TECHNICAL REPORT DATA
(Ftttte retd Ira tractions on the rtvtne before completing]
1. REPORT NO.
hPA/600/8-88/026
3. RECIPIENT'S ACCESSION NO
PB88-179379/AS
4. TITLE AND SUBTITLE
6. REPORT DATE
Health Effects Assessment for Dibenzofuran
«. PERFORMING ORGANIZATION CODE
'. AUTHOR(S)
I. PERFORMING ORGANIZATION REPORT NO
9. PERFORMING ORGANIZATION NAME ANO ADDRESS
10. PROGRAM ELEMENT NO.
11. CONTRACT/GRANT NO.
12. SPONSORING AGENCY NAME AND ADDRESS
Environmental Criteria and Assessment Office
Office of Research and Development
U.S. Environmental Protection Agency
Cincinnati. OH 45268
13. TYPE OF REPORT ANO PERIOD COVERED
14. SPONSORING AGENCY CODE
EPA/600/22
15 SUPPLEMENTARY NOTES
16. ABSTRACT
This report summarizes and evaluates information relevant to a preliminary interim
assessment of adverse health effects associated with specific chemicals or compounds.
The Office of Emergency and Remedial Response (Superfund) uses these documents in
preparing cost-benefit analyses under Executive Order 12991 for decision-making under
CERCLA. All estimates of acceptable intakes and carcinogenic potency presented in
this document should be considered as preliminary and reflect limited resources
allocated to this project. The intent in these assessments is to suggest acceptable
exposure levels whenever sufficient data are available. The interim values presented
reflect the relative degree of hazard associated with exposure or risk to the
chemical(s) addressed. Whenever possible, two categories of values have been
estimated for systemic toxicants (toxicants for which cancer is not the endpoint of
concern). The first, RfD^ or subchronic reference dose, is an estimate of an exposure
level that would not be expected to cause adverse effects when exposure occurs during
a limited time interval. The RfD is an estimate of an exposure level that would not
be expected to cause adverse effects when exposure occurs for a significant portion
of the lifespan. For compounds for which there is sufficient evidence of
carcinogenicity, qi*s have been computed, if appropriate, based on oral and
inhalation data if available.
17.
KEY WORDS AND DOCUMENT ANALYSIS
DESCRIPTORS
b.IDENTIFIERS/OPEN ENDED TERMS C. COSATI Field/Group
18. DISTRIBUTION STATEMENT
Public
19. SECURITY CLASS (This Report)
Unclassified
21. NO. Of PAGES
20. SECURITY CLASS (This page/
Unclassified
22. PRICE
EPA firm 2220.1 (Re*. 4-77) PREVIOUS COITION K OMOUCTC
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EPA/600/8-88/026
June, 1987
HEALTH EFFECTS ASSESSMENT
FOR DIBENZOFURAN
ENVIRONMENTAL CRITERIA AND ASSESSMENT OFFICE
OFFICE OF HEALTH AND ENVIRONMENTAL ASSESSMENT
OFFICE OF RESEARCH AND DEVELOPMENT
U.S. ENVIRONMENTAL PROTECTION AGENCY
CINCINNATI, OH 45268
-------
DISCLAIMER
This document has been reviewed In accordance with the U.S.
Environmental Protection Agency's peer and administrative review policies
and approved for publication. Mention of trade names or commercial products
does not constitute endorsement or recommendation for use.
11
-------
PREFACE
This report summarizes and evaluates Information relevant to a prelimi-
nary Interim assessment of adverse health effects associated with dlbenzo-
furan. All estimates of acceptable Intakes and carcinogenic potency
presented 1n this document should be considered as preliminary and reflect
limited resources allocated to this project. Pertinent toxlcologlc and
environmental data were located through on-Hne literature searches of the
TOXLINE and the CHEMFATE/DATALOG data bases. The basic literature searched
supporting this document 1s current up to May, 1986. Secondary sources of
Information have also been relied upon In the preparation of this report and
represent large-scale health assessment efforts that entail extensive peer
and Agency review. The following Office of Health and Environmental Assess-
ment (OHEA) sources have been extensively utilized:
U.S. EPA. 1983. Health and Environmental Effects Profile for
Tetra-, Penta- and Hexachlorodlbenzofurans. Prepared by the Office
of Health and Environmental Assessment, Environmental Criteria and
Assessment Office, Cincinnati, OH for the Office of Solid Haste,
Washington, DC.
U.S. EPA. 1985. Health and Environmental Effects Profile for
Bromlnated Dlbenzofuran. Prepared by the Office of Health and
Environmental Assessment, Environmental Criteria and Assessment
Office, Cincinnati, OH for the Office of Solid Waste and Emergency
Response, Washington, DC.
U.S. EPA. 1986c. Health Assessment Document for Polychlorlnated
Dlbenzofurans. Office of Health and Environmental Assessment,
Environmental Criteria and Assessment Office, Cincinnati, OH. EPA
600/8-86/018A. NTIS PB86-221256/AS. External Review Draft.
111
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ABSTRACT
There are no pertinent subchronlc, chronic, cardnogenldty, or repro-
ductive toxldty data on dlbenzofuran. Dlbenzofuran was not found to be
mutagenlc In reverse mutation assays and a 2-year bloassay of a related
compound (d1benzo-p-d1ox1n) did not result 1n treatment-related Increases 1n
tumor Incidence. It 1s recommended that a pharmacoklnetlc profile of oral
debenzofuran be developed and that subchronlc and reproductive toxldty
testing be Initiated. Also, further testing for mutagenlclty and clasto-
genldty In mammalian systems and short-term jjn vivo testing for carcino-
genic potential should be performed.
1v
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ACKNOWLEDGEMENTS
The Initial draft of this report was prepared by Syracuse Research
Corporation under Contract No. 68-03-3112 for EPA's Environmental Criteria
and Assessment Office, Cincinnati, OH. Or. Christopher DeRosa and Karen
Blackburn were the Technical Project Monitors and John Helms (Office of
Toxic Substances) was the Project Officer. The final documents In this
series were prepared for the Office of Emergency and Remedial Response,
Washington, DC.
Scientists from the following U.S. EPA offices provided review comments
for this document series:
Environmental Criteria and Assessment Office, Cincinnati, OH
Carcinogen Assessment Group
Office of A1r Quality Planning and Standards
Office of Solid Waste
Office of Toxic Substances
Office of Drinking Water
Editorial review for the document series was provided by the following:
Judith Olsen and Erma Durden
Environmental Criteria and Assessment Office
Cincinnati, OH
Technical support services for the document series was provided by the
following:
Bette Zwayer, Jacky Bohanon and Kim Davidson
Environmental CMteMa and Assessment Office
Cincinnati, OH
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TABLE OF CONTENTS
Page
1. ENVIRONMENTAL CHEMISTRY AND FATE 1
2. ABSORPTION FACTORS IN HUMANS AND EXPERIMENTAL ANIMALS 3
3. TOXICITY IN HUMANS AND EXPERIMENTAL ANIMALS 4
4. CARCINOGENICITY 5
5. REGULATORY STANDARDS AND CRITERIA 6
6. RECOMMENDATIONS 7
7. REFERENCES 8
v1
-------
LIST OF ABBREVIATIONS
DWEL Drinking water equivalent level
HA Health advisory
Koc Soil sorptlon coefficient
ppm Parts per million
RfD Reference Dose
SNARL Suggested-no-adverse-response level
UV Ultraviolet
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>. ENVIRONMENTAL CHEMISTRY AND FATE
The relevant physical and chemical properties and environmental fate of
dlbenzofuran are presented 1n Table 1-1.
In the atmosphere, dlbenzofuran has the potential to undergo direct
photolysis, which 1s due to UV absorption >290 nm, and H may react with
photochemlcally generated hydroxyl radicals (estimated vapor phase ty_ Is
-7 hours). (U.S. EPA, 1982, 1986a). Since part of the dlbenzofuran emitted
to the atmosphere may exist 1n the partlculate form, this part may, as a
constituent of coke dust, grate ash, fly ash, flame soots, etc., transport
over long distances because the partlculate sorbed compound 1s less likely
to undergo chemical reaction than the compound In the vapor state (U.S. EPA,
1982; Llgockl et al., 1985).
In water and soil systems, m1crob1al degradation appears to be the
dominant degradation mechanism of polynuclear aromatic compounds (Sims and
Overcash, 1983). In aqueous systems, dlbenzofuran should bloaccumulate
moderately In aquatic organisms and adsorb to suspended solids and sediments
(Lu et al., 1978, U.S. EPA, 1982; Bjoerseth et al., 1979). In the sorbed
state the compound Is Hkely to be persistent (Bjoerseth et al., 1979).
Estimated K values ranging from 1230-9940 Indicate that dlbenzofuran
should strongly adsorb to soil; however, dlbenzofuran has been detected In a
shallow aquifer under a creosote facility (Bedlent et al., 1984).
Pertinent data regarding human exposure to dlbenzofuran could not be
located 1n the available literature.
0088h -1- 11/26/86
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TABLE 1-1
Physical and Chemical Properties and Half-Lives for Dlbenzofuran
Property
Value
Reference
CAS number
Chemical class:
Molecular weight:
Melting point:
Boiling Point:
Vapor pressure:
Water solubility:
Log octanol/water
partition coefficient:
Bloconcentratlon factor:
Soil adsorption
coefficient (Koc)
Half-lives In
Air:
Water:
132-64-9
Polynuclear aromatic
168.20
82.8-83°C
276°C (760 mm Hg)
287°C (760 mm Hg)
~1.75xlO-2 mm Hg
-3 mg/l at 25°C
4.12
3.18
83, alga (Oedogonlum)
2860, snail (Physa)
947, fish (Gambusla)
1230-4150 (estimated)
9940 (estimated)
<1 day (estimated)
(vapor phase)
years
(adsorbed to sediments)
U.S. EPA, 1982
U.S. EPA, 1982
U.S. EPA, 1982
U.S. EPA, 1982
Hansch and Leo, 1985
Lu et a!., 1978
Lu et al., 1978
Lyman et al., 1982
Sabljlc, 1984
U.S. EPA, 1986a
Bjoerseth et al., 1979
0088h
-2-
11/26/86
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2. ABSORPTION FACTORS IN HUMANS AND EXPERIMENTAL ANIMALS
Pertinent data regarding the absorption of dlbenzofuran after oral or
Inhalation exposure could not be located In the available literature.
0088h -3- 11/26/86
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3. TOXICITY IN HUMANS AND EXPERIMENTAL ANIMALS
The U.S. EPA (1986c) reviewed several studies that Indicated that other
than a few subchronlc toxldty studies of PCDFs 1n rats, chicks and mice,
there are no studies of chronic toxldty. Two of three monkeys died on a
diet containing 5 yg/kg (food) administered over 6 months. It Is highly
probable that continuous exposure at low levels causes cumulative toxic
effects especially 1n view of the lesions observed 1n monkeys at an acute
dose that was <4% of the LD5Q (McNulty et a!., 1981). It appears likely
that PCflFs make a substantial contribution to the toxldty of commercial
PCBs and polychlorophenols.
Since the residence time of 2,3,7,8-T.CDF Is higher In guinea pigs
than other animals tested and guinea pigs are most sensitive to the toxic
effects of 2,3,7,8-T.CDF, loannou et al. (1983) studied bloaccumulatlon
and toxldty of 2,3,7,8-T.CDF 1n male Hartley guinea pigs.. Five- to
six-week-old animals weighing 360-430 g and 16- to 18-week-old adult animals
weighing -800 g were treated by gavage with 2,3,7,8-T CDF dissolved 1n a
mixture of emulphar:ethanol {1:1) diluted 8-fold 1n distilled water. Single
oral treatments of 10 or 15 yg/kg bw 2,3,7,8-T.CDF to adult animals
resulted In Immediate drastic weight loss and death within 2 4 weeks. In
young animals neither single treatments of 4 yg/kg bw nor multiple treat-
ments of 1 vg/kg bw/week for 4 weeks could produce any observable adverse
effects by day 36, when the animals were sacrificed. However, multiple
treatment of young animals with low doses totaling cumulative doses of
between 4 and 12 yg/kg resulted In death of 75X of the animals.
The administration of PCDFs Induces a number of hepatic enzymes, espe-
cially those using 3-methylcholanthrene as Inducer (Poland and Glover, 1974).
0088h 4- 01/27/87
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Structure/activity relationships of PCOFs were studied for the Induction of
AHH and 6-am1nolevul1n1c add synthetase activities 1n chick embryo. The
most acutely toxic Isomers are also the most potent Inducers of AHH
activity. The E05Q of 2,3,7,8-T4CDF on AHH Induction In the rat Is 0.5
yg/kg/day for 3 days (Poland et al., 1976).
Luster et al. (1979) exposed adult Hartley guinea pigs through Injestlon
to 0.05-1 yg/kg/week of 2,3,7,8-T.CDF 1n corn oil for 6 weeks to study
Its effects on Immune function. Thymus-to-body weight ratios were slightly
reduced 1n the 0.5 and 1.0 yg dosage groups. Cell-mediated Immune func-
tions were depressed for the 0.5 yg dosage group as Indicated by lympho-
cyte blastogenesls, delayed hypersensHlvlty reactions and production of
macrophage Inhibitor factors.
TeratogenlcUy
Teratogenlc activities of 2,3,7,8-T.CDF have recently been reported by
Weber et al. (1984) 1n mice. Pregnant C57B1/6N mice were given either a
single dose by gavage on gestation day 10 with 250, 500 and 1000 yg of
2,3,7,8-T CDF/kg bw or dally doses on gestation days 10 through 13 with
10, 30, 50 and 100 yg of 2,3,7,8-T CDF/kg bw. The chemical contained
>98% pure 2,3,7,8-T.CDF. The primary Impurities were found to be
PrCDFs. Each animal was given a total of 10 ml/kg bw at each treatment.
Though these doses were below toxic level to the dams, the animals receiving
dally doses on four gestation days had mild changes 1n liver cells char-
acterized by proliferation of the smooth endoplasmlc retlculum.
In this experiment, the authors found that single administration on
gestation day 10 with 250, 500 and 1000 yg/kg bw resulted In significant
(p<0.05) Increases In fetal mortality. In single as well as multiple dosed
groups there were significant (p<0.01) dose-related Increases In both Iso-
lated cleft palates, and hydronephrosls 1n the fetuses were observed.
0088h -5- 01/27/87
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In utero four exposures of 10 yg/kg/day resulted In significant (p<0.01)
Increases In hydronephrosls of the kidney. This was the lowest adverse
effect level observed 1n this experiment. The right kidney of the fetuses
seems to be affected more severely than the left kidney.
Teratogenlc effects of 2,3,7,8-T CDF have also been reported recently
In BXD recomblnant Inbred strains of mice by Hassoun et al. (1984). No
teratogenlc effects 1n humans have been observed.
Adverse Human Health Effects
The available Information on adverse health effects 1n humans comes
mostly from Japan where In 1968 many people ate rice oil (Yusho) that was
later found to be contaminated with PCBs and PCDFs. In 19681, some 1200
Japanese people consumed high levels of PCOFs 1n rice oil (Yusho) contami-
nated with 800-1000 ppm of a Japanese PCS formulation, Kanechlor 400, which
had leaked from a heat exchanger (Nagayama et al., 1975). This caused a
severe toxic reaction fcnown as Yusho episode. Symptoms of Yusho disease are
described 1n Table 3-1. Several months before this Incident, half a million
chicks were killed by a crude bran oil from the same origin as Yusho oil but
the warning went unheeded (Kohanawa et al., 1969). The composition of
Kanechlor 400 resembled that of Aroclor 1248. However, reports of the total
PCDF content varied greatly from Investigator to Investigator. Some general
symptoms Included the following: retarded growth, abnormal I1p1d metab-
olism, liver disturbances, acneform eruption, skin pigmentation and cutaneo-
mucosal lesions. Liver and adipose tissue of a few patients examined 4
years after the contamination showed retention of PCBs at ppb-ppm levels and
PCDFs at ppb levels. The 2,3,4,7,8-PCDF was found to be retained by the
liver at higher concentrations than other Isomers (Kuratsune et al., 1976;
Klmbrough, 1974).
0088h -6- 01/23/87
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TABLE 3-1
Symptoms of Yusho Disease*
Symptoms
Blackening of nails
Black spots In all pores
Excessive sweating 1n palms
Acnellke skin eruptions
Red spots on limbs
Itching
Change 1n skin color
Swelling of hands and feet
Stiffened soles 1n feet and palms of hands
Pigmentation of mucous membranes
Increased eye discharge
Hyperemla of mucous membranes 1n eyes
Transient visual disturbance
Jaundice
Swelling of upper eyelids
Sense of weakness
Numbness of hands and feet
Fever
Hearing difficulty
Spasms of hands and feet
Headaches
Vomiting
Diarrhea
Males
(X)
83.1
64.0
50.0
87.6
20.2
42.7
75.3
20.2 •
24.7
56.2
88.8
70.8
56.2
11.2
71.9
58.4
32.6
16.9
18.0
7.9
30.3
23.6
19.1
Females
(X)
75.0
56.0
55.0
82.0
16.0
52.0
72.0
41.0
29.0
47.0
83.0
71.0
55.0
11.0
74.0
52.0
39.0
19.0
19.0
8.0
39.0
28.0
17.0
*Source: Kuratsune et al., 1972; U.S. EPA, 1986c
0088h
-7-
01/26/87
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Hutaqenldty
Dlbenzofuran, 2,8-D-CDF, 3,6,-D.CDF, 2,3,7,8-T.CDF and OCDF are
2 d. A
not mutagenlc 1n any of the standard Salmonella strains (Schoeny, 1982).
A mixture of PCDFs containing 3-6 chlorines enhanced slster-chromatld
exchanges In Chinese hamster lymphocyte cultures at 0.1-1.0 mg/8. (Inoue et
al., 1979).
Q088h -8- 01/22/87
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4. CARCINOGENICITY
Animal
Close structural similarity of PCDFs to PCDDs, especially
2,3,7,8-T.CDD which Is a proven animal carcinogen, raises concern as to
the potential cardnogenldty of 2,3,7,8-T.CDF. However, no animal
cardnogenldty bloassay data on PCDFs are currently available 1n the
literature.
The NCI (1979) conducted 2-year d1benzo-p-d1ox1n feeding studies using
rats and mice. This compound Is structurally similar to dlbenzofuran. Rats
and mice of both sexes received 0, 5000, or 10,000 ppm; survivors were
sacrificed after 110-117 weeks (rats) or 91-97 weeks (mice) for hlstologlcal
analysis. Administration of the high concentration accelerated mortality
rate In female rats and mice, and mean body weight gains were generally
lower, which was due to treatment. Nonneoplastlc hepatotoxlc effects
(primarily fatty metamorphosis and necrosis) were concentration-related In
rats and female mice. There were also slight treatment-related Increases 1n
renal lesions, Including renal tubular dllutatlons (female rats) and
Interstitial Inflammation (female mice).
The U.S. EPA (1986c) noted that the biological activity of various
chlorinated dlbenzofurans varies greatly, so that risk assessment by analogy
to any of these more widely studied compounds would not be recommended.
Human
Amano et al. (1984) recently completed a 16-year cohort mortality study
of 1086 Yusho victims In Japan. The 581 males and 505 females sustained a
total of 70 deaths (42 males vs. 45.81 expected and 28 females vs. 31.3
expected). These data are based upon Japanese national death rates
0088h -9- . 01/26/87
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over age 40 through October 31, 1983. In this population, for persons over
40 years of age overall cancer mortality was greater than expected In men
but no difference 1n women. In male Yusho victims 19 cancer deaths occurred
vs. 11.50 expected and 1n female Yusho victims 7 cancer deaths occurred vs.
7.20 expected. However, by organ site, the risk of liver cancer was
consistently found to be high 1n both men and women during the entire
16-year observation period. Even after a 9-year latent period, the risk of
liver cancer In males was significant (observed = 5, expected ~ 0.75,
p<0.01).
As a result of an In-depth review of this study, 1t has been suggested
by CAG (U.S. EPA, 1986c) that a case could be made that PCBs as the compo-
nents of the PCOFs that caused the Yusho Incident In Japan may also have
been responsible for the statistically significant liver cancers seen 1n
these victims.
Dlbenzofuran should be classified as an EPA Group D (U.S. EPA, 1986b) or
an IARC Group 3 chemical. These categories are for compounds In which
evidence of animal cardnogenlcHy 1s Inadequate or limited and there are no
human data.
0088h -1:0- . 06/09/87
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5. REGULATORY STANDARDS AND CRITERIA
Pertinent guidelines and standards, Including EPA ambient air quality
criteria, drinking water standards, EPA or FAO/WHO AOIs (currently RfDs),
EPA or FDA tolerances for new agricultural commodities or foods, SNARLS,
HAs, OWELs, and ACGIH, NIOSH or OSHA occupational exposure limits could not
be located In the available literature.
The U.S. EPA (1975) determined an odor threshold of 120 vq/l for
dlbenzofuran. The U.S. EPA (1982) recommended that this level be considered
an ambient water criteria, based exclusively on organoleptlc properties.
0088h -11- 06/09/87
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6. RECOMMENDATIONS
Physical properties (vapor pressure at 25°C of 1.75xlO-2 mm Hg)
Indicate that dlbenzofuran may not constitute an 1nhalat1onal health hazard.
Olbenzofuran Is Hkely to persist 1n soil sediments and may bloaccumulate In
aquatic organisms. Oral exposure seems to be more environmentally relevant
than Inhalation exposure. Because of the sparslty of toxlcologlcal Informa-
tion, 1t 1s recommended that a complete pharmacoklnetic profile of oral
dlbenzofuran be developed 1n experimental animals. Appropriate subchronlc
and reproductive toxlclty testing using dietary dlbenzofuran should then be
Initiated. Although dlbenzofuran was negative for mutagenlclty 1n bacterial
reverse mutation assays (Schoeny, 1982) and the related d1benzo-p-d1ox1n was
not carcinogenic In 2-year feeding studies (NCI, 1979), mutagenlclty and
clastogenldty assays In mammalian systems and short-term j_n vivo cancer
blossays should be performed.
0088h -12- 01/22/87
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7. REFERENCES
Amano, M., K. Yag1, H. Nakajlma, R. Takehara, H. Sakal and G. Umeda. 1984.
Statistical observations about the causes of death of patients with oil
poisoning. Japan Hygiene. 39: 1. (Jap.)
Bedlent, P.B., A.C. Rodgers, T.C. Bouvette, H.B. Tomson and T.H. Wang.
1984. Ground-water quality at a creosote waste site. Ground Water. 22:
318-329.
Bjoerseth, A., J. Knutzen and J. Ske1. 1979. Determination of polycycllc
aromatic hydrocarbons 1n sediments and musselg from Saudafjord, W. Norway,
by glass capillary gas chromatography. Scl. Total Environ. 13: 71-86.
Hansch C. and A.J. Leo. 1985. Medchem Project Issue No. 26. Pomona
College, Claremont, CA.
Hassoun, E. R. d'Argy, L. Dencker, L.G. Lundln and P. Baswell. 1984.
Teratogenldty of 2,3,7,8-tetrachlorodlbenzofuran 1n BXD recomblnant Inbred
strains. Toxlcol. Lett. 23: 37-42.
Inoue, K., S. Tadayoshl, 0. Yosh1m1tsu, et al. 1979. S1ster-chromat1d
exchanges 1n Chinese hamster cells exposed to polychlorlnated blphenyls
(PCBs) and polychlorlnated dlbenzofurands (PCDFs). Osaka-furotsl Koshl
E1se1 Kenkyusho Kenkyu Hokoku, Shokuhln Elsel Hen. 9: 165-171.
0088h -13- 01/23/87
-------
loannou, Y.M., L.S. Blrnbaum and H.B. Matthews. 1983. Toxldty and
distribution of 2,3,7,8-tetrachlorodlbenzofurans In male guinea pigs. J.
Toxlcol. Environ. Health. 12: 541-553.
Klmbrough, R.D. 1974. The toxlclty of polychlorlnated polycycllc compounds
and related chemicals. CRC Grit. Rev. Toxlcol. 2: 445-498.
Kohanawa, M., S. Shoya, Y. Ogura, M. MoMwakl and M. Kawasaki. 1969.
Poisoning due to an oily by-product of rice bran similar to chick edema
disease. I. Occurrence and toxldty test. Natl. Inst. Animal Health Q.
(Tokyo). 9: 213-219.
Kuratsune, M., Y. Masuda and J. Nagayama. 1976. Some of the recent
findings concerning Yusho. Proc. Natl. Conf. Polychlorlnated- Blphenyls,
Chicago. November 19-21, 1975. U.S. EPA, Washington, DC. EPA-560/6-75-004.
p. 14-28.
L1gock1, M.P., C. Leuenberger and J.F. Pankow. 1985. Trace organic
compounds 1n ra1n-II. Gas scavenging of neutral organic compounds. Atmos.
Environ. 19: 1609-1617.
Luster, M.I., R.E. Faith and G. Clark. 1979. Laboratory studies on the
Immune effects of halogenated aromatlcs. Ann. N.Y. Acad. Sc1. 320: 473-486.
Lu, P.Y., R.L. Metcalf and E.M. Carlson. 1978. Environmental fate of five
radlolabeled coal conversion by-products evaluated 1n a laboratory model
ecosystem. Environ. Health Perspect. 24: 201-208.
0088h -14- 06/16/87
-------
Lyman, W.J., W.F. Reehl and D.H. Rosenblatt. 1982. Handbook of Chemical
Property Estimation Methods. McGraw Hill Book. Co., New York. p. 4-9.
McNulty, W.P., I. Pomerantz and T. Farrell. 1981. Chronic toxldty of
2,3,7,8-tetrachlorodlbenzofuran for rhesus macaques. Food Cosmet. Toxlcol.
19: 57-65.
Nagayama, 3., Y. Masuda and M. Kuratsune. 1975. Chlorinated dlbenzofurans
In Kanechlors and rice on used by patients with "Yusho" disease. Fukuoka
Igaku Zasshl. 66(10): 593-599. (Jap.) CA 84:100394m.
NCI (National Cancer Institute). 1979. Bloassay of d1benzo-p-d1ox1n for
possible cardnogendty. NCI Cardnogenesls. Tech. Rep. Ser. No. 122.
103 p. [Also published as DHEW Publ. No. (NIH) 79-1377]
Poland, A. and E. Glover. 1974. Comparison of 2,3,7,8-tetrachlorodlbenzo-
p-d1ox1n, a potent Inducer of aryl hydrocarbon hydroxylase, with 3-methyl-
cholanthrene. Molec. Pharmacol. 10: 349-359.
Poland, A., E. Glover and A.S. Kende. 1976. Stereospedf 1c, high affinity
binding of 2,3,7,8-tetrachlorodlbenzo-p-dloxln by hepatic cytosol. J. Blol.
Chem. 251: 4936-4946.
Sabljlc, A. 1984. Prediction of the nature and strength of soil sorptlon
of organic pollutants by molecular topology. J. Agrlc. Food Chem. 32:
243-246.
0088h -15- 06/16/87
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Schoeny, R. 1982. MutagenlcHy testing of chlorinated bliphenyls and
chlorinated dlbenzofuran. Mutat. Res. 101: 45-46.
S1ms, R.C. and M.R. Overcash. 1983. Fate of polynuclear aromatic compounds
(PNAS) 1n soil-plant systems. Residue Reviews. 88: 1-68.
U.S. EPA. 1975. Aqueous odor threshold of organic pollutants 1m Industrial
effluents. 20 p. EPA 660/4-75-002. NTIS PB242734.
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