PartMt: *; ..
i* Waato Managaaiant System,
[d«ntifkartton and Uating of
Waatai Notiea off Data Avafiabmty and
ftaquaat for Comments? Supptomant to
Proposed Rule
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18024
Fedora! Register / Vol. 53. No. 97 / Thursday. May 19. 1988 / Proposed Rules
ENVIRONMENTAL PROTECTION
AGENCY
40 CFR Part 261
(FRL33CS-4J
Hazardous Waste Management
System, Identification and Listing of
Hazardous Waste: U«r of « Generic
Dilution/Attenuation factor for
Establishing Regulatory Levels and
Chronic Toxicity Reference Level
Revisions
AGENCY: Environmental Protection
Agency.
ACTION: Notice of data availability and
request for comments; supplement to
proposed rule.
SUMMARY: On June 13.1986, the
Environmental Protection Agency
proposed to amend its hazardous waste
identification regulations under Subtitle
C of the Resource Conservation and
Recovery Act (RCRA) by modifying the
existing Toxicity Characteristic used by
watte generators in determining
whether their solid wastes are
hazardous. As proposed in 1988, the new
Toxicity Characteristic was to be based,
in part, on using chronic toxicity
reference levels along with compound-
sptdfic dilution/attenuation factors
(DAFs) for each of the constituents.
Today's notice solicits comment on an
alternative strategy for setting the DATs
in the Toxicity Characteristic, proposed
on June 13,1988. This notice also
presents revised values and new
information on 14 of the 38 chronic
toxidty reference levels proposed in the
June 13,1938 notice.
DATE: EPA will accept public comments
on this notice until July 5, 198&
ADOftXfSts: One original and three
copies of all comments, identified by the
Docket Number F-88^TCNN-FFFFF
should be sent to the following address:
EPA RCRA Docket (S-212), U.S.
Environmental Protection Agency (WH-
582). 401 M Street SW.. Washington. DC
20460. The EPA RCRA docket is located
in the sub-basement araa-at the above
address, and is open from 9:30 a.m. to
3:30 p.m.. Monday through Friday.
excluding Federal Holidays. To review
docket materials, members of the public
must make an appointment by calling
(202) 475-9327. A maximum of SO pages
of material may be copied from any one
regulatory docket at no cost Additional
copies cost S.20/page.
FOR FUftTHtn INFORMATION CONTACT;
For general information contact the
RCRA Hotline by calling (800) 424-8346
toll-free, or (202) 382-3000. For
information on specific aspects of this
notice, related to the use of a generic
DAP* contact John W. Goodrich-
Mahoney (202) 475-8551 and for the
chronic toxicity reference level
revisions, contact Lisa A. Ratcliff (202)
332-T61. Office of Solid Waste (WH-
562). U.S. Environmental Protection
Agency. 401 M Street. SW. Washington
DC 20460.
SUPIHJMCNTAflY INFORMATIONS
I. Background
II. Discussion of Revisions and Request for
Comments
A. Use of Generic Dilution/Attenuation
Factor
B. Chronic Toxicity Reference Level
Revisions/Data Availability
1. Background
2. Revisions and New Data
III. References
I. Background
Section 3001 of the Resource
Conservation and Recovery Act
(RCRA). as amended, requires EPA to
identify wastes that pose a hazard to
human health and the environment if
improperly managed, One means for
doing this is through identification of
characteristics of hazardous wastes; one
approach in developing characteristics .
is fur the Agency to determine
reasonable mechanisms by which harm
to human health or the environment
might occur, develop models to establish
regulatory levels, and specify methods
for testing the wastes. Characteristics
are established at levels providing a
high degree of certainty that a waste is
hazardous. Thus, a characteristic level is
not intended to be a threshold
identifying hazard but a level that is
dearly hazardous. The Agency may
decide to list other wastes as hazardous
based on the criteria set forth in 40 CFR
281.11.
The Extraction Prcc ,-ure (EP)
Toxicity Characteristic (EPTC) [40 CFR
261.24] has been used to identify wastes
with the potential to produce leachate
containing significant concentrations of
toxicants if the wastes would be
disposed in a sanitary landfill with
municipal trash and garbage (/.&.
codisposal). The Extraction Procedure
(EP) test described in detail in 40 CFR
Part 261. App. II is the laboratory
procedure used to estimate teachability.
Wastes are considered hazardous under
the existing Toxicity Characteristic if
their EP test leachate concentrations
exceed the regulatory levels that are
specified. These levels are set so 'hat
National Interim Primary Drinkic '
Water Standards (DWS) will not a»
exceeded at down-gradient drinking-
water wells: the EPTC assumes the* . •
toxicants will be diluted and/or
attenuated during ground water '
transport by a factor of 100.
On June 13.1986 [51 FR 21648!. the " •-.,
Agency proposed to amer.d :he EPTC
by: (1) Expanding the characteristic to
include 38 additional organic
constituents. (2) introducing a modified
leaching procedure. Method 1311
(referred to as the Toxicity
Characteristic Leaching Procedure or
TCLP) and (3) applying compound-
specific dilution/attenuation factors
(DAFs) for each organic constituent
while retaining the 100-fold dilution/
attenuation factor for the inorganic
constituents.
The Agency's June 1986 proposal
contemplated that state-of-the-art
ground water modeling would allow the
Agency to determine specific DAF's for
each of the organic constituents in the
Toxicity Characteristic. The various
DAFs were to be calculated from a
ground water transport model
incorporating compound-specific
hydrolysis and soil adsorption data.
coupled with parameters describing a
generic underground environment (e.g.,
ground water flow rate, soil gorosity.
ground water, pH, etc.). f
EPA propose^ to use thesejcompouud-
specific DAFs to estimate theVparticubr
reduction in concentration to be
expected for each organic constituent
during transport in the ground water to e
drinking-water source. These values f
would be used in establishing regulatory
levels for organic constituent
concentrations in TCLP (Method 1311)
leachate. For each organic constituent.
the Drinking Water Standard, reference
dose, or risk-specific dose, as
appropriate, would be multiplied by a
specific DAF to establish the regulatory
level. Wastes producing leachate
concentrations above the regulatory
levels would potentially produce
unacceptable toxicant levels at a
drinking water source, and thus would
exhibit the Toxicity Characteristic and
be regulated as hazardous waste.
Wastes producing leachate
concentrations below the regulatory
levels would not exhibit the toxicity
characteristic and would not be
hazardous with respect to that
characteristic.
The Agency has received many
comments on the June 1986 proposal and
will address those comments and
publish revisions to the ground water
transport model and other aspects, of the
proposal at a later time. However, the
Agency is today soliciting comment on
•an alternative approach by which the
Agency would initially regulate certain
wests! with high concentrations of
hazardous constituents while this work
-------
/ Vot. -SS, Na. 9E / TJkBMday.
18B8 /
continues. Th* Agency i*ai*o presentinf
revise&valuejfcand new information on •
14 of the 38 chronic toxicity reference
levels proposed in-ti»*B4fle 1938 notice.
II. DfscussionYof i
forGdmmentftr
kandi'Request
'
..
/I- £foe of aGeneric:DiiutJGn/ .
Attenuation Factor
The Agency is evaluating alternative
approaches for establishing dilution/
attenuation factors (DAFs) for the 38
additional toxic organic constituents
proposed in the Toxicity Characteristic
in June 1986.
One alternative involves setting DAFs
for these constituents in two phases. In
the first phase, the Agency would use a
generic DAF that is sufficiently high to
assure regulative in the short-term of
those wastes with high concentrations
of hazardous constituents. The use of a
• generic" DAF to determine regulatory
levels is notnewto the Agency; a
generic DAF of 100 has been a -'
component of the EPTC [45 FR 33110],
for both organic and inorganic
, con*tittt*nt»t sine* 1980.
The Agency is considering applying
th*^en*rieDAF to those 38 additional
traiocorguik constituent* propoMd for
inclusion; in tfa*TG on Jen* 13. 1988.
Todays itothwdoMrnot affect th*
current regulatory l*vels for the EP
constituent* Th* Agency is not
considering changing the DAF for th*EF
constituents at this time;
fa th* second phas*.' the Agency
would address further the manner in
which DAFs are used to set regulatory
levels* Toe second phase is expected to
result in regulatory levels that an lowers
than: those in this first phase, and thus
. all wastes identified as hazardous in tbs>
first phase will remain classified as
hazardous after completion of th*
second phase. For the second phase.
EPA may. continue to use generic OAF'S,
employ a ground water transport modst
to develop constituent-specific DAFs, ot
use a combination of the two
approaches* '.?^^^i«-
The Agency>isr«MM»Bsidering
promulgating th»Tj^iB one phase, with
use df a generic DAW aidiscussed
above. EPA balieveS* two-phase
approach for promulgating the revised
Toxicity Characteristic is consistent
with sections 3001 (g) and (h) of the
Hazardous and Solid Waste
Amendments of 1984 (HSWA) and the
legislative history of these provision*,
which state that the EPA should take all
necessary action to revise expeditiou*ly
the Toxicity Characteristic {Conference
Report No. 98-1138 (9Bta Congress, 2nd
Session) at 105-108). TW* appnucli
allows th* Agency to proceed with on*
level of regulation as qmclkly as possible
in keeping with its Congressional':
mandate;
The selection of a generic DAF also
allows EPA to expeditiously identify
those wastes .with High concentrations
of hazardous constituents. The Agency
intends to use a sufficiently high DAF
- such that wastes, which are regulated as
hazardous in the first phase, should also
be regulated as hazardous in the second
phase.
Based on the above discussion, the
Agency specifically requests comment
on a two-phased approach, wherein
those wastes with the highest
concentrations of hazardous
constituents would be identified in the
first phase, the most appropriate
dilution/attenuation factor to use under
the two generic phased approach, and
the basis for choosing that DAP. The
Agency specifically solicits comment on
the use of a generic DAF in the first
phase of 100 or 300. . / u
F • - • -"-. ,^iij** •
B. Chronic ToKictty Reference Laval
Revisions/Data Availability",, •• '•"•
1. Background ' .'' ";". '.'"!' .'""'''"
On June 13, 1988 [51 FR 21848J. tb* -
Agency proposed to amend that*, v-. - .
Extraction Procedure Toxicity .-j«: ,;x . .
Characteristic by expanding tb*^?
characteristic to include 3* additional
toxicants, and, using chronic tenacity
referane* levels (combined wttfc
compound-specific. dUutisn/attenuation
. factors)i.t0 calculate leachaftesv
concentration omit* for undivida*!
toxicants which would define * waste
as hazardous. Specifically. BPA^
proposed to us* either too National
while to* value* for aeryjdnitriie«:
chlordane, chlorofornu heptachior, and
methylene chloride have beea revised -
based on changes to their RSD's.
TABLE 1.—SUMMARY OF REVISED CHBON-
sc TOXICITY REFERENCE LEVELS FOR
PROPOSED TOXICITY CHARACTERISTIC:
CONTAMINANTS •
Contaminant
PropOMd-"
chronic
toxicity
Acrytonitrife..
CMORtew
HtptKHor.
MtttiytaMcMaride..
2.3.4.6=
tetraeMD
phtnofc.
V«n*cWorWfc.
0.002
OJX&:
0.005
0.75
O.OOOT
4-
0.075
ftSWMtf
0.0007
0.0003
o.o»-
0.075
0.0000V-
0.05 .
0.0*
;ao(»s;;'
• June 13.19B«f 51FR 21(M«;
It should be noted that in tl
lS98rTC notto* EPA [
apportionaMars
•*'""
Standard (NIPDW3) or the Maximum
Contaminant Lavei 94CL& wher*
available, as th* startiog point tat
establishing (h* reguktory level for each
of th* contaminants. For tbos* toxicants
where NIPDWS or MCL's haw net bean
established, ihe Agency proposed to use
Risk-Specific Dose* (RSO's) for the
carcinogens and Reference Dose*
(RfD's) for the noncarcinogenso
Today's notice presenta revised
chronic toxicity reference level* for a
number of the contaminants thesa
change* (as shown in Tal»l* 1) are
explained in detail below. To v
summarize, the chronic toxicity
reference levels for vinyl chloride and
1.4-dichlorobenz*n* haw been revised
since the MCL's promulgated for th*s*
compounds [July 8, 1987: S3 FR 25MOJ
differ fraa thos* prop*Md 9«ov*abw
13, 198ft MFR 4880X4. Pi»ot.ps«idta*»
and 2A4.8-tnteadriaroplHMtlMmi
different rhrnnin iuatiuty nfavsan*
value* based on changes to their Rftts.
*« -'^w IMWPW* • **^**»fi^'^ •• • «
not addces* sidi*f tn* nra^o**d/
apportionment schawortbircB
risk Ivrsis of conceca: EPA wilt respaod
to tha r*i*t*d commen** <• th* finci ral*.
Th«re
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J8028 Federal Regbte / Vol. §3. No. 97 / Thursday. May 19. 1968 / Proposed Rulea
comments regarding the derivation of
»h« MCL's themselves, or the
appropriateness of the usa-of MCL's as
chronic toxicity refe.'v.-.r* >v<*Ss ;.EPA
ie TC
proposal.}
Chronic Tox.c::y Reference Level:
EPA is revising the chron:c toxicity
reference level for 1.4-dichkirobenzene
from 0.75 to 0.075 ms.'L since the
promulgated MCL differs from the
proposed MCL In particular, on
November 13. 1985. EPA promulgated a
Recommended Maximum Contaminant
Level (RNiCL). now called Maximum
Contaminant Level Goal (MCLG). for
1.4-dlchlerobenzene of 0.7Ji mg/L and
proposed an MCL of 0.75 mg/L [50 FR
46880 and 50 FR 46902. respectively].
The MCLG and proposed MCL were
based on 1,4-dichlorobenzene's
classification as a Group D compound.
I.e.. a chemical not classified or for -
which there is inadequate animal
evidence of carcinogenicity. This
classification resulted from the Agency's
assessment of several negative
careinogenidty studies in rata and mice.
including one chronic inhalation study.
and several subchronic inhalation and
gavage studies. A suggested RfD of 0.1
mg/kg/day for 1.4-dichlorobenzene was
calculated, using a'no-observed-
adverse-effect-level (NOAEL) of 150 mg/
kg/day identified in a Battelle (1980)
subchronic gavage study in rata. and an
overall uncertainty factor of 1000. which
was employed to account for inter- and
intraspecies extrapolation (10 each) and
use of data from an exposure duration
significantly less than lifetime (10). The
MCLG and the proposed MCL were
based on the RfD. a relative source
contribution factor of 20 percent for
drinking water, and body weight and
consumption values of 70 kg and 2 L
water per day. respectively.
Since that time, the Agency received
the results of a long-term study on 1.4-
dichlorobenzene conducted by the
National Toxicology Program (NTP). The
NTP (1988) study was a chronic oral
gavdge bioassay utilizing F344'rats and
B5C3F1 mice. The NTP concluded that
there was evidence of carcinogenicity
both for male rats as shown by an
increased incidence of renal tubular cell
adenocarcinomas. and for mice of both
sexes as shown by increased incidences
of hepatocellular carcinomas and
hepatocellular adenomas. No evidence
of carcinogenicity was seen in female
rats. Based on this new Liformation.
EPA proposed to amend 1.4-
dichlorobenzene's MCLG to zero and
reproposed its MCL at 0.005 mg/L on
April 17.1987 [52 FR 12878). Specifically.
the Agency proposed to reclassify 1.4-
dichlorohenzene as a Group B2
carcir.caeri. However, the r.otics also
indicated '.hat E.FA was considering
classifying 1.4-dichl-jrobenzene tn Group
C instead of Group B2. Thus, the Agency
asked for public comment on the
appropriate classification based on the
weight of evidence.
On July 8.1987 [52 FR 25690). EPA
promulgated an MCL of 0.075 mg/L for
1,4-dichiorobenzene. Because of the
limited evidence of carcinogenic.ity. the
Agency decided to classify 1.4-
dichlorobenzene as a Group C
carcinogen, and as such, its MCLG and
MCL were based on noncarcinogenic
endpoints. using the RfD of 0.1 mg/kg/
day with an additional uncertainty
factor of 10. the relative source
contribution factor of 20 percent, and
body weight and consumption values of
70 kg and 2 L water per day.
respectively. The application of an
additional uncertainty factor to the RfD
in deriving MCLG's and MCL's for
Group C carcinogens is Agency policy
(50 FR 48902, November 13.1985]. Thus.
the revised chronic toxicity reference
level for 1.4-dichlorobenzene, 0.075 mg/
L is the promulgated MCL: it is a factor
of 10 lower than the original proposed
MCL of 0.75 mg/L
Vinyl Chloride
Chronic Toxicity Reference Level:
EPA is revising the chronic toxicity
reference level for vinyl chloride from
0.001 to 0.002 mg/L since the
promulgated MCL differs from the
proposed MCL Based on the statutory
(Safe Drinking Water Act) directive for
setting MCL's. the Agency derives
MCL's from an assessment of a range of
pertinent factors, including the
availability and performance of the
"best available technology" (BAT), the
costs of these technologies for different
size water systems, and the number of
water systems that would have to install
these technologies. The Agency also
evaluates the availability of analytical
methods and the reliability of analytical
results, as well as the resulting health
risks of various contaminant
concentration reduction levels
attainable by BAT. (For more
information on the Agency's process for
deriving MCLG's and MCL's. see 52 FR
46880 and 52 FR 46902. November 13.
1985: see also 52 FR 25690. July 8.1987.)
The "practical quantitation level" (PQL)
is the lowest level that can be reliably
achieved within specified limits of
precision and accuracy during routine
laboratory operating conditions. For
vinyl chloride. EPA originally
established the PQL at 0.001 mg/L and
thus proposed an MCL of 0.001 mg/L for
vinyl chloride on November 13.1985 [50
FR 46902). The chronic tcxicity reference
level in the June 13: 1986:. TC pr-pcs.ii •-
was based on tias proposed MCL. The
Agency subsequer:!v increased ;ht- PQL
for vinyl chloride to 0.002 mg/ L. and on
July 8, 1987. promulgated an MCL based
on this higher PQL [52 FR 25690|. Thus.
the revised chronic toxicity reference
level for vinyl chloride is 0.002 mg/L
Phenol
Chronic Toxicity Reference Level:
EPA is modifying the chronic toxicity
reference level for phenol from 4 to 1
mg/L because the RfD has been revised.
In particular, the Agency's RfD
Workgroup verified a new RfD of 0.04
mg/kg/day on October 28.1986 [1]. This
RtD is based on a Dow Chemical Co.
(1945) study in which slight kidney and
liver pathology was observed in rats
administered phenol by gavage for 6
months. Groups of 10 rats were gavaged
with 0. 50, or 100 mg/kg of phenol. 5
days/week (estimated as 0. 35.7. or 71.4
mg/kg/day on a 7-day basis) until 135 or
136 doses were administered, after
which surviving animals were killed for
histopathologicai^xamination of the
target organs. The" animals receiving 71.4
mg/kg/day of phenol showed a greater
temporary drop in body weight gain
than did the other groups, but the group
rapidly recovered. Surviving animals (6/
10) in this group showed a very slight
amount of cloudy swelling of the liver.
while four animals had some kidney
damage. In the animals that survived (6/
10) treatment with 35.7 mg/kg/day
phenol, there were two that showed a
slight amount of kidney damage;
Mortality was not treatment related. The
low dose (35.7 mg/kg/day) was judged a
lowest-observed-adverse-effect-level
(LOAEL).
The original RfD of 0.1 mg/kg/day.
which was used to derive the chronic
toxicity reference level of 4 mg/L in June
13.1986. TC proposal was based or. the
same study and LOAEL as the new RfD.
However, the new RfD was culr-.-lated
using a larger, overall uncertainty factor
(1000 vs. 500) to account for '.he
uncertainties of concern, i.e.. 10 for the
uncertainty in the interspecies
conversion. 10 for the uncertainty in the
range of human sensitivity, and 10 for
the uncertainty in the use of a less-than-
chronic study. Although a LOAEL
instead of a NOAEL was used in
deriving the RfD, an extra uncertainty
factor was not considered necessary
because of the minimally severe effects
at the low dose. Thus, the revised
chronic toxicity reference level for
phenol. 1 mg/L is calculated using the
-------
F«dMi Register / VoL S3,-.No, 97 / Thursdays May: m:l98fr/
18327
new RfD of 0.04 mg/kg/day and body
weight and consumption values .of 70 kg
and 2 L water per day,* respectively.
the June 13,
comment».were ^,^-.___..__..
recommended tha^K^useJjhie National
Cancer Institute (1980J oral-subchronic
and chronic studies as the basis of the.
RfD for phenol. Specifically, the
commenters criticized the Agency's? - .
selection of the Dow study for two
reasons: (1) the study is unpublished
and has not been peer reviewed, and (2)
the gavage route of administration
employed is not relevant for drinking-
water use. Both commenters asserted
that the National Cancer Institute (NCI)
studies are more relevant for the RfD
determination since the animals were
administered phenolindrinking water.
Agency, Response: The Agency
maintain's-that the Dow study is the
appropriate basis .for the phenol RfD. Kf^
Specifically; EPA disagrees witfi 'the ^
commenters'argument that a gavage
study is not relevant for the
development of an oral1 RfD; the gavage
route of 'administration is a well- m,
established and widely-used means of ^<;;
determining; the toxicity of ingested
substances. However, the RfD
Workgroup: did consider all known
relevant studies before verifying the
RfD. Including the NCI studies. In the 99-~
day NCI subchronic test, no effects in
the liver, kidneys, or any other organs
were observed in mice (1,700 mg/kg/
day) and in rat*|780 mg/kg/day) that
received various doses of phenol in
drinking water. Mice and rats were also
exposed to phenol in drinking water for
103 weeks, and the animals were ..- •
observed for a subsequent 2 weeks;
Mice and rats treated with 313 and 153
mg/kg/day phenol, respectively, showstL
decreased weight gain and reduced -
water intake. In addition, male and
female rats at the 344 mg/kg/day dose
had significantly increased incidences of,
chronic kidney inflamation. The LOAEL- -
identified in the clinic NCI test is 344 ,
mg/kg. It is a sda|i*Ypolicy of the-
Agency to identtf^ilt critical endpoint
used in npncanceggdosg-response
assessments as the one associated with
the highest NOAEL which lies below the
lowest LOAEL or the lowest LOAEL
Therefore, the RfD Workgroup chose to
use the gavage study of Dow since it
produced the lower LOAEL (35.7 mg/kg)
EPA acknowledges the commenters'
criticism that the Dow study is
unpublished, and thus not readily
available. The Agency is attempting to
remedy this problem by placing the
study report along with the IRIS
chemical file for phenol, in the RCRA - -
docket. As for the commenters*
assertion that the study has not been
peer reviewed, the Agency believes that
the study has undergone a thorough
internal review by the RfD Workgroup.
However. EPA welcomes any further
public comment concerning the study
report .
Pyridine.
Chronic Toxicity Reference Level:
EPA is modifying the chronic toxicity
reference level for,pyridine from 0.075 to
0.04 mg/L because the RfD haabeen
revised. The original RfO of 01002 mg/
kg/day was verified on fuly 8.1985,
based on a oubchronic inhalation, study
in rats that was reported iii the 1983
Encyclopedia of Occupational Safety
and Health [2.J. Confidence Jr. the study
was low because of a lack of details
about the study and the identification of
a free-standing LOAEL (2.15 mg/kg/day)
'only. Because of concern regarding
reported neorptoxic symptoms '.'
associated with short-tann, low-level
cJccupational exposure ttfpyridiije
[Encyclopedia of Occupational Safety
hepattclasforiif i» males; bftnir high-dose
group. (SO mg/kg/dayrconipJSi'fed-with 10-
percent incidence in the vefiicie control ;
group. The 0.25 and 1.0 mg/k'g/day dose;"
male rats also showed a lOtpercent ;
incidence of these lesions: however, no-
such lesions were observed in th&lOor
25 mg/kg/day dose groups. In the
females, the frequency of incidsnce of
these lesions was 30 percent in the 50
mg/kg/day group and 10 percent in the
vehicle control group. Based on the data
presented above, the 1 mg/kg/day was
identified as a NOAEL and 10 mg/kg/
day asra LOAEL for hepatic-hypertrophy
in female rats. '.,'"!;.'.' .
ThuSi the RfD Workgroup, verified a
new RfO of 0.001 mg/kg/day^fot-:
pyridine bnAugustilS, 1987 Raising thi
NOAEL of 1 mg/kg/day anid: an owerallr
^p'orted ia
• signs .ifCN^rfllat
"'
rat$*and'izuGer ,—~~
• sponsored »Sttbcttwlu¥oW;--' - - •$=&•
•n«niotojffd«istuaysii?}tt6i JArthur D,
IB thi*«tcidyv Sprague-Oiwley rats, 1O
animals/sen/dbse; were gaViged daily U
with 0,02571.10.25. anid 50mg/kg/day
pyridine forSO days. Data generated
from thi* test included body and organ
weights, food consumption, '•-'
hematologteatand clinical dSemistry
panmetatv^bphthalmologieai
evaluation^ and histopathological
examination* of target organs. Results of
this testindicated a signifiant dose-
ralatedincreaoe in the female Uver-to-
body weight ratios in the1ft 29% and 50
mg/kg/day dose groups* The males of .
the 1 mg/kfl/day dose group showed a
significant decrease in the relative liver
weights. However, the male»in other
dose groups did not show-any: '-
significant differences; thus* this effect
in males exposed to 1.mg/kg/day
pyridine is probably an artifact.
In order to. examine the neurotoxidty
of pyridine. 10 rats/group were perfused
at the time of sacrifice; histopathological
examinations of brain, liver and target
organs were conducted. The?
histopathological examinations did not/
reveal any morphological alterations-in
the brains of exposed and unexposed
animals. However, histopataologicsl
evaluations of target organs showed a
70-percent incidence of non-neoplastic
Agency /tefjwns«rTh« Agencyw
acknowledges that tha;originai RfD was;
, based on a study m wUcfcconfidenca
toxicity test waoa better study •'•>
(although it was available only a* a
draft at that time). Howeve** aa -;:•»
mentioned above* the Agency felt that
the possible CNS^elatedtoxicity of
pyria1n*warraated further tasting.-
EPA's-subchroaic nearotcodcity study
produced aNOAEt of 1 mg/kg/day.
while the NTPsubchronic study resulted
above the LOAEL of. 10 mg/kg/day
identified in EPA's nearotoxicity study.
Thus* in accordance with' Agency; <;;
science policy, utilixation of the higher
25 mg/kg/day NOASL would not have
been snffldentfy protecttye sine* -
advene effects wen demonstrated at a
lower exposure levet T!B» Agency's
neurotoxicity stody and the IRIS-
chemical file for pyridine are available
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18028
FedacaJ Register / Vol. 53, No. 97 / Thursday, May 19. 1966 / Proposed Rales
for review in the RCRA Docket: copies
of tha study are also available from the
National Technical Information Service.
or rlTIS (Nos. PB88-176136 and PB88-
176144).
Chronic Toxicity Reference Level:
EPA is modifying the cnror.ic toxicity
reference level for 2.3.4.6-
tetrachlorophenol from 0.4 to l mg/L
because the RfD has been revised. In
particular, on fury 8.1985. the Agency's
RfD Workgroup verified an RfD of 0:01
mg/kg/day based on a no-observed-
effect-level (NOEL) of 1O mg/kg/day
identified in a 55-day oral gin-age study
(Mattula et aL 19ffl) mrats [3L
However, an inadequate stody design
(few animals per group) aad imparities
associated with tkc coamcnial grade
2,3.4.8-tetraoWoroptiCToi wed i» *ra
study raised some •coacerai about the
validity of the data «mig toxicity reference
level.
Ageacy Response: in the June 13,1986.
TC proposal. EPA apparently was not
sufficienttgr clear in ejq>ktnmg what.
kind of preliminaey data it used to
establish Che Rffl far -2A48-
tetrachiorapheaoL At thai time, the
Agency already had * veaBad KS3
baaed on theHaitoiaataL study!
Howevee. Qu> Agajacgr Uti. U wo*j#l b«
prudent to ooosidar £ha JUD "kiMrim"
until the xasate of th« aiove-mentioned
subchionic iankiiy aad teratoiagy
studlcn Tircra Irrtitivm Thaae stadies and
the IRIS dainucai£le Jar Z3,43-
review ia A* SOLA Dfldirt; copies of
the tezatolqgy Jriudy -aoe ahu> available •
from NTiS (Noa. PB88-17ai51 and PB88-
176169}.
ChraMUS Taxictiy Reference Level:
The chronic toxicity reference level for
tsobutanol is mot being changed from the
value {10-mg/LJ presented in the June 13.
1986. TC proposal. However. EPA is
taking this appartuiuty to make
available for review and comment the
results *f a «ubchcQnic sfcidy which
served as the basis for the RfD that the
Agency's RfD Workgroup verified cm
May 14. 1986 [4], shortly before the TC
proposal was published. In order to
evaluate the toxicity of iaobutanoi. the
Office of Solid Wwte sponsored a 90-
day study hi Sprague-Oawley rats
(Toxicitjr Research Laboratories. 1986).
Thirty animala/iex/doae were
administered daily doses of 0, 100, 316,
or 1.000 mg/k8/day isobutanol by
gavage. No effect «a body weight or
clinical andTmtapathalogical
parameteai waaobaervad atdoaes less
than or equal to 316 aag/kg/iay.
Treatment at the high doM £U880 mg/
kg/ day) ueaWltad ia a miner decrease in
-------
Vol.,53; No. 9? / Thursday, May 19. I98fr/ Proposed Rules
18029
body weight gain during week 2 and "
decreased serum potassium.lavels and
hypoactivity, Hypoactivity was the most
frequently ofaserved,clinjcal sign. It
occu rred1 in evervij|pHsti;h;el.OQtt mg/ kg/
hypoactivity wa9j$§ij^edJj? decreased
by week 4 and oeeurfect'anly'
sporadically theredfteK Ataxia-was also
seen at low incidence in the 1.000 mg/
kg/day dose group throughout the study.
The NOEL was identified as 316 mg/kg/
day,, and an overall uncertainty, factor of
1.000 was applied to it to derive an RfD
of 0.3 mg/kg/day. The uncertainty factor
accounts for the uncertainties in. the
interspecies conversion (10), the range
of human sensitivity (10). and the use of
a less-than-chronic NOEL (10). Thus, the
chronic toxicity reference level foe
isobutanol. 10 mg/L is calculated using
the verified RfD of &3 mg/kg/day and
body weight and consumption values of
70 kg and 2.L water per day.
respectively^, ~ '.''""" ^.,.
Comment Summary: In response to
the JunelS, 198(fctC proposal, three
' comments Wenrreceived that pointed
out that EPA was proposing a regulatory
level for isobutanol. despite stating thaf^
theexisting'data Wewinsufficient for "
I «n BIP/lSl FR 21665]. The
I disagreed with the
Agency-1* decision to set a regulatory
teveMc«isbbiitaRbtufa% preliminary
testing-d* tai and tfcej^qoestfoned the
basis of thVchronfe trodciry reference a
mg/kg/day for mixed cresols based on a
TLV-TWA of 10 mg/m3 [5j. This-TLV
was based on a report of a Russian
study ([Uzhdavine et al.. 1972) in which
rats and guinea pigs were exposed to o-
cresol. However, the report lacks
experimental details, such as 'he size of
the experimental groups. Thus, the
Office of Solid Waste sponsored 90-day
subchronic studies and 90-day
neurotoxicity studies for each isomer.
In the oral subchronic studies
(Microbiological Associates, 1986),
Sprague-Dawley rats. 30 animals/sex/
dose, were administered by gavage the
following doses for 90 days; o-cresol at
0. 50,175, or 600 mg/kg/day; m-cresol at
0, 50.150, or 450 mg/kg/day; p-cresol at
0, 50.175, or 600 mg/kg/day. In the
neurotoxicity studies (Toxicity Research
Laboratories. 1987), Sprague-Dawley
rats, 10 animals/sex/dose, were
administered by gavage the following
doses foe 90 days: o-cresoi at 0,50,175, '
450*or 600 mg/kg/day; m-cresol at 0,50.
150^or-450 mg/kg/day; and p-creaol at 0,
50,175. or 600 mg/kg/day* In the-.,
suochrpnicatudies. the following
param«ter» were evaluated^ body and
Agency Responstfln. the fane 13; 1989,
TC proposal; EPA inadvertently •'•" ":
identified isobutanol a« one of the'
constituents for-which preliminary
toxicity data had been used in deriving
"interim" RfD's, i.e., values to be used .
until- the appropriate testing was ••'.-•
completed [5* FR 21665). The Agency's
subchronic: test for isobutanol was
actually completed in late 1985, and, a* i
mentioned above* the study result* were
reviewed by the RfD Workgroup is May
1986. The study and the IRIS chemical
file for isobutanol are available for
review in the-RdtpJ&cket; copie*of
the study at« ai»«**itafai« from NTIS -
^ ^ _ _ _ and'.
clinical patfeology.i At ssuBrifice* animals
were mexropsied and tisituiisan&organs
were subjected to histopathological
' "~~
dose-related, although these signs
diminished after reaching a peak '
In the subchronic studywith m-cresok •
there was a 20-25 percent reduction in
body weight gain in males and 10-15
percent in females at 450 mg/kg/day;
food intake was reduced by 10-15
percent in males. Also, at this dose there
was a significant increase in the.
incidence of salivation, myotonus. and
tremors. At the 150 mg/kg/day dose.
weight gain was reduced by 10-15
percent in males, though no reduction
was seen in females. At the 50 mg/kg/
day level, there were no significant
adverse effects. The NCAEL identified
for m-creso! from these studies was 50
mg/kg/day.
At 600 mg/kg/day, in the subchronic
study with o-cresol. there was a 47
percent mortality (9/30 males'.: 19/30
females), 30 percent reduction in. body
weight at week 1 and Iff percent at final
sacrifice. Food consumption wa* alao
significantly reduced during, Week* tS:;;
through 8 and fcThte kidney-to-body "V
weight ratio w« ISpwo^ highpr.than; ;
"
that of m« contnsl'vahi«i [
the study, m additfottta-ti
effects; CMS tffscts "
-J
Meta-.
ChronieToxJciiy ffofennce Leva/at
The chronic-toxicity reference levels for
meta-cresok ortho-cresol. and pare-
cresol are/jot being changed from those
values presented in the June 13,1986, TC'
proposal (2 mg/L for each isomer).
Although new toxicological data are
now available from which "new" RfD'a
have been derived, these new RfD's era
the 30010 numerical value as the original
RfD. The RfD Workgroup previously
verified OB July a, 1985*an RfD of 0.05
• j. IQ. thfjnaurotoxicity studies; in
ajddjtioa/ta.iha above-mentioned
parameter*, such signs of neurotoxicity
;afr«alivatiour urination, tremors,
piioerectionj diarrhea, pupil size, pupil
response, lacrimation, hypothermia, '
vocalizationu exophthahuia, palpebral
clofBi%,convulaionsr(typf .and severity),
nspiiation,(rate and type), impaired
gp& positional passivity, locomotor
aca'vity^steireotypy, otsitl* response.
righ^ngdteflax. performance ona wire
nyuuusvatkforelimb strength, positive
gaotrophism. extensor thrust limb
rotation, tail pinch reflejc, toe pinch
reflex, and hind limb splay were also
evaluated. In the neurotoxicity studies,
the lowest dose of each cresol isomer, 50
mg/kg/day, appeared to have caused
some clinical signs of CNS-stimulation
post-dosing; these incidences appeared
predominantly during the first week of
dosing and were sporadic in nature
throughout the course of the studies.
Higher doses of cresol ioomers (greater
than 450 mg/kg/day) produced
significant neurological events, such as
increased salivation, urination, tremors,
lacrimation, palpebral closure, and rapid
respiration. Similarly, high-doae animals
also snowed abnormal pattern* in the
nawpJMJHvtorai tests. In general, most
of theeunieal signs of toxicity were
ited tremor«c*!di^foCthef
each
administration, and on»<»ftiiesVaaimals
became comato«*durint:tiia* ame^At 50
mg/kg/day, no significantadverse -
effects were observed; ThtfNOAlE
identified was 5&mg/kg/dayfOF o-creaol
based on these studies.; ?^*ft->H .v"'
At 600 mg/kg/day in th» subchronic
study of p-cre*ol, there wa»a significant
reduction in weight gain (15 pfircent for
females, 25 percent far malesjt ' •'!
significantiy reduced food consumption
at weeks 1 through 7 and »in males, and
a significantly increased incidence of
CNS signs; such a* lethargy; excessive
salivation, tremor*, and diarrhea; Also,
the liver-to-body weight and kidney-to-
body weight ratio* were significantly
increased. There was a greater •
prevalence of trachea! epithelial :
metaplasia in mis group of animate
compared with the animals-in the
control, low-do** or mid-dose groups.
At the mid-dose group (ITS mg/kg/day).
the reduction in weight gain wa* 5-10
percent in mclec between week* 1 and
3, the liver-to-bcdy weight ratio was
elevated (though not statistically
significantly), and th»kidn*y-tc-body
weight ratio was elevated significantly
-------
18030
«•*••!•"•»«••—
for male*. At tb* SO mg/kg/tlay level
although there was a slight reduction in
weight gain and a small incsease in
iddney-lo-body weight ratio, these
etfects were not stntisr.uaiiy sign;:U.unt.
Ths NOAEL identified irum these
studies was 50 mg/kg/day for p-cresol.
Thus, the RfD Workgroup verified on
Auaust 13,1987, new RfD's of O.OS mg/
kg/day for m-cresol. o-cresol, and p-
cresol. using a NOAEL of SO mg/kg/day
and an overall uncertainty factor of
1.000 (i.e*. 10 to account for the variation
in sensitivity among members of the
human population, 10 to account for the
uncertainty in extrapolating from animal
data to human exposure, and 10 to
account for the uncertainty in
extrapolating from a anbchromc NOAEL
to a chronic NOAEL) (5 ]. Since the
original verified RfD for mixed cresols
and the new verified RfD'a for the
individual isomera are the name value,
the chronic toxicUy reference levels also
remain unchanged. These chronic
toxicity reference levels of 2 mg/L are
calculated asing the new verified RfD's
of OOS mg/kg/day and body weight and
consumption values of 70 kg and 2 L
water pet day. respectivelj'.
Coameat Summary: la response to
the Juaa 13,1984 TC propctal, three
coraraaMts ware received that pointed
OK* that EPA was proposing regulatory
levels for the ctesol isoanets. despite
adapting that d« existing data were
insuffidant far esUfaiisbinjj RfD's [51FR
21685], The oommenters disagreed with
the Agency's decision to sot regulatory
levels for these coBStituents using
preHmiBary testing data, and they
questioned the basis of th« chronic
toxlcity reference fewls.
Agency Reipomie. In thn lone 13. 198ft,
TC proposal, EPA apparently was not
sufficiently clear ia its explanation [51
FR2J6651 of what kind of preliminary
data it used to establish tha BfD's for m-
cresol o-CTBSoi. and p-cre»L At that
time, the Agency already .Bad a verified
RfD of 0.05 lag/kg/dey for nixed
cresola. EPA also had tha preliminary
results of the aboTe-meBsloaed
subchtonic toxicity stadHs: the "in-hfe
portions of these studies-terminated
(e.g. the final sacrifice* oixated) in
December 1985 and Jaaunry «•§. Th»
data from tfcesestodieeaipportad the
choice of tbe RfD of 005 img/kg/day as
well. However, the Agency fait U wooki
be prudent to cooudec the RfD'a
"mtcrim". in case the results of the
ongoini neittolawctty stw*es indicated
otherwise, Tha aabckxamc and
neurotaxicsty stadiaa and the BUS
chemical £l«s for tha crenel ionen ant
a vaJJabia facts**** to tlie RCKA
Docket
Acrylonitrile
Chronic Toxicity Reference Level:
EPA is revising the chronic toxicity
reference '.eva! for acrylonitrile from
0.002 to 0.0007 mg/L because the original
level was derived from inhalation slope
factor rather than an oral slope factor.
The inhalation slope factor. 0.24 (mg/kg/
day)"1, was based on an epidemiological
study [O'Berg. 1980) of textile workers
exposed to acrylonitrile [8], However.
on March 17.1987. the Agency's
Carcinogen Risk Assessment
Verification Endeavor (CRAVE)
Workgroup verified an oral slope factor
of 0.54 (mg/kg/day)™1 for acrylonitrile
[7J. This quantitative potency estimate
wao calculated using the results of three
chronic drinking-water studies in either
Sprague-Dawley or Fischer 344 rats
(Biodynamics, 1900: Biodynamics 1980;
Quast, 1980). In each study, an increased
incidence of brain and spinal cord
astrocytomas. Zymbal gland
carcinomas, and stomach papillomas
and carcinomas waa observed in the
rats. (A brief summary of the dose-
response data reported for these three
studies ts presented in the IRIS chemical
file for acrylonitrile; a copy of the IRIS
file is located hi fee RCRA Docket for
review.) The CRAVE Workgronp
classified acrylonitrile as a probable
human (Group Bl) carcinogen based on
the observation of a statistically
significant increase in incidence of Inng
cancers ia exposed workers and the
observation of tumors, generally
astrocytemao ia the brain, in studies of
two rat strains exposed by various
routes, e.g., drinking water, gavage. and
inhalation [7J.
Thus, using a 10T« risk level as
proposed for greap 1 carcinogens in the
tune 13,19«i TC notice {51 PR 21888J,
an KD of 1* X «r*mg/ks/day is
derived tram *e s*«r oral slope factor
of 054 frdW&err1* The revised
chroni« toxreHy reference tevel for
acrylonttrUe, 0.0007 mg/L. is
subsequently calcalated using the RSD
of 1.9 X W8 mg/kg/day. and body
weight and consumption varnes of 70 kg
and Z L water per day, respectively.
Chlordane
Chfaaic TatiatyBefereace Leyek
EPA iss revisiag the dao»te taxictty
reference tevei for chtordana rrom OM2
to 04003 ntg/L bacaose the onderlying
oral slope factor has been revised, as
weU as the weight of eridaace
ciBDificataB. The original stop* factw.
L81 fms/kx/dafrf', was baaod w a
bag-team aewMng study (brtanwtiaw^
Resanii«sl QswcsopoMt CorpaMttaa,
igja|tewaidin«igciacasttdeaa stated
increase «n kapatocaihilar csceinoniaa
was seen hi both male and female CD-I
mice [8]. Chlordane was also classified
as a Group C carcinogen, so the chronic
toxicity reference level proposed in the
June 13.1986. TC notice was based on *
ID'«risk level [51 FR 21666). On April 1.
1987. the Agency's CRAVE Workgroup
verified a new oral slope factor of 1.3
(mg/kg/day)--' for chlordane [9]. This
quantitative potency estimate was
calculated using the results from the
above-mentioned IRDC study, and an
NCI (1977) study in which male and
female B6C3F1 mice were fed chlordane
for 80 weeks. A significant increase in
hepatocellular carcinomas in both sexes
was also observed in this study. (A brief
summary of the dose-response data
reported for these two studies is
presented in the IRIS chemical file for
chlordane: a copy of the IRIS file is
located in the RCRA Docket for review.)
The CRAVE Workgroup classified
chlordane as a probable human (Group
B2) carcinogen based on sufficient
evidence of liver tumor induction in four
strains of mice of both sexes and in F344
male rats, and inadequate evidence in
humass [9J, jk
Thus. u»inf a 10-*risk level ask
proposed lor Grow 3 carcmogenain Ui®
Tunel3.imTCnB*icef5lFR2|B66|, .
an RSD of 73 X 10'* mg/kg/day Is
derived from tha »ew oral slope factor
' of lJ(mg/k*yd»yrl. The revised
chronic toxicity reference level for
chlordane. 0.0003 mg/L. is subsequently
calculated usiag the RSD of 7A X 10~*
mg/kg/d«y. and body weight and
consumption values of 70 kg and 2 L
water per day. respectively.
Chlofofofm
Chroa'e Taaddty Beferencs Level:
EPA is modifying *» chrome toxicity
reference lewt far cnlBrofocm&«aao05
to 0.06 «g/L because the undssijiug
atope factor has been revised. Tfc»
viginai oral slope factor. 7 x KT*
(mg/kg/day)-1. wa» baaed on two
chronic oral stadtes (NO. 1970: Roe et
al.. 1979) in which statistically
significant increases of hepatocelmlar
carcinomas in male and female B6C3F1
mice, renal epithelial tumors in male
Osborne-Mendel rats, and renal tumors
in male ICI mice were observed (10). On
August 28.19B7. the Agency's CRAVE
Workgroup verified a new oral slope
factor of «.l x WOng/kg/day)"1 *»
chloroform {111. TtSs quantitative
potency estimate wa» caiodated using
(J«Ws0n«t *« «2*"JJ* J-rfrfM
cntorefom was e*luiialsU.red m ttenking
w^vtenmleOsbameAiendel rats and
female WC3W riafe A significant
increase in wna* tamers in mete rats
-------
F«tetai Register /. VoL 53. No.- 9? /
was ob«etvedf th» ft*er tumor incidence
iifcfwnal«miorwa» no* significantly
increased. (A* brief summary of'thedose-
'
located- in
The CRAVE, Wq
chloroform as'a praoa&lermiman (Group
32) carcinogen based on increased
incidence of several tumor types in rats
and; mice, and inadequate- data, in-
humans [li|v
Thus* using a 10~* risk level a*
proposed for Group B carcinogens in the
June" 1988 TC notice [51 FR 21666). an
RSDof 1.6 x 10° mg/kg/day is derived
frbnvthe verified oral slope- factor of 8.1
x 10.-* (mg/kgVdayr l- The revised
chronic loxiciry reference; level for
chloroform. 0.06 mg/L, i* subsequently
calculated using th* RSD of 1.6 x 10'*
mg/kg/day, and body weight and-
consumption value* of ;70 kg and 2 L
. waterjwdajfc tetpectiyely,
C<^m«ir£iOTiOTajy: la response to
ihe June li.^a^TCffropoMi one
consent wiB*Jfeceive4;tIiat criticized
EPA fotus^thlfr NCI study aa the basi«
r for'derivteg tf« brfglrial RSD (e*. its
along f pctor LJftt Qgfflun*"*^ asserted
above-mentioned NCI stndy. and a
2-year feeding study (Davis.1985J using
male and female C3H mice. In the Davis
stu
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18032
, Federal Register / Vol. S3, No. 97 / Thursday. May 19. 1988 / Proposed Rules
I
Until EPA develops a separate risk
assessment procedure for promoters, it
will continue to assess promoters and
initiators in a like manner:
Comments on this notice must be
received by the EPA on or before July 5.
1088. to ensure consideration. It should
be noted that the Agency is reopening
the comment period for only those
issues/revisions discussed in this notice.
Date: April 15.1988.
J.W. McGnw.
Acti.tg Assistant Administrator for Solid
Waste and Emergency Response.
III. References
1. U.S. SPA. 1935. Integrated Risk
Information System (IRIS). Reference
Dose (RED) for Oral Exposure for Phenol.
Online. (Revised: Verification Date 10/
28/88). Office of Health and
Environmental Assessment, •
Environmental Criteria and Assessment
Office, Cincinnati, OH.
2. U.S. EPA, 1985. Integrated Risk
Information System (IRIS]. Reference
Dose (RfD) for Oral Exposure for
Pyridine. Online. (Revised: Verification
Date 06/13/87). Office of Health and
Environmental Assessment,
Environmental Criteria and Assessment
Office, Cincinnati. OH.
3. U.S, EPA. 1965. Integrated Risk
Information System (IRIS). Reference
Doao (RfD) for Oral Exposure for 2.3.4,6-
TetrachlorophenoL Online: Input
Pending. (Revised: Verification Date OS/
13/87). Office of Health and
Environmental Assessment.
Environmental Criteria and Assessment
Office, Cincinnati. OH.
4. U.S. EPA. 1986. Integrated Risk
Information System (IRIS). Reference
Dose (RfD) for Oral Exposure for
Isobutanol. Online. (Verification Date
05/U/B6). Office of Health and
Enuronrr.ontal Assessment,
Environmental Criteria and Assessment
Office. Cincinnati. OH.
5. U.S. EPA. 1985. Integrated Risk
Information System ;;RIS). Reference
Dose (RfD) for Oral Exposure for Meta-.
Ortho-. and Para-Cresol. Online: Input
Pending. (Revised; Verification Date 08/
13/87). Office of Health and
Environmental Assessment.
Environmental Criteria and Assessment
Office, Cincinnati. OH.
0. U.S. EPA. 1983. Health Assessment
Document for Acrylonitrile. Final
Report. Office of Health and
Environmental Assessment
Washington. DC (EPA-600/8-82-C07F).
7. U.S. EPA. 1907. Integrated Risk
Information System (IRIS). Risk
Estimate for Carcinogenicity for
Acrylonitrile. Online. (Verification Date
03/17/87). Office of Health and
Environmental Assessment,
Environmental Criteria and Assessment
Office. Cincinnati. OH.
8. U.S. EPA. 1985. Drinking Water
Criteria Document for Heptachlor,
Heptachlor Epoxide, and Chlordane.
Environmental Criteria and Assessment
Office. Cincinnati. OH. (ECAO-CIN-
406).
9. U.S. EPA. 1987. Integrated Risk
Information System (IRIS). Risk
Estimate for Carcinogenicity of
Chlordane. Online. (Verification Date
04/01/87). Office of Health and
Environmental Assessment.
Environmental Criteria and Assessment
Office. Cincinnati. OH. *
10. U.S. EPA. 1985. Health Assessment
Document for Chloroform. Final Report.
Office of Health and Environmental
Assessment. Washington. DC (EPA/600/
8-84/004F).
11. U.S. EPA. 1987. Integrated Risk
Information System (IRIS). Risk
Estimate for Carcinogenicity of
Chloroform. Online: Input Pending.
(Verification Date 08/26/87). Office of
Health and Environmental Assessment.
Environmental Criteria and Assessment
Office. Cincinnati. OH.
12. U.S. EPA. 1987. Integrated Risk
Information System (IRIS). Risk
Estimate for Carcinogenicity for
Heptachlor. Online. (Verification Date
04/01/87). Office of Health and
Environmental Assessment.
Environmental Criteria and Assessment
Office. Cincinnati, OH.
13. U.S. EPA. 1985. Health Assessment
Document for Dichloromethane
(Methylene Chloride). Final Report.
Office of Health and Environmental
Assessment, Washington. DC (EPA/600/
8-82/004F).
14. U.S. EPA. 1M& IntegratedRisk
Information System (IRIS). Risk
Estimate for Carcinogenicity for
Methylene Chloride. Online.
(Verification Date 12/04/86). Office of
Health and Environmental Assessment,
Environmental Criteria and Assessment
Office. Cincinnati. OH.
[FR Doc. 88-8959 Filed 5-18-48: 8:45 am|
•HJJMO CdMt MM »» M
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