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ENVIKUNMuNi L PROJECTION AGENCY
Um ,..Y, REGION V LISTING BACKGROUND DOCUMENT
Th'e'.jEp.l lowing wastes containing tetra- , penta- , and I/
hexachlor6~dibenzo-£-dioxins (CDDs) or -dibenzofurans(CDFs7
and other toxic constituents:
F020 Wastes (except wastewater and spent carbon from hydrogen
chloride purification) from the production and manufac-
turing use (as a reactant, chemical intermediate, or
component in a formulating process) of tri- , or tetra-
chlorophenol or of intermediates used to produce their
pesticide derivatives. (This listing does not include
wastes from the production of Hexachlorophene from
highly purified 2,4, 5-trichlorophenol .) (H)
F021 Wastes (except wastewater and spent carbon from hydrogen
chloride purification) from the production or manufac-
turing use (as a reactant, chemical intermediate, or
component in a formulating process) of pentachlorophenol ,
or of intermediates used to produce its derivatives. (H)
F022 Wastes (except wastewater and spent carbon from hydrogen
chloride purification) from the manufacturing use (as a
reactant, chemical intermediate, or component in a
formulating process) of tetra-, penta-, or hexachloro-
benzenes under alkaline conditions. (H)
F023 Wastes (except wastewater and spent carbon from hydrogen •
chloride purification) from the production of materials
on equipment previously used for the production or
manufacturing use (as a reactant, chemical intermediate,
M For the purposes of this document the following acronyms and
Definitions are used:
PCDDs = all isomers of all chlorinated
dibenzo-p_-dioxins ;
PCDFs = all isomers of all chlorinated
dibenzofurans;
CDDs and CDFs = all isomers of tetra-, penta-, and
j hexachlorodibenzo-£-dioxins and
-dibenzofurans, respectively;
TCDDs and TCDFs = all isomers of tetrachlorodibenzo-£-dioxins
and -dibenzofurans, respectively;
TCDD and TCDF = the respective 2 , 3, 7-^J.somers .
PeCDDs/Fs and HxCDDs/Fs = the penta-and hexachloro compounds.
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or component in a formulating, process) of tri-, and
tetrachlorophenols. (This listing does not include
wastes from equipment used only for the production or
use of Hexachlorophene made from prepurified 2,4,5-
trichlorophenol.) (H
F026 Wastes (except wastewater and spent carbon from hydrogen
chloride purification) from the production of materials
on equipment previously used for the manufacturing use
(as a reactant, chemical intermediate, or component in
a formulating process) of tetra-, penta-, or hesachloro-
benzenes under alkaline conditions. (H)
F027 Discarded unused formulations containing tri-, tetra-, or
pentachlorophenols, or compounds derived from these chloro-
phenols. (This listing does not include formulations
containing Hexachlorophene synthesized from prepurified
2,4,5-trichlorophenol.) (H)
F028 Residues resulting from incineration or thermal treatment (H)
of soil contaminated with EPA Hazardous Was-te Nos.
FQ20, F021 , F022, F023, F026, and F027: 4
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TABLE OF CONTENTS
Page
I. Summary of basis for listing 4
II. Chemical and physical properties of CDDs
and CDFs. 6
III. Reactions causing the formation of CDDs and CDFs 8
A. Formation of CDDs 9
B. Formation of CDFs 10
IV. Sources of the wastes and typical disposal practices 11
A. Sources: Manufacturing processes causing
formation of CDDS and CDFs. 11
1. Formation of CDDS 11
a. production of ring-substituted
chlorophenols 11
b. Syntheses using tri- and tetrachloro-
phenols 16
c. Manufacturing operations on CDD/
CDF-contaminated equipment 18
d. Manufacture of formulations 19
2. Manufacturing processes associated with
the formation of CDFs 20
3. Miscellaneous processes causing the
formation of CDDS and CDFs 22
4. Other toxicants of concern in these wastes 23
B. Quantities of wastes produced 23
V. Waste management 24 -
VI. Basis for listing these wastes as hazardous 25
A. Hazards posed by the wastes 25
B. Mismanagement incidents and environmental 32
contamination
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Page
C. Health and environmental effects 43
1. Structure - activity relationships in 43
the mechanism of action, toxicity and
persistence of CDDs and CDFs
2. Health and environmental effects of CDDs 45
3. Health and environmental effects of CDFs 55
4. Health and environmental effects of
chlorophenols and hexachlorobenzene
VII. Response to comments
Tables 1-9 63-84
Figures 1-23 85-107
References 108 - 122
4
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I. SUMMARY OF BASIS FOR LISTING
Tetra-, penta-, and hexachlorodibenzo-p-dioxins (CDDs) and
-dibenzofurans (CDFs) are known or expected to the present in wastes
from the production and manufacturing use of tri-, tetra-, and penta-
chlorophenols and from the manufacturing use of tetra-, penta-, and
hexachlorobenzenes under alkaline conditions and elevated tempe-
ratures. CDDs and CDFs likewise are present in wastes resulting
from the production of materials on equipment previously used
for the production and manufacturing use of tri- and tetra-
chlorophenols, and in formulations containing these chlorophenols
and their derivatives. These wastes also contain chlorophenols.
The Administrator has determined that these wastes are acute
hazardous wastes under 40 CFR 261.11(a)(2), since they are capable
of causing or significantly contributing to serious irreversible,
or incapacitating reversible, illness. The Administrator has
further determined that these wastes, including still bottoms,
reactor residues, untreated brines, spent filter aids, spent
carbon adsorbent, and sludges resulting from wastewater treatment,
may pose a present or potential hazard to human health or the
environment when land disposed or incinerated at interim status
facilities, and therefore should be prohibited from being
managed at these types of facilities. The Administrator has
further determined that special permit standards are appropriate
for land disposal and incineration facilities managing these wastes.
This conclusion is based on the following considerations:
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1. These wastes typically contain significant
concentrations of tetra-, penta-, or hexachloro-
dibenzo-p_-dioxins and -dibenzof urans, which are
exceptionally potent toxicants. 2 , 3,7,8-Tetrachloro-
dibenzo-p-dioxin (TCDD) and a mixture of 1,2,3,7,8,9-
and 1,2,3,6,7,8-hexachloro-£-dioxins are among
the most potent animal carcinogens known, and
are potential human carcinogens. In laboratory
studies, TCDD is teratogenic, fetotoxic, and embroytoxic
at extremely low doses. In addition, based on
structure-activity considerations, many CDDs and
CDFs are expected to be extremely powerful acute
toxicants and inducers of the liver microsomal
enzyme system. These substances are all persistent
in the environment.
These wastes also contain signficant concentrations
of tri-, tetra-, and pentachlorophenols and their
chlorophenoxy derivates. EPA's Cancer Assessment
Group (CAG) has determined that 2,4,6-trichlorophenol
(2,4,6-TCP) is a potential human carcinogen. In addition,
certain chlorophenols may cause liver and kidney
damage; some chlorophenoxy compounds are also
potential human carcinogens, and may have reproductive
effects. Although these compounds may undergo
environmental degradation, they are sufficiently
persistent under some environmental conditions
to warrant concern for their human health effects.
2. CDDs and CDFs are capable of causing, or significantly
contributing to serious irreversible illness,
or incapacitating reversible, illness, at extremely
low dose levels. Moreover, these toxicants are
persistent, and can migrate from these wastes. CDDs
and CDFs are present in these wastes in concentrations
orders of magnitude higher than these dose levels.
Since these wastes contain substantial concentrations of
potentent carcinogens, the Administrator has
therefore determined that these wastes are acute
hazardous wastes.
3. The wastes are typically disposed in landfills
or by incineration. Disposal in a landfill in the
presence of solubilizing solvents could result in
leaching of the CDDs or CDFs. The water soluble
chlorophenols and their derivates also can cause
pollution of ground or surface waters. Furthermore,
the constituents of concern in these wastes pose
a threat of pollution of surface waters from
windblown dust, water run-off, erosion, or flooding
of disposal sites. Incineration or burning of
these wastes under improper conditions (too low
a temperature, insufficient oxygen, inadequate
-------
dwell time) may generate, or fail to destroy the
CDDs and CDFs. This could conceivably lead to the
increased formation of these materials from precursor
substances, and emission to air, resulting in human and
environmental exposure.
4. Significant amounts of CDDs and chlorophenols have
been shown to have escaped from these wastes into
the environment. These wastes (i.e., still bottoms,
brines, and spent filtration materials), have
contaminated soil, surface waters, alluvial stream
deposits and fish.
II. CHEMICAL AND PHYSICAL PROPERTIES OF CDDs and CDFs.
Chlorinated dibenzo-£-dioxins and -dibenzofurans are
derivatives of dibenzo-p_-dioxin and dibenzof uran. The
structural formulae of the dioxin and dibenzofuran nuclei,
and the abbreviated structural conventions used in this
report are illustrated below:
Both compounds may have a variety of substituents in the
numbered positions. Theoretically there are 75 different PCDDs
and 135 PCDFs. Almost all of these compounds have been synthe-
sized, but analytical differentiation is difficult. Not all
the CDDs and CDFs have been identified in the environment.
For the chlorinated dioxins and dibenzofurans of interest
in this document, the possible isomeric distribution (USEPA
1980, 1982) is as follows:
7
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tetrachloro derivatives:
pentachloro derivatives:
hexachloro derivatives:
Number of Isomers
dioxins dibenzofuran.s
22 TCDDs 38 TCDFs
14 PeCDDs 28 PeCDFs
10 HxCDDs 1 6 HxCDFs
Of the 22 TCDDs which may occur, 2,3,7,8-TCDD is the dioxin
which is best characterized in terms of toxicity, persistence,
and environmental contamination. Because analyses are
difficult and expensive, it is, for practical or economic
reasons, not always possible to differentiate between
"total" TCDDs and the 2,3,7,8 isomer. For example, in toxicolo-
gical or environmental fate studies, when "total" TCDD is reported,
it is not always clear whether all or only some of the isomers
contribute to the observed effect. In a prior action, relating
to TCDDs in emissions from municipal solid waste resource
recovery incinerators, the Agency determined that, for purposes
of assessing risk related to TCDD exposure, it was prudent to
make the conservative assumption that all TCDD isomers contribute
to the toxicity of TCDD mixtures (USEPA, 1981b). Consistent
with this worst-case assumption, the concern in this document
is with the isomeric mixtures of tetra-, penta- and hexa-CDDs,
rather than, for instance, with the 1,2,3,6,7,8-HxCDD alone. A
similar determination was made for the CDFs. The reasons
for the Agency's determination are explained below (Section V.C.I).
8
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Some of the physical and chemical properties of CDDs
and CDFs are outlined in Table 1. These compounds form
nearly planar molecules of almost identical size, which
form crystalline solids with well-defined melting points.
TCDD is the only compound of the series for which solubilities
have been determined. However, the structural similarity
between CDDs and CDFs gives comparisons of their physico-
chemical characteristics high validity. For example,
because of their low polarizability, all these compounds are
expected to be essentially insoluble in water, considerably more
.soluble in certain organic solvents, lipophilic, and characterized
by strong binding to organic matter, such as soil constituents.
III. REACTIONS CAUSING THE FORMATION OF CDDs and CDFs.
Several reactions, summarized below, are of environmental
importance because they result in the formation of dioxins and
dibenzofurans:
chlorinated chlorinated
chlorophenols > predioxins > dioxins
chlorophenols
+ chlorinated > chlorinated
chlorobenzenes > isopredioxins dibenzofurans
/
/
polychlorinated /
biphenyls /
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A. Formation of CDDs (Esposlto, 1980).
Chlorinated dioxins are formed in an exothermic reaction from
£-chlorinated phenols in the presence of base at elevated tem-
peratures. The reaction, illustrated for TCDD formation as
reaction 1 of Figure 1, shows the participation of an ortho halogen;
the presence of an ortho halogen, however, is not an absolute
requirement for dioxin formation. A compound such as 2-nitro,
4,5-dichlorophenol can also serve as a reactant for TCDD formation;
even relatively weak bases, such as quinoline or pyridine can
effect reaction, and dioxins have been formed at temperatures
as low as 145 °C.
Dioxin formation occurs in several steps, with the intermediate
formation of pre-dioxins, (these compounds have been identified
in waste sludges and commercial products, as well as in the
products of laboratory experiments).
The formation of chlorinated dioxins can also occur indirectly.
For instance, in the course of preparation of polychlorobenzenes
by electrophilic halogens, neutralization of the acidic by-
product with alkali can lead to the formation of a chlorophenol.
y
Subsequent distillation may then produce PCDDs.
In thermal processes, the mechanism forming TCDD has
been estimated from theoretical (thermodynamic) considerations
to take place most efficiently at about 800-1000 °C, while
2y Wastes from the production of chlorinated benzenes are EPA
Hazardous Wastes Nos. K085 and K1Q5. Although the possibility
of the formation of CDDs was mentioned in the Background Document
supporting those listings, they were not cited as toxicants of
concern. Since these wastes are already listed hazardous wastes,
the Agency has no current information on their concentration
of CDDs/CDFs, and judges that these are unlikely to be high, it
was not deemed necessary to list these wastes as acute hazardous
wastes. The presence of CDDs in these wastes and in still
bottoms from chlorobenzene solvent recovery are currently being
studied. Our listing determinations will change if data warrant
such change.
10
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its decomposition is most likely to occur above 1350 °C (Shaub
and Tsang, 1982).
The mechanisms of the condensation reactions outlined above
are exceedingly complex, and may involve molecular rearrangements.
As a consequence, mixtures of chlorinated dioxin isomers are
usually produced. Nevertheless, prevalence of specific isomers
can be predicted in most cases. It is, for instance, possible
to predict that oxidative condensation involving trichlorophenols
will produce an isoraeric mixture containing far more TCDDs than
will the reaction involving dichlorophenols, which produces
I/
a preponderance of dichlorodibenzo-jD-dioxins.
B. Formation of CDFs.
The thermal oxidative cyclization of chlorinated phenols,
A/
polychlorinated biphenyls (PCBs) , polychlorinated diphenyl ethers
(isopredioxins), or chlorobenzenes under alkaline conditions
(reactions 2 and 3 of Figure 1, and Figure 2), are expected to
generate wastes containing CDFs.
As a consequence of these reactions, CDFs can be generated
under manufacturing conditions similar to those under which
CDDs are generated, and are expected to be present in the
_3/ However, the technical products used in commercial practice
seldom are pure with respect to isomeric composition. In actual
practice, therefore, even wastes from operations producing or
using dichloropenols may contain some CDDs and CDFs. The Agency
is investigating this possibility.
4/ There is no domestic production of PCBs, and therefore no
wastes are generated from the production of PCBs. Disposal
of mixtures containing more than 50 ppm of PCBs, however,
is regulated under TSCA (40 CFR 761).
11
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wastes from such process operations.
As is the case for CDDs, many of the CDFs produced differ
from those expected on the basis of the straightforward
reaction mechanism hypothesized in Figure 1. The reactions
discussed above take place via complex mechanisms, involve
intramolecular rearrangements, and generate mixtures of
isomers. As in the case of CDDs, however, it is possible
to predict the prevalence of some CDF isomers over others
IV. SOURCES OF THE WASTES AND TYPICAL DISPOSAL PRACTICES.
A. Sources: Manufacturing Processes Causing Formation
of CDDs and CDFs.
Because of the chemical reactions outlined above, CDDs and
CDFs are found as unwanted contaminants in a variey of
manufactured chemicals, process intermediates, and process wastes.
The following discussion is based in part on the review
by Esposito (1980) .
1. Manufacturing processes associated with the formation of CDDS
Based on the reactions outlined above, CDDs are most
likely to be formed in the following manufacturing processes.
a. Production of ring-substituted tri-, tetra- or penta-
chlorophenolirT
Chlorophenols are used directly as fungicides, flea repellants,
wood preservatives, antispetics, disinfectants, antigumming agents
in gasoline, and as paint removers. They are also utilized for the
synthesis of biocides (chlorophenoxy derivatives), dyes, pigments,
I/
and phenolic resins.
5/ This document does not consider wastes from the production of
cTyes, pigments, and phenolic resins using chlorophenols as feedstock
materials. These wastes will, however, be studied in the course of
our ongoing Industry Studies Program.
12
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Chlorophenols (annual world production about 150,000
kkg (USEPA, 1982a)) are produced by the chlorination of phenol
or by the alkaline hydrolysis of the appropriate chlorobenzene.
The former reaction is preferred, in part, because under these
conditions the formation of CDDs and CDFs is minimized; however,
significant concentrations of CDDs and CDFs are still generated
in using this process. 2,4,6-TCP, 2,3,4,6-TCP, and PGP are
6/
prepared by this process. 2,5-DCP and 2,4,5-TCP are most
readily prepared by the alkaline hydrolysis of chlorobenzenes,
but other methods are available. Figures 3 and 4 illustrate
the possible mechanisms forming CDDs in the course of synthesis
II
of 2,4,6-TCP and 2,3,4,6-TCP. CDFs are also formed, by analogous
reactions, as illustrated in Figure 2.
Chlorination of phenol can be accomplished in either a,batch
or a continuous reactor fashion. The continuous process is
67 Monochlorophenol, 2,4-DCP and £-chloro-jD-cresol are also
prepared by this process, however, wastes from their manufacture
are not listed, because, at this time, the Agency does not have
sufficient evidence that they contain CDDs and CDFs at levels of
concern.
l_l Wastes from the production of DCPs may also contain CDDs and
CDFs. These may, for instance, arise as follows. Technical CDP
typically contains a few per cent 2,4,6-TCP resulting from over-
chlorination (USEPA, 1971). Thus the possibility exists for the
formation of small amounts of, principally, 1,3,6,8-TCDD (Figure 3).
Recent sampling of distillation bottoms generated in DCP manufacture
showed the presence of 70 ppb of 2,3,7,8-TCDD. This finding is
difficult to explain on the basis of reaction chemistry alone, and
may have resulted from equipment contamination resulting from the
manufacturing of 2,4,5-TCP at this plant about seven years
previously. If information is collected that indicates
that CDDs and CDFs are present in the wastes from DCP
manufacture at significant levels, they will also be listed.
13
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much more efficient, and is thus usually employed. Figure 5
is a process flow diagram which generally illustrates the continuous^
process for the production of chlorophenols by the chlorination
of phenol. Figure 6 illustrates the specific process for the pro-
duction of PGP, showing the waste streams of concern. Since increased
chlorination results in increased decomposition of chlorophenols
(Figure 3 reactions 1-4), the chlorination of PGP, for example,
is usually halted when 3-7% tetrachlorophenol remains.
Because the direct chlorination of phenol forms 2,4,6-TCP
rather than the 2,4,5-isomer, more 1,3,6,8-TCDD than 2,3,7,8-TCDD
is formed (reaction 8 of Figure 3). Molecular rearrangements
occur, and other CDDs, including up to 38 ppm HxCDDs
(USDHHS, 1980), as well as CDFs (USEPA, 1981a) are also
formed, and .are found in commercial PGP (see Table 3). ' ^
Because PCP is widely used as a pesticide, there is a
demand for technical formulations free of CDDs. This is
most readily accomplished by distillation. However, one
manufacturer encountered difficulties in this process,
and another, who used to distill PCP in order to purify it
(Figure 6), no longer does so. (USEPA, 1979). The still
bottoms from PCP purification contained concentrations as high
as 2000 ppm of CDDs (des Hosiers, 1982b), and are presumed
to contain CDFs. HxCDDs have also been identified in technical
PCP at 30 ppm (Table 3) (USEPA, 1979; Miles, 1984).
The hydrolysis of chlorobenzenes is another widely used
method for the preparation of chlorophenols. It is used
14
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mainly to prepare chiorophenol isomers which can not readily
be obtained by the chlorination of phenol. Hydrolysis is
carried out in an alkaline aqueous solution, at high temperature
(200-300 °C) and pressure (500 psi), conditions which are
conducive to the formation of CDDs and CDFs. 2,5-DCP,
2,4,5-TCP, and 2,3,5,6-TeCP are prepared by this method. Several
other, more costly methods are available, but are seldom used.
2,4,5-TCP can be efficiently prepared by the alkaline
hydrolysis of tetrachlorobenzene. Its production can result
in the formation of TCDD (reactions 1 and 2 of Figure 7) and
TCDF (Figure 1). A diagram outlining a typical process for
the production of 2,4,5-TCP using this process is illustrated
in Figure 8. The amount' of CDDs formed in this process is a
function of reaction temperature (Langer, 1973; IARC, 1977);
the reaction temperature and pressure depend on the solvent
used (methanol, ethanbl, ethylene glycol, toluene, isoamyl/amyl
alcohols). For example, the process using water or methanol
as solvent operates at around 220-300°C (Kirk-Othmer, 1979).
At this temperature, laboratory experiments show the formation
of about 1.6 g TCDD/kg 2,4,5-TCP. On the other hand, the process
using ethylene glycol is designed to operate at a lower temperature,
and thus should reduce the potential for CDD formation.
Nevertheless, even using ethylene glycol as a solvent can
lead to TCDD formation: two industrial accidents, one in
England (1968) , and one in Italy (1976) , releasing large
8/
amounts of TCDD, involved this process. (USEPA, 1979).
8/ The Agency has recently been advised of a completely
different process for the synthesis of 2,4,5-TCP that
completely avoids the formation of CDDs and CDFs.
15
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The 2,4,5-TCP product, as well as the wastes from this
process -- distillation bottoms, spent filter aids, and reactor
bottoms, if any -- are expected to contain CDDs (including
I/
TCDD) and CDFs, as well as tri- and tetrachlorophenols. These
wastes are generated in considerable amounts: for example, toluene
still bottoms constituted about 5% of TCP production volume
(Harris, 1981). Data in Table 5 (items 12-28) show that the
concentration of TCDDs in still bottoms ranges from 0.6-350 ppm,
averaging 110 ppm. TCDD concentrations in filter aids
(items 25-28) range from 0.008-2 ppm, however, confidential
data in the Agency's files show a range from 0.008-300 ppm,
averaging 27 ppm (15 samples).
In recent years, TCDD contamination has been recognized
as a problem. As a result, changes in manufacturing conditions
have led to a significant decrease in TCDD concentrations
of manufactured products. However, this may not have changed
107
the concentration of CDDs in the wastes. The more
careful control of reaction conditions may reduce but cannot
9_/ In addition, other reaction side products, such as polyethers,
methoxylated and/or ethoxylated aromatics, and polymeric phenols,
are present. The toxicity of these compounds has not yet been
established.
IQ/ In general the data in Table 5 are often for "mixed"
wastes - i.e., for mixtures of wastes generated in TCP and
phenoxyherbicide manufacture (such wastes are apparently
seldom segregated), and for wastes which probably resulted
from manufacturing processes conducted a few years ago.
16
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prevent the formation of CDDs and CDFs, and product purification
techniques may be presumed to increase the concentrations of
contaminants in the wastes. Moreover, the Agency believes
that, even at the current levels of CDD and CDF contamination
of chlorophenols and their derivatives, caution is warranted
in the disposal (as compared with the proper use) of these
materials.
The TSCA (1976) inventory lists few producers of the
higher chlorinated phenols:
PRODUCTION OF SOME CHLOROPHENOLS(a)
CHLOROPHENOL PRODUCER
2,4,5-TCP . Dow, Midland, MI
2,4,6-TCP Dow, Midland, Ml
2,3,4.6-TCP . Dow, Midland/ MI
PCP(b) Reichold, Tacoma, WA
Vulcan, Witchita, KS
(a) TSCA Inventory (1976); data for 1976-1978.
(b) 1978 production capacity 28,000 kkg (Chemical Products
Synopsis, 1979)
There is, at this writing, no domestic production of
2,4,5-TCP, and it is anticipated that the outcome of legal
proceedings on 2,4,5-T and Silvex may influence future production.
ii/
b. Syntheses using tri-, tetra, and pentachlorophenols.
2,4,5-TCP is used as a starting material for the synthesis
of a series of biocides. Since TCDD contaminates one of
11/ Derivatives of dichlorophenols such as the ester and
amine salts of 2,4-D contain lower chlorinated dioxins
(see Table 3). The 1,3,6,8-isomer is the only reported
TCDD in these products. The Agency is studying wastes from
these manufacturing processes.
17
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the starting materials for their synthesis (2,4,5-TCP),
and may also be generated in the formation of the phenoxy
derivatives (see Figure 7 (reaction 2) and Figures 9-12) , it is
expected to be present in the phenoxy derivatives (see
Table 3), as well as the wastes from their manufacture and
processing (Table 5).
A typical process for the manufacture of a phenoxy herbicide
(2,4,5-T) is presented in Figure 13. The process diagram
illustrates the process as it was conducted more than ten years
ago using methanol as the solvent. Process modifications, however,
have been made to reduce the contamination of product with
CDDs (des Rosiers, 1982b). Careful control of reaction
time, temperature, and pH are said to have effected reduction
in TCDD formation (Buzzelli, 1980). The solvent used is
now typically a mixture of ethylene glycol and toluene or
xylene (Anzani et al., 1979), and distillation to remove
solvents is typically part of the process. However, the
product still contain CDDs and CDFs since the distillation
is performed at temperatures and pressures not designed to
remove these impurities. One manufacturer of 2,4,5-T/Silvex
reports the use of activated charcoal adsorption to remove
TCDD (and, presumably, other CDDs and CDFs) from its product
(Buzzelli, 1980). This process, designed to maximize
adsorption of CDDs and CDFs, generates spent carbon adsorbent
as a waste of concern. Figure 13 shows the process wastes,
such as caustic scrubwater, spent filter aids, and/or spent carbon
adsorbent, that are likely to contain CDDs or CDFs (des Rosiers,
1982b). Data in Table 5 (items 8-28) show that these
wastes can be contaminated with CDDs at several hundred ppm.
18
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Another 2,4,5-TCP derivative, the bacteriostatic agent
Hexachlorophene (HCP), is not presently produced by any
U.S. manufacturer. Due to present pharmaceutical specifications,
HCP was, until recently, synthesized (Figure 12) by condensing
a purified grade of 2,4,5-TCP with formaldehyde in a mixture
of concentrated sulfuric acid and ethylene dichloride
(Figure 14). Because the reaction occurs at rather low
temperatures (72-78 °C), and at acid pH, no CDD or CDF
formation is expected to occur. Earlier production techniques
resulted in TCDD contamination of product due to carry-over
of contaminants from the TCP feedstock used (des Hosiers,
1982b). CDDs are reported to be virtually absent «0.1
ppb) from spent acid, wash solutions or recovered solvents
produced in recent years (USEPA, 1979). Thus, wastes from
the production of HCP using prepurified 2,4,5-rTCP are not
included in this listing. The manufacture of several
herbicides (e.g., Erbon, Sesone) entails the use of other
toxic materials, such as the carcinogen ethylene oxide.
Process descriptions, however, make it unlikely that the
wastes from these processes will be contaminated with this
compound, and ethylene oxide is therefore not cited as a toxicant
of concern in these wastes.
The Agency is assessing the reported possible release
of chlorinated xanthenes in the course of HCP synthesis,
as well as the concentration of HCP in these wastes. An
evaluation of the potential risks to human health posed by
these contaminants may show that these wastes should be
regulated.
19
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Table 10 summarizes the processes discussed above and the
wastes of concern in this document.
c. Manufacturing operations on CDD/CDF-contaminated equipment.
Some process wastes may be contaminated with CDDs or
CDFs because they were generated in the course of a manufacturing
process performed on equipment that was previously used for a
CDD or CDF-generating process. Production trains are often
used for the manufacture of different chemicals whose manufacture
necessitates the use of similar process equipment. In the
manufacture of chemicals on a production train previously
used for a process generating, e.g. , CDDs, both the product and
the wastes generated can be contaminated with CDDs. This
was shown to be the case, for instance, for wastes resulting
from the manufacture of 2,4-D, which contain TCDD because
the equipment used, previously employed to produce 2,4,5-T,
remained contaminated with TCDD (See Table 5) after production
12/
shifted to 2,4-D (45 FR 32677, May 19, 1980). It has been
theorized that the 2,4,5-T and TCDD residues remaining in
the equipment would be extracted in on-going 2,4-D processing.
Based on this supposition, one could calculate the number
of process cycles necessary to remove the contamination
(45 FR 32678). There are, however, no sampling data over
time to support this hypothesis, and the Agency has recent
data which indicate that, in the case of another manufacturer,
still bottoms generated seven years after 2,4,5-TCP production
ceased still contain 70 ppb of TCDD.
121 Recent sampling and analysis showed 20 ppm CDDs and 450 ppm CDFs
in the 2,4-DCP still bottoms of a 2,4-D manufacturing facility
where 2,4,5-TCP had been manufactured many years earlier. (Data in
docket file: memorandum from B. Tichenor, October 1, 1982.) See also
footnotes 3 and 6.
20
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d. Manufacture of formulations.
Many chlorophenols, phenoxy herbicides and phenoxy herbicide
formulations are contaminated with CDDs and CDFs, often at concen-
trations of 20-90 ppm (Table 3). More than 1300 such formulations
were found to be contaminated with TCDDs (at unspecified levels)
(Table 4).
2. Manufacturing processes associated with the formation of CDFs.
CDFs are contaminants of polychlorophenols, phenoxyherbicides,
hexachlorobenzene, and polychlorinated biphenyls (PCBs) . The
reactions underlying this contamination we believe are similar to
those illustrated in Figures 1 and 2. In the production of
2,4,5-TCP (Figure 7), for example, CDFs are formed at the beginning
of the reaction, before most of the 1,2,4,5-tetrachlorobenzene
used as starting material reacts, whereas CDDs tend to be
formed near the end of the process, when 2,4,5-trichlorophenolate
formation is favored (USEPA, 1982a).
Identification of CDFs in various commercial products is out-
lined in Table 3. For example, several analyses of commercial PCP
report 130-140 ppra of CDFs (Table 3). There are differences in
isomeric CDF composition of American and European PCPs. The major
CDFs in some American formulations were the 2,3,6,7- and 2,4,6,7-
tetra, the 2,3,4,6,7-, 1,2,4,7,8- and 2,3,4,7,8-penta, and
1,2,3,6,7,8-hexa isomers. European formulations contained
traces of the 2,3,7,8-tetra and 2,3,4,7,8-penta CDFs. These
differences may reflect differences in the methods of synthesis.
13/ This discussion is based in large part on the information and
references discussed in USEPA (1982a).
21
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In the U.S., PGP is manufactured by the chlorination of phenol
(Firestone, I977a); in Europe, both this process and the
alkaline hydrolysis of hexachlorobenzene (at 135-275 °C) have
been used. The product of chlorination tends to contain more
of the comparatively more highly chlorinated CDFs. Typically,
the final pentachlorophenol biocidal formulation consists of
80 - 88 % PGP, and 12 - 20 % 2,3,4,6-TCP, in addition to
PCDDs (1000 - 3000 ppm), PCDFs (200 - 600 ppm) (principally
tetra - octa isomers), and chlorinated diphenyl ethers
(Firestone, 1972; Lamberton et al., 1979). It has been reported
that CDDs and CDFs, principally the hepta- and octa congeners,
but also 30 ppm of the hexa-CDDs and -CDFs, accumulate in the
sludges from wood treatment processing using PGP (Lamberton,
et al., 1979; Table 6, items 28-29). Analysis of tri- and
tetrachloro'phenols shows about 50 ppm of CDFs (see Table 3) .
Until recently much less attention was paid to the presence
of CDFs than to the occurrence of CDDs in herbicides. As
discussed above, phenoxy herbicides are synthesized by
reacting the appropriate haloalkanoic acid with the appropriate
chlorophenol, usually under alkaline reflux conditions
which are conducive to the formation of predioxins, dioxins,
and dibenzofurans (Figure 1). The presence of CDFs in
chlorinated phenoxy herbicides was confirmed for five
herbicide formulations. These data, summarized by EPA
(1982a) are listed in Table 3. The concentration of
CDFs and CDDs are similar. Various 2,4,5-T formulations
contained tri-, tetra-, and penta-CDFs (although not
22
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the most toxic 2 , 3 , 7 , 8-tetra isomer) at concert cratioi 3 up
to 0.7 ppm. All samples showed the presence of chloi Lnated
diphenyl ethers, which are known precursors of CDFs :i pyrolyti
reactions (Rappe, et al., 1978, see below), in concer ^rations
as high as 1%.
3. Miscellaneous Processes Causing the Formation of (DDs and CD s.
Laboratory studies have also established that CDDt and
CDFs are generated in the course of combustion of a \ ariety
of chlorinated aromatic hydrocarbons. These data, r< /iewed
in Esposito (1980), and USEPA (1982a), show that chiccophenates
are the precursors for CDD formation, whereas the thtrmal oxida
tion of PCBs and chlorinated benzenes causes the fom ation of
CDFs. In both cases, oxygen is necessary, and the fcrmation of
CDDs and CDFs decreases with increasing temperature (-Shaub and
Tsang, 1982). Formation of CDDs and CDFs is likely ID occur in
incinerators or other thermal combustion units that c Derate
at 750-900 °C. At temperatures higher than 1200-140( °C,
little CDD or CDF is found (Ahling, 1979; Junk and Richard,
1981; Redford, 1982). In fact, at these temperatures,
thermodynamic calculations show that CDDs (and presun ibly CDFs)
are likely to decompose (Shaub and Tsang, 1982). (see pp. 10 an 11)
The mechanisms forming the various dioxins and ditanzofurans
is still far from certain. Little is known about the
relative contribution of chlorination, dechlorinatioi , and
inter- or intramolecular rearrangements under conditions of
pyrolysis. A thorough understanding of such processes is
necessary in order to estimate the generation of the 3DDs
23
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and CDFs. The Agency's concern with respect to pyrolytic ^
generation of CDDs and CDFs in the management of wastes which
contain their precursors is outlined below (see section V.A.).
4. Other toxicants of concern in these wastes.
The wastes described in this document arise mainly from the
manufacture and synthetic use of chlorophenols. The production
of chlorophenols is almost never isomer-specific, and the wastes
from a plant performing such processes are therefore expected to
contain a variety of chlorophenols. For instance, technical
2,4,5-TCP may contain small amounts of 2,5-DCP (arising from
1,2,4-TCB contamination of the 1,2,4,5-TCB used for its synthesis);
2,4-DCP contains 2,6-DCP (if underchlorinated) and 2,4,6-TCP (if
slightly overchlorinated) (USEPA, 1971); 3,6-DCP may contain 3,4-DCP.
Thus, such wastes as the distillation bottoms resulting from
chlorophenol production, and the neutral aqueous wastes from a
plant producing chlorophenols, or using technical 2,4-DCP or
2,4,5-TCP to produce chlorophenoxy compounds, is expected to
contain variable mixed chlorophenols. In addition these wastes
contain various chlorophenoxy acids (USEPA, 1971). A study
of an aqueous waste at one herbicide manufacturer found
that it contained 13.5 kg/day of mixed chlorophenols and
about 32.7 kg/day of phenoxy acid (USEPA, 1971). A "typical"
untreated aqueous waste stream from phenoxy acid manufacture
contains 112 ppra of mixed chlorophenols and 235 ppm of chlorophenoxy
acids (Sittig, 1980) .
24
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B. Quantities of Wastes Produced.
About 11,600 kkg/year of hazardous wastes were estimated
to be produced in the manufacture of priority pollutant
chlorophenols (2-chlorophenol, 2,4-DCP, 2,4,6-TCP and PCP),
and about 79,000 kkg/year are produced in the manufacture
14/
of phenoxy compounds (Jett, 1982).
IV. Waste Management
Many of the producers of chlorophenols are also engaged in
the manufacture of chlorophenoxy derivatives. Many of the
listed wastes are generated in the production of pesticides.
A recent assessment of the pollution potential of pesticide
production and formulation processes reached some very
general conclusions on the management practices of wastes
from this industry (USEPA, 1978c) .
The aqueous waste stream from the production of chlorophenoxy
herbicides using chlorophenols is expected to contain a
variable mixture of chlorophenols, salts of various chlorophenoxy
acids, chloroalkanoic acids and their by-product hydrolysates,
and mineral salts, as well as the toxicants of principal
concern in this document, i.e^, CDDs and CDFs. Of these,
the first two compound classes (chlorophenols and chlorophenoxy
14/ 2-CP and 2,4-DCP are not covered in this listing; the fraction
oT the total wastes attributable to 2,4,5-TCP, 2,4,6-TCP, tetra-
chlorophenol, and PCP production is not known. At the present time,
because of the 2,4,5-T RPAR proceeding, there is little 2,4,5-TCP
production. Upon its resolution, 2,4,5-TCP production may well
resume.
25
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acids) are amenable biological degradation. One study (USEPA, 1971)
demonstrated that treatment by use of an aerated lagoon £
and a stabilization pond removed 87-94% of chlorophenols
and 49-80% of the chlorophenoxy acids in about two weeks, when
a sufficiently adapted biological population had been developed.
However, CDDs and CDFs are not easily biodegradable (Phillippi,
1981; Huetter, 1982), and accumulate in the sludges and residues
of settling ponds and wastewater treatment plants (see Table 6 -
values as high as 1200 ppm CDDs in settling pond muds). Other
wastes from the manufacture of chlorophenols are generally
land-filled or deep-well injected; treatment wastes are
impounded (Jett, 1982).
Waste management in the course of manufacture of phenoxyacetic
pesticides is a little better characterized: fifteen wastes
from the manufacture of phenoxy acetic acid compounds manufac- ™
tured by five manufacturers are disposed of by landfill, on-site
impoundment (4 manufacturers), and by deep-well injection
(1 generator). Of the five manufacturers, two generate spent
activated carbon, and two manage their solid wastes using
on-site drum storage and impoundment (Jett, 1982).
V. BASIS FOR LISTING THESE WASTES AS HAZARDOUS.
A. Hazards posed by the wastes.
The basis for listing these wastes is the presence of tetra-,
penta-, and hexa-CDDs, and -CDFs, tri-, tetra-, and pentachloro-
phenols, and their chlorophenoxy derivatives.
Several of the CDDs and CDFs are among the most potent animal
carcinogens known, and are considered to be potential human carcino- ^
26
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gens. In laboratory studies, TCDD is teratogenic, fetotoxic,
and embryotoxic at extremely low doses. These substances are
persistent in the environment. Because of their potency as
toxicants, the wastes containing CDDs and CDFs are being listed
I!/
as acutely hazardous.
Data in Table 5 indicates that the level of contamination of
these wastes is significant: distillation bottoms may contain
several hundred ppm of CDDs (Table 5). Still bottoms from
2,4-DCP/2,4-D production resulting from manufacture processes
using equipment previously used for 2,4,5-TCP or 2,4,5-T
production, can also be significantly contaminated with CDDs
(item 10, Table 5). Other wastes (filter aids) from these
processes contain smaller (but still significant) amounts
(8-200 ppb) of TCDDs (Table 5, items 25-28). However,
confidential data indicate that concentrations may be 30,000
times higher than this. Cooling pond muds may contain 1200 ppb
TCDDs (Table 6, item 105). In most of the cases listed in the
Tables, analyses for CDDs other than TCDDs, or for CDFs, were
not performed. Their presence is inferred from knowledge of
reaction chemistry and process technology.
Where carbon adsorption is used to purify a technical
product (as, for instance, in 2,4,5-T purification (Buzzelli,
15/ The RCRA definition of acute hazardous waste is set forth
at 40 CFR 261.11(a)(2). Under that definition, such a material
is not necessarily "acutely toxic" in the way that term is used
by toxicologists. Rather, the term is intended by EPA to
identify wastes which are so hazardous that they may "cause or
significantly contribute'to an increase in serous irreversible,
or incapacitating reversible, illness", regardless of how they
are managed.
27
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1980), the spent carbon filters undoubtedly contain the CDD
and CDF contaminants (since this is the reason for the use
of the carbon adsorbent). Spent carbon from product purifi-
cation is, therefore, an acute hazardous waste.
The chlorophenol and chlorophenoxy content of the wastes
produced in these operations is expected to be variable.
As outlined above, these compounds, because they are water
soluble, are expected to concentrate in the aqueous wastes,
where they are amenable to biological treatment with adapted
organisms. However, some products (i.e., chlorophenoxy
acids, esters, ethers, amines, sulfides, and salts) precipitate
during processing and will contaminate filters, spent
filter aids, etc. In anaerobic environments, and where
microbial adaptation has not occurred, these chemicals
persist. In fact, this has been demonstrated in some of
the damage incidents outlined below which show the persistence
of these 'compounds, and their ability to pollute the environment
The contamination of chemical intermediates and commercial
chemical products with CDDs and CDFs (Table 3) has several
implications. First, the presence of these contaminants
(up to 100 ppm CDDs and 50 ppm CDFs in trichlorophenol,
100 ppm CDDs and 70 ppm CDFs in tetrachlorophenol, and up
to 30 ppm CDDs and 140 ppm CDFs in PGP) will result in the
contamination of the products derived from them (Table 3),
as well as of the wastes generated in product synthesis.
Thus, the contamination of HCP produced in the 1970's was
due to the presence of CDDs in the 2,4,5-TCP used for its
28
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synthesis (Esposito, 1980). The second result of product
contamination is the fact that their disposal thus raises
environmental concerns. The presence of CDDs and CDFs in
biocides and their formulations can be substantial (see
Table 3). Chlorophenols can contain as much as 100 ppm
CDDS and 60-140 ppm CDFs. Phenoxy herbicides, even those
manufactured in the 1970's, may contain as much as 10 ppm
CDDS, and apparently very low levels of CDFs. Older stocks
of herbicides derived from 2,4,5-TCP are much more heavily
contaminated. Thus, the disposal of these herbicides is of
environmental concern, due to the substantial concentrations
of these potent carcinogens.
The damage incidents outlined below, and the data in
Table 6 show that the levels.of contamination cited above
are of environmental concern. CDDs and CDFs can escape
from these wastes and contaminate airborne dust, stream
alluvia, and food (principally fish). For instance, fish
from rivers near industrial installations manufacturing
chlorophenols and chlorophenoxy compounds are contaminated
with TCDFs, and with TCDD at levels up to ten times the
TCDD concentration at which FDA advises fish consumption
should be limited (Table 6, and Figures 16 and 17).
It is very difficult to estimate the total volume of
CDD- and CDF-containing wastes (see pp. 24 and 25). Some
idea of the magnitude of the problem can, however, be
derived from the fact that a waste disposal site used for
29
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over twenty years for the disposal of wastes from the
production of TCPs and phenoxy herbicides, and a tank used
to store HCP production wastes for only two years, are
estimated to contain 120 and 8 kg of TCDD respectively
(des Rosiers, 1982a) .
TCDD, and, given their physicochemical similarities, the
other CDDs and the CDFs as well, are water insoluble and
bind strongly to organic soil constituents. In fact, with
time, TCDD bound to soil becomes more difficult to desorb
(Phillippi, 1981; Huetter, 1982). Therefore these substances
are not ordinarily expected to leach to groundwater aquifers.
However, these constituents have been shown to be quite mobile
(see section B below) possibly because they were co-disposed
with solubilizing solvents (Table 1), or in situations in
which soil binding sites were exhausted. Furthermore,
these wastes pose a threat of pollution of air and surface
waters resulting from windblown dusts, water run-off or
erosion or flooding of waste disposal sites. All these
scenarios have occurred (see Section V. B. below).
Chlorophenols, especially those of higher degree of
chlorination, can likewise pose a threat of environmental
contamination. Although these compounds undergo photolytic
decomposition, and are susceptible to degradation by
adapted microbial communities, they are persistent where
light and adapted microorganisms are absent. Trichlorophenols
have, for instance, been identified at levels of concern in
30
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various media at Love Canal thirty years after their disposal
(N.Y.S., 1981; USEPA, 1982.). 2,4,6-TCP is a potential human
carcinogen, other chlorophenols taint water and fish at very low
(less than ppb) levels (USEPA, 1980f; 1980g). Chlorophenol-
contaminated wastes thus pose a substantial threat to human
health and the environment if mismanaged.
CDDs and CDFs are mobile and persistent. Chlorophenols
and chlorophenoxy acids are also mobile, and persistent in the
absence of adapted microbial communities (USEPA, 1982c; NYS, 1981)
Thus, the listed wastes, if improperly managed, can present
a substantial hazard to human health or the environment.
As discussed in greater detail below (Section V.C.), the
half-life of TCDD in soil has been estimated as 1.5-10 years;
recent experiments would greatly extend this estimate
(Huetter, 1982). Based on structure-activity relationships
it is reasonable to assume that the half-life of CDDs and
CDFs are similar to that established for TCDD (USEPA 1982a).
A further risk to human health is posed by incineration
of wastes containing chlorophenols, chlorobenzenes, or
j.6/
polychlorinated biphenyls. CDDs and CDFs can be created
by incomplete incineration of such materials (Buser and
Rappe, 1979). Table 5 shows that particulates from industrial
16/ Disposal of materials containing more than 50 ppm of PCBs is
regulated under §6(e) of TSCA. The disposal of hazardous wastes
containing less than this concentration of PCBs is not regulated
by TSCA, and is also not adressed in this listing. The formation
of CDFs by incineration of PCBs is used here as illustrative of
the environmental processes forming CDFs.
31
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incineration can contain up to 80 ppb CDDs. The thermal g
production of CDFs from PCBs is of special environmental
importance. Buser and Rappe (1979) showed that when specific
PCBs are pyrolyzed at 500-700 °C, CDFs are obtained in 1-10 %
yield, together with chlorinated benzenes, naphthalenes, and hydroxy
PCBs. The results of a series of experiments identifying
products obtained from specific PCB reactants are depicted
in Table 2. The CDFs of concern in this document are most
likely to be formed in the course of improper (incomplete)
combustion of the more highly chlorinated PCBs. A possible
reaction scheme, which may explain this array of products,
is shown in Figure 2. Such pathways are important in
explaining the origin of the CDFs found in the environment.
Pyrolysis of chlorobenzenes, as well as reaction between |
chlorophenols and polychlorobenzenes, also yields CDFs
(reaction 3, Figure 1). Mechanisms similar to those depicted
in Figure 2 for the oxidative cyclization of PCBs are
probably operative here as well.
Table 5 shows that fly ash and other particulates from
industrial incineration can contain high ppb concentrations of
CDDs and CDFs. Soot from an electrical fire (in which
transformer fluids containing PCBs and chlorinated benzenes
were subjected to heat from the fire), contained several
hundred ppms TCDFs (one sample contained 645ppm (Table 5)).
Although CDDs and CDFs bind very strongly to combustion
particulates, (Silkworth, 1982), improper management of
32
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these wastes (i.e. , residues from incineration) , such as
co-disposal with solubilizing solvents, or disposal under
conditions where dispersion by wind or water run-off can
occur could pose a threat to human health or the environment.
B. Damagea incidents and environmental contamination.
Improper disposal of dioxin-containing wastes has resulted
in the contamination of stream sediments and wildlife, and
may have injured the health of persons who were, as a
consequence, placed at risk. Most of the damage incidents
described below focused on environmental pollution by
TCDDs. It is reasonable to assume, however, that TCDDs
are a marker substance for the CDDs and CDFs, since their
presence can be postulated from knowledge of the reaction
chemistry outlined in Section II, and of the .common fate
and transport properties of the CDDs and CDFs.
0 In 1971 , four horse arenas in Eastern Missouri were sprayed
for dust control with a TCDD-contaminated waste oil sludge,
a mixture of used oil and oily chemical wastes. The soil
of one arena contained 32 ppm of TCDD (Table 6) and 6500 ppm
of trichlorophenol (Kimbrough, 1980). As much as 30 kg of
TCDDs may have been disposed in this manner. As a result
of their contact with the contaminated soil, hundreds of
11/ These residues may pose a hazard to human health. The
Agency is studying ways to prevent their contamination with
CDDs and CDFs.
33
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birds, several cats and dogs, and many rodents died within
a few weeks after the spraying. In the ensuing three
years, 75 horses died, and ten adults and children became
ill with symptoms that included chloracne, urinary tract
infections, gastrointestinal disorders, headaches, and
joint pain. The long-term consequences of these exposures
are as yet unknown (Beale et al., 1977; Kimbrough, 1980).
The mismanagement circumstances surrounding this incident
have been summarized by Carter et al. (1975). The used
oils used for dust control had been collected from many sources
in Eastern Missouri, and include 68,000 liters of distillate
residues from TCP produced for the manufacture of a chlorophenoxy
compound. These distillation bottoms were later shown to contain
about 350 ppm of TCDD, and were mixed with reclaimed motor
oils and lubricants (Carter et al. , 1975; Kimbrough, 1980). .
° The recently discovered environmental pollution in many
localities in Missouri resulted from the (use in the early 1970's)
of similarly contaminated used oils used a dust suppressant.
Recent environmental studies revealed ppm concentrations of TCDDs
in a residential area in Imperial Mo., and in December 1982 concen
trations above 100 ppb TCDD were measured at several sites in
Times Beach, MO. (USEPA, 1983). Because of the potential health
risks posed by these concentrations of TCDD, and the difficulty
and expense of cleanup operations, EPA determined that the
purchase of homes and businesses, and the relocation of the
Times Beach inhabitants, were the best way to prevent
further potential harm. This operation was estimated
34
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to cost $33 million, not including clean-up costs.
0 Chlorophenols and chlorophenoxy derivatives (2,4,5-T, 2,4-D,
and HCP) were manufactured at a facility in the Midwest in the
early 1960's. This facility manufactured Herbicide Orange
in the 1960's, and Hexachlorophene (of unknown purity) from
1969 through 1971. Wastewater from these operations was
for the most part discharged to unlined lagoons. Wastewater
sludges, filter aids, etc., were in part disposed on-site,
but many were (improperly) disposed off-site (see below).
The river which runs through the plant property has
documented water quality problems which date to 1961. These
problems intensified during the period of HCP manufacture.
The plant discharge included chlorophenols and HCP
(USEPA, 1971; I982b). Problems noted (USEPA, 1982b)
included: very high COD and BOD (these indicate the presence
of degradable chemicals), absence of benthic (bottom-dwelling)
organisms in the river below the plant discharge (their
presence was noted upstream from the plant site); overgrowth
of the alga Sphaerotilus below the plant, and fish kills.
In 1971, a spring about two miles downstream from the plant's
discharge was noted to be contaminated (high COD and BOD), and
in late 1981 the sediment of this spring was discovered to
contain 6 ppt of TCDDs (USEPA, 1982b) . The presence of
TCDDs and TCDFs in fish captured in a river near the plant
has recently been confirmed (see data of Table 6, and Figures
15-17). Within the limits of such environmental monitoring
(the habitat of many fish, unless caged, may extend several
miles) , it is apparent that fish near the Verona manufacturing
35
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site may have levels of TCDDs as high as 120 ppt (Figure 15).
Sixty ppt was observed in fish caught 2.75 miles downstream.
These values are 3-6 times higher than the level at which FDA
advises that fish consumption should be limited (USDHHS 1981b).
Eight miles downstream fish contained 6 ppt TCDDs (Fig. 16).
Very low concentrations (0.8, 2.5, 6.2 ppt) of TCDDs were
found in fish as far as 45 miles downstream from Verona
(Figure 17). These studies also show contamination with
TCDFs. As compared with similar fish collected 2-3 miles
upstream or 8 miles downstream, fish caught near Verona
contain about 6-12 times more 2,3,7,8-TCDD (Figures 15
and 16). Fish caught far downriver from Verona have
low levels (110-1070 ppt) of TCDFs (Figure 17). The
source of this contamination, possibly arising upstream
from La Russell (Figure 17) is at present unknown.
Guidelines for CDF consumption have not been established.
In addition, some wastes from this manufacturing facility
[35,000 gal. of 2,4,5-TCP still bottoms (about 350 ppm
TCDDs, see Table 6), spent filter aids (8 ppb TCDDs indicated
in Table 8, but later data indicate that these wastes
may contain 300 ppm and average 27 ppm TCDDs), as well
as a "high strength refractory wastewater" (200 ppb
TCDDs) (Harris, 1981)] were disposed at several sites:
a) According to anecdotal information, some wastes,
both drummed and in bulk, were disposed on-site in unlined
trenches and lagoons. This disposal may be a contributing
36
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factor in the observed contamination of the Spring River
described above. Deep municipal wells in the area have also
187
been shown not to contain TCDDs (DL=100 ppty7 Preliminary
evaluation by a hydrogeologist, of environmental monitoring
data presented in USEPA (1982b) concludes that it is possible
that the Spring River alluvial aquifer may be contaminated
with dioxin, and urges that a monitoring program of the Spring
River be undertaken (Day, 1982). Harris (1981), and USEPA
(1982b) also called attention to the need for long-range dioxin
monitoring studies to define the extent, if any, of CDD/CDF
contamination problems in the Spring River.
b) 30 - 150 drums of the wastes were dumped from the back
of a truck into a trench on a farm site in 1971. These
wastes included drums containing "muddy water" (360 ppb
TCDD), "chemicals" (140 ppb TCDD), and still bottoms (43
19/
and 319 ppm TCDD) (See Table 5). These wastes leached
into the soil, and caused visible contamination. Following
confirmation of the presence of TCDD, based on expert opinion
that migration could occur, and that the site was not suitable
for hazardous waste disposal, remedial measures were undertaken
to prevent exposure to users of shallow ground water and water
from deeper aquifers. TCDDs have migrated vertically in
the soil for several feet. After considerable cleanup and
187 DL = detection limit.
J_9_/ Other data in the Agency's possession show concentrations up
to 2000 ppm CDDs in the still bottoms.
37
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decontamination activity, the soil of the site still contained
up to 500 ppb of TCDD (Table 6, items 40-46).
20/
c) In 1971-1972, aqueous wastes from HCP manufacture were
stored in the open-topped digester of an abandoned concrete
wastewater treatment plant, and in a small open topped
storage tank. The wastes contained up to 2 ppm of TCDDs
(Table 5). The digester, later filled in with debris, leaked
about half of its 225,000 gal waste contents. A report of the
sampling and analysis studies showed that the bottom residues
of the digester contained about 60 ppb of TCDD (Table 6), and
concludes: "although environmental sampling of surface waters
and private wells has not established any public or environmental
exposure resulting from potential ground-water contamination
by the digester contents... the sampling and analysis performed
to date does not confirm that the contents of the digester
have not leaked or are not leaking to groundwater. Indeed,
there is every reason to believe the soil immediately
surrounding the digester is contaminated with TCDD as a
result of a 1971 leak. . .(P)recipitation on previous
fill-in material creates a hydraulic head which. . .can be
expected to force a slow but continuous loss from the digester."
(Harris, 1981). The digester, trench, and areas of sludge
deposits have been fenced and posted.
20/ These wastes resulted from manufacture on equipment which was
previously used for 2,4,5-TCP production. About half a dozen 30
gallon open-top drums with wastes containing TCDD at 7 ppb were
stored on another farm. Results of environmental monitoring are not
yet available.
38
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d) In order to prevent hoof rot in cattle, several farmers
obtained spent filter aids from Hexachlorophene production,
2i/
containing about 8 ppb of TCDD (Table 5), and spread it on
feedlots and gate areas in such a manner that cattle would
walk through it. The soil of one feedlot, sampled nine
years later, contained up to 830 ppt TCDD. One report
summarizing the above contamination incidents concluded
that "the actions of (the companies involved) in the handling
and disposal of their various waste streams are classic
examples of hazardous waste mismanagment" (Harris, 1981).
These practices may have adversely affected the health and
welfare of some individuals, since there are anecdotal
reports of chloracne as well as liver disease among the farm
families concerned.
0 Environmental contamination occurred at a 2,4,5-TCP/2,4,5-T/
2,4-D production facility in Jacksonville AR. Several
thousand drums of toluene still bottoms with up to 300 ppm
of TCDDs, and 2,4-D wastes containing 20 ppb of TCDDs were
improperly disposed at this facility (Table 5, items 8-22).
It was estimated (45 FR 15595) that, in total, these wastes
contained 25 kg of TCDD. The drums corroded over the years,
and their contents slowly contaminated the environment.
21/ These wastes resulted from manufacture on equipment
previously used for 2,4,5-TCP production. Other
data indicate that these materials may contain as much
as 300 ppm, and average 27 ppm of TCDDS.
39
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a) The soil in the area where toluene still bottoms were
stored above ground contains up to 559 ppb of dioxin (Table
6, item 66), most probably from the substance stored in
the barrels leaking onto the ground.
b) High levels of TCDDs (up to 900 ppb) were found in
the sediments of an on-site cooling pond and equalization
basin (Table 6). The sump below the equalization basin
contained 700 ppb of TCDDs (Table 6, item 65).
c) The sediments of two nearby streams, the Rocky Branch
Creek and Bayou Meto contained significant levels of TCDD.
The highest concentration of dioxin was found in the sediment
of Rocky Branch Creek near the plant site, viz., 17000 ppt
(Table 6, item 53), and further downstream at levels up to
384 ppt (item 75). With the exception of one finding of
1600 ppt, the levels of dioxin in the sediment of Bayou
Meto range up to 70 ppt (Table 6).
d) Significant levels (3-8 ppb) of TCDDs were found in
the sediment of the Jacksonville Sewage Treatment Plant
(Table 6, items 73, 74), which received aqueous discharges from
the manufacturing facility.
e) Fish and other aquatic life in Bayou Meto have accumu-
lated dioxin to levels up to 600 ppt. The court evaluating
_22/
these findings, and expert testimony, concluded that "Dioxins
can and have been transported off the ... site on dust, by
22/ Data of Table 6 show that the "dioxins" referred to include
CfDDs and CDFs.
40
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the action of surface water, the infiltration of ground water
into the landfill areas and equalization basin area, and
when people and equipment move to and from the ... site.
Samples show that dioxin has been transported off the ... site
into fish and sediment in Bayou Meto, and also into the
Jacksonville Sewage Treatment Plant". The court found that the
cited environmental contamination constituted "an imminent
and substantial endangerment to the health of persons", justifying
the need for abatement (U.S. vs. Vertac Chemical Corp., 489 F
Supp. 870, 879 (D. Ark. 1980)).
0 The Hyde Park landfill is located in the extreme northwest
Horner of the County of Niagara, New York. From 1953 to 1975,
Hooker Chemical Company disposed of 84,000 tons of hazardous
wastes, including organic solvents, and wastes from the
production of chlorophenols and phenoxy herbicides at this
site (USEPA, 1980a). The landfill is estimated to contain
about 120 kg of TCDD (des Hosiers, 1979, 1982a) . The 15 acre
landfill contains two drainage ditches which empty into
Bloody Run, a tributary of the Niagara River (see Figure 18).
Bloody Run is a small stream, accessible over much of its
length, which flows through a small residential area abutting
the University of Niagara, before emptying into the Niagara River
through a concrete sewer line. A breach in the landfill
contaminated the stream with organic residues, including TCDD.
Off-site monitoring of TCDD indicated 18-220 ppb TCDD conta-
mination (Figure 8, and Table 6, item 86), averaging 70 ppb,
for an estimated 55,000 cubic yards of stream bed sediment in
41
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Bloody Run. Alluvial contamination decreases as a function
of distance from the landfill, but is still 6 ppb at the
stream's discharge face at the Niagara River (see Table 6 ™
and Figure 18). Remedial action for this site has been
estimated to cost more than $12 million.
0 The Love Canal landfill, located in the southeast corner
of the City of Niagara Falls, New York, was used from 1942
to 1953 by Hooker Chemical Company for the disposal of
21,800 kkg of hazardous waste, including those containing
CDDs, CDFs, and chlorophenols (N.Y.S., 1981; USEPA, 1982c).
Two hundred thirty-nine homes and a grammar school were
built on land around the "canal". Numerous natural drainage
features and three storm sewers underlie the area, and
ultimately flow into two small streams, Black Creek and
Bargholy Creek. The monitoring data summarized in Tables 6 ^
and 9 and illustrated in Figures 22 and 23, illustrate the
fact that TCDDs and chlorophenols have persisted (they were
present 25 years after disposal ceased), and have migrated
into the environment, resulting in the contamination of soil
and sediment at a considerable distance from the dump site.
The high TCDD levels found in some storm sewer sediments (up
to 655 ppb) are particularly worrisome because of frequent
local flooding from sewers. (USEPA, 1982d). TCDD was also
found in the stream beds of local streams (up to 37.4 ppb),
and in crayfish from those streams (3.7 ppb). Remedial actions
now underway, are estimated to cost in excess of $45 million
(USEPA, 1980a). Many legal suits resulting from the contamination
42
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have been filed, and are now in litigation. A judgment approving
settlement (U.S. vs. Hooker Chemical and Plastics Corp., Civil
Action 79-989, January 1981) stipulated cleanup levels which
are technically feasible (i.e., based on analytical detection
levels in water (1-10 ppt) and soil (10-50 ppt) .
0 Disposal of CDD/CDF-containing wastes and/or incineration
of industrial wastes at an industrial facility may have
resulted in the contamination by CDDs and CDFs of the Tittabawassee
River in Michigan, and of fish living in the river. This
contamination is thought to have resulted at least in part
from the discharge of CDD-contaminated scrubber water from
the facility's incinerator (Table 5). Fish in the Tittabawassee
and Saginaw rivers contain up to 80 ppt of TCDD,
up to 240 ppt of TCDDs, and 373 ppt of CDDs (Table 6 and Figure
21). One fish sample contained 255 ppt of CDFs (Table 6, item
199). These values show the potential for CDDs and CDFs to
accumulate to levels of concern: in the case of TCDDs the
concentrations in fish are almost five times those determined
by FDA to be the acceptable limit of TCDD in fish for human
consumption (USDHHS, 1981b).
0 Eighty thousand gallons of Herbicide Orange were stored
from 1968-1977 at a military facility near Gulfport, MS.
Leaking drums caused TCDD contamination of the storage
area and its surroundings. The mean concentration of TCDD
in the soil at the spill sites in July 1977 was 240 ppb
(Gross, 1980). Figure 20 illustrates environmental sampling
43
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results. TCDD levels in soil and in biota (composite
crayfish/mosquito fish samples) decrease as a function of
distance from the storage site. However, even 2.2 miles
downstream of the site there was 20 ppt TCDD in fish. The
statement summarized: "these observations appear to be at
odds with the commonly held view that TCDD in soil is
immobile" (Gross, 1980).
These damage incidents amply demonstrate that these
wastes contain high concentrations of CDDs and CDFs, that
these toxic substances can migrate from the wastes if they
are mismanaged, that they persist in the environment, and can
become part of the human food chain, posing a threat to human
health of serious irreversible or incapacitating disease.
In addition, the following damage incidents concerning
PGP were identified from O.S.W.E.R Superfund and O.S.W enforcement
23/
action files, as well as from Regional sources.
0 Selma, CA. This Superfund site covers 12 acres, and is located
about half a mile from a residential area including light industry
and agriculture. Wood treating operations began at this site in
1936; pressure treatment was used since 1965. Pressure treatment
solutions used included PCP dissolved in mineral spirits, heavy
oil, ketones, or aromatic oils. More than a million Ib of PCP
were used between 1970 and 1979. Process wastes were discharged
into an off-site drainage ditch, several on-site disposal wells,
23/ Wastes resulting from the use of PCP in wood preservation
operations are not covered by this listing-.
44
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and an unlined pond. Sludge removed from tanks was placed in piles
on-site. Elevated levels of PGP were found in soil and ground
water, both on- and off-site. An aquifer that is the sole source
of water in the area is located about 25-30 feet below the site.
Soil is contaminated with 0.002-4500 ppm of PGP; ground water con-
24/
tained 0.001- 2.3 ppm of PGP. (Schultz, 1983.)
0 Haverford, PA. Wood preserving facility from 1947-1963. Liquid
wastes were disposed into a well beneath the plant. A nearby tribu-
tary, Naylor's Run, was contaminated. (Superfund priority site.)
The environmental consequences of the management at this site are
in the peer-reviewed literature, and show 230 ppb PGP in creek water
one mile downstream from the facility in 1974. (Fountaine, 1976.)
0 Mena, AR. Active wood processing plant. Waste products from
previous operations (1967-1977), including PGP, have contaminated
surface and possibly subsurface waters. Monitoring found 0.036
ppb PGP in drinking well water, and 118-2000 ppm PGP in the soil
of surrounding residential areas. (Superfund priority site.)
0 Denver, CO. A wood treating facility occupying 64 acres
in an industrial section. From 1964 to 1981, PGP was used to
treat and preserve wood. Contamination of soil, ground water,
and surface water has been documented. Ground water north of the
facility contains 1.1 ppm of PGP. An unlined irrigation ditch
along the northern boundary of the site also contains traces of PGP.
24/ The Ambient Water Quality Criterion for PGP, which was based on
organoleptic criteria, is 0.03 - 1.0 ppm. (USEPA, 1980).
45
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Pensacola, FL. Currently inactive wood treating facility
operated from the early 1900's to 1981. Wastewater contaminated
with PGP was discharged into two 80,000 gal. percolation ponds.
6ppm PGP was found in ground water near the facility. (Superfund
priority site) .
0 Live Oak, FL. Abandoned wood preserving facility (1964-1977)
that used creosote and PGP. Wastewater was stored on-site in a
five acre surface impoundment. Soil, and possibly ground water
and a surrounding wetland, are contaminated. Surrounding residences
use private wells as a water source. (Superfund priority site) .
0 Whitehouse, FL. The 11 acre site of a wood preserving company
located in a residential district, whose residences obtain drinking
water from private wells. The facility has treated wood with PGP
since 1950. Complaints of oily residues on the ground, and an
abnormal taste in the water of one of the private wells led to an
investigation. 4-12 ppm of PGP was detected in two monitoring wells
but in none of four private wells tested. In addition, chlorophenol,
dichlorophenol, and tetrachlorophenol were identified, but not
quantitated. (Superfund priority site.)
0 Caldwell, ID. Site of a lumber company. Spillage occurred
from tanks and drums containing PGP. Ground-water contamination
was detected in the aquifer used for the city water supply.
(Superfund priority site).
0 Pocatello, ID. This site was used by a railroad company to
treat rail ties, probably with PGP, at an unknown location in the
46
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company's yard. In 1980, the State sampled wells in the vicinity
and detected PGP at parts per trillion. In March 1983, EPA
found 9 ppm of PGP in the sludge, and 4.5 ppm PGP in the liquid
phase of an unlined impoundment on-site. (Superfund Priority
Site.)
0 Galesburg, IL. Railroad tie treatment facility, operating
since 1907. Ground water in the vicinity of waste sludge
ponds, the drip track area, and a spray irrigation field is
contaminated with significant levels of phenols. The
contaminated water is leaching into surface water: monitoring
data showed <0.4 ppb to 17 ppm PGP. The possibility of ground-water
pollution is of great concern because the site is located
over an aquifer that is the water supply for local residents.
There is potential for surface water contamination of nearby creeks
as well.
0 Joplin, IL. Operations at a wood preserving facility using
creosote and PGP have contaminated the aquifer underlying the
plant, as well as contiguous surface waters. In ground water, PGP
concentrations range up to 3.4 ppm; 120 ppb and 9 ppb were measured
in two springs, on- and off-site, respectively. 2 ppm was detected
in Joplin Creek, downstream from the site. (International Paper
Co., 1983)
0 Pere Marquette, MI. Landfill one mile east of Lake Michigan,
operating from 1971-1978 resulted in ground water contamination
with PGP and other compounds. (Superfund priority site).
47
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Libby, MT. Ground-water contamination with PGP by unknown
or undefined wood preservative and/or paper mill practices.
Three wells showed detectable levels of PGP; two wells approached
or exceeded ambient water quality criteria levels. (Superfund
priority site) .
0 Newport, DL. Wood preserving plant (in operation from 1929-1972).
In later years, the pressure injection process, using PGP containing
"traces of dioxin", dissolved in fuel oil was used. A sump was used
for effluent collection. Standing water sample contained 20 ppm of
PGP. There is possible ground water, surface water, and soil
contamination.
0 Cass Lake, MN. Wood preserving operation. This facility dis-
charged 12,000 gal. of wastewater daily into an unlined aerated
pond. PGP was detected in ground water at concentrations exceeding
ten times the EPA AWQC level, and there is contamination of local
wells and a nearby beach.
0 Brooklyn Center, MN. A wood treatment facility using PGP
since 1965. From 1965 until 1980, a pond was used for the disposal
of waste from this process. In addition, general burial of sludges,
and at least two large wood treating solution spills, in 1953 and
1968, occurred at the site. Ground water beneath the site is conta-
minated with PGP: up to 50 ppb PGP was detected in drinking
water wells in the surrounding community, and 3.8 ppm of PGP has
been detected in groundwater beneath the site. (Minnesota (MNCPA),
1983.)
48
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0 New Brighton, MM. Site of two wood treatment facilities
operating on a 68-acre site using PGP. Sludges from this operation
f
were discharged to a surface impoundment in a wetland on the site.
Contaminants from the site have migrated from the impoundment into
the surrounding ground water. Nearby wells periodically contain
low levels of the chemicals used at the site. Standing water and
soil on-site contain up to 3300 ppm (average, 1400), and 140 ppm
of PGP, respectively. Miscellaneous debris contains per cent levels
of PGP. The State is considering plans to remove the sludge and
contaminated soils. Hexachlorinated dioxins were identified (but
not quantitated) in the standing water. (Superfund priority site.)
0 Broken Bow, OK. Wood preserving facility using surface im-
poundments for storage and recovery of PGP. Wastes contained 5.9 ppm
of PGP. There is contamination of soil,.ground water, and a nearby
creek: soil near the creek contains 0.32 ppm PGP; sediment in the
creek contains 1-9.9 ppm of PGP.
°Laramie, WY. A tie treating facility covering 100 acres,
just southwest of the city. The facility has been in operation
since the 1880s. Pollutants, including PGP, have migrated
from unlined surface impoundments contaminating the shallow
ground water beneath the site, as well as the Laramie River.
The extent of the contamination problem has not yet been
defined. (Superfund Priority Site.)
° Conroe, TX. Contamination of soil with PGP and HxCDDs, and
of water with PGP was recently discovered in a residential area
49
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bordering a wood treatment facility. At the border of the facility,
soil samples contained <1 - 110 (average 28) ppm of PGP; samples
taken from residential yards showed <1 - 30 (average 12) ppm
of PGP. Total HxCDD values were 1.5 - 12 (average 4) ppb, and
HxCDFs were found in 1.7 - 21 (average 9.5) ppb concentration.
(Superfund Priority site.)
An extensive fish kill in a Swedish river was traced to the
release (caused by vandalism) of a chlorophenolic wood treating
solution. One week after the release, 2,4,6-TCP, 2,3,4,6-TCP,
and PGP were distributed throughout the 15 km long system of
streams and lakes that was sampled. About 8 km downstream
from the release point, the total concentration of these three
chlorophenols was 19 ppb about a month after the incident
soil/sediment concentrations were not measured). Fish caught
about 10 km downstream accumulated 0.57-1 ppm of these chlorophenols ^
in liver. These analyses illustrate the persistence and bioaccumulation
of these toxicants. (Renberg et al. 1983).
0 Extensive contamination of soil and water with chlorophenols
occurred in the vicinity of two finnish sawmills using chlorophenol
wood preservatives. Up to 45 ppm PGP (60-80% of the total chlorophenols)
was found in the soil of one saw mill. The main components of the
wood preserving solution (2,4,6-TCP, 2,3,4,6-TCP and PGP) were the most
abundant at most sites, indicating the environmental stability of
these chlorophenols in soil. Lakes near these saw mills contained about
40 ppb chlorophenols (mostly 2,3,4,6-TeCP) (these levels are 40 times
greater than EPA's WQC for this chlorophenol). (Valo et al., 1984).
0 Another documented damage incident concerns the accidental
release, in December 1974, of wastewater containing PGP in fuel
50
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oil, which overflowed the banks of a wastewater impoundment at
the Davis Timber Company in Hattiesburg, MS. The oil and PGP
entered a creek leading to a lake, resulting in an extensive
fish kill. An additional fish kill was observed two years later.
This incident has been described in the open literature (Pierce
et al., 1980). These investigations showed that, despite some
environmental degradation, PCP remained the primary contaminant,
and caused "thorough contamination of lake sediment". Two years
after the release, PCP concentration in sediments was about
0.05-0.3 ppb, ten to one hundred times higher than background
concentrations found in sediment samples from an isolated pond
that received no industrial or agricultural drainage.
In addition, there are several studies illustrating the fact
that PCP and HxCDDs have contaminated the human food chain. For
several years, the FDA has surveyed foods for the presence of
PCP and HxCDDs. This sampling leads FDA to estimate that PCP
levels in the adult total diet result in average daily ingestion
of about 3 mg PCP/kg/d.ay. The majority of this ingestion results
from two food composites: "meat, fish and poultry", and "oils,
fats and shortenings." (P. Lombardo, 1983). The possible
long-term sequelae of these exposure levels has not been determined.
In 1983, FDA found that rendered fat and meat and bone
meal samples derived from PCP-treated sheepskins, and used
for the preparation of poultry feed, contained up to 78 ppm
PCP and "total dioxins" (HxCDDs, HpCDDs and OCDDs) up to 94
ppb. This resulted in eggs contaminated with up to 0.3 ppm
PCP and about 221 ppt of HxCDDs, HpCDDs and OCDDs. (Hill,
1983). Although this contamination did not result from the
mismanagement of industrial waste, it illustrates the ease
51
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The above damage incidents amply illustrate that PGP wastes
are frequently mismanaged, that PGP can migrate from the wastes if
they are mismanaged, that PGP persists in the environment, and
that PGP and HxCDDs can enter the human food chain. The resulting
potential for harm to human health through irreversible or
incapacitating disease is outlined below.
C. Health and Environmental Effects.
The health and environmental effects of the CDDs, CDFs,
and chlorophenols are more fully described in the Health
and Environmental Effects Profiles.
1. Structure-activity relationships in the mechanism of
action, toxicity, and persistence of CDDs and CDFs.
The toxicokinetics of these substances is the subject
of two excellent recent reviews by Poland and Knutson (1982),
and by Neal et al. (1982). The extreme toxic potency of the
CDDs and CDFs (see below) suggests that these substances
affect some fundamental cellular processes. Studies of
the biochemical effects of CDD and CDF intoxication have
focussed on some of these fundamental proceses , viz. induction
of hepatic microsomal AHH monooxygenase activity, in vitro
keratinization, and stereospecific binding to a specific
cytosolic protein (Kende and Wade, 1973; Poland and Glover,
1974; McConnell et al., 1978; Poland et al., 1979; Bradlaw,
1979, 1980; Moore, 1980; Knutson and Poland, 1980; McKinney
and McConnell, 1982).
There is a strong correlation between the systemic
toxic potency of CDDs and CDFs, their potency as enzyme
inducers, their response in the in vitro keratinization test,
and their ability to bind to the cytosol receptor.
52
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Those CDD and CDF congeners which have high acute toxicity,
which are potent enzyme or keratinization inducers, and which
bind strongly to the cytosol receptor, share certain structural
features:
1) they have halogen atoms in at least three lateral
(2,3,7,8) ring positions; and
2) they have at least one unsubstituted ring position.
The Agency recognizes that within congener groups there
are differences in toxicity (Bellin, 1984; Kociba, 1984).
There is, for instance, a 370-fold difference in acute
toxicity between the 1,2,3,7,8- and 1,2,4,7,8- PeCDD isomers
(see Table 7), and 1,2,3,7,8-PeCDD is 100 times more active
than 1,2,3,7,9-PeCDD in the j.n vitro keratinization test
(Knutson and Poland, 1980). (However, even the less toxic
isoraer has extremely high acute toxicity (LD50,gp =1.1
mg/kg), and therefore is of concern to the Agency). The
ED50 for AHH induction in rat hepatoma cells is 50 times
greater than that for 1,2,3,8-TCDD, and several penta- and
hexa-CDDs and CDFs are not responsive in this assay (Bradlaw,
1981).
Because most of the isomers of the listed congeners are
toxic, albeit to different degrees, and because the Agency
believes that most of these wastes contain a certain
percentage of the most toxic (TCDD) components, it is
appropriate and permissible to rely, in part, on the known
structure-activity relationships to establish the potential
toxicity of these wastes. Moreover, the identification and
analysis of individual isomers would be quite costly, and not
necessary because of the toxic nature of the CDDs/CDFs. The
53
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Agency thus determined that dibenzo-p_-dioxin congeners are
toxicants of concern in these wastes.
2. Health and Environmental Effects of CDDs.
The Health and environmental effects of CDDs are
extensively discussed in three peer reviewed documents
prepared by EPA (USEPA 1984a; USEPA 1984c; and the HEP
prepared for this listing. The following highlights this
material.
a. Exposure: environmental fate and transport of CDDs.
It has been estimated that the fraction of human exposure
that can be directly attributed to drinking water alone is
probably low (USEPA, 1981c).
The low solubility of CDDs (0.2 ppb for TCDD, Table 1) and their
high affinity for soils with high organic content (Kearney, 1972; '
Ward and Matsumura, 1978; Homberger, 1979) would seem to
decrease the likelihood of ground-water contamination
(Helling, 1973; Matsumura and Bezenet, 1973). However, in
soils with low organic content, or soils whose binding
capacity is exhausted, or where CDD-containing wastes are
co-disposed with solubilizing solvents (see Table 1), the
likelihood of ground-water contamination by CDDs increases
greatly. CDDs could also conceivably reach ground-water
via channelization due to fracturing, or as a consequence
of desorption due to changes in soil pH (USEPA, 1981c).
In some instances, despite their low solubility, water
transport can be appreciable. (Helling et al., 1973). For
example, studies on the fate of TCDD in a microagroecosystem
54
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show very little vertical movement of TCDD in soil (Nash
and Beal, 1978), but water transport can nevertheless occur:
only 7 weeks after three applications of Silvex® containing
7500 ppb of 2,3,7,8-TCDD, water leachate contained 50 - 60
ppt of TCDD. In areas of heavy rainfall and/or sandy soil,
vertical soil migration, and lateral displacement via soil
erosion and runoff also can occur (Esposito, 1980).
Estimates of the half life of TCDD in soil range from 1.3
to more than 10 years (USEPA, 1981 a; NRCC, 1981). Laboratory
studies show that the half-life of TCDD in sediment-containing
Wisconsin lake waters is about 1.5 years; the half life in
water without sediment was longer (Ward and Matsumura, 1977).
However, these values may greatly underestimate the true value,
since it has recently been shown that radiolabelled TCDD adsorbed
to soil becomes progressively more resistant to extraction
during incubation experiments (Phillippi et al., 1981; Huetter,
1982). Additionally, TCDD is highly resistant to microbial
degradation. (USEPA, I981a; NRCC, 1981).
One of the major environmental concerns regarding CDDs
focuses on their persistence in sediments, because of the
biological magnification which may result. From studies on
model systems, it has been estimated that sediments and suspended
solids accumulate a million times more TCDD than the water in
which they occur. Biota which live in sediments containing
adsorbed CDDs ingest these contaminants, and bioconcentrate them.
Bioconcentration of TCDDs has been determined in model
ecosystems in studies which were reviewed by Esposito (1980).
55
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Bioaccumulation ratios are species dependent. For the mosquito
fish, the value was 4875 after 7 days of exposure. In a different
study, at soil concentrations as low as 0.1 ppb, ^C-TCDD
accumulated in the organisms tested with accumulation ratios
as high as 24,000 for mosquito fish, and 2,000 for catfish.
The weighted average bioconcentration factor for TCDD in
the edible portion of aqueous organisms consumed by Americans
is estimated as 122,000 (USEPA, I981a).
The largest portion of the daily intake of CDDs probably
comes from the fatty portion of foods such as milk, beef, and
fish. Their contamination could be importantly affected by
concentrations of CDDs in soil, dust, and water sediments.
TCDD has been reported in the edible portion of many fish, and
is highest in bottom feeders like catfish, suckers, and carp
(see Table 6). Animals feeding on contaminated forage accumulate
TCDD in their adipose tissue (Table 6), posing a danger of
human exposure. Human exposure could result from inhalation and
ingestion of airborne particulates, or from ingestion of water
contaminated with such particulates. Wind dispersion of airborne
contaminated dust particles is a known dispersion mechanism
for dioxins. Airborne dust from improperly disposed hazardous
wastes was shown to contaminate contiguous areas. For example,
near the Hyde Park landfill, dust on the rafters of an industrial
facility at which no internal TCDD contamination could occur,
contained 700 ppt TCDD (Table 6, item 103).
56
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b. Metabolism of CDDs.
Studies of the metabolism and biological storage of CDDs have
been carried out only for TCDD, and the rat, mouse, and dog are the
species best studied (Rose et al., 1976; Hay, 1981 Koshakji, 1984).
About 70-86% of orally administered TCDD is absorbed, with
an elimination halflife of about a month. As compared to
TCDD dissolved in ethanol, adsorption of TCDD to soil causes a
30% reduction in its biological availability (Poiger and Schlatter,
1980 McConnell, 1984). Fecal elimination is the major route
in the hamster, mouse, and rat (53% of the ingested dose),
with about 13 and 3 percent of the ingested dose appearing in
urine and exhaled air, respectively. Dermal absorption of
CDDs occurs (USDHHS, 1980b), but, in the case of wastes, has
not been quantified. There are also no data to indicate what
fraction of inhaled CDD adsorbed onto respirable dust particles
is absorbed.
Most of the absorbed TCDD which is stored (mainly in pancreas,
liver and fat) is not metabolized (Hay, 1981). However, about 1%
of the absorbed material is metabolized to poleracidic metabolites
which are converted to glucuronides before excretion in urine and
feces (Koshakji, 1984). It has been proposed that TCDD may be
metabolized to (DNA-reactive) arene oxides (Guenther et al.,
1979). Long term incubation with adapted microbial cultures
likewise showed minimal conversion to hydroxylated metabolites
(Phillippi et al., 1981).
A protein which strongly binds halogenated dioxins (and
57
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dibenzofurans) has been isolated from the cytoplasm of several
tissues of rats and mice (Carlstedt-Duke, 1979; Greenlee and
Poland, 1979; Okey et al., 1979).
The total body burden of TCDD in human beings is low (Table
6), but it is persistent; thus, CDDs (CDFs) can be detected
in blood years after exposure (Hay, 1981). TCDD has been
detected at levels from 20 to 173 ppt in adipose tissue of
three Vietnam veterans who were heavily exposed to Agent Orange.
Tissue samples from other Vietnam Veterans and controls contained
less than 20 ppt TCDD (Gross, 1984).
c. Health Effects.
TCDD is the isoraer whose biochemical and toxicological
effects have been best studied in the laboratory.
The pathologic effects produced in a given species by the
toxic CDD congeners are similar to those of TCDD, differing
only in the intensity of the effect produced by a given isomer.
CDDs are among the most acutely toxic substances known with
LD50's (in the relatively resistant rat) in the ug/kg range
(see Table 7). The structure/activity relationships outlined
above are readily apparent; species differences in LD50 are
considerable, and are thought to result from species differences
in the metabolism of these compounds. The systemic effects in
animals of long-term, low level exposures were recently reviewed
(USEPA, 1981c). Even at very low doses (0.001 - 0.01 ug/kg)
various studies observed some mortality, lethargy, decreased
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body weights, liver pathology, including biochemical evidence
of liver damage, thymic atrophy, decreased lymphatic tissues,
disturbances of porphyrin metabolism and mild adverse effects
on reproductive systems.
1. Biochemical effects.
TCDD has a dramatic influence on various enzyme systems in
many species, including man (Esposito, 1980). TCDD is by far
the most potent known stimulator of the microsomal enzyme
system, including hepatic amino levulinic acid synthase (ALAS)
and aryl hydrocarbon hydroxylase (AHH) (Poland and Glover, 1974)
It also induces other enzymes, such as ligandin (a protein
which transports organic anions), and enzymes important in
glucose and heme metabolism, such as ALAS.
2. Effects in human beings.
Because human exposure to CDDs usually occurs along with
exposure to other chemicals (e.g., 2,4,5-T, chlorophenols,
CDFs), the clinical effects observed are not always
ascribable to CDDs alone. However, by extrapolation of the
known effects of CDD exposure in animals, the chronic human
effects can be estimated.
Human CDD exposures have resulted from 23 accidents in
the manufacture of 2,4,5-TCP and from use of phenoxy herbicides
contaminated with CDDs. As is the case in animals, the
appearance of the toxic effects of exposure to dioxins is
somewhat delayed. The body systems that are affected are
the skin, nervous system, liver, lipid metabolism, general
metabolic state, cardiovascular system, blood forming organs,
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and (perhaps) the immune system.
Chloracne is commonly found in workers exposed to halogenated
aromatics (Taylor, 1979) and is said to be a sensitive indicator
of overexposure to TCDD (Reggiani, 1981). The acnegenic
potency of CDDs is related to their structure. TCDD is
one of the most potent chloracnegens known (Beljan, 1981;
Taylor, 1979).
Severe nervous system effects also occur with CDD exposure,
including pain and weakness in the lower extremities, often
accompanied by difficulty in walking and limb coordination.
Peripheral neuropathy, hyperirritability, sleep disturbances, and
"neurasthenia" have been reported.
Effects on the liver range from abnormalities in liver
enzymes and toxic hepatitis to porphyria cutanea tarda, a
systemic disease with high fatality rates. Elevated serum
cholesterol and serum lipids, urinary tract infections,
joint pains, and gastro-intestinal disorders have also been
enzymes and toxic hepatitis to porphyria cutanea tarda, a
systemic disease with high fatlaity rates. Elevated serum
cholesterol and serum lipids, urinary tract infections,
joint pins, and gastro-intestinal disorders have also been
noted (Beljan, 1981; Reggiani, 1981; Pasderova-Vejlupkora,
1980; USEPA, 1981c).
3. Reproductive, teratogenic, and mutagenic effects.
TCDD and HxCDD produce adverse reproductive and teratogenic
effects in rodents and monkeys at extremely low dose rates.
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These effects were recently reviewed (USEPA, 1981c), and
are outlined in greater detail in the Health and Environmental
Effects Profile (HEP). In brief, reproductive effects are
seen in rats dosed at 0.125 ug/kg/day throughout pregnancy
(fetal mortality, fetal intestinal hemorrhages, early and
late resporptions), with no signs of maternal toxicity. In
mice and rats, 1 ug/kg/day on day 6-15 of gestation results
in increased incidence of kidney abnormalitites, cleft palate
formation, and intestinal bleeding in offspring. Certain mouse
strains (C57B/6J) are more susceptible than others (AKR/g)
to these teratogenic effects (Pratt, 1984).
In a three generation reproductive study Murray et al. (1979)
noted that 0.1 ug/kg/day significantly decreased fertility of
rats. For the F1 and F2 generations there were significant de-
creases in fertility, litter size, gestation, and postnatasl
survival even at 0.01 ug/kg/day. Although there also was a
statistically significant decrease in these last two parameters
at 0.001 ug/kg/day, the authors interpreted this dose as a NOEL
for reproductive effects. From a critical re-evalaution of the data,
Nesbit and Paxton (1982) concluded that 0.001 ug/kg/day is an
effect level for TCDD, and that a NOEL has not been established
in this study. Schantz et al. (1980) determined that studies
such as Murray's (1979) study stood "only a poor chance ... at
detecting a significant effect". A reproductive study in
monkeys noted abortions, stillbirths, and failure to conceive
at a calculated daily dose of 0.0015 ug/kg/day (Schantz, 1979).
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Administration of TCDD to pregnant rats results in the
induction of many enzymes in several fetal tissues. Exposure
of newborns to TCDD by lactation causes enzyme induction.
TCDD is concentrated in the milk, and, particularly early in
lactation, the pup can actually receive a higher dose (in
ug/kg) than was administered to the mother (Berry et al.,
1977; Lucier and McDaniel, 1979). Pregnant monkeys are
"unexpectedly sensitive" to TCDD,... "as susceptible to TCDD
poisoning as the... guinea pig." (McNulty, 1984) These
investigators found that TCDD is fetotoxic in the monkey, but
the high rate of abortion (even at a dose of 0.2 ug/kg)
prevented conclusions as to its teratogenic potential. Schwetz
et al. (1973) studied the effects of 0.1 - 100 ug/kg/day HxCDD
in rats. There was a significant-, dose-related, increase in . .
maternal body weight gain, increased liver pathology, decreased
body fat, and increase in late resorptions. At 100 ug/kg/day
there was an increase in cleft palate formation, abnormal
vertebrae and split sternebrae.
4. Carcinogenic effects.
TCDD is carcinogenic in mammals at extremely low doses (see
Figure 21). In an oncogenic study in rats, 100 ng of TCDD/kg/day
increased the incidence of liver, lung, and nasal tumors. At
10 ng/kg/day, an increase in neoplastic liver nodules was
noted, and at 1 ng/kg/day some pre-neoplastic liver changes
were observed (Kociba et al., 1978). These studies suggest
that TCDD is an order of magnitude more potent a carcinogen
than aflatoxins. Two NCI bioassays also concluded that TCDD
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is carcinogenic in rats and mice when administered orally, or
by dermal application (DHHS I980a,b).
An NCI bioassay (DHHS,1980a) showed that oral administration
of a mixture of HxCDDs is carcinogenic in rats and mice.
Dermal application of these hexachloro isomers resulted in
a statistically significant increase in fibrosarcomas of the
skin, but, in line with the NCI/IARC criteria, such results do
not demonstrate the material's carcinogenicity when applied by
this route.
EPA's determination that the mixture of HxCDDs is carcinogenic
has been disputed by Dr. Squire, who reviewed the NCI data
(Squire, 1983), and noted a lower incidence of neoplastic
nodules in female rats than that reported by NCI (and originally
accepted by EPA). He evaluated several of the lesions diagnosed
as tumors by NCI as non-neoplastic regenerative nodules, and
concluded that there is only "equivocal" evidence that these
HxCDDs are potential human carcinogens.
As a result of these comments, experts from GAG and from
the National Toxicology Program (NTP) have reviewed both
Dr. Squire's evaluation and the histology slides gathered in
the NTP study. As a result of their re-evaluation, they again
concluded that there is sufficient evidence that the mixture of
HxCDDs is carcinogenic, as indicated by a statistically significant
increased incidence of liver tumors in female rats and in mice
of both sexes (Haberman and Bayard, 1983; McConnell, 1983).
The review led GAG to estimate that the carcinogenic potency
of the two HxCDDs ranges from 0.59 per ug/kg/day (male rat) to
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11 per ug/kg/day (male mouse). GAG recommended that 6.2 per
ug/kd/day, derived from hepatocellular carcinoma and adenoma
data in male mice and female rats (the test systems in which
the response was most strongly evident), be used as the upper
limit potency estimate for HxCDD (McGaughy, 1984). Either of
these estimates makes HxCDD one of the most potent carcinogens
identified by the Agency.
The mechanism of carcinogenic action of TCDD and HxCDD is
not yet established. Several recent studies investigating the
interactions between TCDD and various carcinogenic PAHs, demonstrate
the complexity of the interactions between TCDD and other
carcinogens in vivo (Pitot et al., 1980; Berry et al., 1979;
Cohen et al., 1979; Giovanni, 1979). Based on the experiments
of Kociba (1978), CAG's most recent estimate of the potency
factor for TCDD in humans, q-|*, is 1.56 x 10-" per mg/kg/day, ™
showing that TCDD is a more potent carcinogen than aflatoxin
(USEPA, 1980c). However, the rodent bioassay may greatly
underestimate the potential low dose risks of exposure to TCDD
in the presence of other environmental carcinogens that are
activated by AHH (Longstreth and Hushon, 1982).
There is impressive epidemiologic evidence associating
soft tissue sarcomas, lymphomas, and stomach cancer with
and exposure to phenoxy herbicides and/or TCDDs (USEPA 1980d,
I981g; Acheson, 1982; Blair, 1981). These studies cover agricul-
tural and forestry workers exposed to herbicides, as well as
industrial workers exposed to TCDD. Workers in occupations
associated with exposure to PGP are also at increased risk of M
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several forms of cancer (see below). Since these are reports
of occupational exposure, the -etiologic agent cannot be unambiguously
identified. However, since HxCDDs are potential human carcinogens,
and since these contaminants are present in commercial PGP in
concentrations averaging about 15 ppm, they could be responsible.
5. Immunotoxic effects.
Thymic atrophy is a pronounced effect of the CDDs. The
immunotoxic effects of TCDD are outlined in the HEP. Recent
investigations show that HxCDD is responsible for some of the
immunosuppressive effects of technical grade PGP. Daily oral
exposure of adult female mice for 14 days to 10, 30, or 100 mg
technical grade PGP/kg body weight suppressed the peak (day 4)
IgM antibody response to sheep red blood cells by 44%, 53%,
and 72%, respectively. Similar exposure to purified PGP had
no effect. Exposure to 1,2,3,6,7,8-HxCDD at 0.2, 1.0, and 4.0
ug/kg (concentrations corresponding to those resulting from
the exposure to technical PGP) achieved 30%, 47%, and 62%
suppression of the peak antibody response. Addition of 0.1 ug
of'1,2,3,6,7,8-HxCDD or 1,2,3,7,8,9-HxCDD to spleen cells of
untreated mice caused 80% suppression. (Holsapple et al., 1984)
d. Aquatic toxicity (EPA, I981c)
TCDD is toxic to fish and invertebrates at levels as low
as 1 ng/1 (ppt). At 200 ppt TCDD, invertebrates show moderately
reduced rates of reproduction resulting from 17 to 55 day
exposures. Fish exposed at 1 and 56 ppt for 24 to 96 hours
suffer 50 - 100 % mortality, expressed several weeks after
cessation of exposure. No data are available concerning the
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toxicity of TCDD to saltwater aquatic life, nor on its effects
on aquatic or terrestrial plants.
e. Existing guidelines and standards.
From studies on carcinogencity in rats, EPA has estimated
257
that lifetime exposure of people to 6 fg/kg/day engenders an
excess cancer risk at the 10~6 level. (USEPA 1984). The
resulting draft ambient water quality criterion for the protection
from the potential carcinogenic effect of exposure to TCDD
from the ingestion of contaminated water and aquatic organisms,
based on a 10~6 excess cancer risk, is 1.3 x 10~8 ppb. (USEPA,
1984).
The above exposure/risk estimates are based on upper boundary
estimates for the dose-response extrapolation, and may be
overestimates
The National Research Council of Canada (NRCC, 1981) has
estimated that ingestion of less than 30-90 fg/kg/day
should be sufficient to protect for the risk of cancer at
the 10~6 risk level.
The FDA (USDHHS, 1981b) advises that fish containing
25-50 ppt of dioxins should be eaten only twice a month by
permanent residents, who ordinarily might eat a fairly
large amount of fish from the area, and only once a week by
sport fishermen, and that fish containing more than 50 ppt
should not be eaten. Canada has established a guideline of
20 ppt for TCDD in commercial fish found in Lake Ontario.
2_5/ 1 fg = 10-15 gm.
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(USDHHS, I981b). The Canadian guidelines were based on
chronic systemic toxicity considerations and do not consider
cancer risk. The FDA determined 300 ppt (i.e., 0.3 ug/kg)
as a level of concern for the presence of HxCDDs in chicken
and eggs (Bolger and Biddle, 1983).
No draft criterion is available to protect fresh and
saltwater species from TCDD toxicity.
Criteria or guidelines to protect against the risks inherent
in exposure to other CDDs have not been developed. However,
from the point of view of potential carcinogenicity, at any
risk level, the allowable dose for HxCDDs is only about
twenty times that calculated for TCDD (USEPA, I984c).
3. Health and environmental effects of CDFs.
a. Exposure: environmental fate and transport (USEPA, I982a)
The widespread use of the many chlorinated chemicals of
commercial importance which are contaminated with CDFs render
them fairly continuously available to ground water and run-off
water. However, the similarity in molecular configuration,
vapor pressure, and calculated partition coefficient between
CDDs and CDFs (Table 1) provide a reasonable basis for the
following comparisons. In common with CDDs, CDFs are expected
to be almost insoluble, and to adsorb strongly to organic
soil components. As is the case for CDDs, this suggests
that transfer to water may occur only where soil binding
sites are exhausted, where these chemicals are co-disposed
with solubilizing solvents (Table 1), or where entrainment
by run-off water or windblown dust can take place.
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CDFs are also expected to be persistent in the environment.
The molecular similarity between CDDs and CDFs implies that
CDFs will be found to be as resistant to microbial degradation
as are CDDs.
CDFs have been detected in the water of a river receiving
industrial waste from a chemical manufacturing plant, and
in the bay draining this river (Table 6). Thus, there is
potential for low-level contamination of ground water,
rivers, and streams with CDFs. Data currently available
are not sufficient to estimate the magnitude of the exposure
to CDFs in ambient water.
CDFs are expected to bioaccumulate in a manner similar
to that of the CDDs, and they have in fact been found in
wildlife and in exposed human beings (Table 6). BCF's have
not been experimentally determined for these substances,
but the physicochemical properties of CDFs, in particular
the Kow (Table 1) lead one to expect a BCF similar to that
estimated for TCDD, i.e., about 50,000 - 100,000.
b. Metabolism.
The absorption, distribution, and clearance of CDFs have
been studied in guinea pigs, rats, and monkeys, using mixtures
of isomers, and also using pure C^ ^--labelled TCDF.
These studies show large differences in species sensitivity
and biological half-life (Table 8). In all three species
(guinea pig, monkey, and rat), fat and liver are the most
significant repositories, but the guinea pig (by far the
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most sensitive to the acute effects of CDFs) absorbs much
more of the administered CDF than do the rat or the monkey,
and the biological half-life and acute toxicity are greater
in the guinea pig than in the rat. It has been suggested
(Birnbaum, 1980; loannou, 1983; Poiger, 1984) that the
ability to metabolize and clear TCDF may explain the rat's
relative ability to resist the acute toxic effects of this
compound. Although the disposition of TCDF in the monkey
and rat is similar, monkeys and guinea pigs clear TCDF
more slowly, and are more sensitive to this chemical (Birnbaum
et al., 1981 lannou, 1983; Poiger, 1984). Experiments
with mice have shown that CDFs (including TCDF and 2,3,4,7,8-PeCDF)
are transferred to offspring via the placenta and in milk
(Nagayama, 1980). In rats and mice, with a half-life of
days, TCDF is more readily eliminated than TCDD.
In rats, TCDF is cleared only in metabolized form; the
tetrachloromethoxy-, trichloromethoxy- and two trichloromethyoxy
dibenzofurans were identified as the major metabolites
(Poiger et al., 1984).
PCDFs have been found in human beings. In Japanese who
consumed contaminated "Yusho" oil, CDFs were detectable in
liver and fat (0.16 - 17.6 ppb) nine years after their
ingestion of the contaminated oil (USEPA, 1982a). The
liver of one "Yusho" patient was estimated to contain 0.01
and 0.9 % of the tetra- and pentaCDFs, ingested 44 months
previously (Kuroki and Masuda, 1978) . A study of the
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retention of CDF isomers in the tissues of a Taiwanese
patient who died about two years after ingesting rice-bran
oil contaminated with PCBs and CDFS showed that the liver
contains the highest concentration of GDFs. The major CDF
isomers found were the most toxic, laterally-substituted
ones including 1,2,3,4,7,8-HxCDF, 2,3,4,7,8-PeCDF, and
1,2,4,7,8-PeCDF (Kunita, 1984).
Rappe and Buser (1981) have reported PCDFs in the blood
of sawmill, textile, and leather workers exposed to 2,3,4,6-TCP,
PGP, or PCP laurate. Their blood was shown to contain the higher
chlorinated CDFs at the ppt level (see Table 6).
c. Health Effects.
1. Toxic effects in animals.
The pattern of toxicity of CDFs is indistinguishable- from
that produced by TCDD (Moore, 1978). In the guinea pig,
the species mo'st sensitive to CDFs (Moore et al., 1979a) ,
the oral 1059 for TCDF is 5-10 ug/kg, only 2-4 times
greater than that for TCDD. As with CDDs, the acute toxic
effects of CDFs are species-dependent. Studies on the
accumulation and distribution of TCDF in guinea pigs administered
small daily doses demonstrate that, when a body burden of
about 6 ug/kg is attained, the toxicity of the compound in
this species is irreversible, and results in progresive
weight loss and death. (Decad et al, 1981). The systemic
effects of chronic low level exposure are reviewed in
USEPA (1982a). At 500 ug/kg/day, rats develop chloracne-like
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lesions on the ears, loss of body weight, reduced thymus,
ventral prostate, and seminal vescicle weight, and altered
serum lipids. Rhesus monkeys fed 5 ug/kg/day show atrophy
or squamous metaplasia of the sebaceous glands, involution
of the thymus, and bone marrow hypoplasia. In addition,
the clinical appearance in Rhesus monkeys was exactly the
same for TCDF as for TCDD, although the acute toxicity of
TCDF was estimated to be approximately one tenth that of
TCDD (McNulty et al., 1980).
2. Biochemical effects.
PCDFs are potent inducers of the' liver microsomal enzyme
system. The induction spectrum resembles that of 3-raethyl-
cholanthrene (SMC), inducing AHH activity. The approximate
ED5o for AHH induction in the rat, 0.5 ug TCDF/kg/day x 5
days, is about the same as that reported for TCDD administered
as a single injection, i.e., about 30,000 times more potent
inducing ability than SMC (Goldstein, 1977) . CDFs are also
potent inducers of ALAS, the rate-controlling enzyme of
heme biosynthesis (Goldstein, 1977; Oishi and Hiraga, 1978).
Limited information is available concerning the effects
of CDFs on immune function. Chlorinated aromatics in general
depress many aspects of immune function. CDFs may affect
the host defense mechansim, since toxic doses cause severe
thymic atrophy in the guinea pig, mouse, and chicken, and
lymphopenia in the chicken.
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3. Human health effects.
The severe systemic, chronic, reproductive, and teratogenic
effects which were observed in the Japanese Yusho patients
(USEPA, 1982a) are undoubtedly due in part to their CDF
exposure, since it has been demonstrated in rabbits that
the concomitant effects of CDF and PCB exposure can be
differentiated (Vos and Notenboom-Ram, 1972). The contaminated
"Yusho" oil contained 5 and 20 ppm PCDFs (USEPA, 1982) and
led to the accumulation of up to 25 ppb PCDFs (including
the CDFs) in the liver, kidney and adipose tissues of
those exposed. Kunita et al (1984) showed that the 2,3,7,8-
TCDF, 2,3,4,7,8-PeCDF, 1,2,4,7,8-PeCDF and 1,2,3,6,7,8-HXCDF
found in the adipose tissue of Taiwanese patients were
"the main causative agents in the pathogenesis of Yusho
disease". It is, however, impossible to estimate the
magnitude of the contribution of the CDFs to the problems
experienced by Yusho patients (or by exposed workers), or
to what extent their symptoms relate to the other toxic
components of the chemical products to which these people
were exposed.
4. Teratogenic, reproductive, and mutagenic effects.
The teratogenic potential of 2,3,7,8-TCDF has been
studied in the (Ah-responsive) C57BL mouse. TCDF was
administered as a single dose (0.1 - 0.8 mg/kg) i.p., on days
10, 11, 12, or 13 of gestation. A dose dependent increase was
observed in the frequency of fetal resorptions and fetal
death (day 10-11) and in cleft plate and hydronephrosis (day
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11-12). 0.1 mg/kg, administered on day 12, produced marked
thymic hypoplasia. The authors established 0.2 mg/kg as
the ED5Q in a single dose regimen for cleft palate production
(Hassoun et al. 1984).
CDFs may also cause reproductive effects: oral administration
to rats, at 1 and 10 ppm, of a mixture of CDFs resulted,
at the higher dose level, in decreased testosterone levels
in testes and decreased seminal vesicle weights.
There are few mutagenicity studies on pure CDFs. TCDF
and octa-CDF were not mutagenic in the Ames assay (USEPA,
1982i). However, as is the case for CDDs, such a study is
limited by the extremely low water solubility of the CDFs,
and the Ames test system is notoriously insensitive to aromatic
hydrocarbons.
Inoue et al. (1979) have shown that a mixture of CDF isomers
containing 3 to 6 chlorine atoms markedly increased sister
chromatid exchanges (SCEs) in cultured hamster lymphoma
cells at 0.1 ppm, whereas PCBs do not. An increase in SCEs
is taken as indicative of chemical interaction with or damage
to DNA. TCDF and octa-CDF were negative in a recombinant
DNA assay (Schoenig, 1981, quoted in USEPA, 1982a).
5. Carcinogenicity.
Halogenated CDFs are now being tested for carcinogenicity.
Because of the chemical and biological similarities between
CDDs and CDFs, the carcinogenic properties of CDDs may be useful
models for the carcinogenic properties of CDFs. Several studies
(summarized above) have shown that TCDD, and a mixture of
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two HxCDDs are very potent animal carcinogens by oral and
dermal routes (see above). The potential carcinogenicity
of the analogous CDFs may therefore be postulated with
some confidence.
Several epidemiologic studies of populations exposed to commercial
products contaminated with CDFs and CDDs (chlorophenoxy acids,
chlorinated phenols, PCBs) show an increased risk of cancer, but
do not allow a conclusion of the role of the individual contaminants
relative to that of the parent compounds.
d. Aquatic Toxicity.
The few available studies were summarized by EPA (1982a).
Young Atlantic salmon, fed a mixture of di-, tri-, tetra-
and octa-CDFs, showed a median time to death of 120 days.
Only the octa-CDF accumulated in the tissues. Immature
brook trout exposed to 2,8-DCDF, and to a mixture of tri-
and tetra-CDFs accumulate the higher CDFs more than the
2,8-isomer.
e. Existing Guidelines and Standards.
No standards or guidelines have been formulated for these
compounds.
3. Health and environmental effects of chlorophenols and their
derivatives, are described in the Health and Environmental
Profiles. In the case of PCP, additional information is
available in the position documents prepared by EPA's Office of
Pesticide Programs (USEPA, I981a; 1984). However, several recent
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reports of human health effects not mentioned in those documents
are discussed here.
A recent review of acute PGP poisoning episodes (Wood et al. ,
1983) provides added support for the fact that dermal absorption
of PGP and TCP is an important route of exposure.
There are now many reports in the literature indicating that
workers in occupations associated with PGP exposure are at
increased risk of nasal and nasopharyngeal cancer, stomach
cancer, and non-Hodgkins lymphoma (Grufferman et al., 1976;
Bishop and Jones, 1981; Hardell et al., 1982; Williams, 1982;
Gallagher and Threlfall, 1984). Because these are reports
of occupational exposure, it is of course not clear whether
the etiologic agent is PGP, or its associated CDD or CDF
impurities. Although, one report (Olsen and Jensen, 1984).
does not support the hypothesis that nasal cancer can be associated
with chlorophenol exposure, in toto these reports reinforce
EPA's concerns regarding the hazardousness of PGP.
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Berry, D.L. et al. 1979. Studies with chlorinated dibenzo-p_-
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87
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o
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o
Smith, R.M. et al. I981a. Analysis of 2,3,7,8-tetrachlorodi-
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0 Tumasonics, G., and L. Kaminsky. 1982. Chick embryos as a probe
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industrial effluents. EPA 660/4-75-002.
o
o
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Science Advisory Board.
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U.S. EPA 1979. Toxic Substances Assessment: Chlorinated dioxins
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by Technical Resources, Inc., P. E. des Hosiers, Project Officer.
Confidential document.
* U.S. EPA 1980a. Damages and Threats caused by hazardous material
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* U.S. EPA 1980d. Risk Assessment on (2,4,5-trichloro-phenoxy)
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(Silvex), and 2, 3, 7 ,8-tetrachlorodibenzo-jp_-dioxin (TCDD) .
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* U.S. EPA 1980e. Second Annual Report: Chemicals Identified
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* U.S. EPA. 1981f. Chemicals identified in human biological media, a
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Region 6.
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o
U.S. EPA 19811. Incineration of PCBs, Summary of Approved Actions,
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13:835-844.
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biphenyl mixture in rabbits. Toxicol. Appl. Pharmacol. 23:563-578.
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tional hazard. Am. Ind. Hyg. Assoc. J. 43: 799-810.
Wood, S., et al., 1983. Pentachlorophenol poisoning. J. Occup. Med.
25: 527-530.
Yamagishi, T. et al. 1981. Polychlorinated dibenzo-p-dioxins
and dibenzofurans in commercial diphenyl ether herbicides,
and in freshwater fish collected from the application area.
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Zingeser, M.R. 1979. Anomalous development of the soft
palate in rhesus macaques (Macaca Molatta) prenatally
exposed to 2,3,7,8-tetrachlorodibenzo-£-dioxin. Teratology
19:54A-55A. (Abstract).
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RE: SJ2405
VII. Response to Comments
A number of comments were received which addressed the
Agency's proposed listing of CDD- and CDF- containing wastes.
The Agency1s response to many of these comments were described
in the preamble to the final regulation for these wastes.
In the following material, we further amplify some of our
responses, and address other comments that were received.
1. One commenter stated that EPA had improperly applied its
criteria in determining the listed wastes to be acute toxic
wastes. In particular, the commenter believes that it is
improper to cite data indicating the toxicity of the "pure"
material rather than that of the waste material in which
it is contained. The commenter argued that EPA did not
(but should) cite studies which demonstrate that the
listed wastes (rather than its constituents) pose a
potential hazard.
The Agency agrees that no data on the directly-
.. established toxic effects of these waste were cited.
However, there are no studies directly showing the
animal or human effects of these wastes nor do we
believe that such studies are necessary for a determination
concerning the need to regulate wastes as acute
hazardous wastes. The toxicants of concern are
known to leach from these wastes and are otherwise
bioavailable (e.g., ingested when absorbed to soil).
Determination of the degree of hazard posed by
wastes (or other materials) known to contain certain
concentrations of toxicants is routinely made, as
in these regulations, by accepted toxicologic methods
of hazard assessment. Such methods use dose and
species extrapolations to estimate the potential
hazards to human health. The Agency ,therefore, does
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not agree with the commenter that an estimation of
the degree of hazard must await a bioassay. It
should be noted, however, that the Office of Research
and Development is developing and validating protocols
for this purpose (i.e., developing bioassays which
would enable a direct assessment of the hazardous
nature of the waste). The conceptual and methodologic
problems encountered in the development of such an
assay particularly for systemic effects of chronic
exposure are far from trivial, and an accepted
test may be difficult to achieve.
One commenter argued that 1 kg or less per month
of an acutely hazardous substance is not necessarily
an appropriate or magical number to exempt a generator
from regulation. The commenter stated that other factors
should be considered in setting the level, and that
hazardous wastes that have an oral LD50 of 5 mg/kg or
less, and that are persistent in the environment should
also be regulated.
The Agency agrees that in establishing a small
*
quantity generator (SQG) level policy decisions need
to be made. We established a 1 kg per month small
quantity generator (SQG) exclusion limit for acute
hazardous wastes, since these are deemed by the
Agency to present more of a hazard to human health
since only a relatively small quantity of the wastes
need get into the environment to present a risk of
serious or fatal illness. (In the industrial setting,
the SQG limit is, for all intents and purposes, equal
to zero.) The Agency also agrees that other factors,
including persistence and bioaccumulation of the
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toxicants of concern, quantity of waste, current
management practices, history of mismanagement, etc. are
also appropriate in determining whether a waste should
have a one kg SQG limit (i.e., wastes that are toxic (T)
may also be designated as having a 1 kg/mo level rather
than the general level of 1000 kg/mo). In fact, all
these factors were used by the Agency in setting a
1 kg/mo SQG limit. The present regulation, and
this background document illustrate that decision.
One commenter stated that distinguishing between the different
isomers of the CDDs and CDFs would not be a regulatory burden;
however, the commenter also stated that inclusion of all
isomers on Appendix VIII would create a regulatory burden
and an analytical nightmare.
The Agency perceives these comments as contradictory.
It would, we agree, be extremely costly, and therefore
burdensome to regulate these wastes in such a fashion that
isomer-specific analysis would be required (e.g., if we
list all isomers on Appendix VIII, persons subject to the
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Several commenters state that EPA has failed to demonstrate
that PCP and its contaminants are acute hazardous wastes.
They argue that EPA1s criteria for this listing are imper-
missibly vague, because the Agency failed to identify what
it considers to be serious irreversible or incapacitating
reversible illness. They also state that EPA improperly
used structure-activity relationships to extrapolate the
health effects of 2,3,7,8-TCDD to PCP and its contaminants;
that EPA must consider the wastes containing PCP on the
basis of the toxicity of PCP itself, and not on the
basis of its contaminants; and that PCP and its contaminants
do not cause chronic health effects.
The comments are to some extent contradictory,
for the same persons who state that EPA has failed to
define what it considers to be "serious irreversible
or incapacitating reversible" illness also state that
neither PCP, nor PCP - containing wastes meet this
criterion. The criteria for defining acute hazardous (H)
wastes to which these commenters refer, are directly
based on the statutory language of RCRA §1004(5>(A).
No one challenged the statutory provision as impermissibly
vague, nor did we receive any comments on this criterion
during the comment period following the promulgation of
§261.11(a)(2) on May 19, 1980.
Furthermore, in the preamble to that regulation,
EPA stated its intention to apply this standard to wastes
"containing substantial concentrations of potent carcinogens..."
(45 j[R 33107). TCDD and HxCDD are among the most potent
carcinogens tested in rodents, and are present in
these wastes in substantial concentrations (see above and
Table 3).
We disagree with the comment that EPA improperly
extrapolated the health effects of TCDD to PCP and
its contaminants. As discussed more fully in the
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preamble to the final version of this regulation, and
discussed elsewhere in this document, we believe that it
is appropriate and permissible to place reliance on the
biochemical and toxicity structure-activity relationships
for these compounds. It should also be noted that the
Agency is not evaluating the toxicity of the HxCDD and
HxCDF conquers - the chlorinated dioxins and -dibenzo-
furans most prevalent in wastes from PCP production and
manufacturing use—solely by reference to structural
similarity with TCDD and TCDF. We are, however, relying
on structure activity relationships in stating that all
forms of HxCDDs and HxCDFs are constituents of concern.
As to the basis for the Agency's concern requiring
the toxicity.of PCP and its contaminants, the principal
basis for listing these wastes as acute hazardous
wastes is the presence of substantial concentrations of
both HxCDDs and HxCDFs and of PCP. As discussed in the
preamble for the final version of the regulation and in
this document, the Agency determined that a mixture of
two HxCDDs is a potential human carcinogen of high
potency. Moreover, based on biochemical-structure
activity relationships (receptor induction, receptor
binding strength, enzyme induction, cell keratinization,
etc. (Bellin, 1984; Kociba, 1984)) the Agency also
determined that HxCDDs and HxCDFs may have chronic
systemic effects similar to those established for TCDD.
Additionally, the levels of HxCDDs in PCP wastes
are of concern in terms of the potential for serious
98
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harm if they are released to water or air, either in
soluble form, or adsorbed to soil particulates. 10~7
to 10~6 is an appropriate estimate for a water quality
criterion for HxCDDs, based on that for TCDD and the
difference in the carcinogenic potency values of HxCDD
and TCDD. This value is a minisule fration (10~^-°) of
the concentration of HxCDDs in PCP wastes. The Agency,
therefore, concludes that the potential toxicity of HxCDDs
at the level found in PCP are of regulatory concern.
5. Concerning the degree of toxicity of PCP and its HxCDD
contaminants, several commenters further stated that HxCDD
is not a carcinogen, and that, if it is a carcinogen, it is
a promoter, rather than an initiator of carcinogenicity. These
commenters further argue that PCP is not acutely toxic to
people, and that, in any case, the concentration of HxCDD in
PCP is so low that acute toxic effects of PCP would be
observed before HxCDD exposure would be sufficient to cause
a teratogenic response. (The commenters noted that in the
rat a teratogenic response to HxCDD was found at a dose of
100 ug/kg body weight.) They thus conclude that the conta-
minants in a dose of PCP will be no more toxic than the PCP
itself, and that the Agency erred in designating these
wastes as acute hazardous wastes.
The Agency disagrees with these comments. The carcino-
genicity of a mixture of two HxCDDs was established by the
positive response obtained in animal bioassay studies. The
data from these studies were recently reviewed by an expert
reviewer employed by the commenters, and by NTP and EPA1s
Carcinogen Assessment Group (CAG). While the commenter's
expert concluded that there is only "equivocal" evidence of
HxCDD1s carcinogenicity, scientists from both NTP and EPA
disagreed with this evaluation. The CAG concluded that the
tested mixture of HxCDDs is an extremely potent human carcinogen
They estimate the carcinogenic potency of the HxCDD mixture
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is between 0.59 per ug/kg/day (male rat) to 11 per ug/kg/day
(male mouse). The CAG recommended that 6.2 per ug/kg/day
derived from hepatocellular carcinoma and adenoma data in
male mice and female rats (the test systems in which the response
\
was most strongly evident) be used as the upper limit potency
estimate for HxCDD (Haberman and Bayard, 1983; McGaughy, 1984).
There are at present no scientific methods which have sufficient
general acceptance to allow one to establish an unambiguous
mechanism of action for this carcinogenic response. HxCDD
may be a promoter, a co-carcinogen, or a complete carcinogen.
There is at present no valid scientific basis for a risk
extrapolation assumption other than the no-threshold model
presently used by CAG for the cancer hazard extrapolation.
The Agency agrees that.the PCP dose for acute lethality
(about 160 mg/kg body weight) does not classify PCP as an
acutely toxic substance (as distinct from acute hazardous
waste), such as those listed in §261.33(e). Indeed, the
Agency judged that it should not be so listed. (45 FR
78533, November 25, 1980). However, the carcinogenic
and teratogenic effects or HxCDD are of significant
regulatory concern, and the Agency strongly disagrees
that the acute toxicity effects of PCP are of greater
concern than its teratogenic effects. It is true that
acute toxicity (LD50) is more easily observed and evaluated
than carcinogenicity or teratogenicity: fewer animals
need be observed, and the lethal endpoint is more
unambiguously noted. This, however, does not lessen
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the concern for the possible serious irreversible and
chronic systemic health effects of PCP and its contaminants.
Even evaluating the commenters1 remarks at face value, however,
one notes that lifetime exposure to one hundredth of the
LD50 of commercial PCP containing 15 ppm of HxCDDs would
,26/
incur an excess cancer risk of 10 J . Someone exposed
to a dose approaching the median LD50 would receive a
dose 1800 times larger than the ADI established for the
27/
reproductive effects of HxCDDs.
The Agency therefore judges that the designation
of PCP-containing wastes as acute hazardous (H) wastes
was appropriately drawn.
6. Several persons commented that EPA1s determination that
wastes containing PCP are acute hazardous wastes should be
peer-reviewed by an impartial scientific panel, similar to the
Science Advisory Board.
The Agency feels that the usual regulatory procedures
suffice in the case of PCP-containing wastes, as they do for
other wastes, to ensure that implementation of RCRA is properly
achieved. The administrative process, consisting of extensive
interagency review and comment, regulatory proposal, review of
public comments, modification of the proposed regulation, and
further interagency review before finalization suffices to
26/ 1/100 x LD50 x 15 ppm HxCDD/PCP=10~2 x 120 mg PCP/kg x
(15xlO~6 mg HxCDD/mg PCP) x 103 ug/mg = 0.018 ug HxCDD/kg/day,
Risk=potency x exposure = 6.2/ug/kg/day x 0.018 ug/kg/day =
0.1
27/ Exposure/ADI=(15xlO~6 mg HxCDD/mg PCP x 120 mg PCP/kg/day x
10~5 ng/kg = 1800 ng/kg/d / 1 ng/kd/d = 1800.
101
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ensure that there is ample opportunity for comment and review
from many points of view. Moreover, a judgment on technical
and policy issues is made and reviewed by many persons within
the Agency. In the case of these wastes, technical, scientific
and administrative issues concerning the CDDs and CDFs were
reviewed by the Chlorinated Dioxin Workgroup, by a committee
of scientific and technical experts meeting in Cincinnati in
July 1983, and by the Agency's Dioxin Monitoring Taskforce.
The health and environmental effects of chlorophenols were
prepared and evaluated by scientists from a contractual agent,
and were reviewed by scientists in several EPA offices.
The Agency therefore judges that additional outside
peer review is not needed.
7. Several comments were received in response to EPA's question
regarding the desirability, practicality,.and advisability
of developing a "characteristic" definition of hazardousness
under 40 CFR 261.24 for these wastes. Whereas some commenters
suggested that this would be a desirable regulatory goal, others
felt that this might not be a suitable regulatory alternative,
since it might encourage dilution as a means for circumventing
disposal. One commenter argued that EPA should develop a charac-
teristic definition of hazardousness for the CDD and CDF contaminants
of PCP, stating that adequate data exists in the RPAR rulemaking
docket to define such a level. The commenter stated that failure
to set such a level would unjustifiably cause all wastes containing
PCP to be classified as acute hazardous wastes, and argued that
the delisting mechanism places an undue burden on the regulated
community. One commenter recommended that the Agency set 1 ppm of
CDD or CDF as the lower limit of concern for any waste.
On reconsideration, the Agency concluded that with
presently available data, it is not possible to develop
a characteristic definition of hazardousness for these
wastes. This is true even for wastes from 2,4,5-TCP or
those containing PCP: 2,3,7,8-TCDD and a mixture of HxCDDs
102
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(the only CDDs whose potency has been estimated) are
the principal, but not the only CDD/CDF contaminants
of concern in these wastes. Qualitative and pragmatic
considerations dictated the selection of all CDDs
and CDFs as toxicants of concern (48 FR 14515). However,
a quantitative risk assessment is needed to develop a
"characteristic" definition. Such a risk assessment
would need to consider the carcinogenic or teratogenic
potency of the individual toxicants of concern. In the
case of the listed wastes, that would mean a detailed
knowledge of the response for each of the CDD and CDF
isomers cited as toxicants of concern. There are no
data sufficient for this purpose. Moreover, the Agency
continues to judge that the delisting process is a more appropriate
means to deal with the question of the limit of concern for
human health and the environment — especially for these very
toxic wastes.
8. One commenter questioned the regulatory relevance of the
criteria used by EPA to define the listed wastes as acute hazar-
dous wastes. In particular the commenter questioned the relevance
of the application of these criteria to PCP, because "EPA has
neither controlled wastes containing (PCP) under TSCA, nor
implicated wastes containing (PCP) in a series of damage
incidents." The commenter also argued that, since EPA has
failed to conduct a risk assessment, it has not proven that
these wastes are likely to pose a substantial risk to human
health and the environment.
The Agency disagrees with these comments. The criteria
used by EPA to determine whether a waste should be subject
to control under RCRA are derived from the definition of
hazardous waste in Section 1004 of that statute, and are
stated in 40 CFR 261.11. These regulations state that the
103
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Administrator shall list a solid waste as acutely hazardous
if it is capable of causing or significantly contributing
to an increase in serious irreversible, or incapacitating
reversible, illness. The commenter correctly calls
attention to the fact the EPA did not cite mismanagement
incidents concerning PCP-containing wastes. Although it
is not necessary to do so in order to list these wastes
as acute hazardous wastes, we have incorporated a description
of eighteen such mismanagement incidents in the revised
Background Document.
Furthermore, the Agency's determination that a
waste is an acute hazardous waste may be qualitative,
and need not be based on a quantitative risk assessment.
It is difficult to develop an exposure scenario which
can satisfactorily encompass the many possible exposure
conditions presented by the myriad individual waste
management situations which one can envision. There are
no potency criteria for many of the toxicants of concern,
and it is difficult to estimate the exposure factors
resulting from waste mismanagement in a generic (i.e.,
not site-specific) fashion. A scientifically meaningful
quantitative risk assessment is therefore difficult to
develop. The Agency's Exposure Assessment Group (BAG),
however, has been working on this problem.
One comment was received stating that the regulation should
clearly state whether the surrogate used for the trial burn
showing acceptable destruction and removal efficiency (DRE)
is to be found in the waste, can be spiked into the waste,
or if a trial burn can be conducted solely on the surrogate.
The commenter also asked EPA to include a requirement for
continued hydrocarbon monitoring.
104
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The dioxin regulation follows the format of the present
incinerator standards. §264.342 clearly states how POHCs
(surrogates) are selected. In general, a trial burn surrogate
is a substance more difficult to decompose than the substance
whose ORE is to be assured. In the case of CDDs and CDFs, a
substance such as carbon tetrachloride would be acceptable.
Detailed guidance is provided in the incinerator guidance
manual (U.S. EPA, 1983d), which explains how to use the
POHC/surrogate system.
At the present time, the Agency does not share the
commenter's confidence in continous hydrocarbon monitoring.
The Agency has no data showing a corelation between ORE
and total unburned hydrocarbons, except where the DRE drops,
and unburnt carbon (UNC) increases. Carbon monoxide is still
the best indicator of process upset and the Agency will continue
to require a CO monitor. We will, however, continue to support
research which tries to correlate DRE with other measurable
conditions.
10. Several comments were received concerning the listing of wastes
that are generated in the course of a manufacturing process
performed on equipment that was previously used in a process
that generated CDDs or CDFs. The commenters argue that,
despite evidence that such contamination can occur, EPA's concern
is not warranted, because cross-contamination can be avoided.
The commenters thus conclude that extending regulation to such
wastes is not warranted. _.
The Agency disagrees with these comments. The history
of contamination of the wastes from manufacturing operations
at the Vertac Chemical Company (outlined in this Background
Document) suffices as a basis for EPA1s determination.
105
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The commenters submitted no proof of their statement that
process equipment contaminated by CDDs or CDFs can be readily
rendered free of contamination. The Agency requested substan-
tiating data, but received no reply. Furthermore, the many
unsuccessful attempts that have been made to decontaminate
manufacturing equipment that was contaminated as a result of
industrial accidents show that decontamination of reaction
equipment is, in fact, very difficult. As a consequence, in
several instances, contaminated equipment was buried.
(Bleiberg, 1964; Goldmann, 1973; Jirasek et al., 1973; Hay, 1977)
The Agency thus concludes that the best way to control
the possible route of environmental pollution resulting
from contaminated equipment wastes is to presume them to be
acute hazardous wastes, leaving the possibility of a showing
of non-hazardousness to the delisting process. In a
delisting petition one needs to demonstrate either with
historical records of equipment use, or otherwise, to show
that the CDDs and CDFs of concern do not occur at levels
of regulatory concern. The Agency has no data showing how
cross-contamination can be avoided. In fact, the discussion
in this document (Supra) shows that such contamination does
occur.
11. One person commented that the proposed regulation does not
adequately address the management of dioxin-containing waste. The
commenter considered the proposed regulation to be a weakening
of existing regulation under TSCA. In particular, the
commenter argued, the proposed rules do not address the
management of CDD/CDF-containing cleanup materials, do not
establish sufficiently stringent regulatory limits, and do not
address dioxin detoxification processes.
106
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The Agency does not agree with the commenter that this
regulation has more limited regulatory effect than the TSCA
regulation which it replaces. The less extensive and less
stringent TSCA regulation was, in all respects, subsumed
into this regulation. Moreover, the commenter appears to
have misinterpreted the regulation. Thus, the small quantity
generator exclusion limitation for these wastes (i.e. , 1
kg per month) applies to the waste, not to its CDD or CDF
content. The Agency agrees that, except for residues of
incineration or thermal treatment, this regulation does not
specifically list wastes from detoxification processes.
The regulations (40 CFR 261.3(c)(2)) already state that a
waste resulting from the treatment of an EPA hazardous
waste is a hazardous waste, unless it is delisted.
Moreover, as a consequence of this listing, facilities
wishing to treat these wastes, will now become subject to
regulation.
12. One commenter stated that, for optimal efficiency in
regulating hazardous waste, EPA should integrate its regulatory
efforts under RCRA and TSCA. The commenter suggested that
questions concerning possible waste management problems should
be an integral part of the TSCA §3 (premanufacture notification)
review process, and that data collection to support these
regulatory evaluations should be required of an applicant
pursuant to authority under RCRA and TSCA.
We agree that consideration of possible hazardousness
of the wastes generated by the manufacture, or the significant
new use of a newly manufactured chemical is extremely
important. Such consideration considerably enhances EPA1s
hazardous waste regulatory activities. It is for this reason
that there is considerable interaction among the Agency's
107
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office regulating hazardous waste management, and that conducting A
premanufacture review. Aspects of waste management are indeed
considered in the course of the PMN review process, and applicants
are asked to provide relevant data where these are 'needed.
There is, however, no mechanism under RCRA enabling the Agency
to obtain data for chemicals or processes which have not been
previously manufactured.
13. One person commented on the need to clarify the effect of
requiring full permit status for mobile treatment units in an
emergency response situation.
The final regulation requires incinerators or other
thermal treatment units burning these wastes to demonstrate
that they can achieve six 9s destruction and removal efficiency
(ORE) on POHCs in the waste. Under §265.352 interim status ^
incinerators or other thermal treatment units may burn these
wastes if they receive certification from the Assistant Administrator
for Solid Waste and Emergency Response that they can meet the
technical standards of Subpart 0 of Part 264 when they burn
these wastes.
This approval process must provide an opportunity for
public comment. (See the preamble for this regulation.) In
appropriate circumstances, emergency permits for burning these
wastes may be issued (see §270.61).
14. One commenter stated that EPA has failed to cite evidence that
chlorinated dioxins are present in the environment due to
their production in combustion (including woodburning) processes
that bear no relationship to deliberate manufacturing operations.
The commenter states that, before adopting this regulation, EPA
should consider whether a background level exists. ^
108
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in discussing the generation of CDDs and CDFs (in the
Background Document for this regulation), the Agency alluded to
this theory, known as the "Trace Chemistry of Fire" hypothesis.
In view of the known reaction chemistry underlying the formation
and decomposition of these chemicals, and the widespread
occurrence of chlorinated compounds in the environment, the
known occurrence of CDDs and CDFs in the combustion residues from
many sources is not surprising. Recent data (Czuczwa and Kites,
1984) on the occurrence of CDDs and CDFs in sediment cores from
several of the great lakes, as well as from three Swiss lakes,
lead to the conclusion that increased CDD/CDF deposition in
these sediments may be mostly due to atmospheric inputs, began
in 1940 and increased only after development of the chlorinated
organic chemical industry. While these data are preliminary,
they reinforce the Agency's conclusion that there is a need to
ensure the proper management of these wastes. As part of the
Dioxin Strategy (USEPA, 1983b), the potential hazards of combustion
sources such as incineration of hazardous and municipal waste,
incineration at wire reclamation facilities, internal combustion
engines, home heating units (e.g. woodburning stoves), boilers
and inadvertent combustion sources (e.g. transformer fires) will
be evaluated (Tier 7 sources). Results from these investigations
will indicate to what extent these activities contribute to
environmental pollution with CDDs and CDFs, and may
indicate that disposal of wastes from some of these sources
should be regulated.
109
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15. One commenter stated his concern that, as acute hazardous
wastes, these wastes were improperly proposed to be listed under
40 CFR 261.31 rather than under 40 CFR 261.32. The commenter is
concerned that this will result in "indiscriminate inclusion
and regulation of ill-defined wastes from diffuse sources as
acutely hazardous waste."
The Agency judges that these wastes are properly
listed as hazardous wastes from non-specific sources,
for they result from several processes. The criteria
for listing wastes under both sections are identical
(§261.11). There is therefore no basis for the commenter's
fears.
16. One commenter did not agree with EPA1s determination not to
list CDD- and CDF-containing wastes such as certain fly ash
materials, or wastes resulting from wood preservation, until
it has analytical monitoring data showing the potential hazards of
such wastes. The commenter argued that the Agency should list
these wastes now, on the basis of present knowledge of reaction
chemistry and process technology. The commenter stated that
EPA is imposing a burden to regulation that is unjustified in
fact or law, because RCRA "does not require a smoking gun": the
Agency must prove that a solid waste must be regulated if it
may "pose a substantial present or potential hazard to human
health or the environment...".
In the preamble to the proposed regulation, the Agency
outlined its concern that wastes other than those covered in
this listing may contain CDDs and CDFs. The suspected processes
are being studied in order to verify whether these concerns
can be substantiated. Until such verification is achieved,
however, and a demonstration of their potential hazard
is made, the Agency cannot list these wastes. In order
to substantiate a finding that a waste " "may pose a
substantial present or potential hazard.." the Agency
may not act on mere suspicion. Under OSWs industry
110
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studies program, the Agency is gathering data on
the processes and technologies of concern, and additional
data are derived from ongoing activities in other Agency
offices including data being gathered under Tier 4 of
the Dioxin Strategy. If those data lend support to a positive
listing decision, the Agency will bring the appropriate wastes
under RCRA regulation.
17. One commenter suggested that the Agency develop a regulation
indicating how materials subject to the regulation could be
made suitable for delisting. The commenter suggested that
such a regulation should specify a specific delisting method,
should emphasize that alternative technologies can be used,
and that a method of delisting the treated waste exists.
The Agency judges that is not necessary to develop
a special regulation on delisting. As the commenter points
out, the RCRA regulations already provide a mechanism for
delisting wastes at specific facilities. 40 CFR 260.22
lists the criteria which must be demonstrated in order delist
an acute hazardous waste or at least to demonstrate that the
waste is only toxic.
Treatment, storage, and disposal of a waste is subject
to the permitting requirements of the RCRA regulations. In
general, these permits neither proscribe nor prescribe specific
treatment modalities. It would be stifling of technological
innovation to specify a requirement for the use of specific
technologies for the treatment of wastes. Some of the
factors raised by the commenter may, however, be discussed
in the management standards for these wastes, whose development
is presently in progress.
Ill
-------
18. Comments received on the analytical method.
a. One person commented that, in the directions for the
extraction procedure (Section 9 of the method), no information
was provided on the identitiy or quantity of solvent needed.
The Agency agrees with this comment. Step 9.7.3
will be added as clarification, and will direct the transfer
of sample extract with a small volume of methylene chloride.
b. Several comments were received on the use of HPLC in the
sample clean-up procedures. One commenter felt the procedure
description to be inadequate. Another respondent commented
that additional chromatography, using disposable pipets,
would be preferable to the use of HPLC, because it would
prevent the possibility of cross-contamination. A third
person doubted that the clean-up procedures are sufficient
to prevent interference.
The Agency judges that the method description provides
adequate discussion of the HPLC clean-up procedures, since
these procedures are discussed in greater detail in-the
Solid Waste Test Manual (USEPA, I982e). With respect to
the comment on cross-contamination, good analytical
technique, which includes adequate rinsing between sample
injections, should suffice. Moreover, the Agency has no
data supporting the effectiveness, for these wastes, of
additional column chromatography. The commenter did not
provide data in support of this suggestion. Therefore the
Agency judges that the elimination of the HPLC clean-up
procedure is not warranted. As to the efficacy of the
clean-up procedure, the Agency agrees that no practical
clean-up procedure will suffice to eliminate all interfering
substances. The developers of the method have shown that
112
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the suggested clean-up procedure is, for the wastes to be
analyzed, efficacious under most conditions.
c. One person commented that EPA should specify a limit
of quantitation, and also called attention to the fact that the
analytical method for the detection of PCBs is 10 ng per
resolvable GC peak as a reasonable estimate of the smallest
amount a GC/MS instrument can measure. The commenter questioned
whether the specified 0.015 ng/peak detection limit can be
achieved, especially in the expected presence of co-eluting
substances. Another person commented that the footnote
to Table I in the method description is inaccurate.
The Agency agrees that a limit of quantitation can
be calculated if the limit of detection is known, but
disagrees that such a calculation is useful or necessary
if results specify the limit of detection that was achieved,
The Agency also agrees that the analytical method for PCBs
required a higher detection limit than the one specified
here for the analysis of CDDs and CDFs. The two methods
were developed for different regulatory purposes, and a
comparison of their detection limits is therefore not
appropriate. Our data show that the lower detection limit
is achievable but continued evaluation of the method may
show that it" is not realistic for some matrices. If so,
the Agency will modify the procedure appropriately. The
Agency also agrees that the footnote to Table I of the
method needs revision; it has been modified accordingly.
d. One commenter stated that the method requires the use
of very costly GC/MS equipment, and notes that most labo-
ratories do not have such equipment.
The Agency agrees that the needed equipment is intri-
cate and costly, but without such equipment it is not
113
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possible to properly analyze for CDDs and CDFs at levels
of regulatory concern. Many, if not most, large industrial
anayltical laboratories have such equipment (GC/EC, low-
resolution GC/MS, and optional HPLC) .
e. Several comments were received relating to the use of
standards. One commenter stated that GC/MS standardization
does not require the use of specific labelled isomers,
that the use of expensive Cl5 and CLg isomers should not
be required (even if the analysis for 015 and Clg compounds
is required), and that the use of isomers should not be
restricted to chlorine isomers. One respondent stated that
it is not valid analytical methodology to use the 2,3,7,8-TCDD
and its congeners as surrogate standards for the quantitative
measurement of all CDDs and CDFs. Another person stated
that the procedure'does not clearly state how calculations
for quantitation of 015 and Cl5 compounds are to be performed.
The use of surrogate compounds is often justified,
e.g., when the surrogate has the same extraction charac-
teristics and chromatographic elution rate as the compound
that is being determined. Unfortunately there is, at present,
no satisfactory surrogate for the CDDs and CDFs. Further-
more, experience show that accurate analysis at the extremely
low concentrations needed for the CDDs and CDFs can only
be achieved by standardization of the use of an internal
standard.
The Agency agrees with the commenter regarding the
need, in general, to use a specific isomer as the standard
for a particular compound. However, at present, very few
isotope-labelled CDD or CDF isomers are commercially
available. Moreover, this method is not intended for
isomer-specific analysis, since it is intended to fulfill
the regulatory need to establish the presence of the ,
114
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total CDDs and CDFs. The use of specific isomers as a
standard for each possible isomer or congener is therefore
not absolutely necessary. Nevertheless, the Agency may
re-evaluate this method in the future, and, if warranted,
require the use of additional isomers when these become
commercially available. Although bromine compounds
might be adequate as surrogates for the chlorinated
compounds, their use also would sacrifice accuracy,
and there use would probably not result in the
reduction in cost or convenience.
f. One person commented that the proposed rule applies
to chlorophenols and to phenoxy acids, but noted that the
proposed method does not include a procedure for their
analysis. This commenter also states that analytical
procedures should not be mandated, but should allow for a
different procedure.
The proposed method was intended only for the
determination of CDDs and CDFs. EPA's document describing
test methods for evaluating solid wastes (U.S. EPA I982e)
contains a method for chlorophenols and chlorophenoxy
compounds. The RCRA regulations (40 CFR 260.21) provide
for the use of a method other than the one required.
g. One person commented on the proposed laboratory disposal
requirements, stating that the amounts of the compounds in
working standards and sample extracts are no more hazardous
than many other compounds used in the laboratory, and should
be allowed to be disposed with other laboratory wastes.
Alternatively, the commenter suggested that CDD/CDF laboratory
wastes should be allowed to be disposed with plant wastes.
The method procedures specify that, as a general
analogy, laboratory wastes containing CDDs and CDFs may
be disposed in a manner similar to that used for radioactive
115
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or infectious waste. Thus, they should not simply be
poured into the laboratory drain, but should be separately
collected and disposed as hazardous waste.
g. Additional comments received related to specific statements
in the stated procedure. The Agency has responded by
revision of the method where this was appropriate.
116
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s—*
rH
00
en
rH
. s-X
rH
OO OC
en C
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CO
-H
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C cO
cfl
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3
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erf x:
S CO
sea and Jones (1975). m. Sarna et al . , 1984. Log P values for
DCDF and OCDF are about the same as those
for the corresponding dioxins.
c
cu
CD
1— 1
cO X) OTJ 0) MH
-------
TfiBLE 2
FORMATION OF CDBFs FPOM THE PYSOLYSIS OF SPECIFIC PCBs. a
PCS Pyrolyzed
CDBFs Formed
Tetra;
2,3,4,5-
2,3,5,6-
2,6,2',6'-
Penta;
2,3,4,5,6-
2,4,5,2',5'-
2,4,5,3',4'-
2,4,6,2',4'-
2,3,6,2',5'-
Hexa;
2,4,5,2',4',5'-
2,4,6,2',4',6'-
2,4,5,2',4',6'-
2,3,4,2',3',4'-
2,3,5,2',3'/5l-
2,3,6,2',3',6'-
3,4,5,3',4',5'~
*2,3,4; 1,2,3,4-
1,2,4-
1,9; 1,4,9-
*1,2,3,4; small amounts of 1,2,4-;
2,3,4-;
*2,3,3; small amounts of 2,3,6,3-
plus three other tetra; 1,3,4,6,9;
*2,3,7,8-; 2,3,6,7-; 1,3,4,7,8-
*1,3,7-; 1,3,6,7-; 1,3,7,9-; 1,3,4,7-;
1,4,8-; 1,2,8-; 1,4,6,8-; 1,2,6,8-;
*l,2,4/8-; 1,2,5,9-; 1,4,6,9-;
*2,3,7,8-; 2,3,4,7,8-; 1,3,4,7,8-
1,3,7,9-; 1,3,4,7,9-;
*1,3,7,8-; 1,3,4,7;8-; 1,3,4,7,9-;
*3,4,6,7,-; 1,2,3,6,7-;
2,4,6,8-; 1,2,4,6,8-;
*1,2,4,8-; *1,2,3,9-; 1,2,4,6,9-(?);
1,2,4,8,9-
2,3,4,6,7,8-; small penta-CDBFs
[continued)
-64-
-------
Table 2 (cont'd)
Hepta:
2,3,4,5,2',3',4'- 2,3,4,6,7-; 1,2,3,4,6,7-;
1,2,3,6,7,3-; 1,2,3,4,7,3,9-;
1,2,3,4,6,7,8-; 1,2,3,4,6,7,9-;
2,3,4,5,2',4',5'- *2,3,4,7,8-; 1,2,3,4,7,8-;
•*1,3,4,6,7,8-; 2,3,4,6,7,8-;
1,2,3,4,6,7,9-;
Octa;
2,3,4,5 *2,3,4,6,7,8-; *1,2,3,4,6,7,8-;
2',31,4',5'- octa-.
a. Source: Buser and Rapper, 1979.
* = Most abundant PCDBF
-65-
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TABLE 4
COMMERCIAL PRODUCTS POTENTIALLY CONTAMINATED
WITH TETRAChLORO or BROMODIOXINSa'b
NUMBER OF COMMERCIAL
PRODUCTS CONTAINING
COMPOUND TCDDs
Erbon (2-(2,4,5-trichlorophenaxy)-ethyl 20
2, 2-dichloropropionate.'
Hexachlorophene (2,2'-methylene-Dis(3,4,6- ^68
trichlorophenol)
*
Ronnel (U-2,4,5-trichlorCphenyl-U,0-aimethyl- 325
thiophosphate)
Silvex or'Fenoprop (2-(2,4,5-trichlorophenoxy)- 376
propionic acid, esters and
salts)
2,4,5-T (2,4,5-trichlorophenoxy acetic acid) 443
2,3,4,6—Tetrachlorophenol ' • 1
2,4,5-Trichloropnenol 12o
2,4,6-Trichlorophenol _ 22
(a) based on Esuosito et al.,
;b) Survey of data 6/15/78 - 1/6/80
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-------
TABLE 7
Estimated single oral lethal dose 50-30 values of certain
polychlorinated dibenzo-p-dioxin and dibenzofuran isomers a
Chlorine isomer
2,3,7,8 d
1,2,3,7,8
1,2,4,7,8
2,3,4,7,8
1,2,3,4,7/3
1,2,3,6,7,8
1,2,3,7,8,9
2,3,4,6,7,8
Guinea - pig
ug/kg
CDD CDF
0.<3;2C 5;10e
3
1,125
<10f
73
70-100
60-100
12 Of
Mouse
ug/kg
CDD CDF
284 660 Ci e
132;6203
338
>5,000
825
1,1250
Rat
ug/kg
CDD CDF
2 2 ; 4 5 c 5 f
Il9b
>2500b
i
1
413b
625b'e
1
720b
|
i
I
(a) adapted from Huff, 1979, except as otherwise indicated.
(b) estimated from body surface conversion ratio factor
(equivalent area dose): rat (mg/kg) = !_ mouse (mg/ky).
(Casarett and Doull, 1981) 2
(c) for male and female animals, respectively (Schwetz et al., 1973).
(d) LD50 for TCDD (115 ug/kg) = 70 in monkey (McConnell et al., 1978)
115 in the rabbit (Schwetz, 1973); >300 in the dog (Schwetz, 1973
5000 in the hamster (Henck, 1981).
(e) Schwetz et al. (1973) report that 1 of: 2 male rats given
100 mg/kg orally was killed; no deaths occured in 4 female
mice given 2 g/kg, or in 2 female rats given 1 g/kg.
These authors report an approximate value of 100 mg/kg for
the oral LD50 of a mixture of 3 HxCDDs of unknown composition.
(f) Decad et al., 1981.
(g) C57BL/6j(Ahr) and DBA/2J(And) mice, respectively (Weal, et al,
1982).
-------
TABLE 8
Toxicity, Distribution and Whole-body Half Life of the
Radioactivity Derived from 14C-TCDBF
- J 3 - d O
Percent Dose Recovered
Guinea pig
3 days"
DISTRIBUTION3
Liver 29. 3 _+ 0.6
Adipose 56 .9 +_ 7.6.
Skin 17. 1 + 0.6
Muscle - 15.6 +_ 4 .5
Feces 4.7
Urine 2.3
HALF LIFE (days) >20
LD50, oral, ug/kg 5-10
LD50/30, TCDBF 2
LD50/30, TCDD
Monkey Rat Mouse
21 days° 3 days13
1.0+0.8 5.9^0.3
3.7 + 2.8 11.6 + 2.3
2.4 + 1.6 1.2 +_ 0.3
1.6 + 0.1 _ 0.3+0.3
71.5 62.1
13.2 . 2.0 ^
8 2
1000 6 6600
20 23
aSource: Decad et al., 1981
^Days after iv administration of l^C
guinea pig: 6 ug/kg; monkey and rat: 30.6 ug/kg
-------
TABLE 9
Environmental Monitoring Data From Love Canal
SAMPLE
CIRCUMSTANCES
CH EM I C AL ( o ob
RE 5 E RE i
TCDD
CHLOROPHENOLS
tn tetra penta
IR
Homes near canal
ND'
ID
a, c
SOIL
near canal
near canal
<.002 -
0.312
no
670 -
ysooo
i
i
o , o
a
LEACttATE
1.56
WrxTER
.
SUMPS
• water
sediment
STORM SEV/ER
shallow wells
near canal
near canal
_
•
ND
ND
ND, .02,0. 5
0. 5,9570
I
30
734
C
1 «
14
r*
A
sediment ! near canal
away from canal
further awav
306
655
ND-5
95900,
STREAM SEDIMENT
Black and
Berg hoiz Creeks
Niagara River
| ND-37.4
! .02,.06,.10J
* References: a = EPA, i9a'2c; D = N'YS 1982; c = t\YS 1979.
** N.D. = oelcw aetection limit; ID = oresent iut not cuantitatea.
-------
TABLE 1'J
SUMMARY O? CHLOROPHENOL AMD CHLOROPHEN*
MANUFACTURING PROCESSES AND WASTES
PROCESS
PHENOL/CHLOROPHENOL
FEEDSTOCK
PRODUCT! S)
WASTSS/RS5 1 DU E
Manufacture of chloroohenols.
a. chlorir.ation of ohenol.
I phenol
! phenol; 2, 4-DC?
2,4-DCP
2,4,6-TC?
2,3,4,6-TC?
PC?
( spent carbon from HC1
( purification;
( "distillation octtor.s;
<( "reactor residues;
( chlorination reaccor
( scrubber liquid.
hvc'rolvsis of chloro benzenes .
" ! " • !
! 1,2,5-TC3
! 1,2,.4,5-TCH
2,5-DC3
2,4,5-TCP
"reaccor residues; "scenz
<( filter aids; "d is t ilia t io.-
( bet tons.
M anu f a c ture _o_f pesticides_derived from 2,4,5-TC?^
! 2,4,5-TC? !
2,4,-5-T
2,4,5-T?
Ronnel
Sesone
Srbon •
HCP, Isobacc
"reactor resdues;
buttons; aqueous effiuen:
from separator; "residues
fron procuct filcracion
or centri fucacion ; "sper.-
filter aids.
* Pastes listed in this Background Document.
-• Because of process variations at individual facilities, not all cr.ese
residuals occur at every facility.
"*• In many instances, these cnlorophenols are no-: isolated, ouc are used
directly as feedstocks for subsequent syntheses.
:- Present processes use purified 2,4,5-TC? and do noc generate wastes
of concern.
• This tabulation is illustrative, not definitive: similar waste
resale ing fron the production of chlorphenates fron other tri-,
tetra-, or oencachlorcohenols are also of concern.
-------
98
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FIGURE 2
POSSIBLE REACTION SCHEMES FOR THE PYRCLYSIS OF
2,2'/4,4',5,5'-hsxachlorobiphenyl.
C! Cl
loss of :
onno C!
loss of ortho !-:
and Cl witn
Cl snirt
loss of ortno
h ana Cl
loss of rwo
orno H
13.7.3-;.2tra-CC5.=
ci .c:
2.3.4.7,3-oema-COSr
C!
Source: acantad from Busar and Raooe, 1979.
-------
Cl
246-TC?
sc:
246-TC? radical (A)
2346-TeC?
e»
rCP
ct
a
FCP ,
c:.
c: s
a
2346TeC? radical (3)
• 0
A "r^V V . .„,
•ci
Cl Cl
c:
- a
- a
Ci
Cl Cl
Cl C
PC? radical (C)
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7IGT7SZ 4
OF 2,2,4,5-rzr-lACZLC3.0PEZ^CL
OH
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JT" PFCCUCITCN Ci GJLQrCFfiSCCLS 3Y DIRECT
CF PHENOL.
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Noncorract heating
•^Caolmg Coils
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Purification or Sale
Aluminum
Chloride
Catalyst
Svoroouc:
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50 NA
Tcs»j> 36
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NA 15
CONCENTPATICNS
?CDD/rCDBI
TISH , Ncr
Source: ETA, '.1982b.
,3/7 r*} Fish La]
Whole
Univ of JE
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Univ" of Ni
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niv of NZ
Whole V^icle/Fillet
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: not analyzed
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k ):±:
-------
FIGURE Ifl; TCDD/TCDBF CO!TTlv1TT70^rTTTnNr?; IN FISH, SPRING RIVLR,
VEKHA, MO. , NOVEMBER 19.81.
rn.^-ts:
1 •*"!' ' ' y
\ • v y>.
^ i x' ' » rntt^tt
w-— -—- —• p^~ — - •»i— -
; r\ r^.. ^\
M 'J^0
Fish Lab Univ of NE
(Whole)
NA NA <8
NA NA <8
2,3,7,8
Total TctiiS
Lab Univ of NZ
Whole
SCALE 1:24000
o
F1sh Sample Collection Point^Downstream from Verona,
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^ J.SJW*'—* *»J • __ ,
Concentrations of TCDDs ar.d TCDBFs in
(Sources: -cited in Table 5) .
fish(1970-1977)?
a. Valuer in ( )-= TCDD; values with
Values in C ] = CDDs.
All data are in sg/g (??t).
See also Table 6~, iter:^"l92 ff.
b. TCDBFs = 37 ppt.
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FTGD3E 22: TCED :CNTICP^7G DATA SI I£tfE GMSL
- - O- - ^PCUNO WA7s3 '
Scares: Z?A, 19S2c.
-------
RGURS. 23
DICXJN: LOVS CANAL SAMPLES
SIACX C3f£X S708M
5ID1MINT: SIOIMfNTi
Hppb 31ppb
« AT FISH
IN StRGHOtTZ
3.7 pco
JTORM
S£Ot.M{Nr :
CAflSON fSOM
T3£ATM£NT P1.ANT:
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S70R
t ?S£DIM£NT:
son. ACSOSS
572 E;T
SANO LfNSI:
ppr
SUSfA« SOIt. F5OM
SOUTHERN SIC7ION
Of LOVt CANAL: 5.
Sourci: NY5r IS 82
•/-r
------- |