaundice, abdominal
pain, edema, ascites, and decrease in liver size. At autopsy
the liver is small and necrotic with evidence of fatty meta-
morphosis, a condition called acute yellow atrophy, with
less exposure the course can be long enough for the develop-
ment of a postnecrotic-type of cirrhosis or liver scarring.
At the time of death, common findings in addition to severe
liver damage include evidence of damage to the heart, pancreas,
gallbladder, lungs, adrenal glands, and kidney tubules (Green-
berg, et al. 1939; Strauss, 1944). With even less exposure
there may be few or no clinical findings and only mild-to-
moderate laboratory evidence of liver dysfunction that resolves
with time (Cotter, 1944).
Acute, Sub-acute, and Chronic Toxicity
Almost invariably, clinical evidence of damage from
polychlorinated naphthalene exposure has occurred only after
repeated exposures. Consequently, there have been few tests
of acute toxicity. Cornish and Block (1957) in investigating
metabolites of polychlorinated naphthalenes, gave groups
of three rabbits single oral doses of various compounds
at a level of 500 mg/kg and followed their course for 7
days. No mortality or illness occurred in the rabbits treated
with mono-, di-, or tetrachloronaphthalenes. One of the
three treated with pentachloronaphthalene died. All the
rabbits treated with a solution of hepta- or octachloronaph-
thalene died.
C-15
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Beginning in the 1930's a number of herds of cattle
were afflicted with a mysterious 'X-disease' or hyperkeratosis
of cattle. Severely afflicted individuals developed coarse,
wrinkled skin, a chronic cough and shortness of breath,
weight loss with associated inflammation of the upper portion
of the gastrointestinal tract, pancreatitis and pancreatic
scarring, kidney damage, gallbladder disease, severe liver
damage, hair loss and reversible suppression of spermatogenesis
(Vlahos, et al. 1955). In addition, animals were found
to be more susceptible to a viral infection, proliferative
stomatitis, which caused warty growths of the mucosal lining
of the nose, mouth, and intestinal tract (Olson, 1969).
This disease was eventually traced to the ingestion (either
by licking farm equipment or by eating contaminated food
pellets) of oil or grease containing polychlorinated naphtha-
lenes. The investigation of the origins of this illness
stimulated several studies on the subacute and chronic toxi-
city of polychlorinated naphthalenes taken orally. Although
many of the studies were performed using calves or cattle
(Table 5), a number of studies were done with several other
species (Table 6). Polychlorinated naphthalenes containing
three or fewer chlorine atoms were found to be nontoxic.
Tetrachloronaphthalene resulted in mild liver disease at
levels as high as 0.7 mg/kg/day (Bell, 1953). The higher
chlorinated naphthalenes produced more severe disease at
lower doses. Because of their insolubility, hepta- and
octachloronaphthalene were less toxic when given in suspension
than when given in solution.
C-16
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TABLE 5
Oral Toxicity of Polychlorinated
Naphthalenes in Cattle
No. of
chlorine atoms Dose Duration Results Reference
(mg/kg/day) (days)
2 0.9 7 no effect Bell, 1953
3 0.49-0.54 7-10 no effect Bell, 1953
4 0.48-0.70 10-18 slight
hyperkeratosis Bell, 1953
5 0.35-0.49 5-10 severe systemic
disease Bell, 1953
6 0.23-0.65 5-10 severe systemic
disease Bell, 1953
6 0.83-1.66 60 severe systemic
disease Sikes, et
al. 1952
7 0.14-0.49 7-9 severe systemic
disease Bell, 1953
8 0.21-0.70 9-13 moderate systemic
disease Bell, 1953
8 0.88 13 severe systemic
disease Sikes, et
al. 1952
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TABLE 6
Oral Toxicity of Polychlorinated Naphthalenes
Dose
Duration
(days) Results
Species Reference
0.3 g/rat/day
50 mg/rat/day
100 mg/rat/day
0.23 mg/kg/day
2.3 mg/kg/day
2.3 mg/kg/day
3.4 mg/kg/day
3.5 mg/kg/day
3.6 mg/kg/day
4.1 mg/kg/day
136 slight liver
damage rats
63 all moribund
or dead rats
55 all moribund
or dead rats
135 cirrhosis sheep
23-35 all dead or
moribund sheep
(acute yel-
low atrophy)
10 no effect pigs
8 slight
decrease in pigs
Vitamin A
Marked
decrease in
Vitamin A
Bennett, et
al. 1938
Bennett, et
al. 1938
Bennett, et
al. 1938
Block, et
al. 1957
Block, et
al. 1957
Link, et al. 1958
Link, et al. 1958
pigs Link, et al. 1958
10 1 of 3 dead pigs
10 3 of 3 dead pigs
Link, et al. 1958
Link, et al. 1958
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Synergism and/or Antagonism
Drinker, et al. (1937) exposed rats to an average of
3 3
1.31 mg/m of trichloronaphthalene or to 1.16 mg/m of a
penta-/hexachloronaphthalene mixture in air for 6 weeks
with only minor liver effects. When a similarly exposed
group of rats was challenged with a sublethal dose of an
ethanol/carbon tetrachloride mixture, no effect was seen
with the trichloronaphthalene-exposed rats but 7 of the
10 penta-/hexachloronaphthalene-exposed rats died. No other
data are available on potentially synergistic or antagonistic
effects.
Teratogenicity, Mutagenicity, and Carcinogenicity
No animal or human studies have been carried out on
the carcinogenicity, mutagenicity, or teratogenicity of
polychlorinated naphthalenes.
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CRITERION FORMULATION
Existing Guidelines and Standards
The only standards that presently exist for polychlori-
nated naphthalenes are the Occupational Safety and Health
Administration's standards which were adopted from and are
identical to the ACGIH Threshold Limit Values. The rigor
of these standards increases as the number of chlorine atoms
present increases on the assumption that vapor toxicity
is proportional to the number of chlorine atoms present
in each compound. The present Threshold Limit Values are:
There are no state or federal water quality or ambient air
quality standards for chlorinated naphthalenes.
Current Levels of Exposure
Polychlorinated naphthalenes have not been identified
in drinking water samples, market basket food samples, or
at standard ambient air stations. Near point sources, concen-
trations in water can range as high as 7.0 /ig/1 (Crump-Wiesner,
3
et al. 1973) and concentrations in air as high as 2.9 jjg/m
(Erickson, et al. 1978). Near a point source one fish sample
had a level of 39 jug/kg for the whole fish, and a sample
of apples contained 90 jig/kg of polychlorinated naphthalenes
(Erickson, et al. 1978). Polychlorinated naphthalenes have
been detected in several samples of PCBs, compounds that
Trichloronaphthalene
Octachloronaphthalene
Tetrachloronaphthalene
Hexachloronaphthalene
Pentachloronaphthalene
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are known to be widely distributed in the aquatic environment.
Measurements of chlorinated naphthalenes in environmental
samples have not been widely performed using current sensitive
measurement techniques for these compounds.
Special Groups at Risk
Because of the possible potentiation of the toxicity
of higher chlorinated naphthalenes by ethanol and carbon
tetrachloride, individuals who ingest enough alcohol to
result in liver disfunction would be a special group at
risk. Individuals (e.g., analytical and synthetic chemists,
mechanics, and cleaners) who are routinely exposed to carbon
tetrachloride or other hepatotoxic chemicals would also
be at a greater risk than a population without such an expo-
sure. Individuals involved in the manufacture, utilization,
or disposal of polychlorinated naphthalenes would be expected
to have higher levels of exposure than the general population.
Basis and Derivation of Criterion
There are insufficient animal toxicity data available
on which to base a criterion for polychlorinated naphthalenes.
However, industrial exposure to vapors of polychlorinated
naphthalenes has resulted in systemic toxicity, and this
toxicity is the basis for the present ACGIH threshold limit
values (TLV). Such a TLV can be used as a basis for devel-
oping water criteria for polychlorinated naphthalenes.
It is recognized that the ACGIH TLVs apply primarily to
normal adult working males and do not incorporate safety
factors for sensitive populations. In order to provide
a reasonable margin of safety, calculation of an acceptable
C-21
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concentration of polychlorinated naphthalenes in drinking
water as proposed by Stokinger and Woodward (1958) should
include a safety factor of 100 as illustrated below:
TLV (mg/m3) ' 50 m3/wk = acceptable
7 days/wk • 100 intake
where 50 m /wk = average amount of air inhaled by a
normal adult in a 40 hour work week;
7 days/wk = conversion factor for daily intake;
100 = safety factor for sensitive populations
(NAS, 1977).
Since no pharmacokinetic data are available to compare
absorption efficiency by the inhalation route versus the
oral route, it is assumed that absorption efficiency is
the same by either route.
Using the ACGIH TLV levels, the acceptable daily intakes
for polychlorinated naphthalenes would be as follows:
Acceptable Daily
' Intake (mg)
Trichloronaphthalenes 0.36
Tetrachloronaphthalenes 0.14
Pentachloronaphthalenes 0.036
Hexachloronaphthalenes 0.014
Octachloronaphthalene 0.007
-------
Assuming an average intake of 18.7 g of fish per day
with a biomagnification factor of 4,800 for edible portions
of aquatic species as derived in the Exposure section, and
a water intake of 2 1/day, then criteria levels for the
above polychlorinated naphthalenes in water would be as
follows:
Criterion
Level (jug/1)
Tr ichloronaphthalenes
Tetrachloronaphthalenes
Pentachloronaphthalenes
3.9
1.5
0.39
0.15
0.08
Hexachloronaphthalenes
Octachloronaphthalene
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