United States
Environmental Protection
1=1 m m Agency
EPA/690/R-07/012F
Final
6-11-2007
Provisional Peer Reviewed Toxicity Values for
Dibenzofuran
(CASRN 132-64-9)
Superfund Health Risk Technical Support Center
National Center for Environmental Assessment
Office of Research and Development
U.S. Environmental Protection Agency
Cincinnati, OH 45268

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Acronyms and Abbreviations
bw	body weight
cc	cubic centimeters
CD	Caesarean Delivered
CERCLA	Comprehensive Environmental Response, Compensation and Liability Act
of 1980
CNS	central nervous system
cu.m	cubic meter
DWEL	Drinking Water Equivalent Level
FEL	frank-effect level
FIFRA	Federal Insecticide, Fungicide, and Rodenticide Act
g	grams
GI	gastrointestinal
HEC	human equivalent concentration
Hgb	hemoglobin
i.m.	intramuscular
i.p.	intraperitoneal
IRIS	Integrated Risk Information System
IUR	inhalation unit risk
i.v.	intravenous
kg	kilogram
L	liter
LEL	lowest-effect level
LOAEL	lowest-observed-adverse-effect level
LOAEL(ADJ)	LOAEL adjusted to continuous exposure duration
LOAEL(HEC)	LOAEL adjusted for dosimetric differences across species to a human
m	meter
MCL	maximum contaminant level
MCLG	maximum contaminant level goal
MF	modifying factor
mg	milligram
mg/kg	milligrams per kilogram
mg/L	milligrams per liter
MRL	minimal risk level
MTD	maximum tolerated dose
MTL	median threshold limit
NAAQS	National Ambient Air Quality Standards
NOAEL	no-observed-adverse-effect level
NOAEL(ADJ)	NOAEL adjusted to continuous exposure duration
NOAEL(HEC)	NOAEL adjusted for dosimetric differences across species to a human
NOEL	no-observed-effect level
OSF	oral slope factor
p-IUR	provisional inhalation unit risk
p-OSF	provisional oral slope factor
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p-RfC
provisional inhalation reference concentration
p-RfD
provisional oral reference dose
PBPK
physiologically based pharmacokinetic
PPb
parts per billion
ppm
parts per million
PPRTV
Provisional Peer Reviewed Toxicity Value
RBC
red blood cell(s)
RCRA
Resource Conservation and Recovery Act
RDDR
Regional deposited dose ratio (for the indicated lung region)
REL
relative exposure level
RfC
inhalation reference concentration
RfD
oral reference dose
RGDR
Regional gas dose ratio (for the indicated lung region)
s.c.
subcutaneous
SCE
sister chromatid exchange
SDWA
Safe Drinking Water Act
sq.cm.
square centimeters
TSCA
Toxic Substances Control Act
UF
uncertainty factor
Hg
microgram
(.imol
micromoles
voc
volatile organic compound
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PROVISIONAL PEER REVIEWED TOXICITY VALUES FOR
DIBENZOFURAN (CASRN 132-64-9)
Background
On December 5, 2003, the U.S. Environmental Protection Agency's (EPA's) Office of
Superfund Remediation and Technology Innovation (OSRTI) revised its hierarchy of human
health toxicity values for Superfund risk assessments, establishing the following three tiers as the
new hierarchy:
1.	EPA's Integrated Risk Information System (IRIS).
2.	Provisional Peer-Reviewed Toxicity Values (PPRTV) used in EPA's Superfund
Program.
3.	Other (peer-reviewed) toxicity values, including:
~	Minimal Risk Levels produced by the Agency for Toxic Substances and Disease
Registry (ATSDR),
~	California Environmental Protection Agency (CalEPA) values, and
~	EPA Health Effects Assessment Summary Table (HEAST) values.
A PPRTV is defined as a toxicity value derived for use in the Superfund Program when
such a value is not available in EPA's Integrated Risk Information System (IRIS). PPRTVs are
developed according to a Standard Operating Procedure (SOP) and are derived after a review of
the relevant scientific literature using the same methods, sources of data, and Agency guidance
for value derivation generally used by the EPA IRIS Program. All provisional toxicity values
receive internal review by two EPA scientists and external peer review by three independently
selected scientific experts. PPRTVs differ from IRIS values in that PPRTVs do not receive the
multi-program consensus review provided for IRIS values. This is because IRIS values are
generally intended to be used in all EPA programs, while PPRTVs are developed specifically for
the Superfund Program.
Because new information becomes available and scientific methods improve over time,
PPRTVs are reviewed on a five-year basis and updated into the active database. Once an IRIS
value for a specific chemical becomes available for Agency review, the analogous PPRTV for
that same chemical is retired. It should also be noted that some PPRTV manuscripts conclude
that a PPRTV cannot be derived based on inadequate data.
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Disclaimers
Users of this document should first check to see if any IRIS values exist for the chemical
of concern before proceeding to use a PPRTV. If no IRIS value is available, staff in the regional
Superfund and RCRA program offices are advised to carefully review the information provided
in this document to ensure that the PPRTVs used are appropriate for the types of exposures and
circumstances at the Superfund site or RCRA facility in question. PPRTVs are periodically
updated; therefore, users should ensure that the values contained in the PPRTV are current at the
time of use.
It is important to remember that a provisional value alone tells very little about the
adverse effects of a chemical or the quality of evidence on which the value is based. Therefore,
users are strongly encouraged to read the entire PPRTV manuscript and understand the strengths
and limitations of the derived provisional values. PPRTVs are developed by the EPA Office of
Research and Development's National Center for Environmental Assessment, Superfund Health
Risk Technical Support Center for OSRTI. Other EPA programs or external parties who may
choose of their own initiative to use these PPRTVs are advised that Superfund resources will not
generally be used to respond to challenges of PPRTVs used in a context outside of the Superfund
Program.
Questions Regarding PPRTVs
Questions regarding the contents of the PPRTVs and their appropriate use (e.g., on
chemicals not covered, or whether chemicals have pending IRIS toxicity values) may be directed
to the EPA Office of Research and Development's National Center for Environmental
Assessment, Superfund Health Risk Technical Support Center (513-569-7300), or OSRTI.
This document has passed the STSC quality review and peer review evaluation indicating
that the quality is consistent with the SOPs and standards of the STSC and is suitable for use by
registered users of the PPRTV system.
INTRODUCTION
RfD and RfC values for dibenzofuran (DBF) were not available on IRIS (U.S. EPA,
2007) or in the HEAST (U.S. EPA, 1997). There is a Class D cancer assessment on IRIS (U.S.
EPA, 2007). Dibenzofuran was included in a Drinking Water Toxicity Profile from 1992 (U.S.
EPA, 1992), although no oral toxicity value was listed. The Office of Water did not include
dibenzofuran on the latest Drinking Water Regulations (U.S. EPA, 2006a) or the Drinking Water
Contaminant Candidate List (U.S. EPA, 2006b). The CARA list (U.S. EPA, 1991, 1994)
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included a Health Effects Assessment (HEA) (U.S. EPA, 1987) and a Reportable Quantity
Document (U.S. EPA, 1989) for Dibenzofuran. The HEA concluded that additional toxicity
testing was necessary and did not derive a toxicity value due to the lack of data (U.S. EPA,
1987). The 1987 HEA for Dibenzofuran neither identified nor included discussion of Thomas et
al. (1940), the primary source of data used in this PPRTV document. By contrast, the 1989
Reportable Quantity Document for Dibenzofuran (U.S. EPA, 1989) used Thomas et al. (1940) as
the basis for derivation of composite scores and the corresponding reportable quantities for
dibenzofuran.
ATSDR had not published a Toxicological Profile for dibenzofuran (ATSDR, 2006).
NTP did not study the toxicity of dibenzofuran (NTP, 2006). WHO (2006) provided no relevant
information. Available data on carcinogenicity, mutagenicity, metabolism, and other biological
effects were summarized for dibenzofuran by the National Cancer Institute (NCI, 2000). Data
on the adverse health effects of various halogenated dibenzofurans were available; however, the
biological activity varies greatly among these congeners. U.S. EPA (1986a) did not recommend
risk assessment by analogy to any of these more widely studied chemicals. NCI (2000) reported
that the most structurally related chemical was dibenzo-p-dioxin. NCI (1979) reported that no
excess tumors were induced in rats or mice fed dibenzo-p-dioxin up to 10,000 ppm in the diet.
Updated literature searches for noncancer and cancer data were conducted for data
available through April 2006. The databases searched included: TOXLINE, MEDLINE,
CANCERLIT, CCRIS, TSCATS, HSDB, RTECS, GENETOX, DART/ETICBACK, and
EMIC/EMICBACK. Inhalation RfC values were not derived for dibenzofuran, because no
human or animal inhalation data were found and the marginal ingestion data seemed inadequate
to consider for inter-route extrapolation. However, a subchronic oral p-RfD value was derived,
based on a LOAEL point of departure (POD) in Thomas et al. (1940). Chronic toxicity of
dibenzofuran is discussed in the appendix. No data were identified from which to derive cancer
risk values.
REVIEW OF PERTINENT DATA
Human Studies
Two cross-sectional studies of exposed workers were identified in the OPPT TSCATS
database (Koppers 1980a,b). However, these studies reported exposures to dibenzofuran only in
complex mixtures of coal tar products. Neither report noted adverse health effects that could be
attributed to dibenzofuran exposure. Existing review documents and a detailed literature search
identified no other data regarding the toxicity of dibenzofuran in humans.
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Animal Studies
The only long-term toxicity data available for dibenzofuran were from a 200-day rat
feeding study reported by Thomas et al. (1940). However, this document also will address the
NCI (1979) data for dibenzo-p-dioxin, which NCI (2000) considered to be the chemical most
structurally related to dibenzofuran.
NCI (1979) reported that unsubstituted dibenzo-p-dioxin, a structural analog of
dibenzofuran, exhibited very low toxicity and no evidence of carcinogenicity in Osborne-Mendel
rats and B6C3F1 mice, even when the maximum tolerated dose was approached (10,000 ppm in
diet). Groups of 35 rats of each gender ingested dibenzo-p-dioxin at 5000 or 10,000 ppm in diet
for 110 weeks. Groups of 50 mice of each gender ingested the same doses for 87 or 90 weeks.
Controls consisted of groups of 35 untreated rats of each gender and 50 untreated mice of each
gender. Mean body weights of the dosed male and female rats and mice were lower than those
of the corresponding controls; the depression in the amount of weight gained in the dosed male
mice was, however, relatively slight. Except for the male rats, survival at the end of the bioassay
was lower in the dosed groups of both rats and mice than in the corresponding control groups. At
week 90, at least 57% of the rats and 54% of the mice were still alive. In some male and female
rats there was a dose-related increase in the incidence of hepatotoxic alterations characterized by
fatty metamorphosis or necrosis. Also in mice, toxic hepatic lesions including liver degeneration,
necrosis, fibrosis and/or cirrhosis were observed in slightly increased numbers in the dosed mice
— particularly in the high-dose females. No tumors were induced in rats or mice of either gender
at incidences that were significantly higher in the dosed groups than in the corresponding control
groups. The authors concluded that unsubstituted dibenzo-p-dioxin exhibited very low toxicity
and was noncarcinogenic in Osborne-Mendel rats and B6C3F1 mice, even when the maximum
tolerated dose was approached (10,000 ppm in diet).
The Thomas et al. (1940) report consisted of two studies, a primary 200-day
dibenzofuran feeding study and a follow-up 78-day study. In the primary study, groups of five
female albino rats (strain not specified), approximately 30 days old, consumed 0, 250, 500, 1000,
2000, or 4000 ppm of dibenzofuran in their food for 200 days. In addition, two female rats
consumed 8000 ppm of dibenzofuran in their diet for a shorter period (approximately 100 days).
According to the authors, none of the animals exhibited any abnormal activity or behavior, nor
was food intake appreciably altered by dibenzofuran administration, although it was noted that
the rats receiving dibenzofuran tended to consume more water than controls. The authors also
reported no effect on body weight gain at any dose during the exposure period; however,
decreases in body length and absolute organ weights were observed in all dibenzofuran-exposed
groups at necropsy. The authors also reported that the treated animals had unusually large
amounts of abdominal fat, which they interpreted as accounting for the lack of effect on body
weight gain. Quantitative data were not provided to support the assertions of no appreciable
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changes in food intake or body weight gain, decreases in organ weight and overall length, and
excess abdominal fat. In addition, the authors did not report whether a dose-response effect was
observed for changes in body length or organ weight, or for excess abdominal fat.
Histological examination of the liver, kidney, spleen, heart, and adrenals was performed
in rats exposed to dibenzofuran at 500 ppm and higher, and in the control animals (Thomas et
al., 1940). The low dose group (250 ppm) apparently was not examined for histopathology. In
the kidney, histological examination of rats exposed to concentrations of 500 ppm and higher
revealed fine, brown-pigmented granules in the epithelial cells of proximal convoluted tubules in
the deeper parts of the renal cortex. This effect was noted among all rats receiving dibenzofuran,
and both the amount of pigmented material within cells and the frequency of occurrence among
cells increased with dose of dibenzofuran. In addition, the two rats fed diet containing 8000 ppm
dibenzofuran exhibited prominent, irregular dilatation of the collecting tubules with coagulated
material resembling protein; other tubules in these two rats were slightly dilated and contained
more granular and amorphous material than controls. These effects were reported as occurring
without cellular degeneration or glomerular abnormalities. Some (frequency not specified) of
the kidneys from rats receiving 4000 ppm showed similar, but less severe, changes. These
lesions were not reported among rats fed the lower doses of dibenzofuran. However,
quantitative data were not reported. In the spleen, slight hyperplasia of the Malpighian bodies
was reported among several rats (frequency not given) in the 4000 and 8000 ppm groups. No
alterations, other than reduced organ weight, were noted in the liver, heart, or adrenals of the
treated rats.
In the follow-up study to determine whether dietary dibenzofuran affected water balance,
an effect noted qualitatively (increased water consumption) in female rats receiving
dibenzofuran in their food, Thomas et al. (1940) exposed groups of five male rats (average initial
body weight 255 grams) to 0 or 5000 ppm of dibenzofuran in the diet for 78 days. Treated rats
exhibited greater water consumption and urine output than controls, suggesting that
dibenzofuran altered water balance. The excess in urine output was greater than the excess in
water consumption in the treated group, suggesting a slight dehydration of tissues. The authors
reported that no alterations in hematological parameters were observed (hemoglobin and
erythrocyte, leukocyte, and reticulocyte counts). Tables 1 and 2 have summarized the
hematological data reported in the 78-day study.
TABLE 1. Blood cell types in rats exposed to DBF in normal diet for 78 days
Dose
Rats "N"
Hemoglobin
Erythrocytes
Reticulocytes
White cells
0
10
16.3%
8.12 x 106
3.0%
1.44 x 104
5000 ppm
5
16.6%
9.07 x 106
2.35%
1.65 x 104
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TABLE 2. Average differential white blood cell counts in 78-day exposed rats
vs. "normal rat blood"
Dose
Rat
s
"N"
Lymphocytes
Polymorphonuclear
nutrophils
Monocytes
Basophiles
Eosinophils
"Normal"
...
67.9%
27%
5.3%
0.77%
2.1%
5000
ppm
5
63.8%
33.5%
1.18%
0.64%
0.94%
In contrast to qualitative observations reported among the female rats exposed to similar
concentrations in the 200-day primary study, the male rats treated for 78 days tended to consume
less food than the controls and had a slightly lower rate of body weight gain than the control
group. These data and water consumption data are summarized in Table 3. The authors noted
that the odor and taste of dibenzofuran at 5000 ppm in the food was distinctly noticeable and
may have contributed to this effect. Histological examination was not performed on tissues from
these rats.
TABLE 3. Weight gain in male albino rats fed DBF for 78 days vs. controls
Dose
Rats "N"
Weight gain
Food ingestion
Water ingestion
0
5
321 g
6108 g
9652 cc
5000 ppm
5
243 g
5482 g
10,316 cc
Difference

78 g (24%)
626 g (10%)
664 cc (6.9%)
The literature search revealed additional, peripheral data for dibenzofuran, including
those for soil nitrification organisms (Sverdrup et al., 2002), drought resistance of certain insects
(Sjursen et al., 2001), plant seedling growth (Sverdrup et al., 2003), fungi-specific enzyme
systems (Kurihara et al., 2002), and a study of human intellectual effects of exposure (Schantz,
2001) that mistakenly refered to unhalogenated dibenzofuran. Abstracts for these studies
reported the following conclusions.
• 75 mg DBF/kg (soil) NOEL for soil nitrification and no effects on soil bacterial
diversity (Sverdrup et al., 2002)
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No dose-related decrease in drought tolerance in adult soil-dwelling insects,
Folsomia fimetaria (Sjursen et al, 2001)
20% reduction in plant seedling weight when exposed to 43-93 mg DBF /kg soil
(Sverdrup et al, 2003)
No change in expression of NADH-ubiquinone oxidoreductase (NUO) among DBF-
exposed fungus, Phanerochaete chrysosporium (Kurihara et al., 2002)
DERIVATION OF A PROVISIONAL SUBCHRONIC ORAL
RfD VALUE FOR DIBENZOFURAN
The only subchronic or chronic toxicity data available for dibenzofuran were from the
200-day and 78-day feeding studies described by Thomas et al. (1940). These studies, though of
apparently high quality for their era, had a number of major short comings, including the
following:
•	only qualitative data were reported for most endpoints
•	only five organs were examined in the pathology
•	the lowest dose group was not subjected to pathology examinations
No pertinent developmental or reproductive data were found for dibenzofuran. The
LOAEL data from the Thomas et al. (1940) 200-day feeding study provided the POD for this
derivation, because no NOAEL was reported. Data from the 78-day study were used to confirm
food ingestion rates estimated using default rates in U.S. EPA, 1986b. Benchmark dose
modeling was considered infeasible because adverse effects and the dose-response nature of the
response were reported only qualitatively.
The lowest dose tested in the 200-day Thomas et al., 1940 study, 250 ppm in diet, was
selected as the LOAEL POD for the aggregate critical effects of reduced length and organ
weight, and excess abdominal fat. Ingestion data from the 78-day study was used to estimate the
actual doses to the animals treated at the LOAEL, as follows. The 78-day feeding study was
conducted under the same conditions as the 200-day primary study. This estimation made the
following assumptions.
•	Data from the 78-day study (Thomas et al., 1940) were more likely to represent
actual food intakes than the default reference food factor from U.S. EPA, 1986b
•	Rats in the 200-day study (Thomas et al., 1940) eating a diet treated with 250
ppm dibenzofuran consumed quantities of food closer to the control amounts
(6108 g/diet/5 rats) than to the quantities of food treated with 5000 ppm
dibenzofuran (5482 g/5 rats) in the 78-day study
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•	Growth of rats eating the 250 ppm diet in the 200-day study (Thomas et al.,
1940) more closely approximated controls than those eating 5000 ppm, and that
the 78-day weight provided a reasonable average weight for the 200 day study
period.
In the 78-day study, Thomas et al. (1940) reported that a group of 5 control rats ingested
a total of 6108 grams of food over the 78 days and grew from 1.273 kg to 1.594 kg/group, while
experimental rats ingested 5482 g of food treated with 5000 ppm dibenzofuran and grew from
1.274 kg to 1.517 kg/group of 5 treated rats. The following calculations used food consumption
data from the 78-day study to estimate dibenzofuran consumption in the 200-day study at the
POD (250 ppm) for the critical effect of reduced length and organ weight, and excess abdominal
fat among the exposed rats.
(6108 g diet/5 rats) / 78 days = 78.3 g/diet/5 rats/day
(78.3 g/5 rats/day) x (250/106) = 0.0196 g DBF/5 rats/day = 19.6 mg/5 rats/day
19.6 mg DBF/5 rats/day / (1.594 kg/5 rats) = 12.3 mg DBF/kg/day
The estimated dibenzofuran dose of 12.3 g/kg/day was essentially the same as the dose of 12.5
g/kg/day calculated using the EPA default reference food factor (U.S. EPA, 1986b).
Based on the data available, the following uncertainty factors were applied to derive a
subchronic oral p-RfD.
•	10 for variability in human susceptibility
•	10 for the uncertainty in animal-to-human extrapolation
•	1 for using data from a 200-day study (in rats) to derive a subchronic p-RfD
•	3 (10°5) for using a minimal LOAEL instead of a NOAEL
•	10 for deficiencies in the database, including the lack of reproductive and
developmental data, and the minimal data details reported in the key study
The uncertainty factors noted above provide a composite UF of 3000 (103 5).
In the absence of a NOAEL, a LOAEL could be several orders of magnitude above the
actual no adverse effect dose, since it merely represents the lowest dose tested. Nevertheless, the
uncertainty factor for using a minimal LOAEL instead of a NOAEL was reduced from 10 to 3
(100 5) because the following findings suggested that the smaller uncertainty factor would be
more appropriate in this case. While many of the dose levels tested and the organism effects
considered in the following reports would be difficult to relate to humans, together they seem to
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emphasize the relatively low toxicity and mild effects of dibenzofuran across a variety of
species.
•	The Thomas et. al (1940) study noted relatively minor effects in rats, even at very high
doses, up to thirty times the LOAEL dose selected as the POD
•	Peripheral data in other species indicated very minor effects or no effects among
organisms exposed to dibenzofuran
•	75 mg DBF/kg (soil) NOEL for soil nitrification and for soil bacterial diversity
(Sverdrup et al, 2002)
•	No dose-related decrease in drought tolerance in the adult soil-dwelling insects,
Folsomia fimetaria (Sjursen et al, 2001)
•	20% reduction in plant seedling weight when exposed to 43-93 mg DBF /kg soil
(Sverdrup et al, 2003)
•	No change in expression of NADH-ubiquinone oxidoreductase (NUO) among
DBF-exposed Phanerochaete chrysosporium fungi (Kurihara et al, 2002)
•	NCI (1979) reported no tumors and relatively low toxicity among rats and mice fed diets
containing 5000 ppm and 10,000 ppm dibenzo-p-dioxin, a structural analog to
dibenzofuran. Effects reported were hepatic lesions, slight reductions in weight gain and
nephropathy (in male rats)
Applying the composite UF of 103 5 (-3000) to the dietary LOAEL POD of 12.3 mg
DBF/kg-day for the combined critical effects of reduced length and organ weight and excess
abdominal fat observed in female albino rats allowed the following calculation of the subchronic
p-RfD.
Subchronic oral p-RfD = LOAEL / (UF x MF)
= (12.3 mg/kg/day) / (103 5x 1)
= 4x10"3 mg/kg-day
= 4 (j,g dibenzofuran/kg-day
The data were insufficient to derive a chronic oral p-RfD value using an acceptable
composite uncertainty. However, the Appendix of this document contains a Screening Value
that may be useful in certain instances. Please see the attached Appendix for details.
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DERIVATION OF PROVISIONAL INHALATION
RfC VALUES FOR DIBENZOFURAN
Provisional inhalation RfC values were not derived for dibenzofuran because no useful
inhalation exposure data were identified and data were insufficient to attempt inter-route
extrapolation from the marginal ingestion data.
STATEMENT OF CONFIDENCE
Confidence in the principal study is low. Thomas et al. (1940) examined a number of
endpoints, including histological examination of several major organs. The study had an
adequate number of dose groups, but was limited by inclusion of only five rats in each group.
Although only female rats were used for the 200-day portion of the study, male rats were used
for the shorter water balance study (78 days). Thomas et al. (1940) did not report whether the
critical effect selected displayed a dose-response relationship. However, the reductions in
growth and organ weights, and the increase in abdominal fat were supported by histological
changes noted in the kidney and impairment of water balance at higher doses. Because the
critical effects were observed among rats receiving the lowest dose tested, one cannot be certain
that the effects noted at 250 ppm (12.5 mg/kg-day), would not have been present at lower doses.
Thus, it is uncertain whether 250 ppm is a true LOAEL. Confidence in the database and the
resulting RfDs is low because of the limited toxicity data base for dibenzofuran, including lack
of human studies and chronic, developmental, or reproductive oral animal studies. However,
some confidence is gained from the relatively low toxicity and lack of tumors among rats and
mice fed high doses of dibenzo-p-dioxin (NCI, 1979), the chemical identified by NCI (2000) as
most structurally related to dibenzofuran. Nevertheless, risk managers are advised to consider
any other available data before applying this p-RfD.
Suppliers and users of dibenzofuran should be encouraged to conduct toxicology studies,
such as that initiated by EPA in 1978 (NCI, 2000) but then terminated because of lack of
funding. The absence of inhalation, toxicokinetic, and metabolic data would justify especially
encouraging studies to seek such information.
REFERENCES
ATSDR (Agency for Toxic Substances Disease Registry). 2006. Toxicological Profile
Information Sheet. U.S. Department of Health and Human Services, Public Health Service,
Atlanta, GA. Examined May 2, 2006. Online, http://www.atsdr.cdc.gov/toxpro2.html#-D-
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Koppers Company. 1980a. 1979 Cross-Sectional Health Study of Workers at the Garwood, Hew
Jersey Plant of Koppers Company, Inc. (unpublished).
Koppers Company. 1980b. 1979 Cross-Sectional Health Study of Workers at the Chicago,
Illinois Plant of Koppers Company, Inc. (unpublished).
Kurihara, H., H. Wariishi and H. Tanaka. 2002. Chemical stress-responsive genes from the
lignin-degrading fungus Phanerochaete chrysosporium exposed to dibenzo-p-dioxin. FEMS
microbiology letters (Netherlands). 212(2): 217-20.
NCI (National Cancer Institute). 1979. Bioassay for Dibenzo-p-Dioxin for Possible
Carcinogenicity (CAS No. 262-12-4). Technical Report Series No. 122; NIH Publ. No.79-1377,
Research Triangle Park, NC. p. 1-122. http://ntp.niehs.nih.gov/ntp/htdocs/LT rptsZtrl22.pdf
NCI (National Cancer Institute). 2000. Summary of Data for Chemical Selection: Dibenzofuran.
December 12, 2000. Online.
http://ntp.niehs.nih.gov/ntp/htdocs/Chem Background/ExSumPdf/Dibenzofuran.pdf
NTP (National Toxicology Program). 2006. Testing Status: Dibenzofuran. Examined May 2,
2006. Online.
http://ntp.niehs.nih. gov/index.cfm?obiectid=6DE08B91-FlF6-975E-7C2FCEB6EE6E83AA
Schantz, S.L. 2001. Developmental neurotoxicity of PCBs: overview and update.
Neurotoxicology. 22(1): 140.
Sjursen, H., L.E Sverdrup and P.H. Krogh. 2001. Effects of polycyclic aromatic compounds on
the drought tolerance of Folsomia fimetaria (Collembola, Isotomidae) Environ. Toxicol. Chem.
20 (12): 2899-2902.
Sverdrup, L.E., F. Ekelund, P.H. Krogh, T. Nielsen and K. Johnsen. 2002. Soil microbial toxicity
of eight polycyclic aromatic compounds: Effects on nitrification, the genetic diversity of
bacteria, and the total number of protozoans. Environ. Toxicol. Chem. 21 (8): 1644-1650.
Sverdrup, L.E., P.H. Krogh, T. Nielsen, C. Kjaer and J. Stenersen. 2003. Toxicity of eight
polycyclic aromatic compounds to red clover (Trifolium pratense), ryegrass (Lolium perenne),
and mustard (Sinapsis alba). Chemosphere. 53(8): 993-1003.
Thomas, J.O., R.H. Wilson and C.W. Eddy. 1940. Effects of continued feeding of diphenyl
oxide. Food Res. 5:23-30.
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U.S. EPA. 1986a. Health Assessment Document for Polychlorinated Dibenzofurans. 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, EPA-600/8-86/018A.
U.S. EPA. 1986b. Reference Values for Risk Assessment. 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. 1987. Health Effects Assessment for Dibenzofuran. 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. 1989. Reportable Quantity Document for Dibenzofuran. Prepared by the Office of
Health and Environmental Assessment, Environmental Criteria and Assessment Office,
Cincinnati, OH for Office of Solid Waste and Emergency Response, Washington, DC,
U.S. EPA. 1991. Chemical Assessments and Related Activities (CARA). Office of Health and
Environmental Assessment, Washington, DC, April.
U.S. EPA. 1992. Drinking Water Toxicity Profiles. Human Risk Assessment Branch (WH-
586). Office of Science and Technology, Office of Water, Washington, DC, September 1992.
OHEA-I-127. NTIS/PB93-122406. p. 17-22.
U.S. EPA. 1994. Chemical Assessments and Related Activities (CARA). Office of Health and
Environmental Assessment, Washington, DC, December 1994.
U.S. EPA. 1997. Health Effects Assessment Summary Tables. FY-1997 Update. Prepared by
the Office of Research and Development, National Center for Environmental Assessment,
Cincinnati, OH for the Office of Emergency and Remedial Response, Washington, DC, July,
1997. EPA/540/R-97/036. NTIS PB 97-921199.
U.S. EPA. 2006a. Drinking Water Regulations and Health Advisories. Examined May 11,
2006. Online. http://www.epa.gOv/ogwdw/mcl.html#mcls
U.S. EPA. 2006b. Drinking Water Contaminant Candidate List. . Examined May 11, 2006.
Online, http://www.epa.gov/ogwdw/ccl/index.html
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U.S. EPA. 2007. Integrated Risk Information System (IRIS). Office of Research and
Development, National Center for Environmental Assessment, Washington, DC. Examined May
2, 2006. Online, http://www.epa.gov/iris/
WHO (World Health Organization). 2006. WHO website Search. Examined May 11, 2006.
Online, http://www.who.int/research/en/
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APPENDIX
DERIVATION OF A SCREENING VALUE FOR
DIBENZOFURAN
For reasons noted in the main PPRTV document, it is inappropriate to derive provisional
toxicity values for Dibenzofuran, chronic RfD. However, information is available for this
chemical which, although insufficient to support derivation of a provisional toxicity value, under
current guidelines, may be of limited use to risk assessors. In such cases, the Superfund Health
Risk Technical Support Center summarizes available information in an Appendix and develops a
"Screening Value." Appendices receive the same level of internal and external scientific peer
review as the PPRTV documents to ensure their appropriateness within the limitations detailed
in the document. In the OSRTI hierarchy, Screening Values are considered to be below Tier 3,
"Other (Peer-Reviewed) Toxicity Values."
Screening Values are intended for use in limited circumstances when no Tier 1, 2, or 3
values are available. Screening Values may be used, for example, to rank relative risks of
individual chemicals present at a site to determine if the risk developed from the associated
exposure at the specific site is likely to be a significant concern in the overall cleanup decision.
Screening Values are not defensible as the primary drivers in making cleanup decisions because
they are based on limited information. Questions or concerns about the appropriate use of
Screening Values should be directed to the Superfund Health Risk Technical Support Center.
The Thomas et al. (1940) study provided insufficient data to derive a chronic oral p-RfD
value with uncertainty in an acceptable range. The 200-day rat minimal LOAEL POD of 12.3
mg/kg-day was considered to derive a screening chronic oral reference dose by applying a
composite uncertainty factor of 10,000 (104), including 10 for variability in human susceptibility,
10 for animal-to-human extrapolation, 3 (100 5) for extrapolating from 200-day rat data to a
chronic screening value, 3 (10°5) for using a minimal LOAEL instead of a NOAEL, and 10 for
deficiencies in the database, including the lack of developmental data and the minimal data
details reported in the key study.
Applying the minimal LOAEL dietary POD of 12.3 mg DBF/kg-day and the composite
uncertainty factor of 10,000 (104) allowed the following calculation:
Screening chronic oral p-RfD = LOAEL/UF
= (12.3 mg/kg-day)/104
= 1x103 mg/kg-day
= 1 (j,g dibenzofuran/kg-day
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Confidence in the key study was low, because of the lack of detail on the critical effects
and other deficiencies noted in this document. Given the lack of additional studies, confidence in
the database also was low, leading to low overall confidence in the screening toxicity value. Users
are advised to consider any other available data and to consult with the STSC before using this
screening p-RfD.
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