REPORT OF THE AD HOC STUDY GROUP ON
PENTACHLOROPHENOL CONTAMINANTS
December 29> 1978
ENVIRONMENTAL HEALTH ADVISORY COMMITTEE
SCIENCE ADVISORY BOARD
U.S. ENVIRONMENTAL PROTECTION AGENCY
WASHINGTON. D.C. ZWfeO
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EPA NOTICE
This report has been written as part of the activities
of the Environmental Health Committee of the Science
Advisory Board, a public advisory group providing
extramural scientific information to the Administrator and
other officials of the Environmental Protection Agency- Hie
Board is structured to provide a balanced expert assessment
of the scientific matters related to problems facing the
Agency. Hiis report has not been reviewed for approval by
the Agency, hence its contents do not necessarily represent
the views and policies of the Environmental Protection
Agency, nor does mention of trade names or commerical
products constitute endorsement or recommendation for use.
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TABLE OF CONTENTS
1. SUMMARY AND CONCLUSIONS
1-1 Background 1
1.2 Discussion........ 2
1.3 Conclusions 6
2. SUMMARY OF CHEMISTRY AND ENVIRONMENTAL
BEHAVIOR OF PENTACHLOROPHENOL AND ITS
CONTAMINANTS
2.1 Pe n t ac h 1 orophe no1 and its Uses 9
2.2 Manufacture of Pentachlorophenol
and its Contaminants................... 9
2.3 properties of Pentachlorophenol
and its Contaminants....... 11
2.4 Detection and Quantification of
PCP and its Contaminants 11
2.5 Environmental Chemistry 11
3. TOXICOLOGY
3.1 Toxicity of PCP in Laboratory Animals.. 17
3.2 Toxicology of Chlorinated Dioxins
and Dibenzofurans...................... 30
3.3 Human Poisonings Involving PCP 36
3.4 Human Poisonings Involving Exposure
to Chlorinated Dibenzo-p-dioxins....... 40
4. MECHANISTIC RELATIONSHIPS IN THE
TOXICITY OF COMPOUNDS STRUCTURALLY
RELATED TO THE CHLORINATED DIBENZO-p-
DIOXINS. . * . ... 43
APPENDICES
5. A - Study Group Members and their
Affiliations..................... 47
6. i - Charge to Study Group 48
7. C - Chemistry of Pentachlorophenol
and its Contaminants 49
8. D - Testimony and Comments of
Interested parties Concerning
Initial Draft Report at EHAC
Review of April 3, 1978..... 99
iii
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List of Tables
2.1 Comparison of Composition of Commercial Grade
and Purified Grade Fentachlorophenol . 10
2.2 Chlorodioxin Isomer Distributions in Commer-
cial Grade PCP (Dowicide 7) and PCP-Na
Samples 10
2.3 Physical Properties of pe ntachloropheno 1 12
2.4 Physical Properties of Various Chlorodioxins .... 13
2.5 Solubility of Several Chlorodioxins in various
Solvents 14
3.1 pentachlorophenol-Compositions reported for
Some Samples used in Toxicity Testing.. 18
3.2 Biological Activity Purified vs. Technical
Samples of PCP. 22
3.3 Toxicology Data Summary 32
3.4 Distribution of Human Episodes Resulting from
Exposure to,fentachlorophenol by Medical
Attention and Circumstances 39
7.1 Comparison of Composition of Commercial Grade
and Purified Grade Pentachlorophenol 52
7.2 Chlorodioxins and Chlorofurans in Dow PCP
Products. S3
7.3 Hex a- and Octachlorodioxins in Domestic PCPs 53
7.4 GC-MS Analyses of Monsanto PCP. S4
7.5 Chlorodioxins in a Commercial PCP and PCP-Na
Sample 55
7.6 Hexachlorodioxin Isomers in Three Dow Products... 55
7.7 Chlorodibenzofurans in Dow PCP Products...., 56
7.8 Reactions in Chlorination of Trichlorophenol..... 57
7.9 Dioxin Congeners in Commercial PCP 58
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List of Tables (Cont.)
7.10 Physical Properties of Pentachlorophenol {PCP)... 60
7.11 Physical Properties of Various Chlorodioxins..... 62
7.12 Solubility of Several Chlorodioxins in Various
Solvents 6 3
7.13 Properties of Chlorinated Dibenzofurans. 64
7.14 Melting Points of Chlorodiphenyl Ethers,.. ,. 6 5
7.15 Chlorinated Dibenzofurans, GLC Retention Times
Relative to 2,3,7,8-Tetrachlorodibenzo-p-dioxin... 66
7.16 Chlorinated Dibenzo-p-dioxins, GLC Retention Times
Relative to 2,3,7,8-Tetrachlorodibenzo-p-dioxin... 67
7.17 Estimated Half-Lives of Several Chlorodioxins
in Refluxing KOH Solution 71
7.18 Chlorinated Dibenzodioxins and Dibenzofurans
X5Onters and Souroes75
7.19 Dibenzo-p-di©xin (D): Approximate Activity of
Congeners in Chick Embryo Assay for Induction
of Aryl Hydrocarbon Hydroxylate 77
7.20 Dibenzofurans {FJ s Approximate Activity in Chick
Embryo Assay for Induction of Aryl Hydrocarbon
Hydroxylase . 7 8
7.21 Estimated Vapor Density and Rate of Evaporation
of Chlorodioxins " 79
7.22 Estimated Vapor Density and Rate of Evaporation
of Chlorinated Dibenzofurans 79
7.23 Major Registered Uses of PCP*. 86
7.24 Some Potential Sources of Occupation Exposure to
PCP and PCP Impurities 87
7.25 Some Potential Sources of Incidental Exposure
to PCP and PCP Impurities 87
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1. SUMMARY and CONCLUSIONS
1,1 Background
In the fall of 1970, the C.S, Department of Agri-
culture (US DA) expressed concern about the presence of
certain chlorodioxins in some "economic poisons." in
January 1971, the USDA held a meeting with industry
officials to discuss the problems of these chlorodioxins in
pentachlorophenol (PCP). At that time the hexa- and
heptachlorodibenzo-p-dioxins (dioxins) were identified as
the contaminants of major concern in PCP. Since that time
the intensity and breadth of concern about the health
implications of polychlorinated dibenzo-p-diox ins have
increased. This concern has no doubt been stimulated by
the development and widespread publication of knowledge of
the extremely high toxicity of 2,3,7,8-tetrachlorodibenzo-
p-dioxin (TCDD). Although TCDD is or has been a contaminant
of great concern in several well publicized cases, it
should be noted that TCDD has not been identified as a
contaminant of pentachlorophenol"*manufactured in the united
States. Frequent references to TCDD in subsequent
discussions are because it is the only polychlorinated
dibenzo-p-dioxin that has been the object of comprehensive
toxicologic research. Several other polychlorinated
dibenzo-p-dioxins and related polychlorinated dibenzofurans
have now, however, been identified as contaminants of
commercial samples of pentachlorophenol. A commercial
process has been developed and patented which enables
production of pentachlorophenol with greatly reduced
concentrations of these contaminants. This development, as
well as the scheduled reregistration procedures required
under the amended Federal Insecticide, Fungicide,
Rodenticide Act CFIFRA), stimulated the SPA to five
extensive consideration to whether or not the
polychlorinated dibenzodioxins present in PCP have
contributed to increased health hazards or environmental
degradation associated with PCP use.
The SPA requested that the Science Advisory Board
(SAB) consider this issue. The request was referred to the
Environmental Health Advisory Committee of the SAB. On
January 12, 1977, the Chairman of the Environmental Health
Advisory Committee appointed an Ad Hoc Study Group on
Pentachlorophenol Contaminants and charged it to review and
report on available information about the chemistry and
toxicology of the chlorinated dibenzodioxins and
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d ibenzofurans. Additionally, to the extent possible, the
study group was a'sked to comment on the potential hazard to
humans which could be attributed to registered uses of PCP
and the extent to which this hazard might be mitigated
by use of a commercial process which results in lower
levels of chlorinated dibenzodioxins and related
contaminants (see Charge to Study Group—Appendix B).
Early in its deliberations the Study Group recognized
that the breadth of the chefrge, as well as the relative
paucity of information on the chemistry and toxicology of
poiychlorinated dibenzo-p-dioxins and dibenzofurans,
precluded an early or comprehensive response. By
consensus, the Study Group agreed to respond to the charge
by attempting to identify the areas of information needs
required to evaluate the problem of PCP contamination with
dioxins and related compounds. The Study Group would
supply specific information when possible and would attempt
to identify the information gaps which limit conclusions
regarding both specific regulatory questions concerning POP
and the broad issues of total environmental contamination
by chemically and. toxicologically related halogenated
dioxin-like substances.
1.2 Discussion
Pentachlorophenol is produced and used extensively.
Production in the U.S. is estimated at approximately 50
million pounds per year; the vast majority of which is used
as a wood preservative. However, there are other uses
including use as an herbicide, a fungicide, a bacteriocide,
a sliraicide and as a preservative for leather.
Numerous contaminants have been identified and
quantified in samples of pentachlorophenol from several
major commercial producers. The quantity and proportions
of the contaminants differ somewhat from batch-to-batch of
the technical grade product and are discussed in more
detail in Appendix C. The contaminants include
tetrachlorophenol (5—10% ), trichlorophenol {ID,
chlorinated phenoxyphenols (about 5%) and poiychlorinated
dibenzo-p-dioxins and dibenzofurans ranging in
concentration from thousands of ppnt in the case of
octachlorodibenzo-p-dioxin to tens to hundreds of ppm for
the hexa- and heptachlorinated dibenzo-p-dioxins and for the
octa-, hepta- and hexachlorodibenzofurans.
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While it is technically feasible to produce
commercially purified PCP that can meet reasonable
regulatory constraints relative to chlorinated dibenzo-p-
dioxins and dibenzofurans, the production of this more
purified product entails increased production costs and,
according to some industry representatives, results in a
product that may be more difficult to handle. A patented
commercial process exists which enables the production of
PCP which contains much lower concentrations of
contaminants reducing the hepta- and octachlorodibenzo-p-
dioxins to 10 to 20 ppm and most of the other
polychlorinated dibenzo-p-dioxin and dibenzofuran
concentrations to 1 or 2 ppm. However, the production of
the purified product results in another serious problem of
how to safely handle and dispose of the concentrated
residual waste created in the removal of the contaminants.
The matter of disposal has been a subject of serious
consideration by a previous advisory committee and by
industry representatives. {See Appendix D.) There is no
question that the handling, transport and disposal of any
residual toxic product from the purification process must
proceed under the strictest standards-. Possible disposal
methods include a suitable licensed disposal- site (none is
known according to Reichhold, Appendix D) and either land
or sea incineration. Presently, the Dow Chemical Company's
Midland, Michigan petrochemical complex uses incineration
to destroy the wastes associated with PCP purification.
(See letter of Robert Johnson to Ernst Linde, Appendix D.)
With regard to the possibility of human exposure to
PCP and/or its contaminants, it is useful to consider
certain physico-chemical properties of PCP relative to its
contaminants. The chlorinated dibenzo-p-dioxin and
dibenzofuran contaminants are less volatile and less water-
soluble than the un-ionized form of PCP and are, therefore,
less readily transported by vaporization and air transfer
or by surface water. Furthermore, the dioxins tend to bind
strongly to soil and wood, which further limits their
transport. On the other hand, the contaminants are
generally more persistent than PCP, as they are only slowly
biodegradable with half-lives in soil on the order of a
year or longer. Although there are considerable data on
the environmental persistence of TCDD, for which
photodecomposition on surfaces and microbial metabolism are
major factors in its environmental degradation, data are
very sparse on the environmental persistence and transport
of the chlorinated dibenzo-p-dioxin and dibenzofuran
contaminants of pentachlorophenol.
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A key problem to overcome in order to make an adequate
evaluation of the relative hazard of PCP and its
contaminants is the lack of ready availability of suitably
sensitive and specific analytical methods. Although much
progress has been made in developing appropriate analytical
capability, routine analysis has been hampered by the
unavailability of suitable analytical standards for some of
the isomers. In fact, the availability of appropriately
specific analytical methods may be the rate limiting factor
in assessing the hazard of dioxins and related chemicals.
Thus, when there are several isomers with widely differing
toxicities, as is the case with hexachlorodibenzo-p-
dioxins, analyses of the isomers as a group only permit
assessment of hazard based upon the most toxic isomer. Ttiis
approach may, indeed, lead to overestimates of hazard, but,
in the absence of more definitive analyses of specific
toxic chemical species, it is necessary to treat
contamination data on a toxicologically worst-case basis.
The toxicological information necessary to make the
evaluation of relative hazard of purified versus standard
commercial PCP is also deficient. Pentachlorophenol Is a
toxic chemical in its own right. A set of signs and
symptoms characteristic of uncouplers of oxidative
phosphorylation has been described in several cases of
accidental or suicidal poisonings. The chlorinated
dibenzo-p-dioxins and dibenzofurans, on the other hand,
have quite a different syndrome in acute poisoning. This
syndrome is characterized by a delayed onset and involves
widespread degenerative changes in several organs, in
particular the liver, thymus, and skin. There are limited
data on the acute toxicity (LDS0) of the chlorinated
dibenzo-p-dioxin and dibenzofuran contaminants of PCP, but
there are virtually no data on the chronic toxicity of the
contaminants. Although the acute toxicity of purified PCP
is generally less than that of contaminated technical
samples, there are insufficient data to permit such a
comparison for chronic toxicity. Studies of acute toxicity
of technical PCP suggest that some of the effects, e.g.,
liver damage, are more consistent with a dioxin effect than
with purely a PCP effect. .Induction of aryl hydrocarbon
hydroxylase {AHH) activity appears to offer a means of
comparing the relative biological activity of poly-
chlorinated dibenzo-p-dioxins and dibenzofurans and cor-
relates quite well with acute toxicity measurements. How-
ever, a problem is that this test has not been validated
for assessing relative potential for chronic injury from
the contaminants. Recent reports of the induction of
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neoplasms by TCDD (Van Miller et al., 1977? Kociba, 1977)
raises the specter that the polychlorinated dibenzo-p-
dioxin contaminants of PCP may also have this potential.
At least some of these contaminants, e.git
octachlorodiben«o-p-dioxin, have been started in the
National Cancer Institute's (NCI) carcinogenesis screening
program, but no data have yet been made available from NCI
on PCP itself. (See section 3.1.4 for discussion of
purified PCP.5 A paper dealing with long term studies of
TCDD and HCDD was recently presented at the New York
Academy of Sciences Science Week (Holmes et al., 19785.
A recent incident of illness in a herd of cows housed
in a newly constructed barn in Michigan stimulated an
investigation into possible contamination of tissue by
residues of pentachlorophenol and its dioxin contaminants.
Both fCP and some of the polychlorinated dibenzodioxins
were found in tissues of these cows (Moore, 1977, see
section 3.2.3). This finding of low,, but detectable,
levels of chlorinated dibenzo-p-dioxins in tissues of these
animals is a matter of public health concern? however, the
biological significance of this finding is not presently
known.
There have been reports of occupational exposure to
chlorinated dibenzo-p-dioxins resulting in adverse health
effects in man. usually chloracne has been the predominant
sign of toxicity, although signs and symptoms of systemic
poisoning (some of which are consistent with dioxin
poisoning in laboratory animals) have also been reported in
association with these industrial exposures. Hi ere is
insufficient information concerning the identity and dosage
of dioxins involved to allow these observations in man to
be useful in a quantitative assessment of the relative
hazard of purified PCP versus commercial products
containing dioxin contaminants-. There are no data that
permit an estimate of the relative susceptibility of humans
to systemic effects of the dioxins and related contaminants
of pcp. The widespread (though of relatively brief
duration) exposure of humans to TCDD in Seveso, Italy
during an industrial accident in 1976 may yet provide
information that will permit some estimates of human dose-
response relationships to that dioxin. As yet, there is no
quantitative information which permits a comparison of the
toxicity of dioxin to humans ,versus other animals.
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1.3 Conclusions
1. Toxic polychlorinated dibenzo-p-dioxin and
dibenzofuran isomers are known to be present in commercial,
technical pentachlorophenol (PCP). The most toxic dioxin
known, TCDD, has not, however, been found in PCP*
2. Analytical methods and preparation of standards for
analysis of the various isomers of the hexa-, hepta-, and
pentachlorinated dioxins have been developed. The method-
ology and equipment required, however, have limited their
widespread use.
3. Among the chlorinated dioxins there are marked
differences in acute toxicity of the isomers; therefore
when analysis of a PCP sample is expressed in terms of
total isomers, such as hexachlorodibenzo-p-dioxins,
evaluation of potential hazard must be based upon the
most toxic of the hexachlorinated isomers.
4. The polychlorinated dibenzo-p-dioxin and '
dibenzofuran contaminants are more stable and persistent,
but less mobile, in the environment than PCP.
5. There is evidence that the dibenzo-p-dioxin and
dibenzofuran isomers can migrate from PCF-treated wood into
animal tissues and products that are consumed by man. "the
toxicological impact of this exposure cannot be quantified
with present data and information, but, conservatively, any
exposure by this route must be considered undesirable and
attempts should be made to prevent exposure.
6. Numerous cases of acute human poisonings with PCP
have occurred, and some occupational exposures to PCP have
resulted in chloracne and other signs suggestive of
dibenzo-p-dioxin or dibenzofuran poisoning. The data and
information related to these reports are inadequate to
assess the toxic hazard of PCP and its contaminants to man.
7. itie most probable opportunity for human exposure
to toxic quantities of PCP and its contaminants is in the
PCP production and utilization industries. Any major
changes in the application of PCP must consider the
implication to this high risk occupational group.
Environmental exposures of humans are likely to be limited
and most probably would occur from direct contact with PCP-
treated wood, from exposures through ingestion of food
contaminated by residues, or from occupational exposure
from inhalation of off-gassing vapors from improperly
treated wood.
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8. Certain uses of PCP, e.g., application to wood
used in human or animal housing or to wood that may com© in
contact with foods or feeds, increases the probability of
exposure to man. Restrictions on such uses might be a
first step in reducing the likelihood of injury from PCP
and its contaminants.
9. There are insufficient quantitative data to rank
the relative contribution o-f PCP to the overall
environmental contamination with dibenzo-p-dioxins and
dibenzofurans. However, because of PCP's extensive use, it
may be a major source of chlorinated dioxins in the
environment. As regards the dibenzofurans, PCP probably
represents a lesser source. However# the similar
toxicological effects produced by the polychlorinated
dibenzo-p-dioxins, dibenzofurans* and other related
compounds (chloroazobenzenes, chloroazoxybenzenes,
chlorinated napthalenes, and polyhalogenated biphenyla)
suggest the potential for additive hazard from the many
sources of these contaminants. Quantitative data on the
total environmental contaminants, the fractional
contribution of the major sources of these contaminants,
and the toxicological response to mixtures of contaminants
are urgently needed.
10. Technology is now available which could markedly
reduce the levels of diben20-p-dioxin and dibenzofuran
contaminants in PCP. It would seem prudent, therefore, to
control the contaminants to the extent possible by best
manufacturing practice. This might best be accomplished by
a phasing in of improved processing. Ttois phasing in of
the use of the more purified product must take into account
the economic impacts as well as the possible trade-offs of
occupational hazards related to residue handling, transport
and disposal..
\
Addendum: Coincident with the final review of this
report, an - article appeared in Science (vol. 202, p.
1166-1167, December 15, 1978) suggesting that "Dioxins"
were produced in trace quantities during the combustion of
a wide variety of materials and could be expected to have
ubiquitous distribution in the environment. A preliminary
review of some data that formed the basis of this report
indicated that the quantities produced in most combustion
activities would contribute extremely minute quantities or
no dioxins to the* environment. Etowever, combustion of
highly chlorinated materials in improperly fueled
incinerators resulted in sufficient quantities of
chlorinated d i ben z o-p-d i ox i ns to warrant attention and
further investigation as to a possible source of
environmental contamination.
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1.4 References
Holmes, p.A., j.h. Rust, W.R. Richter, and A.M. Shefner
(1978). Long term effects of TCDD and HCDD in nice
and rats. In; Abstracts of N.Y. Academy of Sciences,
Science Week (June 21-30, 1978) on The Scientific
Basis for the public Control of Environmental Health
Hazards.
Kociba, R.J., Dow Chemical (1977), Letter and attachments
to Thomas Holloway, EPA. September 7, 1977.
Moore, J.A. (1977). Memorandum to Director, NIEHS (March
21, 1977). Subject: Studies on Possible
Pentachlorophenol/Dibenzodioxin Intoxication progress
Report #2.
Van Miller, J.P. , J.J. Lalich, and J.R. Allen (1977).
Increased incidence o£ neoplasms in rats exposed to
low levels of 2,3,7,8- TCDD. ChetnosDhere 6 (9):
537-S44.
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2. SUMMARY of CHEMISTRY and ENVIRONMENTAL BEHAVIOR
of PENTACHLOROPHENOL and ITS CONTAMINANTS
2.1 Pentachlorophenol and its Uses
Pentachlorophenol (PCP) is a compound of high and
diversified biological activity. It has been shown to be
an effective contact poison against bacteria, fungi and
higher plants and is also toxic to animals. PCP has been
registered for a wide variety of uses, including as a wood
preservative, an herbicide, a sliraicide, a preservative for
hardboard and paper, a leather preservative, an additive
in paints, and a treatment in greenhouses. The principal
use of PCP, however, is in wood treatment as either the
free phenol dissolved in a petroleum carrier or as the
sodium salt in a water based dip treatment. PCP has been
used for over 40 years in wood treatment. The current
level of production and use in the United States is
probably in excess of 50 million pounds per year, Tfce
manufacturing capacity is estimated to be approximately 70
million pounds per year.
2.2 Manufacture of PCP and its Contaminants
PCP in the United States is manufactured from phenol
by a catalytic chlorination process. During chlorination,
the temperature must be maintained above the melting point
of the products formed; this, it is felt, contributes to
the side reaction that gives rise to contaminants.
Commercial technical PCP contains other chlorinated
phenols, among them the 2,3,4,6-tetra isomer, traces of
trichlorophenol, chlorinated dibenzo-p-dioxins, chlorinated
dibenzofurans, chlorophenoxy phenols, chlorodiphenyl
ethers, chlorohydroxydiphenyl ethers, and traces of even
more complex reaction products of phenol. Most
chlorobenzodioxins are the by-products about which there
are the greatest concerns. Analyses of PCP have revealed
that the principal chlorodioxin and chlorodibenzofuran
contaminants are those containing six to eight chlorines.
The highly toxic 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD)
has not been identified in any sample of PCP that has been
analyzed. The compositions of a sample of commercial PCP
and of a sample of purified PCP are given in Table 2.1. A
representative distribution of isomers is given in Table
2.2.
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TABLE 2.1
Comparison of composition of commercial grade
and purified grade Pentachlorophenol (PCP)
Analytical Results
Component Commercial3 Purifiedb
(Dowicicfe*~7) (Dowicide EC-7)
Pentachlorophenol 88.4% 89.8%
Tetrachlorophenol 4.4% 10.1%
Trichlorophenol 0.1% 0.1%
Chlorinated phenoxyphenols 6.2%
Octachlorodioxins 2500 ppm 15.0 ppn
Heptachlorodioxins 125 ppm 6.5 ppn
Hexachlorodioxins 4 ppm 1.0 ppm
Octachlorodibenzofurans 80 ppm 1.0 ppm
Heptachlorodibenzofurans 80 ppm 1.8 ppm
Hexachlorodibenzofurans 30 ppm 1.0 ppm
^Sample 9522 A
Technical grade PCP reduced by distillation
TABLE 2.2
Chlorodioxin isomer distributions in commercial
grade PCP (Dowicide 7) and PCP-Na samples,
(Buser, 1975;197 6)
Chlorodioxin
PCP
PCP-Na
l,2,3f6,7,9-Cl6D
1
0.5
1,2,3,6,8,9-ClgD
3
1.6
1,2,3,6,7,8-ClgD
5
1.2
1,2,3,7,8,9-CL6D
0
0.1
1,2,3,4,6,7,9-Cl?D
63
16.0
l,2,3,4,6,7,8-Cl7D
171
22.0
l,2,3,4,6,7,8,9-ClaD
250
110.0
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2.3 properties of PCP and its Contaminants
The physical properties of a compound play an
important role in how the compound behaves under different
conditions. These properties influence the mobility of a
compound in air or water, its ability to adsorb to
surfaces, and its disappearance due to some type of
degradation. This behavior relates to the route and rate
of exposure by which a compound might be received by man or
other organisms. For these reasons the properties of PCP
and its principal contaminants, dioxins and dibenzofurans,
so far as possible, were evaluated in this report. (See
Tables 2.3-2.5.) From these tables of physical properties
it is ascertained, that PCP has a higher vapor pressure, a
higher water solubility, and a lower capacity for
adsorption than the dioxins or dibenzofurans. For these
reasons PCP is likely to be far more mobile than the
dioxins or the dibenzofurans. The dioxins and
dibenzofurans would probably show an enhanced propensity
for adsorption and hence a,low availability.
2.4- Detection and Quantification of PCP and its
Contaminants
There are a number of methods that may be used for
analyzing PCP; these include colorimetry, spectro-
photometry, and gas chromatography (GC). Gas
chromatography is probably the most sensitive and widely
used method. It is routinely applied for detection and
quantification of PCP down to the parts per billion range.
Analytical methods employing gas chromatography and mass
spectrometry have been devised for the chlorodibenzodioxins
and chlorodibenzofurans. The current state of the art for
TCDD provides a reliable analysis.down to the low parts per
trillion range. Gas chromatography alone is adequate only
for the higher concentrations.
2.5 Environmental Chemistry
PCP has been found in a number of different
environmental samples such as house dust, air, water and
urine of presumably non-exposed humans. Frequently the
appearance of PCP in non-biological samples can be
explained by the proximity of a source of PCP, but in the
case of the urine of presumably non-exposed humans the
explanation is more elusive. It may be that
exposure to treated wood or the use of PCP as a
preservative in certain items affords human exposure, but
another possibility that cannot be ruled out is the
generation of pentachlorophenol in chlorination of water or
perhaps even the generation of PCP by natural processes.
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TABLE 2.3
Physical Properties of Pentachlorophenol (PCP)
Molecular Weight
Melting point
Boiling Point
Dens ity
Vapor Pressure
Solubility 1^0
Solubility of sodium salt, H20
Partition Coefficient
Molar Refraction
266.35
191°C
3lO°C (decomposes)
1.98?
1.6 X 10"4mm Hg (25°)
1.2 X I0_1mm Hg (1GQ°C
40 mm Hg (2ll°C)
20 ppm at 30°C
33g/100g
1 X 10:
53.5
*S.01
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TABLE 2.4
Physical Properties of Various Chlorodioxins
Chlorodioxin
Hoi. Wt.
M.P.
C
»p»
Value*a)
Estimated
Vapor (b)
Pressure
Molar
Refraction
UV Max
(CHCI) nm
2,7,-Cl2
253.08
__
0.76
6.0 x 10~6
*i f ¦
302
2,3,7-Gl3
287.53
162
0.86
3.6 x 10"6
—
305
2,3,7t8,-Cl4
321.87
306
0.51
1.7 X 10"6
71.4
310
1,2,4,7,8-Clj
356.42
206
—
72.6
307
1,2,3,7#8-Ci5
356.42
241
— —
308
1,2,4,6,7,9-Cig
390.86
240
0.MW>
6.6 x 10~7
—
310
1,2,3,6,8,9-Clg
390.86
—
—
81.1
—
1,2,3,6,7,8-Clg
390.86
. 205
—
316
1,2,1,7,3,9-C16
390.86
243
--
—
317
1,2,3,4,6,?.9-C17
425.31
0.9C
3.0 x 10"7
8S.9
—
1,2,3,4,6,7,8-Cl7
425.31
—
0.90
—
1,2,3,4,6,7,8,9-Clg
459.75
331
0.90
1.8 x 10~?
90.7
318
(a) Beroza, M. and M.C. Dowrtidn, "p" value determined for dioxin between hexane and acetonitrile,
J. Assoc. Offic. Anal. Chcro. 48:3 58-370 0.965).
(b) Vapor pressure estimated from data of Wool son (Woolson et aK, 1973).
(c) Estimated by summing atomic refractions.
(d) "p" value determined for mixture of hoxachlorodioxin isomers.
-------
TABLE 2.5
Solubility of Several Chlorodioxina in Various Solvents3
Solubility in mg per
liter
Solvent
TCDO HxCDD
OCDD
acetone
90
5
anisole
2600
1700
benzene
470 1600
1000
chloroforn
5 50
560
methanol
1Q
toluene
1800
1500
o-xylene
3600
water
0.0002
— indicates no data
Ea^ Firestone observed that I,2,3,6,7,8-HxCPD is considerably
less soluble in organic solvents than other HxCDD isomers.
The solubility of the 1,2,3,6,7,8-isomer in isooctane is
about 20 mg/1.
^ Dow standard 8Z-h, a mixture of 71% 1,2,3,6,7,8-HxCDD and
291 1,2,3,6,7,9-HxCDD and 1,2,3,6,8,9-HxCDD.
14
-------
Additionally, exposure to hexachlorobenzene {HCB} results
in excretion of significant amounts of PCP in urine. Uptake
of PCP by living organisms occurs quite readily, whether by
oral, respiratory, or dermal routes. The material is
excreted in urine either as free phenol or as conjugated
metabolites. The length of time for loss of the ingested
amount varies with the species and ranges up to 90 hours.
The distribution of the dibenzo-p-dioxins and
dibenzofurans in the environment has been les3 widely
studied. For the most.part, in the studies that have been
conducted exposure was likely to have occurred through use
of materials containing these contaminants. Upon direct
exposure, both the chlorinated dibenzodioxins (CDDs) and
the chlorinated dibenzofurans
-------
on the other hand, was found to be very rapid in the
presence of hydrogen donors such as oils and 2, 4 ,5 -T.
The principal dioxin contaminant of technical
pentachlorophenol is the octachlorodibenzo-p-dioxin, or
OCDD. There is concern that this compound and the other
chlorodioxins might be generated in burning treated paper
or wood. Studies of R.H. Stehl and L.L. tamparski (1977J
and B. Ahling and L. Johansson (1977) indicate that low
levels of the chlorodioxins might thus be generated under
certain conditions of combustion. The levels are
sufficiently low, however, as probably not to be a serious
source of exposure.
Further discussion and documentation of the chemistry
for PCP and its contaminants may be found in Appendix C,
Section 7.
2.6 References
Ahling, s. and L. Johansson (1977). Combustion experiments
using pentachlorophenol on a pilot scale and
full-scale. Chemosphere 6_ (7)s 425.
Stehl, R.H. and L.L. Laraparski (1977). Combustion of
several 2,4,S-trichlorophenoxy compounds: formation
of 2,3,7,8-tetrachloro-dibenzo-p-dioxin. Science 197:
1008.
16
-------
1
3. TOXICOLOGY ••
3.1 Toxicity of pentachlorophenol in Laboratory Animals
The widespread use of pentachlorophenol (pep) as an
antimicrobial agent and the likelihood of commercial
products being contaminated with certain highly toxic
polychlorinated dibenzo-p-dioxins and dibenzofurans
necessitate a review of the toxicological information
currently available. Although this review is primarily
concerned with data on PCP per ser available data on
commercial samples are included "Tor comparative purposes.
Results of acute toxicity studies by oral, dermal,
and injection routes, repeated oral exposures of 3-8
months, a two-year oral test with PCP containing very low
levels of contaminants, mutagenic and teratogenic studies,
and a recent study on the effects of PCP on metabolising
enzymes are reviewed.
3-1-1 Sample Studies
Table 3.1 lists the composition of the samples used
in the long term studies. The PCP content varies from 8 5%
to 99%. There no evidence of the presence of 2,3,7,8-
tetrachlorodibenzo-p-dioxin {TCDD), the most toxic of the
polychlorinated dibenzo-p-dioxins. The 1,2,3,6,7,8-
hexachlorodibenzo-p-dioxin (HxCDD) is the major hexa isomer
(Buser, 1975;1976). The 1,2,3,7,8,9-isomer has been
reported to produce chick edema. (Cantrell et al., 1969).
The octachlorodibenzo-p-dioxin (OCDD) has shown little
toxicity, possibly because of its low solubility. The
objective in recent years has been to reduce the levels of
polychlorinated dibenzo-p-dioxins and polychlorinated
dibenzofurans to a minimum in the commercial samples.
3.1.2 Acute Toxicity
Oral: The LDS0 for PCP in male rats has been
reported as 78 mg/kg (Deichmann et al., 1942), 90 mg/kg
(Gabrilevskaya and Laskina, 1964), 146 mgA<3 (Gaines, 1969)
and 205 mg/kg, the last being Dowicide EC-7 (relatively
pure). For, the female rat, it was-135 mg/1cf (Dow Chemical
Co. Summary, 1969) and 175 mg/kg (EC-7) (Gaines, 1969).
The LDen for nice was reported as 130 + 9.5 mg/kg
(Pleskova ana Bencze, 1959); 100-130 mg/kg for rabbits
(Deichmann et al., 1942); for guinea pigs, 250 ragAg
(Gabrilovskaya and Laskina, 1964);and for swine 120 mg/kg
17
-------
TABLE 3.1
PKNTACIILOROPMENOL - COMPOSITIONS REPORTED FOR SOME SAMPLES USED IN TOXICITY TESTING*
PURIFIED COMMERCIAL •
Aldrich Dowieide EC-7 Dowicide 7 Monsanto
_ J_1) (3) (2) (4) (6) (1) (3)
Pentachlorophehol >
Tetrachlorophenol <
Trichlorophenol
Higher Chlorophenols
Caustic Insolubles (max)
2,3,7,B-Tetrachlorodibenzo-p- <
dioxins
PenLachlorodibenzo-p-dioxins *
Hexachlorodibenzo-p-dioxins <
Heptachlorodibenzo-p-dioxina *
Gctachlorodibenzo-p-dioxin 5
Tetrachlorodibenzofurans <
Pentachlorodibenzofurans <
lie xach I o rod ibenzof urans <
Ileptachloradibeivzofurans *
Oetaehlorodibenzofuran <
*unless otherwise stated
(1) Analyses by GC-MS - Sensitivity 0.1 ppm
(2) Analyses by GC-MS - Sensitivity 0.05 ppm
(3) J. A. Goldstein et al. <1977)
(4) 11. A. SchewLz et al. (1976)
(5) Uuser (1975) reported 1,2,3,7,8,9 HxCDD as major isomer (toxic)
(fi) n . 1.. Johnson et al. (1 'J7 J)
99%
0.1
90.4 + 1.0%
10.4 + 0.2
< 0.1
0.1
< 0.05
0.1
0.1
0.1
0.1
0.1
0.1
0.1
0.1
0.1
1.0 + 0.1
6.5 + 1.0
15.0 ~ 3.0
3.4 + 0.4
1-8 ± °-3
< 1
85-90%
4-8 %
< 0.1
2-61
1
None
84.6%
3 %
0.1
9.27
575-2510
Detected
Detected
Detected
< 0.1
a (5)
520
13H0
< 4
40
90
400
260
-------
(Harrison, 1959). Dreisbach {1963) has reported an estimated
dose for man to be as low as 29 mg/kg.
These data would suggest that PCP has moderate acute
oral toxicity, but that the LD50 value may vary with the
quality and quantity of contaminants. Man would appear to
be more susceptible than the rodent and the female to be
more susceptible than the male.
Skin Absorption: When PCP in an organic solvent was
applied to rabbit skin under occlusion for 24 hours, 200
mg/kg was lethal, but 100 mg/kg and 50 mg/kg were not {Dow,
1969). The LD5q for rats has been reported as 96 mg/kg,
105 mg/kg, and 320 mg/kg (Deraidervko, 1966? Noakes and
Sanderson, 1969? Gaines, 1969) and that for mice as 261 + 39
ragAg (Pleskova and Bencze, 1959).
Subcutaneous injection; The LDe0 for the rat was
100 mg/kg, for the rabbit 7 0 mg/kg (SI in olive oil)
(Deichmann et al., 1942), for mice 63 + 3.2 mg/kg (Pleskova
and Bencze, 1959).
Intravenous Injection: The lowest dose of PCP
reported to kill raboits was 22 mg/kg (Kehoe et al., 1939),
when it was instilled' as a 1% aqueous sodium pentachloro-
phenate.
inhalation; Exposure to 5 mg/1 dust for one hour did
not kill male and female rats (Reichhold Chemicals, 1974).
Demidenko (1969) reported the LD^q by inhalation to be 225
mg/kg for rats and 355 mg/kg for mice. The exposure
concentration and the calculations to arrive at the£#Dso
dose were not given in the abstract. Workers have reported
that the dust is irritating to the mucous membrane of the
nose and throat.
Irritancy 'Tests: Rabbit eyes exposed to solid material
showed slight conjunctival and slight iritic congestion, in
one of.four eyes. Exposure of rabbit skin under occlusion
caused minimal irritation oh intact skin and slightly more
on abraded skin (Dow, 1969).
Commercial samples have produced chloracne in the
rabbit ear bioassay, whereas the purified material has not.
Positive reactions could be produced by topical or oral
application {Johnson et al., 1973).
Allergic contact dermatitis has not been a problem in
handling the chemical.
19
-------
Clinical Effects; Acute animal exposures have, in
general, caused anorexia, diarrhea, stimulation of the
central nervous system, increase in body temperature,
anuria, paralysis of the hind legs and functional
cardiovascular changes leading to death (Deichraann et al. ,
1942; Gabrilevskaya and Laskina, 1964; Pleskova and Bencze,
1959; Denidenko, 1966).
3.1.3 Subchronic Feeding Studies
Johnson et al. (1973) compared the toxicity of
commercial PCP with improved process PCP and with a purified
PCP. (The commercial sample contained 8 5-901 PCP, 9-26 ppnt
of HxCDD and 575-2150 ppnt OCDD and produced chlorance of
rabbit ears and chick edema in bioassays. The improved
process PCP contained 88-931 PCP, 30 ppm OCDD and 1.0 ppm
HxCDD. Neither the improved process PCP nor the chemically
pure PCP produced chloracne or chick edema.) Three, 10 and 30
mg/kg per day (mixed with diet) were fed to Sprague-Dawley,
Spartan strain rats for 90 days. The purified and the
improved process PCP caused increase in liver weight at 30
mg/kg and 10 mg/kg and increased kidney weight at 30 mg/kg.
The commercial sample caused a decrease'in hematological
values, an increase in alkaline phosphatase, a decrease in
serum albumin, and an increase in liver weights at all
levels; and focal hepatocellular degeneration and necrosis at
the 30 mg/kg level. The authors concluded that the
impurities causing toxic effects had been eliminated by the
new process.
Knudson et al. (197 4) fed PCP (Dynastit-Nobel)
containing 200 ppm OCDD, 82 ppm pre-OCDD and no detectable
TCDD to rats (SPF-Wistar) at levels of 0, 25, SO and 20 0 ppm
in the diet. Liver weight was increased in rats fed 5 0 and
20 0 ppm PCP and was accompanied by increased activity of
microsomal liver enzymes. There were fewer calcium deposits
in the kidneys of test rats; Twenty-five ppm was considered
the no-effect level.
Kimbrough and Linder (197 5) fed purified PCP to one
group of ten male rats and commercial PCP to a second group
for 90 days. A level of 1000 ppm in the diet, equivalent to
approximately 50 mgAg per day, was chosen for the purpose of
examining liver changes by light and electron microscopy.
Enlargement of hepatocytes was observed in the livers of rats
fed pure PCP, whereas technical grade PCP caused foamy
20
-------
cytoplasm* vacuoles, inclusions, single hepatocellular
necrosis, slight interstitial fibrosis, and prominent brown
pigment in macrophages and Kupffer cells. By electron
microscopy, there was ail increase in the smooth endoplasmic
reticulum in the group fed technical PCP with less change
in the rats fed pure PCP, There were many lipid vacuoles
in the former group and some in the latter. Atypical
mitochondria were.observed in the livers of both groups.
Goldstein (1977) subsequently studied the differences
between the hepatic effects produced by commercial and
purified FCF with respect to drug metabolizing enzymes and
presence of porphyria. Chemical analyses of the samples
used are listed in Table 3-1. Use technical grade material
contained significant amounts of PCDD's and PCDF's, whereas
the purified material contained less than 0.1 ppm of each
isomer, the level of sensitivity of the method. Groups of
six Sherman female weanling rats were fed pure or technical
PCP at levels of 0, 20, 100 or 500 ppm mixed with Purina
Chow. Animals were sacrificed after eight months and
hepatic enzyme activity and hepatic porphyrins were
determined. '
Technical pentachlorophenol produced hepatic porphyria
and increased hepatic aryl hydrocarbon hydroxylase
activity, glucuronyl transferase activity, liver weight,
cytochrome p-450, and microsomal heme, but not N-
demethylase activity. The peak of the CO-difference
spectrum of cytochrome p-450 was shifted to 448 nia, and
there was a dramatic increase in the 455/430 ratios of the
ethyl isocyanide difference spectrum. The enzyme changes
were observed at 20 ppm of technical pentachlorophenol.
Porphyria occurred at 100 and 500 ppm. Pure
pentachlorophenol had no significant effect on aryl
hydrocarbon hydroxylase activity, liver weight, cytochrome
p-450, microsomal heme, the ethyl isocyanide difference
spectrum, or N-demethylase activity at any dose level, but
did increase glucuronyl transferase at 50 0 ppm. in
contrast, both pure and technical pentachlorophenol
decreased body weight gain comparably at 500 ppm. It was
concluded that technical pentachlorophenol produces a
number of liver changes which cannot be attributed to
pentachlorophenol itself, but which are consistent with the
effects of biologically active chlorinated dibenzo-p-
dioxins and dibenzofurans. See Table 3-2.
21
-------
TABLE 3.2
BIOLOGICAL ACTIVITY
PURIFIED VS TECHNICAL SAMPLES OF PCP
Technical
Pure Grade
Chick edema - +
Chloracne - +
porphyria - +
Increase in liver weight/body wt. +
Increase in liver enzyme activity + +
Presence of pigment in liver cells +
Liver h istopathology less *
Depressed body weight + +
Enbryotoxicity + +•
- indicates no presence
+ indicates presence
22
-------
3.1.4 Two-year Feeding Study
Schwetz et al. (1976) carried out a two-year oral
study with Dowicide EC-7, a substance which the Johnson 90-
day study had shown to act more like purified material than
commercial preparations. Analyses of-the samples used are
given in Table 3.1.
Weanling Sprague-Dawley (Spartan-substrain) rats were
divided into five groups of 25 males and 2 5 females each.
They were fed a test diet of ground Purina Laboratory Chow
mixed with PCP (dissolved in anisole), the amount being
adjusted on a monthly basis to provide dose levels of 0, 1,
3, 10 or 30 rag/kg per day. The male rats, were terminated
after 22 months because of high mortality in both control
and test groups. The female groups were terminated after
24 months. Gross and histopathologic*! examinations were
performed.
Effects, which the authors attributed to ingestion of
PCP at the highest dose level of 30 ng/kg per day, were.
(1) a significant decrease in body weight among female
rats? (2) a significant increase in serum glutamic pyruvic
transaminase activity in male and female rats; (3) an
increase in the specific gravity of urine among female rats
at the end of one year but not at two years; (4) an
accumulation of pigment in the liver and kidneys. An
accumulation of pigment in the liver and kidneys was also
observed in females fed 10 mg/kg per day. There were no
other significant differences between test and control
groups with respect to clinical observations, hematological
changes,.blood and urine chemistry, terminal organ weights
and pathological changes, ttere was no evidence of
carcinogenic effect, tumors being similar in number and
kind "in both test and control groups, nor was there a' life-
shortening effect attributable to the test material.
It was concluded, therefore, that doses of penta-
chlorophenol as high as 30 mg/kg per day fed throughout the
life span produced only mild changes which did not shorten
the life span or alter the incidence of tumors.
The results are consistent with those found by
Goldstein (1977) when doses of approximately 25 mg/kg per
day of purified material fed for eight months, caused weight
loss. However, dark pigment in the liver reported by
Schwetz et al. (1976) was observed by Kimbrough (1972)
23
-------
in the livers of rats fed technical materials, bat not in
those fed purified PCP at doses of 50 rag/kg. An 18-month
feeding study with mice at 130 ppm did not elevate 'the
incidence of tumors (Innes, 1969).
3.1.5 Chronic inhalation Exposures
& Russian study has reported that chronic exposure to
3 mg/M J caused threshold changes in an unidentified
organism, but no details are given in the abstract. Based
on this study and on observations in the workplace, maximum
allowable concentrations were determined to be 0.1 mg/M3
(Demidenko, 1969).
The American Conference of Governmental Industrial
Hygienists (ACGIH) has established a threshold limit value
(TLV) of 0.5 mg/M3 (0.046 ppm), a level below which
irritation to the nose, throat and eyes is minimal (ACGIH,
1971).
3.1.6 Mutagenic-Cytotoxic Potential
PCP has not shown mutagenic activity in the Ames test
(Anderson et al., 1972), the host-mediated assay
(Buselmaier et al., 1973), or the sex-linked lethal test on
drosophila (Vogel and Chandler, 1974).
3.1.7 Teratogenic and Embryotoxic potential
PCP did not cause deformities, but it was highly
embryolethal and embryotoxic following oral administration
to rats of 15,30, or 50 mg/kg per day on days 6-15 of
gestation. No effects were produced at S mg/kg (Schwetz
and Gehring, 1973? Schwetz et al., 1974). Purified PCP,
with its low nonphenolic content, wag slightly more toxic
than the commercial grade (Schwetz et al., 1974).
Oral administration of PCP to the goIdem Syrian
hamster at levels ranging from 1.25 to 20 mgAg daily from
days 5 to 1Q of gestation resulted in fetal deaths and/or
resorptions in three of six teat groups. PCP was found in
the blood and fat of the fetuses (Hinkle, 197 3).
Pregnant rats (Charles River-CD Strain) were given
60 mg/kg of labeled PCP on days 8 through 13 of gestation and
were sacrificed on the 20th day. Only a small amount of PCP
crossed the placental barrier and only slight teratogenic
effects were noted (Larsen et al., 1975).
24
-------
3.1.8 Summary
Laboratory studies to evaluate the toxicity of PCP as
a wood preservative or pesticide began in the 1930*s and
have continued to the present time. PCP is considered a
toxic compound, an economic poison, whose toxicity may vary
depending upon the quality and quantity of contaminants
which vary with different manufacturing procedures.
Samples were not adequately characterized until recently
when some insoluble contaminants were recognized to be the
highly toxic polychlorinated dibenzodioxins and furans. Due
to the difficulty of separating the isomers and in
obtaining standards for analyses, there are many gaps in
the toxicity data, creating uncertainty in any evaluation
of the potential hazard,
m attempt must be made to differentiate between the
clinical and" pathological effects of PCP, the related
phenols, and its likely contaminants, reported as (1) hexa-,
hepta- and octachlorodibenzgdioxins and (2) hexa-, hepta- and
octachlorodibenzofurans. In addition there may be
chlorophenoxyphenols and chlorinated diphenyl ethers
(reported in European samples) whose identification, amounts,
and toxicity have not been evaluated.
The increasing oral LD5fl values through the years
are probably'related to improved process procedures,
being reported in 1942 as 78 mg/kg and in 1969 as 205 mg/kg
for male rats. PCP is easily absorbed through the skin,
the LD5q for rabbits being similar to that by oral
dosing when the material was applied in a. lipid solvent
under occlusion.
In-general, acute exposure of, animals- has led to rapid-
development of high body temperature, increased respiratory
rate, moderately elevated blood pressure, hyperglycemia,
and muscle weakness, terminating in asphyxial convulsions
with cardiac arrest, which tends to occur in less than 24
hours. Pathological examinations showed extensive damage
to the cardiovascular system. These changes resemble those
produced by the related phenolic compound dinitro-
orthocresol (DNOC). Barnes (19575 concluded that both DNOC
and PCP interfere with production of high energy phosphate
compounds essential to cell respiration. *Chis interference
causes stimulation of the cell metabolism .to the toxic
stage with accompanying fever and the other clinical signs
described above.
25
-------
Most chlorinated dihenzodioxins, on the other hand,
show a very different clinical picture. Oxidative
phosphorylation is not affected. The effects are usually
delayed (several weeks to months) and may be accompanied by
effects on the liver, the hemopoietic system, and the
lymphatic system with thymic atrophy and lymphoid
depletion. There is a marked increase in liver microsomal
enzyme activity and eventual histological change. There is
a striking difference in susceptibility among species, the
guinea pig being the most susceptible and the female being
more susceptible than the male.
Comparative chronic studies with purified and
commercial PCP have been limited. in essence, however,
studies show a marked difference,in effect on the liver.
The no-effect level for the relatively pure material in a
90 day test was 3-10 mg/kg; the no-effect level for
commercial material was not established. A life time oral
study was done only with new process material at dose
levels of 3, 10 and 30 mg/kg. The data showed that at
higher levels there were some functional changes which did
not result in a shortening of the life span, higher
incidence of tumors or significant pathology,
3.1.9 conclusions
1. Experience has shown that dermal absorption is the
primary hazard to man from the use of PCP as a wood-
preservative.
2. The chemical has a low vapor pressure and is a
respiratory irritant which has acted as a warning. No
complaints have been noted when the concentration does not
exceed the TLV.
3. In the United States there have been no reports of
chronic injury to those workers exposed for as long as 3 5
years while manufacturing this material. Hi is conclusion
is supported by Western Electric (Ochrymowych, 1978), whose
utility poles were treated with commercial grade PCP, with
no reports of injury in over two decades of service. Deaths
and injuries have arisen from mishandling of the material
in the wood treatment process. There has been a complaint,
however, when treated wood was used in a home interior
without further finishing, a procedure which is not
recommended.
4. Trace contaminants in the form of chlorinated
dioxins and chlorinated dibenzofurans are present in bio-
logically active amounts. Due to limited knowledge of the
amounts and toxicity of the isomers present, only tentative
conclusions as to their contribution to the total toxicity
picture and the extent of the hazard to the general public
can be made.
26
-------
3.1.10 References
ACGIH (1971). Documentation of TLV's for Substances in
Workroom Air, Uiird edition.
Amer, S. M. and E.M. Ali (1969), Cytological effects of
pesticides. IV. Mitotic effects of some phenols.
CytQlogia 34(4): 533-40 (CA 73j24223h).
Anderson, K. J., E.G. Leigh ty, and M.T.Takahashi
(197.2). Evaluation of herbicides for possible mutagenic
properties. J. Agr. Food Chem. 20: 649-56.
Buselmaier, W., G. Roehrborn, and P. Propping (1973).
Comparative investigations on the mutagenicity of
pesticides in mammalian test systems. Mutat. Research
21(1): 25-6. ~~
Buser, H-R (1975). Polychlorinated dibenzo-p-dioxins,
separation and identification of isomers by gas
chromatography - mass spectrometry. J. Chromatog- 114;
9 5-108. . "* •
Buser, H.-R (1976), High resolution gas chromatography of
polychlorinated dibenzo-p-dioxins and dibenzofurans. Anal.
Chem. 48:1553.
Cantrell, J. S., N.C. Webb, and A.J. Mabis (1969). The
identification and crystal structure of a hydro-
pericardium-producing factor; 1, 2, 3, 7, 8, 9-
hexachlorodibenzo-p-dioxin. Acta Cryst. B25s 150-156.
Deichmann, W. B., W. Machle, K.V, Kitzmiller, and
G. Thomas (1942)~ Acute and chronic effects of
pentachlorophenol and sodium pentachlorophenate upon
experimental animals, J. Pharm. Exptl. Therap. 76: 104,
Demidenko, N. M. (1966). Toxicological properties of
pentachlorophenol. Gig. Toksikol. Pestits. Klin.
Otrayleni, (4): 234-9.
Demidenko, N. H., (1969). Maximum permissible atmospheric
concentration of pentachlorophenol. Gig. Tr. Prof, Zabol.
13 (9): 58-60, (CA 72:47095M).
Dow Chemical Co. (1969) Toxicity Summary for Dowicide 7.
27
-------
Dreisbach, R. H. (1963). Handbook of Poisoning: diagnosis
and Treatment, p, 256.
Fed. Proc. (1943). Fed. Am. Soc. Exp. Biol. 2:16.
Gabrilevskaya, L. N. and V.P. Laskina ( 1964)'. Maximum
permissible concentrations of PCP and Na-pentachloro-
phenolate in water reservoirs. Sanit.Okhrana Vodoemov ot
Zagryazneniya Prom.Stochnymi Vodami, (6): 2S1-272
(CA 6 2115304d).
Gaines, T. H. (1969). Acute toxicity of pesticides.
Toxicol. Appl. Pharmacol. 14(3): 515-34,
Goldstein, J. A. (1977). Effects of pentachlorophenol on
hepatic drug metabolizing enzymes and porphyria related to
contamination with chlorinated dibenzo-p-dioxins and
dibenzofurans, (In press).
Grant, W. F. (1973). Cytological effects of environmental
mutagens - pesticides. Mutat. Res. 21(45: 221-2.
Harrison, D. L. (1959). The toxicity of wood preservatives
to stock, Part I; Pentachlorophenol. New Zealand Vet. J.
7: 89-98 (CA 55:238l4e).
Hinkle, D. K. (1973). Fetotoxic effects of pentachloro-
phenol in the golden Syrian Hamster. Tox. and
Appl. Pharmacol. 25(3): 455 (abstract).
innes, J. R. M. et al. (1969). Bioassay of pesticides and
industrial chemicals for tumorigenicity in mice: A
preliminary note. J. Natl. Cane. Inst. 42; 1101-14.
Johnson, R. l., P.J. Gehring, R.J. Kociba, and B.A. Schwetz
(1973). Chlorinated dibenzodioxins and pentachloro-
phenol. Environ. Health Perspect. 5: 171-5.
Kehoe, r. A., W. Deichmann-Gruebler, K. V. Kitzmiller
(1939). Toxic effects upon rabbits of pentachlorophenol
and sodium pentachlorophenate. J. Indust. Hyg. 4 Toxicol.
21: 160-172. "
Kimbrough, R. D. (1972). Toxicity of chlorinated hydro-
carbons and related compounds. Arch. Environ, Health
25(2): 125-31.
28
-------
Kirabrough, R. D. arid R.E. Linder (1975). The effect of
technical and 99% pure pentachlorophenol on the rat liver.
Light microscopy and ultrastructure. Toxicol. Appl.
Pharmacol. 33; 131-132. (Abstrac t).
Knudson, I., H.G. Verschuuren, E.M. Den Tonhelaar,
R. Kroes, and P.F.W, Helleman (1974). Short-term
toxicity of pentachlorophenol in rats. Toxicol. 2:
141-152.' :
. Larsen, R. V., Q.S. Born, W.V. Kessler, S.M, Shaw,
D.C. Von Sickle (1975). Placental transfer and
teratology of pentachlorophenol in rats. Environ. Lett.
10(2): 121-8.
Lehman, H. J. (1951) Quart. Bull. Assoc. Food and Drug
Officials 15: 122-157" ;
Levin, J-0,C. Rappe, and C. -A Nilsson (1976). Use of
chlorophenols as fungicides in sawmills. Scand. J.
• Wor^ Environ, and Health ^2: ~71-81.
Noakes, D. N. and D.M. Sanderson (1969). A Method for
determining the dermal toxicity of pesticides.
British J. of Indust. Med. 26; 59-64.
Gchrymowych, J., Western Electric (1978). Personal
commiin i cation.
pleskova, A. and K. Bencze (1959). Toxic properties of
pentachlorophenol. Pracovni lekerstvi 11; 348-54.
Reichold Chemicals (1974). Report of May 28, 1974.
Schwetz, B. A. and P.J. Gehring (1973). The Effect of
tetrachlorophenol and pentachlorophenol on rat
embryonal and fetal development. Toxicol. Appl.
Pharmacol. 25 (3); 455 (Abstract).
Schwetz, B. A., P.A. Keeler#P.J. Gehring (1974). The
Effect of purified and commercial grade penta-
chlorophenol on rat embryonal and fetal develop-
ment. Toxicol. Appl. Pharmacol. 28(1); 151-61.
Schwetz, B. A., J.F. Quast,C.G. HumistonrC.E. Wade,
G.C. Jersey, R.W. Lisowe, and R.J. Kociba (1976).
Results of a toxicological evaluation of pentachloro-
phenol sample XD 8108.00L administered to rats by the
dietary route on a chronic basis. (Dow Chemical Co.
Report - unpublished).
Vogel, E. and J.L.R. Chandler (1974). Mutagenicity
testing of cyclamate and some pesticides in drosophila
melanogaster. Experientia 30(6): 621-3.
29
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3.2 Toxicity of-Chlorinated Dioxins and Dibenzofurans
3.2.1 Toxicity of Chlorinated Dibenzo-p-dioxins
It has been reported that hexachlorinated, heptachlor-
inated, and octachlorinated dibenzo-p-dioxms are found in
pentachlorophenol. Of the ten hexachlorodibenzo-p-dioxin
isomers theoretically possible, only six are predicted and
have been found in pentachlorophenol (Stehl and Crummett,
1977; Vogel 1977). Of these six, two (1,2,3,7,8,9- and
1,2,3,6,7,8-hexachlorodibenzo-p-dioxin) would be expected
to have marked toxicity given that the 2,3,7,8, positions
are halogenated. Previous toxicity studies have shown that
the single oral LD5Q of these two isomers in guinea pigs
ranges between 60 and 100 ug/kg (McConnell et al. , 1978).
The comparative toxicity of various dibenzodioxin isomers
does show a positive correlation between in vivo toxicity and
the ability of these isomers to induce aryThydrocarbon
hydroxylase {AHH) enzyme systems in chick embryos (Poland
and Clover, 1973). Utilizing AHH induction data to predict
toxicity, one predicts several orders of magnitude decrease
in the toxicity of the other four hexachlocodibenzo-p-
dioxin isomers (1,2,4,6,7,9-, 1,2,4,6,8,9-, 1,2,3,6,7,9-
and 1,2,3,6,8,9-). Specific toxicologic evaluation of the
other isomers has not been performed.
Chronic (two year) toxicity studies of a mixture of
two hexachlorodibenzodioxins is in progress at the Illinois
Institute of Technology Research Institute through an NCI
contract. The two isomers present in this mixture are the
1,2,3,6,7,8 and 1,2,3,7,8,9-hexachlorodibenzodioxins. A
hexa-chlorodibenzodioxin mixture (the specific isomer
composition is unknown) has been found to induce chloracne
in the rabbit ear bioassay as indicated by the formation of'
comedones (Schwetz et al., 1973). in teratology studies,
this hexachlorodibenzodioxin mixture was found to cause
maternal toxicity in rats at a dose of 10 0 ug/kg/day; doses
of 10 or 100 ug/kg/day of hexachlorodibenzo-p-dioxins were
highly lethal to fetuses during late gestation. The weight
and length of surviving fetuses were also significantly
decreased. A significant increase in fetal abnormalities
was observed in offspring from rats that received the 100
ug/kg/day dose. Subcutaneous edema of the fetuses was
observed at a 1 or 10 ugA
-------
There are two heptachlorinated dibenzodioxin isomers
possible, both of Which have been found in pentachloro-
phenol. Of these two, the 1,2,3/4,6,7,8- isomer would be
expected to be the more toxic. Specific toxicity studies
on this isomer are incomplete. In a.guinea pig toxicity
study, animals survived a single oral dose of 180 ug/kg
with little or no toxicity observed (McConnell et al.,
1978). Further studies are currently in progress at the
National Institutes of Environmental Health Sciences
(NIEHS) in which guinea pigs are receiving doses of 200,
400, or 600 ugAf.
The toxicity of oetachlorodibenzo-p-dioxin is not
known. Oral doses of 1 g/kq did not cause death in five
female rats or in four male mice that received 4 g/kg
(Schwetz et al., 1973). In a teratology study with
octachlorodibenzodioxin, no signs of maternal toxicity were
observed in rats that received either 100 or 500 mq/kg/<3ay
of OCDD. No increase in fetal absorptions or fetal
anomalies was observed at the 500 mg/kg dose. The
incidence of subcutaneous edema was significantly
increased. In a chick edema bioassay, edema was not
observed in chicks that were maintained on a diet
containing 0.5% OCDD for 21 days (Schwetz et al., 1973).
Table 3.3 summarizes relative dibenzo-p^dioxin/
diben2ofuran toxicity where data are available. Comparative
toxicologic data show that the pattern of toxicity caused
by dioxin isomers is the same as that produced by TCDD
(McConnell et al., 1978). Experiments with carbon 14—
labelled TCDD indicated that dioxins pass.the placental
barrier and are secreted in milk (Moore et al., 1976). It
has been shown that TCDD causes immunosuppression (Vos and
Moore, 1974); increased susceptibility to bacteria (Thigpen
et al., 1975),* and fetal death or birth defects (Courtney
and Moore, 1971).
3.2.2 Dibenzofurans
Relatively little work has been directed toward the
specific indentification of dibenzofuran isomers present in
pentachlorophenol. Preliminary work reported.by Stehl and
Crummett (1977) records the presence of the 2,3,6,7- and
2,4,6,7-tetrachlorodibenzofurans and the 2,3,4,6,7-,
1,2,4,7,8- and 2,3,4,7,8-pentachlorodibenzofurans as well
as the 1,2,3,6,7,8-hexachlorodibenzofuran. Quantification
of the levels of these isomers in pentachlorophenol was not
done due to interferences with other chemicals (chlorinated
diphenyl oxides). Of the isomers reported, the 2,3,4,7,8
31
*
-------
TABLE 3.3
TOXICOLOGY DATA SUMMARY
D J Bf.N7.OD I OX I US
LD30 (xtngla doae) pn/k»
Culnea Pig
lilce
Mt
)%>»fcey (Rheaua)
AJIH Induction In Chick Eafcyro
Relative to TCKD
Teratogenic Itoae |ig/kg
Vctotoxlc &>!• Uln/kft
Mice
Ktt
3-Centrallun Study - Rat m/KR
Reproduction - frlmataa
90-Day Study - kt Vtlf-t
2-tear Study
Chloracna
Chick Edcna lloaiaay (21-day)
Irvc it card Diseeaa
Suucvptlblllty
Tctra
Ciiloro
——— —" " ¦ ' J —•¦-»—— ' i '
* lltxncliloro-
lleptachtaro-
Pet a
Chlqco-
Tetr*
Chloro
Ftnl a
Chloro
i'.cxi-
Chlorc
tllxcure of
llcsa
lacunae*
1,2.1,
6.2,0
1,2.3.
?.«.«
1,1.4.
6,1,9
1,2,4,
6,8,9
1.2,3.
6,*,9
1,2,3.
6.M
1,2,3,4.
6,1.8
1,2.3,4.
6,7.9
1.2, J,4,
5.6,2,8
2,1,2.6
2,3.4.
M
1,2.1
t.2,5
2
lumi
n
ao
10-100
1250
60-10U
>1440
>100
>1,000.COO
14,000.000
> 5<10
>6000
> 1Q00
1UOO
>3
-------
and 1,2,3,6,7,8 would be of prime toxicologic interest.
Toxicity studies with the 2,3,4,7,8-pentachlorodibenzofuran
have been performed in guinea pigs ( Moore, 1977). A single
oral doge caused death in 6/6 animals that received 30 or
10 ugAf. All animals survived a 30-day observation period
subsequent to receiving 3 or 1 ug/kg. Toxicity was
observed at the 3 ug/kg dose while only an increase in
liver size was seen at the 1 ug/kg dose, the pattern of
the toxic response is similar to that reported in studies
using the 2,3,7,8-tetrachlorodibenzofuran (Moore et al.,
1975).
3.2.3 Chlorinated Dibenzo-p-dioxin/Dibenzofuran Toxicity/
Contamination Associated with Exposures to PCP
The dibenzofurans and dibenzo-p~dioxins present in
pentachlorophenol have been responsible for animal health
problems. The chick edema disease problem of the 1950 's
and 1960's was in part traceable to pentachlorophenol
contaminants {Firestone,1973). ,
. Recent studies at the National Institute of
Environmental Health Sciences have identified the presence
of hexa-, hepta-, and octachlorinated dibenzo-p-dioxins in
tissues from a dairy herd in Michigan. The results of
dioxin analyses of tissue samples taken from the herd are
summarized as follows:
Number of Number of Samples in which Detected
Tissue Samples Octadioxln Heptadioxin Bexadioxin
Liver 15 -15 15 9
Fat 7 7 6 1
Range (ppb) 0.23-47.0 0.03-12.0 0.01-1.3
A possible source of these tissue contaminants was PC?-
treated wood used in the construction of a new barn in
which the cows were housed and fed (Moore, 1977).
Although the presence of toxic chlorinated dioxins in
tissues of food animals is a matter for serious public
health concern, there is insufficient evidence to conclude
that contaminants from PCP-treated wood were the cause of
illness in the Michigan cows. Van Gelder (1977) concluded
that although the contaminants were more toxic than the PCP
itself, they were not present in sufficient amounts to
cause illness. Controlled dosing experiments, recently
completed, may help answer questions raised by the Michigan
field studies concerning the pharmacokinetics and toxicity
of PCP and its contaminats in cattle (Moore, 1978).
Results of these experiments are expected in late 1978.
33
-------
3.2.4 References"
Courtney# K. D. and J.A. Moore (1971). Teratology studies
with 2,4,5-trichlorophenozyacetic acid and 2,3,4,8-
tetrachlorodibenzo-p-dioxin. Toxicology and Applied
Pharmacology 20: 396-403
Firestone, D. (1973). Etology of chick edema disease.
Environmental Health Perspectives, Experimental issue
Number 5:59^66.
McConnell, I. E., J.A. Moore, J.K, Haseman, and M.W. Harris
(1976). The Comparative toxicity of chlorinated
dibenzo-p-dioxin isomers in mice and guinea pigs.
Toxicology &_ Applied Pharmacology 37: 14 5, abstract
(Manuscript in preparation).
Moore, J. A. (1977). Memorandum to Director, NIEHS (March
21,1977), subject; Studies on Possible Pentachlorophenol/
Dibenzodioxin Intoxication Progress Report #2.
Moore, J.a. (1978). NIEHS. Personal communication. August
1978.
Moore, J. A., B.N. Gupta and J.G. Vox (1975). Toxicity
of 2,3,7,8-tetrachlorodibenzofuran - - preliminary
results. National Conference on Polychlorinated
Biphenyls, (November 19-21, 197 5), Chicago, Illinois,
Conference proceedings, EPA-560/6-75-004.
Moore, J. A. , M.W. Harris and P.W. Albro (1976). Tissue
distribution of carbon 14 tetrachlorodibenzo-p-dioxin
in pregnant and neonatal rats. Toxicology Applied
Pharmacology 37 :146, abstract (Manuscript in
preparation).
Poland, A. and E. Glover (1973). Chlorinated dibenzo-p-
dioxin: Potent inducers of -aminolevulinic acid
synthetase and aryl hydrocarbon hydroxylase. II. A
study of the structure—activity relationship.
Molecular Pharmacology 9_, 736-747.
Schwetz, B. A., J.M. Norris, G.L. Sparschu, V.K. Rowe
P.J. Gehring, J.L. Emerson, and C.G. Gerbig (1973).
Toxicology of chlorinated dibenzo-p-dioxins.
Environmental Health Perspectives, Experimental Issue
Number 5: 87-100.
34
-------
Stehl, R. and W.Crujnmett (1977). Letter to Dr. Thomas
Bath, EPA. "
Thigpen, J. E., R.E. Faith, E.E. McConnell, and J.A. Moore
(1975). Increased susceptibility to bacterial
infection as a sequela of exposure to 2,3,7,8-
tetrachlorodibenzo-p-dioxin. Infection and Immunity
12 (6): 1319-1324. '
Van Gelder, G. A« (1977). Prepared statement on the
toxicity of pentachlorophenol and chlorodioxins in
cattle and laboratory animals and results of field
investigations of dairy farms in Michigan. Statement
presented at administrative hearing, Michigan
Department of Agriculture, Lansing, Michigan
July 18-22, 1977).
Vogel, S". H. (1977). Presentation to PCP Ad Hoc Working
Group (March 3, 1978),
Vos, J. G. and J.A. Moore ( 1974). Suppression of
cellular immunity in rats and mice by maternal
treatment with 2,3,7,8-tetrachlorodibenzo-p-dioxin.
International Archives of Allergy and Applied
Immunology 47:777-79r4T
35
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3.3 Human poisoning Involving PCF
The SPA Pesticide Episode Review System Report (PERS)
No. 6 0 describes poisoning espisodes involving
pentachlorophenol which occurred from 1966 to September 1,
1976. A total of 64 alleged episodes were located, 47 of
which involved humans. Of these, 42 involved adults, four
involved children, and one did not specify the age group.
Tfcree of the episodes involving children occurred at home
and one at a job site. Eleven episodes involving adults
(over 17 years old) occurred in the home and 28 at various
job sites. Four of the human-related episodes involved
combinations of pentachlorophonel and active ingredients
other than chlorophenols and petroleum distillates.
Twenty-nine episodes involving humans (one a child
less than 6 years old) were associated with occupational
activities. Sight of these occurred at lumber-treating
establishments.
Six episodes occurred during construction activities.
Four of these involved individuals who were* painting or
otherwise applying the chemical to structures, and two
involved carpenters who were working with treated lumber.
Five episodes occurred during occupationally-related
agricultural activities. One of these involved a child who
was splashed with the chemical while watching a man apply
it to a post. The remaining four episodes involved adults.
Two episodes involved commercial pest control
operators engaged in application of the chemical. In one
episode, a man sprayed PCP in the crawl space beneath a
house. He developed symptoms of weakness, headache, double
vision, tachycardia, nausea and hyperpyrexia. He recovered
after a short period of hospitalization. In the other
episode, an individual working for a pest control company
accidentally splashed the chemical into his eyes. This was
diagnosed as mild chemical conjunctivitis.
In another job-related incident, an employee at a
greenhouse worked for several weeks around benches which
were treated with the chemical; he subsequently developed
headaches and chronic coughing.
In one incident the affected person was working inside
a school building while pentachlorophenol and bromacil were
being applied nearby. A quantity of the mixture was drawn
into the building through an air intake duct and blew
directly into the face of a teacher. The only symptoms
reported were shortness of breath and weakness.
36
-------
Six episode reports concerning incidents associated
with occupationally-related operations did not specify the
tyge of job the affected individual was engaged in at the
time of the accident. Five of these were minor reactions
to the chemical; however, the remaining episode resulted in
the death of the victim. In this episode the individual
ingested the pesticide which was in an unmarked bottle.
The man mistakenly thought the bottle contained water; he
died enroute to the hospital.
In addition to those episodes which occurred during
job-related activities, 14 others took place in the home.
Of these, 11 involved adults and three involved children.
Of the three episodes involving children, one
occurred when a child spilled the chemical on himself,
resulting in a mild dermatitis; one involved a 5-year old
who took a small amount of the chemical into his mouth
without swallowing and recovered, the only symptoms to
develop were nausea and vomiting; and one in which the
report did not specify the circumstances of the episode.
All of the episodes affecting adults in the home were
the result of application of products containing
pentachlorophenol to the honva. Five of these involved
reactions of persons other than the applicator to the
chemical after it was applied. Commonly reported in this
type of involvement,was a protracted period of illness
which increased in severity over time. Three episodes were
reported in which individuals who applied the material were
affected. One of these was a minor reaction; however,
those remaining were quite severe and persisted for an
extended period. One involved an individual who applied
the chemical to the exterior of an addition to his home.
The man developed a severe cough persisting from at least
August through November 1974. This was allegedly in
response to an initial period of chemical application, with
more severe symptoms occurring after a second period of
application, the man was hospitalized for an extended
period. In the other incident the subject had a number of
manifestations compatible with poisoning by penta-
chlorophenol or other polychlorinated phenols shortly after
exposure to the product. These included excess
perspiration, nausea without vomiting, abdominal pain, dry
mouth, listlessness, and generalized dermatitis. Shortly
afterwards she also developed generalized pruritus and
several peripheral nerve manifestations, particularly
numbness and pain in the left first dorsal segment.
37
-------
generalized paraesthesia and Herpes Zoster of the tenth
right dorsal segment.
Two additional episodes involved individuals who were
opening cans of the chemical and were sprayed by the
material in the process. Symptom development was not
reported in either case. The final episode report was
submitted with no reference to circumstances of exposure or
the effects therefrom.
Pour reports did not specify the episode location.
One of these did not contain information about the circum-
stances of exposure, one involved a can which exploded in a
man's face while he was opening it, one was an attempted
suicide, and one involved a 68 year old man who accident-
ally swallowed a mouthful of 2.5 percent pentachloropheno 1
and recovered after hospital treatment.
Table 3.4 presents data showing the degree of
medical attention required In the 47 episodes of alleged
human poisoning from pentachlorophenol along with the
circumstances surrounding the episodes.
A study (Sato et al., 1978) conducted in Hawaii from
1967 to 1973 examined the clinical findings in workers
exposed to PCP. The concluding statement reads as
follows:
"The information gathered in this study suggests that
despite high chronic exposures to PCF, individuals in
the wood treatment group of workers had not undergone
any serious health effects from this exposure. The
only evidence of tangible health effects, part of
which could have been caused by exposures to chem-
icals other than PCP, were the low-grade infections
or inflammations of the skin and subcutaneous tissue,
of the protective membrane of the eye, and of the
raucous membrane of the upper respiratory tract. No
long-time (sic) effects could be elicited in the exposed
group."
3.3.1 References
Sato, N.M., H.W. Klemmer, L, Wong, E.L. Reichert, R.J.
Korsak, and N.N. Rashad (1978). Clinical findings in
workers exposed to pentachlorophenol. Draft report
USEPA, Washington, D.C.
38
-------
TABLE 3.4
Distribution of Human Episodes Resulting
from Exposure to Pentachlorophenol by Medical
Attention and Circumstances
(PERS 1966 to September 1, 1976)*+
Medical Attention
Circumstances
Total Number
of Episodes
Hospitalization followed
-Ingestion
' 1
- by death
-Chronic Exposure
1
-Unspecified
1
Hospitalization followed
-Treated wood at home
2
by recovery
-Attempted" suicide
1
-Ingestion
1
-Exposed during nearby
1
application
-Contacted chemical during
1
. application
. -Spill
1
-Reaction to treated home
1
-Unspecified
1
Medical attention at a
-Contacted chemical during
9
doctor's office or
application
emergency room
-Exposed to treated object
4
-Container exposed
1
-Reaction to treated home
1
-Ingestion
1
-Exposed during nearby
1
application
-Contacted contaminated
1
object
-Unspecified
8
Effects not requiring
-Opening container
2
-medical attention
-Reaction to treated home
2
-Contacted chemical during
2
application
-Working with treated wood
1
i
-Unspecified
2
•
TOTAL
47
*A cause-effect relationship has not been confirmed between the
pesticide and reported* reactions for all of these episodes.
+From the EPA Pesticide Episode Review System Report No. 6 0
39
-------
3.4 Human Poisonings Involving Exposure to Chlorinated
Dibenzo-p-dioxins
Over the last 30 years a number of cases of human
poisoning have occurred as a result of industrial exposure
to the chlorinated dibenzo-p-dioxins. Although less well
documented, it is also possible that human poisoning has
occurred as a result of industrial and non-industrial
exposure to the chlorinated dibenzofurans. The references
on the next two pages list reports on cases of human
poisoning from industrial exposure to the chlorinated
diben2o-p-dioxins« Most of these are exposures to tCDD.
Some of these reports (Baader and Bauer, 19 51; Jirasek et
al., 1973? Jirasek et al., 1974; Fazderova et al., 1974)
represent dioxin poisoning in factory workers involved in
the manufacture of pentachlorophenol? these would represent
exposures to chlorinated dibenzo-p-dioxins other than TCDD.
Chloracne was the predominant sign of toxicity
reported in these workers. However, a number of other
symptoms have been reported. These include emphysema,
myocardial degeneration, toxic nephritis, hypertension,
peripheral edema, anorexia, g'astritis, weight loss,
bursitis, peripheral neuropathy, paraesthesia, headaches,
vertigo, coordination disturbances, fatigue, loss of
libido, easy fatigability, emotional instability,
pancreatic necrosis, polyneuritis,, encephalomyelitis,
hyperpigmentation, hirsutism, eye irritation, oiliness of
the skin, hyperlipidemia and hypercholesterolemia.
A report recently issued from a January meeting of an
NIEHS/IARC ad hoc Working Group summarizes available
epidemiological and laboratory research on chlorinated
dibenzo-p-dioxins and dibenzofurans (NIEHS/IARC, 1978).
The report includes exposure incidents and discusses
several aspects of toxicity including chloracne, hepa-
toxicity, embryotoxicity and teratogenicity.
40
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3.4.1 References
Baader, E.w. and H.J. Bauer (1951). Industrial
intoxication due to pentachlorophenol, Industr. Med.
Surg. 20: 286-290. '
Bauer, H., K.H. Schultz, and U. Spiegelberg (1961).
Beruflich vergiftungen bei der herstellung von
chlorphenol-verbindunge. Arch. f. Gewerbepath. und
Gewerbehyg. 18: 533-55 5.
Bleiberg, J., M. Wallen, R. Brodkin, and I.L. Applebaum
(1964). Industrially acquired porphyria* Arch. Dermatol.
89: 793-798. ' "*
Dugois, P. and L. Colomb (1957). Remarques sur l'acne
chlorique. J. Med. Lyon 38: 899-903.
Goldman, P. J. (1973). Schwerste akute chloracne, eine
Massenintoxikation durch 2,3,6,7-tetrachlorodibenza-
dioxin. Der Hautarzt 24; 149-152.
Jirasek, L., J. Kalensky, and K. Kubec (1973). Acne chlorina
and porphyria cutanea tarda during the' manufacture of
herbicides. Cs Derm. 48: 306-317.
Jirasek, L., J. Kalensky, K. Kubec, j. Pazderova, and
S. Lukas (1974). Acne chlorina, porphyria cutanea tarda and
other manifestations of general intoxication during the
manufacture of herbicides. Cs Derm. 49: 145-157.
Kimmig, J. and K.H. Schultz (1957). Occupational acne
(so-called chloracne) due to chlorinated aromatic cyclic
ethers. Deriaatologica 115; 540-546.
May, G. (1973). Qiloracne from the accidential production of
tetrachlorodibenzodioxin. Brit. J. Ind. Med. 30:
276-283. "~
NIE1S/IARC. (1978). Long term hazards of polychlorinated
d ibenzodioxins and polychlorinated dibenzofurans.
Joint NIEHS/IARC Working Group. International
Agency for Research on Cancer. Lyon, France 1978.
Oliver, R. M. (1975). TOxic effects of 2,3,7,8-
tetrachlorodibenzo 1,4 dioxin in laboratory workers.
Brit. J, Ind. Med. 32: 49—53.
41
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Pazdecova, J,, E. Lukas, M. Nemcova, M. Spacilova, L.
jirasek, J. Kalensky, J. John, A* Jirasek, and J.
Pickova (1974). Chconic intoxication by chlorinated
hydrocarbons produced during the manufacture of sodium
2, 4, 5-trichlorophenoxyacetate. Prac. Lek. 26: 332-
339.
Poland, A. P., D. Smith, C. Metter, and P. Fossick (1971).
A health survey of workers in a 2, 4-D and 2, 4, 5-T plant.
Arch. Environ. Health 22: 316-327.
Schultz, K. H. (1957). Untersuchungen zur atiologie der
Chloracne. Arch. Klin, exp. Derm. 206: 589-596.
Schultz, K. H. (1968). Clinical picture and etiology of
chloracne. Arbeitsmed. - Socialmed. - Arbeitshyg. -3; 25-29.
Taylor, J. S. (1974). Chloracne - A continuing problem.
Cutis 13: 585-591.
42
-------
4. Mechanistic Relationships in the Toxicity of Compounds
Structurally" Related to the Chlorinated
Dibenzo-p-d ioxina
The chlorinated dibenzo-p-dioxina appear as trace
contaminants in the commercial synthesis of certain
chlorinated phenol products. Clinical-epidemiologic
investigations of industrial and environmental accidents
involving these compounds and laboratory investigations
have established the extraordinary toxic potency of certain
chlorinated dibenzo-p-dioxins and the potential human
health hazards they pose. Less well appreciated is the
similar spectrum of toxic effects produced by certain
chlorinated dibenzofurans, chlorinated azoxy- and azo-
benzenes, polychlorinated biphenyls and polybrorainated
biphenyls. We wish to draw attention to these compounds as
a group: 1} their similar toxic spectrum, 2) their
isostertsm in chemical structure, and 3) their similar
biochemical actions.
The prototype dibenzo-p-dioxin, 2,3,7,8-tetra-
chlorodibenzo-p-dioxin 1TCDD), produces a number of well
defined toxic actions in laboratory animals and human
beings. 1) Lethality - While the cause is unknown there is
an order of species sensitivity--guinea pigs and chickens
are very sensitive, rats and mice much less so. 2} Chlor-
acne and Hyperkeratosis - Reported .in humans, rabbits anS
hairless mice.3) Involution of Lymphoid Tissue -
Particularly thymus, also in spleen and lymph nodes. In
young animals this is reported to be accompanied by
suppression of the immune response. Thymic involution has
been seen in guinea pigs, rats and mice. 4) Terato-
fenicity, Embryo Toxicity and Fetal Wastage - Has Been
emonstrated inrats and mice. '"s) edematous Syndrome-Young
chickens (and occasionally in mice). 6} Liver Toxicity -
Seen in rats, rabbits and mice. Liver necrosis is greatest
in rats and rabbits; distinct histologic damage is seen in
mice. Little or no damage is seen in guinea pigs. 7)
Disturbance in porphyria metabolism - Induction of
aminolevulinic acid (ALA) synthetase in chicken embryos-.
Porphyria in mice and chickens and presumably the causative
agent of porphyria cutanea tarda seen in factory workers.
The administration of TCDD and certain other
chlorinated dibenzo-p-dioxins to chicken embryos, rats and
mice induces a number of hepatic enzyme activities, the most
well studied of these being aryl hydrocarbon hydroxylases
(AflH) (Poland and Glover, 1973* 1974) and 6 -aminolevulinic
acid (ALA) synthetase (Poland and Glover, 197 3). Ike
capacity of halogenated dibenzo-p-dioxin isomers to induce
43
-------
hepatic ALA syn the tase and A HI! activities (in the chicken
embryo) was found_ to have a well-defined structure activity
relationship: 1)*halogens in at least three and preferably
four of. the lateral ring positions (positions 2, 3, 7, and
8)j 2) the order of potency for substitution was 3r> CI> F>
wn . *7 \ a +¦ 1 naef r.rid iinenhcV 1 v* i nn r\r% c^iapj —
This structure activity relationship for the
induction of AHH or ALA also corresponds to the structure
activity relationship for the lethality of these compounds
in experimental animals.
Recently, a binding protein has been identified in
the cytosol fraction of mouse liver which binds 7CCD
reversibly with a high affinity (Poland and Glover, 1976a).
The binding affinity of other chlorinated dibenzo-p-dioxin
and halogenated aromatic compounds for this protein
corresponds to their biological potency to induce AHH; this
and other evidence suggest that this cytosolic binding
species is the receptor for the induction of AHH activity.
Recently it has been shown that certain chlorinated
b iphenyls show symptoms cf toxicity similar to the
chlorinated dibenzo-p^dioxins when administered to chickens
and to rats. Thus, 3,4,5,3',4',5* -hexachlorobipnenyl
causes marked involution of the thymus, loss of
subcutaneous and visceral adipose tissues, li-ver necrosis
and hydropericardi un when administered to chickens
( Mc Kinney et al,, 1976). Quite similar symptoms are seen
in chickens administered either 2,3,7, O-tetrachloro-
dibenzofuran or 2, 3, 7,8-tetrachlorodibenzo-p-dioxin. The
compound 2,3,4,3',4'-pentachlorobiphenyl has an LD5q of
about 12 mg/kg in the rat with death occurring in about 11
days {Yaraamoto et al., 1976). A narked decrease in body
weight, disappearance of fat from adipose tissues and liver
necrosis were the primary symptoms of toxicity in these
animals. These symptoms are very similar to those s«en
upon administration of 2,3,7,8-tetrachlorodibanzo-p-dioxin,
2,3,7,3-tetrachlorodibenzofuran and other chlorinated
difcenzo-p'-dioxins and dibenzofurans to rats.
octachlorodibenzo-p-dioxin is very weak or inactive
9
44
-------
The major symptom of toxicity in man exposed to the
halogenated dibenzo-p-dioxins is chlo?-acne. Hie outbreak
of chloracne in workers exposed to 3, 4, 3 ' ,4'-tetra-
chloroazoxyben2ene and 3,4,3 .4'-tetrachloroi20bensane has
recently been reported (Poland and Glover, 1976b).
These compounds, like 2,3,7,8-tetrachlorodibenzo-p-
dioxln and 2,3,7,8-tetrachlorodibenzofuran, are potent
inducers of arylhydrocarbon hydroxylase. They also have a
high affinity for a receptor for 2,3,7,8-tetrachloro-
dibenzo-p-dioxin recently described in rat liver by Poland
and Glover (1976a).
Although the data is not extensive at this tine,
there appears to be a strong correlation between toxic
symptoms produced by a number of halogenated aromatic
compounds. The prototype compounds are shown below:
c'ToT
ci
\^c»
2,3,7,8-tetrachloro-
dIbenzo-p-d iox in
3,4,3*,4'-tetrachloro-
azoxybenzene
Q. .CI
O /—ci
2,3,7,8-tetrachloro-
dibenzofuran
3,4,31,4'-tetrachloro-
biphenyl
In examining these prototype compounds planarity is
important. In the biphenyl series, substitution at the
2,2*,6, or 6* position leads to nonplanarity and
inactivity. The general structure necessary for these 0
toxic effects appears to be a rectangle of about loA by 3A
with halogens in three or preferably four of the corners of
the rectangle.
The current data suggest we should not view
chlorinated dioxins, chlorinated dibenzofurans, PCBs or
PSBs, and chlorinated azoxybenzenes separately, but rather
as a class. This permits anticipation, of other potentially
hazardous compounds which might be isostereoraers.
45
-------
4.1 References
McKinney, J.D. , K. Chae, B.N. Gupta, J.A. more, and
J.A. Goldstein, (1976}. Toxicology assessment of hexa-
chlorobiphenyl isomers and 2,3,7,8-tetrachlorodibenzofuran
in chicks. Toxicol. Appl. Pharmacol. 36: 65-80.
Poland , A. and" E. Glover (1973). Chlorinated dibenzo-p-
dioxins: Potent inducers of 6 -aminolevulinic acid
synthetase and aryl hydrocarbon hydroxylase. Mo1.
Pharmacol. 9: 736-747.
Poland, A. and E. Glover (1974). Comparison of 2,3,7,8-
tetrachlorodibenzo-p-dioxin, a potent inducer of aryl
hydrocarbon hydroxylase, with 3-methylcholanthrene. Mol.
Pharmacol. 10: 349-359.
Poland, A. and E. Glover (1976a). Stereospecific, high
affinity binding of 2,3,7,8-tetrachlorodibenzo-p-dioxin
by hepatic cytosol. J. Biol. Chen. 251: 4936-4946.
Poland, A. and E. Glover (1976b). 3,4,3' ,4'-tetra-
chloroazoxybenzene and azobenzene: Potent inducers of aryl
hydrocarbon hydroxylase. Science 194(4265): 627-630.
Yanamoto, H., H. Yoshimura, A. Fujita, and T. Yamamoto
(1976). Metabolic and toxicological evaluation of
2,3,4,3',4'-pentachlorobiphenyl in rats and mice. Chem.
Pharm. Bull. 24: 2168-2174,
46
-------
5. Appendix A
SCIENCE ADVISORY BOARD
ENVIRONMENTAL HEALTH ADVISORY COMMITTEE
Ad hoc Study Group on pentachlorophenol Contaminants
Chairman:
Dr. Sheldon D. Murphy, Professor of Toxicology, Department
of Pharmacology, university of Texas Medical School at
Houston, P.O. Box 20708, Houston, Texas 77025
Members:
Dr. Donald G. Crosby, Professor and Tbxicologist,
Department of Environmental Toxicology, University of
California, Davis, California 95616
Dr. David Firestone, Division of Chemistry and physics,
HFF-147, Food and Drug Administration, 200 C Street, S.W.,
Washington, D.C. 20204.
Dr. Virgil H. Freed, Department of Agricultural Chemistry,
Oregon State University, Corvallis, Oregon 97331
Ms. Dorothy B. Hood, Consultant, Toxicology, Haskell
Laboratory for Toxicology and Industrial Medicine,
E.I. du Pont de Nemours and Company, Wilmington,
Delaware 19898
Dr. John Moore, National Institute of Environmental Health
Sciences, P.O. Box 12233, Research Triangle Park,
North Carolina 27709
Dr. Robert A. Neal," Director, Center * in Toxicology,
Department of Biochemistry, Vanderbilt Medical School,
Nashville, Tennessee 37323
Dr. Alan Poland, Assistant Professor, McArdle Laboratory
for Cancer Research, university of Wisconsin, Madison,
Wisconsin 53706
SAB Staff Officers:
Mr. Ernst Linde, Scientist Administrator, Science Advisory
Board, A-1Q1, U.S. Environmental protection Agency,
Washington, D.C. 20460 Phone: (703) 557-7720
Mr. A. Robert Flaak, Science Advisory Board, A-101, U.S.
Environmental Protection Agency, Washington, D.C. 2046 0
47
-------
6. APPENDIX 3
Kik ^
^^7 * UNITED-STATES ENVIRONMENTAL PROTECTION AGENCY
WASHINGTON. O.C 2C460
January 12, 1977
orncc or t*c
A0MINl3f«*T0*
SUBJECT: Ciarge to ad hoc Study Group on Pentachlorephenol Contaminants
FROM: Ghaiir.in, Environmental Health Advisory Cosaittee
TO; ^ Study Group Masters
A recent inquiry frcn EPA has been referred to the Environmental
Health Advisory Ccnmttee (EHAC). The request (attached) asks tor
opinion as to the implications regarding hazard to hxnan health of the
observed presence of various chlorinated dicentcaioxin iscnters i-*
pentachlorophenol (?€?].
•The Environmental Health Advisory Ccraittee feels that this inquiry
provides a tir^ly opportunity to review, rather sore crcadly than the
original inquiry icslied, the toxicology and analytical nethodaU ;y
pertinent to both the chlorinated difeensofurans and the dibenzodicxSn
isomers.
Accordingly, we ask the study group to review and report in sunrtary
form on the available information (with" particular ertphasis an recent
*ork) on the chesistxy and toxicology of the dibenaodioxins and dibenso-
furans. . •
To the extent possible, it would also be desirable to concent on
the potential hazard to hisans which can be attributed to registered
uses of PC? and the extent that this hazard nay be litigated by use of
the cocrsercial prccess which results in lower levels of the contaminants
of interest. It umild be cost helpful if you can ccnnlete your %ork by
March 2S so that the Ccsnittee will have an opportunity to study your
report before acting to advise the Agency at its April 19 meeting*.
•Norton Kelson
ce: Ernst Linde
48
-------
7* APPENDIX C
7.1 Chemistry of PCP and its Contaminants
7.1.1 Commercial Synthesis of PCP and
Formation of By-products 50
7.1.2 Composition of Commercial PCP 52
7.1.3 Formation of Chlorodioxins and
Chlorofurans During Commercial
Synthesis of PCP. 56
7.1.4 Chemical and Physical Properties
of PCP, Chlorodioxins and
Chlorofurans 60
7.1.5 Reactions....... 65
7.1.6 Hethods of Analysis.72
7.2 Environmental Contamination and Exposure
7.2.1 Environmental Behavior of PCP and
its Contaminants76
7.2.n Occupational Use and Exposure..... — ... 82
7.2.3 Environmental Transport and Exposure.... 83
7.2.4 Food and Feed 84
7.2.5 Biological uptake and Concentration 84
7.2.6 Sources of Exposure 86
49
-------
7. Appendix C
7,1 Chemistry of Pentachlorophenol and its Contaminants
7.1.1 Commercial Synthesis of PCP and Formation of
By-Products
Chlorinated phenols, including PCP, are excellent
bactericides and fungicides and have been widely used for
these purposes since the 1930s. Two comnerical processes
are available for the manufacture of PCP. One process in-
volves the alkaline hydrolysis of hexachlorobenzene, and
the other process involves direct chlorination of phenol or
a mixture of chlorophenols (Doedens, 1964; Sittig, 1969).
pentachlorophenol is produced in the United States
solely by the chlorination of phenol (American wood
Preservers Ins-titute, 1977). The overall reaction
follows;
OH OH
f/^Vl AICU (catalyst) C'Tr\Y
[OJ - 5 ct2 1- ~ TOI - 5 HC.
I30 C Ti
Phenol Cl
The chlorination is carried out at substantially
atmospheric pressure using two reactors. The temperature
of the phenol in the primary reactor at the start is in the
range of 65-130°C (generally 105°C) and is held in this
range until the melting point of the product reaches
95°C. About three to four atoms of chlorine are added at
this point:
50
-------
OH : CH
ct CI
The temperature is progressively increased to maintain
a temperature of about 10°C above the product melting
poini, until the reaction is completed in 5-1S hours. The
reaction mixture, containing about 80% PCP is a liquid so
that no solvent is required, but catalyst concentration is
critical. Generally, 0.0075 tnol of anhydrous aluminum
chloride is used per mol of phenol.
The off-gas from the primary reactor, {largely HC1
initially and chlorine near the end) is sent to a second
reactor (scrubber-reactor system) containing excess phenol.
The reactor is held at such a temperature that the chlorine
is almost completely reacted to yield lower chlorinated
phenols, which may be separated and purified or returned to
the primary PCP reactor. The residual gas is substantially
pure HC1.
In the chlorination of phenol to form PCP, there is a
progressive increase in temperature to keep the reaction
mixture fluid. The higher temperature not only favors the
primary synthetic reaction but also, to some extent favors
formation of the various.contaminants found in PCP.
The composition of technical PCP from different
sources varies somewhat. The PCP content is in the range
of 85-90%. Several percent of other chlorophenols are also
present, as well as a number of impurities including
chlorophenoxy chlorophenols, chlorodibenzo-p-dioxins,
chlorodioxins (1500-3000 ppm), chlorofurans (200-600 ppra)
and chlorodiphenyl ethers. The structure of these various
impurities is shown below.
The presence of hydroxydiphenyl ethers in tetra- and
pentachlorophenol has been discussed by Swedish chemists
(Jensen and Renberg, 1972; Nilsson and ftenberg, 1974; Rappe
and Nilsson, 1972).
CMorodfoxln Chlerofuran Chlorophenoxy chicrophenol
vniorewiwAi" <. (preoioxm)
¦Cl* C,^'0'V^"C,y
On .
chlorophenoxy chlorcphenol chlorodiphenyl ether
(kopredloxin)
ehIo rod!hydrexydIpheny1 ether
-------
7,1.2 Composition of Commercial PCP
Results of analysis of a commercial PCP (nowicide 1,
Sample 9522 A), produced by Dow Chemical Company in June
1970 (Dow Chemical Co., 1971), and a purified grade of PCP
prepared by distillation of Dowicide-7 are shown in Table
7.1. *
The results of recent analyses of a number of domestic
(Dow) PCP samples for chlorodioxins and chlorofurans by
Swiss workers (Buser and Bosshardt, 1976) are shown in
Table 7.2,
The results of analyses of hexa- and octachlorodioxin
in various domestic PCPs (Crummett, 1975) are presented in
Table 7.3.
TABLE 7.1
Comparison of composition of commercial grade
and purified grade Pentachlorophenol (PCP)
Analytical Results
Component
Commercial*
(Dowicide 7)
Purified*3
{Dowicide EC-7)
pentachlorophenol
Tetrachlorophenol
Trichlorophenol
88.4%
4.4%
0. It
6.2%
89.81
10.1%
0.1%
Chlorinated phenoxyphenols
Octachlorod ioxins
Heptachlorod ioxins
Hexachlorod ioxins
2500 ppm
125 ppm
4 ppm
80 ppm
80 ppm
30 ppm
15.0 ppm
6.5 ppm
1.0 ppm
1*0 ppm
1.8 ppm
1.0 ppm
Octachlorod ibenzofucans
Heptachlorodibenzo£urans
Hexachlorodibenzofurans
^Sample 9 522 A
Technical grade PCP reduced by distillation
52
-------
Table 7.2
Chlorodiaxins and Cfclorofurans in Ocw PC? Products
(3usar and Bosshardt, 1976)
PCOO^onm PCDF^ocn
Samoles
Hexa-
recta-'
Octa-
'ie?ra-
Psnza-
Hexa-
He0"2-
Cc-s-
PC?(£C-7)
'0,15
1.1
5.5
0,45
0.03
0.3
0.5
0.2
PC?(£C-7)
0.03
0.6
3.0
<0.02
<0,03
<0.03
»—
•
O
V
<0,1
PGpCc)
9.5
125
16Q
<0.02
0.05
15
95
105
pCpCc)
9.1
180
220
0.05
• 0.25
36
320
210
PCP-Na^
3.4
40
115
<0.02
0.05
11
50
24
PC?
10.0
130
210
0.20
0.20
13
70
55
PC?
5.4
130
370
0.07
0.20"
9
60
65
(a) PCCD =» Polych 1 ordibenza-?-
-------
A composite lot of ?CP (Lot MB-306) was recently
prepared from samples from each of the three domestic
producers of technical PCP. This sample, analyzed by
Monsanto (Vogel et al. , 1976)/ gave the following results
(see also Table 7.4 below, which gives results of GC-MS
analysis of a sample of Monsanto PCP):
Hexa- Hepta- octa-
PCDD, ppm 11 199 1170
PCDF, ppm 19 81 137
Since the structure-biological activity relationships
of the individual hexa- and heptachlorodioxin isomers vary
considerably (Poland et al., 1976? McConnell et al.,
1978), it is also necessry to determine the levels of
individual isomers in PCP samples. However, little
information is available on the levels of individual
chlorodioxin or chlorofuran isomers in PCP. Estimates of
the relative amounts of hexa- and heptachlorodioxin isomers
in PCP (Dowicide 7) and a sodium pentachlorophenate
(PCP-Na) sample examined by Buser (1975, 1976) are given
in Table 7.5. The levels- of individual dioxins were
estimated from chromatogram or mass fragmentogram peak
heights and the total recorded concentration of hexa- and
heptachlorodioxins.
Table 7.4
GC-MS Analyses of Monsanto PCP
(Goldstein et al., 1977)
HxCDD
8
ppm
HCDD
520
ppm
OCDD
1380
ppm
PCDF
40
ppm
HCDF
90
ppm
Hp CDF
400
ppm
QCDF
260
ppm
The Dow Chemical Co, has been engaged in research
directed towards fractionation and identification of
contaminants present in various grades of PCP (Stehl and
Crummett, 1977). Results of examination of three Dow
products for hexachlorodioxin isomers are shown in Table
7.6.
54
-------
. . Table 7.5
Chlorodioxins in a Commercial PCP and PCE-Na Sample
(Buser, 1975, 1976)
ppm Chlorodioxin in
Chlorodioxin PCp-Oowicide 7 PCF-Na
1,2,3,6,7,9-ClgD 1 0.5
1,2,3,6,8,9-ClgD 3 1.6
1.2.3.6.7.8-ClgD 5 1.2
1.2.3.7.8.9-ClgD 0 0.1
1,2,3,4,6,7,9-C1,D 63 16
1,2,3,4,6,7,8-CI7D 171 22
1,2,3,4,6,7,8,9-ClgD .250 110
Table 7.6
Hexachlorodioxin (HxCDD) Isomers in Three Dow products
as Determined by Gas-Liquid Chromatography (GLC)
(Stehl and Crumraettr 197 7)
GLC Relative Isomer %, HxCDD Concentration
Peak HxCDD Isomer . DowicideQ Dowicide 7 Dow Std 8^A
A 1,2,4,6,7,9- 35 25
(or 1,2,4,6,8,9-)
B 1,2,3,6,8,9- 43 50 , 29
(or 1,2,3,6,7,9-)
C 1,2,3,6,7,8- 20 25 71
D 1,2,3,7,8,9- • 2 Trace
Ratios of 25-50-25 (Dowicide 7) for the A-B-C isomers
compare with Buser'a values of 10-35-55.
55
-------
Table 7.7
Chlorodibenzofurans in Dow PCP Products
Tetra Penta Hexa
2,3,6,7- 2,3,4,6,7- 1,2,3,6,7,8-
2,4,6,7- 1,2,4,7,8-
2,3,4,7,8-
A list of chlorodibenzofurans tentatively identified
by Dow chemists in Dowicide or EC-7 is shown in Table 7.7,
7.1.3 Formation of Chlorodioxins and Chlorofurans during
Commercial Synthesis of PCP
Chlorodioxins may be prepared in condensation
reactions from ortho-substituted chlorophenoxy radicals
(Kulka, 1961) or anions {Pohland and Yang, 1972), Accord-
ing to S.L. Vogel, Monsanto Industrial Chemicals Co.
(Vogel, 1977), dioxin formation occurs during commercial
synthesis of PCP via a series of reactions involving
phenoxy radicals. Phenoxy radicals are produced from
decomposition of polychlorocyclohexadienone produced by
over-chlorination of tri-, tetra-, or pentachlorophenol.
The phenoxy radical (an electrophile) attacks electro-
negative sites (ortho or para positions) on a polychloro-
phenol molecule toform phenoxyphenols which undergo
further reaction to form chlorodioxins.
The decomposition of tri-, tetra-, or pentachloro-
phenol can also be catalyzed by chlorine (the chlorine
radical is the. initiator). The tetrach1orophenol present
in commercial reaction mixtures (very little trichloro-
phenol is present) serves as a substrate for chlorine
radicals, limiting the chain reaction with PCP molecules
which accelerates PCP decomposition. The chlorination is
normally stopped when 3-7% tetrachlorophenol remains.
Further chlorination results in increased decomposition
(Table 7,8).
56
-------
TABLE 7,8
Reactions in Chloriiucion of Triehlorqphenol
*- CI
ci A
o a
MOi * Cl
C« A c'^v«
* Jj ' 4-
W V*ci i X CJ
a ci
Gl ""LOT JOX^ IQXnJQXr
q"Vci ey/^ Cl^r 0
a' + IQi" ISLr*IQl,Jyi-*
&°Igra
Ci
*HCI
pi- rd
CT +HCl
+ HCl
Ct C* u £1
+¦ HCl
57
-------
Rearrangement via a spirocyclic anion (Smiles
rearrangement) can yield additional isomers (Gray et al.,
1D75). Highly alkaline conditions are required for
efficient operation of, the Smiles rearrangement since the
reaction involves rapid equilibration of the anion forms of
a phenoxyphenol through a spirocyclic intermediate. This
is illustrated by the formation of 1,2,3,6,7,8- and
1,2,3,7,8,9-hexachlorodibenzc-p-dioxin from 2,3,4,6-tetra-
chlorophenol,
In the manufacture of pentachlorophenol a considerable
amount of HC1 is present, so the Smiles rearrangement is
unlikely- Dioxin congeners formed by normal and
spirocyclic rearrangement vs. the levels of individual
dioxin found in PCP (vogel, 1977) are shown in Table 7.9.
The hexachlorodioxins found agree with those predicted to
form without the Smiles rearrangement.
Tmiz 7.9
Dioxin Ccr.aer.ers in Commercial PC?
Possible Cioxin Cdnccntrs in ?C?
No Smiles
Rearrancgnent
1,3,5,3 (1CG3)
1,2,4,7,9 (73)
1,2,3,7.9 (255)
1,2,3,6,3,9 (5CS)
1,2,3,6,7,3 (2=2)
1,2,4,6,7,9 (255)
1.2,3,4,5,7-9 (755)
1,2,3,4,6,7,3 (252)
With S-niUs
Rearrangement
1,3,5,a (252)
1,3,7,9 (735)
1,2,4,7,9 (31.251)
1,2,3,7,9 (252)
1,2,4,5,3 (43.753)
1,2,3,6,7,9 (31,253)
1,2,3,5,3,9 (18.755)
1,2,4,5,7,9 (12.52)
1,2,4,6,8,9 (12.52)
1,2,3,7,3,9 (13.733)
1,2,3,5,7,8 (6.252)
1,2,3,4.5,7,9 (735)
1,2,3,4,5,7,8 (255)
1*2,3,4,6,7,3,9(1002) 1,2,3,4,0,7,3,9(1002)
(a) PC? producers composite sample.
Relative i
Issuers Found
None
None
40-50
20-40
Trace
20-40
ca 60
ca 40
100
PC? in ccrn
(a)
N.O.
H. 0,
ca 15
ca 2C0
ca 10C0
-------
Little information is available on the formation of
dibenzoCurans during PCP production. Formation of
dibenzofurans can be explained by the production of
polychlorodiphenyl"ether intermediates (Kulka, 1961;
Plinroer, 1973? Acsenaul.t, ,1976) which can lose chlorine to
yield dibenzofuran.
Cleavage of the poly^hlorodiphenyl ether in the
presence of HCl yields PCP and hexachlorobenzene.
Various free radical reactions might also yield a
number of biphenyl compounds.
Cln * CI# Ci2 +
CI
n-l
f 1
CI
m
CI
OH
a*
ci.
OH
CI
n
59
-------
Mass spectral data obtained from analysis of contaminants
in PCFs {Firestone ,et al., 1972) suggested that
polychlorchydroxyb{phenyls were present in these products.
7.1.4 Chemical and Physical Properties of PCP, Chloro-
dioxins and Chlorofurans
7.1.4.1 pentachlorophenol
The chemical and physical properties of compounds play
an important role in their behavior, persistence in the
environment, and biological effects. Properties of PCP are
given in Table 7.10. PCP is volatile in steam and soluble
in most organic solvents# although of limited solubility in
CClj and in paraffinic petroleum oils (British Crop
protection Council, 1971}. Also see Bevenue and Beckman
(1967) for data on solubility in various solvents.
Differential thermal analysis of PCP (Langer et al.,
1973) revealed a solid state transition at 75°C, followed
by melting below 200°C and vaporization above 300°C,
Prolonged heating in bulk atapve 2QQ°C resulted in
formation of octachlorodioxin in a tar residue. Heating
the PCP in a sealed capillary at 250°C for ten hours
resulted in formation of about 50% polychlorophenoxyphenol
and a small amount of octachlorodioxin. Sodium
pentachlorophenate exhibited a strongly exothermic reaction
at about 36Q°C; upon cooling, essentially pure octa-
chlorodioxin crystallized.
. TABLE 7.10 ;
Physical Properties of Pentachlorophenol (PCP)
Molecular Weight
Melting Point
Boiling Point
Density
vapor Pressure
Solubility HjO
Solubility of sodium salt, H2°
Partition Coefficient
Molar Refraction
266.35
191°C
310°C (decomposes)
1.987
1.6 X 10~4mm Hg (25°)
1.2 X 10-Imm Hg, (100°C)
40 mm Hg (21l°C)
20 ppm at 30°C
33g/100g
1 X 105*01
53.5
-------
7.1.4.2 Chlorodioxins
Properties of- various chlorodioxin congeners are given
in Table 7.11. The solubilities of 2,3,7,8-tetrachloro-
dibenzo-p-dioxin (TCDO), hexachlorodibenzo-p-dioxin (HxCDD,
a sample of mixed isomers), and octachlorodibenzo-p-dioxin
(OCDD) in several solvents (Stehl and Crummett, 1977) are
shown in Table 7.12.
The visible absorption spectra and electron spin
resonance spectra and g factors of a number of chlorodioxin
cation radicals have been reported (Pohland et a!., 1973).
The crystal structures of several chlorodioxins have been
determined by x-ray diffraction studies. The compounds
studied included 1,2,3,7,8,9~hexachlorod ibenzo-p-d iox in
(Cantrell et al., 1969), and 2,7-dichloro-2,3,7,8,-
tetrachloro- and octachlorodibenzo-p-dioxins {Boer et al.,
1973), The x-ray diffraction data indicate that the
C-Cl distances shorten with increasing chlorine
substitution on the rings. This effect could result from a
reduction in effective electronegativity difference between
CI and C as more electron density is drawn from the
aromatic ring, which should, in turn, result in increased
covalency of the C-Cl"bonds- and give shorter distances
{Boer et ali, 1973).
Infrared spectra and characteristic frequencies of a
number of chlorodioxins as well as 2,8-dichloro- and
octachlorofuran have been reported by Chen (1973).
7.1.4.3 Chlorofurans
Little information is available to date on the
physical and chemical properties of chlorofurans. It is
presumed that in the immediate future increased emphasis
will be placed on identification of specific chlorofuran
isomers occurring in cofflmerical PCP and synthesis of these
compounds for chemical and toxicological study. Some
properties of several chlorofurans (Gray et al., 1976?
Page, 1976) are given in Table 7.13.
7.1.4.4 Chlorodiphenyl Ethers "and Ghlorophenoxy phenols
Data on the physical and chemical properties of
chlorophenoxy phenols are limited. Lundstrom and lutzinger
(1976) prepared several chlorodiphenyl ethers and also
cited a number of ..these compounds prepared by other workers
via various routes. Hie melting points of some of the"
chlorodiphenyl ethers are given in Table 7.14.
61
-------
TABLE 7.11
Physical Properties of Various Chlorodioxins
Cnlorcdioxin
Hoi. Wt.
M.P.
C
Hp II
Value
Estimated
Vapor (b)
Pressure
Molar
Refraction
uv y.z x
tCI-CI) r.-n
2 , 7,-Cl_
' ' 2
253.08
—
0.76
6.0 x
10"6
—
T 302
2,3,7—CIj
287.53
162
0.86
3.6 x
10~6
—
305
2,3,7,8,-Cl^
321.87
306
0.51
1.7 x
10"&
71.4
310
1,2,4,7,8-C1.
356.42
206
—
—
72.6
307
l,2/3,7,8-Cl5
356.42
241
—
,—
308
3.,2,4,6,7, 9-Cl6
390.86
240
0.94
6.6 x
10"7
—
31«1
1,2,3,6,3,9-Clg
390.86
—
__
81.1
—
1,2,3,6,7,8-Clg
390.86
285
—
—
316
i,2,3,7,8,9-Clg
390.06
243
—
—
317
1,2,3,4,6,7,9-Cl^
425.31
—
0.90
3.0 x
10~7
65.9
—
1.2,3,4,6,7,8-C17
425.31
—
0.90
—
1,2,3,4,6,7,8,9-Clg
459.75
331
0.90
1.8 x
10"7
90; 7
316
(a) Bcroza, M. and M.C. Bowman, "p" value determined for dioxin between hexane and acctor.itrile,
J. Assoc. Offic. Anal. Chem. 48:358-370 <1965).
{b} Vapor pressure estimated from data of ttoolson (Woolson et al., 1973).
i
(c) Estimated by summing atomic rerractions.
{d) ' p" v-luc determined 'icc mixture of he::achlorodioxin isomers.
-------
TABLE 7.12
Solubility of Several Chlorodioxins in various Solvents3
Solubility in mg per
liter
Solvent
TCDD HxCDD
OCDD
acetone
90
—
5
anisole
2600
1700
benzene
470
1600
1000
chloroform
550
—
560
methanol
10
— ,
—
toluene
1800
1S00
o-xylene
—
—
3600
water•
0.
0002
~ indicates no data
(a) pirestone observed that 1,2,3,6,7,8-HxCDD is considerably
less soluble in organic solvents than other HxCDD isomers.
The solubility of the 1,2,3,-6,7,8-isonier in isooctane is
about 20 mg/1. •
Dow standard 8 2-A, a mixture of 71% 1,2,3,6,7,8-ffxCDD and
29% 1,2,3 # 6# 7,9-HxCDD and 1,2,3,6,8,9-HxCDD.
63
-------
DIchloYo
2,4
3.7
2,0
Trir.hloro
2.4.6
2,3,0
2.4.7
2.4,0
TctracJiloro
Molecular
He l«|ti t
209.1
243,5
278.1
Molting
Totnt B€
TABLE 7.13
Properties of Chlorinated Dibenzofurans
(a)
10Q
(c)
116-117
109-191
Va[ior Pressure
(tsLinated) 25"C
7.3 x 10"
7.0 x 10;
fi.B X 10"
4.0 x
3.7 x
10
10
-6
1,4,6,0
/,il
2.5
X
10
2,4,6,0
190-2001^1
2.5
X
10
2,3,6,0
202-203* '
2.2
X
10
2,4,6,7
2.1
X
10
1.2,7,0
227-220^
2.0
X
10
2,3,7,0
2.0
X
10
2,3,6,7
1.9
K
10'
3,1,6,7
1.0
X
10
I'entachluro
312.6
1,3,4,7,0
234-235^
1.3
X
10
1,2.4,7,0
1.3
X
10
1,2,3.6,7
l.l
X
10
2,3,4,7,0
1.1
X
10
llejitachluro
301.6
4.4
3.6
3.0
X
X
X
10
10
10
Octacliloro
416.1
1.9
X
10
6
6
6
-6
-6
6
•6
-6
-7
7
7
7
Molar
Refraction
IIV max
(CJIC1 j) mn
60,2
65.0
69.0
74.6
04.2
09.0
256,302,313
257,294,310,323
250,309,316
263,272,297,320
256,266,297
(a) from diitii supplied by fir. Jkwid Firestone—private communication.
(b) Calculated from Table of Atomic Refraction.
cj II. Giliiuii, et al., .1. Aw, CIujim. Soc., tjf>:2473, 1934.
I il) A J'. Gray, ef £[., J. Or"«j."(:heiu., 4104^:2420, 1976.
-------
Table 7.14
Melting Points of Chiorodiphenyl Ethers
piphenyl ether MLF.°C
2,4,4'- 51-52
2,2»,4,4'- 70
2,3',4,4'- oil
3,3',4,4'- Oil
2,3,4,5,6- 132-133
2,2',4,4*5- Oil
2,3',4',5'- 65-67
2,2' ,4,4' ,5 Oil
2,3* #4,4',6— 36
2,2',3,4,5,6,6'- 147-148
Deca- 224-225
7.1.4.5 Gas Liquid Chromatography (GLC) Behavior of
Chlorodioxin and Chlorophenol Congeners
The GLC behavior of various chlorodioxina and
chlorofurans on nonpolar (QV-1Q1) and Polar (Silar 10-C)
columns is recorded in Tables 7.15 and 7.16. Retention
times depend on the number and location of chlorine atoms
in the ring system. Order of elution and retention times
of chlorodioxins on glass capillary columns is reported by
Buser (1975, 1976).
7.1,5 Reactions
7.1.5.1 Pentachlorophenol
FCF is relatively stable and will not decompose when
heated up to its boiling point; however, it is rapidly and
extensively degraded by ultraviolet irradiation in the
laboratory and by sunlight (when FCP is in solution) and is
decomposed by strong oxidizing agents (Bevenue and Beckiaan,
1967).
Similar to any phenol, the phenolic hydroxyl of PC?
takes part in nucleophilic reactions, e.g., it forms esters
with organic and inorganic acid and ethers with alkylating
agents such as methyl iodide or diazoaethane. Electron
withdrawal by the ring-chlorines causes PCP to be unusually
acidic (pKft5.26), roughly comparable to propionic acid
(pK»4.9), and causes it to be a relatively weak nucleo-
phile while stabilising its salts (sodium pentachloro-
phenate is a stable item of commerce). While the high
degree of chlorination makes the aromatic ring sufficiently
electropositive to form stable charge-transfer complexes
with electron donors, the ring chlorines are as resistant
to nucleophilic displacement under normal conditions as are
those of the chlorinated aromatic hydrocarbons.
65
-------
TABLE 7.15
Chlorinatac Oiisnzorjrars
GLC Retention Tinies Relative tc
2,3,7,3-Tetrachlorcdicsnza-p-uicxin (TCDC)
RR-'1'
Cor.qerer QV-101^ Silar 10C^
2,4,-CI- 0.24 0.38
3,7-Cl J° 0.2S , 0.40
2,S-C1| 0.26 ' 0.47
2.4.6-Cl <, 0.44 0.73
2,3,8-Ci: 0.47 0.83
2.4.7-Cli — 0.64
2,4,3-C'^ — 0.54
1.4,0,2-CI, 0.70
2,4,6,S-CU 0.70
2,3,6,8-Cl? 0.80
2,4,6,7-Cn 0.32 1.26
1 ,2.7,3-Cl, 0.89 1.04
2.3,7,3-Ci: 0.S9 ' 1.50
2,3,5,7-Cl ^ 0.93 1.55
3»4.S,7-C1^ 0.55 1.78
1,3,4,7 >3—01 1.35 1.27
l,2,4,7,3-Cl: 1.35 1.27
1.2.2.5.7-C"- 1.52 1.55
2.3.4.7.8-Cl2 1.63
Cl7 ¦ — 3.95
CU — 4.73
CI; — 5.37
Clg 8.3 3.73
(1) KST =» retanti'cn tine relativa to TCDO.
(2) Data of O.'.-f. Pfcillipson, fQA; 2 m x 0.2 cn i.d. colussn packed with
1% 0V-101; calurcn tsristratur*, 200"C.
(3) Dcta of O.K. Phillipscn, ?0A; 2 m x 0.4 cn i.d, calunn packed with
2% Siiar IOC; column tacperar^rs, 200*0.
66
-------
TABLE 7.16
Chlorinated Oicar.zo-o-cnoxins,
GIC Retention Tic.es Reiativa to-
2,3,7,8-Tetracr.larcctbenzc-p-ciioxi.n (TCCD)
Concener
2,7,-Cl20
1 t2,4-C1,D
2,3,7-Clp
•1,3,6,3-ClJ)
1,3,7,3-cno
2,3,7,3-Cl ,9
1 ,2,3,4-ClTO
1,2,3,3-ClJo
1,2,4,'7,2-Cl-Q
1 ,2,3,4,7-Cl-Q
1 ,2,3,7,3-ClgO
1,2,4,6,7,S-CUQ
1,2,3,5,7,3-Cl-2-
1,2,3,4,7,3-CnO
1,2,3,6,7,3-Clfo
1 ,2,3,7,S,9-€l!3
Q
1 ,Z,3,4,o,7,9-Cl-3
1,2,3,4,5,7,8^0
ClgD
RRT
t(U
M)
'-101^
Silar 1OC(3 ^
cu sesponsa
(Silar ICC Co 1 u.th}
0.30
0.90
0.49
0.52
0.38
0.55
0.54
0.40 -
0.76
0.52
0.32
0.38
0.78
0.41
1.00
1.00
Q.4Q
0.97
1.01,
0.25
0.S9 .
1.04
—
1.57
1.56
0.41
1.70
1.76
0.41
l.SO
1.82
0.33
2.4a
2.52
0.23
2.73
2.S2
0.36
3.05
3.11
0.40
3.10
3.23
0.37
3.24 .
3.55
0.42
4.73
5.41
0.60
5.32"
6.20-
*. • 0.70
9.1
.10.3
0.34
(1} RRT - retention time relative to 2,3,7,S-ClaO.
(2) Data of Q. Firestone, FDA; glass coil, 2o x 0,4 cm i.d., packed with
25 0V-1C1 on SC-1C0 mesh Chromasorb WHP; column temperature 21CC.
(3} Oata of 0. Firestone; glass coil, 2ra x 0.4 cm i.d., packed with 1.2S
Silar ICC an 80-100 mesh Chromcsc-b WHP; column tamperature 2G0°C,
(4) EC Response « nanograms to give 1/2 full seals deflection (127 sm)
at 15 x attsnuation, Hewlett-Packard Model'S713A §as chromatagrach.
67
-------
Chlorination of PCP (or overchlorination of phenol
during PCP manufacture) can give rise to a series of
interconvertible nonaromatic cyclic ketones including
hexachloro-2,5-cyclohexadien-l-one, hexachloro-3-
cyclohexen-l-one, heptachloro-3-cyclohexen-l-one, and
octachloro-3-cyclohexen-l-one. Reduction of these
compounds under mild conditions or treatment with base
provides chlorophenols; for example, PCP is formed from
heptachloro-3-cyclohexen-l-one by boiling with aqueous
acetone or from hexachloro-2,5-cyclohexadien-l-one by
reduction with aqueous sulfur dioxide or potassium iodine.
Heat (as in a gas chromatography also generates phenols
(Svec and Rubelka, 1975).
Pentachlorophenol, being a weak acid, reacts with
strong bases to give the corresponding water-soluble salts
at a pH of 5.0; the solubility of the sodium salt is about
79 ppm; at pH 8.0, the solubility is greater than 4000 ppra.
PCP is readily converted to the ether derivative, which is
useful for analysis by gas chromatography. PCP is a
powerful uncoupler of oxidative phosphorylation in various
tissues and apparently reacts with bovine serum albumin
(anion-anion reaction) to form a stable complex from which
the PCP can be liberated with strong base. PCP forms
colored electron acceptor complexes as do other phenol
derivatives (Hutzinger, 1969); these complexes are useful
for chromogenic detection and mass spectrometric
identification.
Treatment of PCP with powerful oxidizing agents
produces pentachlorophenoxyl radicals which combine
reversibly to form "diners." For example, in the presence
of fuming nitric acid or nitronium fluoroborate, PCP
provides 2,3,4,5,6-pentachloro~4-pentachlorophenoxy-2,5-
cyclohexa-dienone (Chang, 1962). Hie radicals or their
dinters can be oxidized further to 2,3,5,6-
tetrachlorobenzoquinone (chloranil). Chemical oxidation of
PCP under anhydrous conditions was found to result in
production of the radical dimer 2,3,4, Sje-pentachloro^-
pentachlorphenoxy-S, 5-cycla~hexadienone (Denivelle and
Fort, 1954).
Pyrolysis of alkali metal salts of PCP (3 00°C)
results in condensation of two molecules to form OCDD,
1,2,3,4,6,7,8,9-octachlorodibenzo-p-dioxin (Sandermann et
al., 1957). The reaction proceeds through an intermediate
phenoxyphenol, now called a "predioxin," which is readily
detectable in technical PCP. Nonvolatile, polymeric
phenylene ethers are formed concurrently by reaction of the
chlorophenol at positions other than ortho. Small amounts
of initiators such as chlorine or hexachloro-2,5-cyclo-
hexadien-l-one allow OCDD formation to take place at
comparatively low temperatures (200°C) in high yield from
PCP rather than its salts (Kulka, 1961); and pyrolysis of
the chlorinated cyclohexenes themselves smoothly provides
OCDD (731 yield from hexachloro-2,5-cyclohexadien-l-one at
270 - 280°C), probably through a pentachlorophenoxy-
pentachlorocyclohexadiene such as 2,3,4,5,6-4-pentachloro-
phenoxy-2,5-cyclohexadienone.
-------
Results of conbusting wood and paper treated with-PCP
or PCP-Na indicate that actachlorodioxin was not fomed
during combustion with PCP. However, ppm levels of
octachlorodioxin are formed during combustion of paper
treated with PCP-Na (Stehl and Lamparski, 1977? Ahling and
Johansson, 1977).
The absorption of light energy rather than heat allows
PCP to undergo a number of reactions under very mild
conditions; maximum light absorption lies in the ultra-
violet region (245 and 318 nm). In either water or organic
solvents, PCP undergoes photochemical reduction to isomeric
tri- and tetrachlarophenols (Crosby and Hamadmad, 1971).
Nucieophiles, such as bromide ion, can displace chloride
from the PCP ring (Crosby and Wong, 19,76), and in water the
predominant reaction is¦replacement of an ortho-, meta-, or
para-chlorine by hydroxyl to provide tetrachlorocatechol, .
tetrachlororesorcinol, and tetrachlorohydroquinone,
respectively. The pentachlorophenoxide anion can also
displace chloride in sufficiently concentrated solution
with eventual cyclization to OCDD in water at ambient
temperatures (Crosby and Wong, 1976),
Photoreactions of PC? in organic solvents result
primarily in reductive dechlorination (Zabik et al. , 1976).
The sodium salt of PCP in aqueous solutions yields a
variety of colored products when irradiated with sunlight
including phenoxybenzoquinones, chloranilic acid (2,5-
dichloro-3,6-dihydroxybenz.oquinone) , and 2, 4,5,6-tetra-
chlororesorcinol (Munakata and Kuwahara, 1969). P.1 inuner et
al. (1973) showed that alkaline aqueous solutions of PCP,
irradiated with light in the 300-350 nn» region, yielded
octachlorodibenzo-p-dioxin. Although a free radical
mechanism was proposed to account for the observed products
of unsensitized photolysis of PCP-Na (Munakata and
Kuwahara, 1969), Crosby and Wong (1976) demonstrated that
octachlorodibenzo-p-dioxin is generated photochenically
from PCP in dilute aqueous sodium hydroxide by a cycli-
zation process analogous to its generation from PCP by heat
(Sandernann et al., 1957). This mechanism involves
photonucleophilic displacement of chloride ions from PCP by
pentachlorophenoxide ion.
CI
CI
CI
CJ
CI
CI
CI
CI
69
-------
7.1.5.2 Chlorinated Dibenzodioxins
OCDD and related cyclic ethers appear to be rather
stable chemically, perhaps due to their planar and
electropositive rings. For example, OCDD distills
(sublimes) unchanged at 3 50°C and can be recovered
quantitatively from hot sulfuric acid {Sandermann et al, ,
195?). However, these poiychlorinated ethers share with
PCP the facile photochemical reduction upon ultraviolet
irradiation. For example, in the presence of an organic
solvent as hydrogen donor, 2,3,7,8-tetrachlorodibenzo-p-
dioxin is rapidly dechlorinated via tri- and dichloro-
dioxins {Crosby et al,, 1971); di-and octachloro-dibenzo-
furans are dechlorinated more slowly, and the rate of OCDD
photoreduction is still slower although transient hepta-
and hexachiorodioxins are detectable.
These compounds are relatively stable and only slowly
biodegradable. When dissolved in concentrated sulfuric
acid -or trifluoromethanesulfonic acid with oxidizing
agents such as or KNO^ or with ultraviolet
irradiation, blue to blue-green colored species are
obtained, due to formation of cation radicals (Pohland et
al., 1973,* Yang and Pohland, 1973).
TCDD (2,3,7,8-tetrachlorodibenzo-p-dioxin) is quite
stable to 700°C (50% decomposition at this temperature
after 21 second exposure), whereas decomposition is com-
plete at 800°C after 21 second exposure (Stehl et al.,
1973).
TCDD is stable in refluxing aqueous alkali solution
(SO ml of 321 aqueous KOH solution plus 20 ml ethanol)
whereas other higher chlorinated dioxins decompose at
varying rates (first-order reaction), presumably due to
hydrolysis (nucleophilic displacement of halogen by
hydroxyl groups) (Firestone, 1977). Estimated half-lives
(t 1/2) of several dioxin congeners in reflux ing KOH
solution are shown in Table 7.17.
70
-------
Table 7.17
Estimated Half-Lives {t 1/2) of
Several Chlorodioxins in Re fluxing KOI Solution ^a'
t 1/2
1.2.3.5.7.8
1.2.4.6.7.9
9-OCDD
9-HxCDD 7 hrs
a-HxCDO 2 hrs
23 rain
16 niln -
4.5 min
(a) 10-40 ng chlorodioxin refluxed gently with 50 ml of 32%
aqueous KOH solution and 20 ml ethnol.
Crosby et al. (1971, 1973) found that TCDD is
rapidly photodecomposed (by reductive dechlorination) in
alcohols whereas octachlorodioxin is much more stable. In
either sunlight or simulated sunlight, 2,7-dichloro-,2,
3,7-trichloro- and 2,3,7,8-tetraehlorodibenzo-p-dioxins (5
mg/1 in methanol) were entirely decomposed in a few hours.
Sim et al. (1975) irradiated various chlorodioxin
congeners in isooctane as well as in methanol, ifie
photolysis rates of the chlorodioxins in methanol solvent
were sinilar to those reported by Crosby et al. (1973).
While photochenical dechlorination is by far the most
rapid known reaction of these compounds, three conditions
are required: the dioxin or dibenzofuran must be accom-
panied by an organic, hydrogen-donating solvent (such as a
pesticide or formulating agent), UV light in the wavelength
region of 290-320 nm must be present, and the light must
penetrate the solvent (CCosby and Wong, 1977). The rate of
photoreduction is inversely proportional to the degree of
chlorination, and, therefore, dechlorinated products do not
accumulate. tJnlike PCF and 2,8-dichlorodibenzofuran, pure
OCDD and tcdd do not appear to be photolyzed in water at
appreciable rates due, perhaps, to their very low
solubility.
It has been reported that a hydrogen-donating solvent
is not required for photolysis to occur, There are
indications that a cellulose substrate will permit
photolysis.*
*£ee Testimony of RobertD. Arsenault, Koppers
Company, Inc., April 3, 1973, in "Testimony of Interested
Parties," section 8,2.3 of this report.
71
-------
It seems probable that the observed hexa- and hepta-
chlorodioxins are formed thermally from o-phenoxyphenols
(predioxins), detectable in technical PCP and originating
in the small proportions of tri- and tetrachlorophenol
present {Jensen and Renburg, 1973). (In environmental
samples, these dioxins can arise by similar ring closure by
photoreduction,) Other phenoxyphenols ("isopredioxins")
are also detectable and may account for the observed
dibenzofurans; dibenzofurans can also be formed photochemi-
cally by rearrangement and subsequent dehydration of o-
phenoxyphenols (Crosby et at., 1973). The original
pyrolytic conversion of a PCP salt to OCDD was accompanied
by a large proportion o£ hexachlorobenzene (Sandermann et
al., 1957), suggested to arise from decomposition of
decachlorodiphenyl (Kulka, 1961), but this reaction has not
been confirmed.
7.1.6 Methods of Analysis
7.1.6.1 Pentachlorophenol
The review of PCP by Bevenue and Beckman (1967)
discusses a variety of colorimetric and chromatographic
methods of analysis, including gas chromatography.
Colorimetric methods suffer from lack of sensitivity and
frota spectral interferences. Gas chromatographic methods
usually involve preparation of the methyl ether derivative
with diazomethane. Argauer (1968) prepared the
chloroacetate for detection of chlorophenols including PCP
by electron-capture gas chromatography (EC-GLC). Rudling
(1970) described a method for determining PCP in tissues
and water by acetylation of extracted PCP and analysis by
EC-GLC. The identity of PCP in sample extracts was con-
firmed by combined gas chroma tography-niass spectrometry
(GC-MS). Farrington and Munday (1976) described the pre-
paration of chlorophenyl 2,4-dinitrophenyl ether for EC-GLC
determination of trace amounts of PCP and other
chlorophenols.
Barthel et al. (1969) described a method for deter-
mination of PCP in blood, urine, tissue and on clothing in
which the extracted, underivatized PCP was injected on a
GLC column containing 3% diethylene glycol succinate (DECS)
plus 2% syrupy phosphoric acid.
Fountaine et al. (1975) reported a procedure for
determining PCP in water by ultraviolet ratio spectro-
photometry. Fritz and Willis (1973) described the
chromatographic separation of PCP and other phenols using
an acrylic resin, and Renberg (1974) reported an ion
exchange technique for determination of PCP in fish and
water.
72
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Yip (1571) reported a modified method for PC? and
chlorophenoxy acid herbicides in total diet samples
involving extraction of the sample with acetonitrile or
chloroform, nethylation, Florisil chromatography to sep-
arate PCP from the other herbicides, and EC-GLC analysis.
Modifications, based on Yip's method, are currently used by
FDA for total diet analyses. However, the method suffers
from low and erratic recoveries, particularly for high-fat
samples at the limits of detection (ca 0.01-0.02 ppm). In
sona instances diethyl ether or diethyl ether-petroleum
ether (1:1) have been used as extracting solvents in an
effort to improve recoveries of PCP.
7.1-6.2 Chlorodioxins, Chlorofurans and Other
Contaminants in PCP
PCP contains a number of hexa-, hepta- and octachloro-
dioxins as well as other contaminants (Firestone et al.,
1972; Woolson et al., 1972; Buser, 1975). Until recently,
EC-GLC had been used mainly for chlorodioxin analysis. But
because of the presence of other components, mass
spectrometry has come into use for specific detection and
confirmation of chlorodioxins as well as chlorofurans.
Villanueva et al. (1975} compared four methods
(Firestone et al.> 1972; Jensen and Renberg, 1973; Crummett
and Stehl, 1973; Rappe and Nilsson, 1372) for analyzing for
chlorodioxins in PCP. The Cruntmett and Jensen method,
which involved extraction of non-acidic material in PCP
with etherhexane (1:1), gave the best recoveries, although
the Crummett method, employing ion exchange to remove the
acidic components, was simpler than the Jensen method.
Crummett and Stehl (1973) employed GC-MS for
determination of hexa- and octachlorodioxin in PCP. Buser
(1975) developed a specific method for analysis of
chlorodioxins and chlorofurans in PCP and other chloro-
phenols. Phenolic compounds were extracted vith alkali and
the neutral material chromatographed on a basic alumina
micro-column to eliminate polychiorinated benzenes and poly-
chlorodiphenyl ethers. Hie fraction containing
chlorodioxins and chlorofurans was then subjected to mass
fragmentographic (GC-KS) analysis at selected m/e values.
It is important to remove ortho-phenoxyphenoI isomers from
the extract since they can undergo ring closure by
elimination of HC1 upon injection in the gas chromatograph,
resulting in formation of a chlorodioxin (Jensen and
Renberg, 1973).
73
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Recoveries were determined with hexachlorodiox in j the
values ranged frorn 85% at the 0.2 ug level (0.05 ppm) to
over 951 at the 10" ug level (2.5 ppm) .
Buser and Bosshardt (1976) employed the GC-MS
procedure to examine a number of commercial PCP and PCP-Na
samples. Chlorodioxins and chlorofurans were detected by
mass fragmentography and their presence confirmed by
complete mass spectral analysis. Hexachlorodioxins were
recovered from PCP and PCP-Na samples with 80-95%
efficiency (0.1-30 ppm), and octachlorodioxins with 95%
efficiency (10-30 ppm).
Buser (1976) prepared glass capillary columns with QV-
101, OV-17 and Silar 10C stationary phases for high
resolution gas chromatography of chlorodioxins and
chlorofurans. The best separations of hexachlorodioxin
isomers were obtained with the OV-17 glass capillary column.
Sample introduction was effected by a isothermal splitless
injection technique, using n-tetradecane as the solvent for
column temperatures in the range of 205-225°C. The use of
high resolution glass capillary columns permits the
detection and quantization of individual isomers.
Pfeiffer (1976) investigated the use of liquid
chromatography for determination of chlorodioxins in PCP,
The technique was found to be useful for paid examination of
non-phenolic impurities in PCP. Samples could be analyzed
in four hours with detection limits of 0.2 ppm for hexa-
chlorodioxin and 0.1 ppm for octachlorodioxin.
Vogel et al. (1976) evaluated three methods for ana-
lyzing for chlorodioxins in PCP. In method (A) (Blaser et
al., 1976) phenolics are removed by ion-exchange chrom-
atography, and hexa- and octachlorodioxin are determined by
GC-MS. in method (B), proposed by J.P Hieure and 0. Hicks,
Monsanto industrial Chemical Co., phenolics are, removed by
chromatography on slightly deactivated basic alumina, and
chlorobenzenes, chlorobiphenyls and chlorodiphenyl ethers
are removed by activated (super 1) basic alumina. Quant-
ization of chlorodioxins and chlorofurans is accomplished by
GC-MS. In method (C), also proposed by Mieure and Hicks,
chlorodioxins and chlorofurans are isolated by chromato-
graphy on activated basic alumina and examined by GC-MS (or
GLC). Good agreement was obtained between the three methods.
Method (8) was considered the most sensitive when MS
detection was used? methods (A) and (C), however, required
less time for analysis.
74
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Hass (1977) reported a procedure for analysis of
chlorodioxina in beef liver and fat samples involving solvent
extraction, H2SO4 cleanup, chromatography on basic
alumina and mass spectral analysis using either electron
impact (EI) mass spectrometry or negative chemical ionization
(NCI) mass spectrometry (Hunt et al., 1975) in the selected
ion monitoring mode. Limits of detection of hexa-, hepta-,
and octachlorodioxin in liver (17-25 g sample) were 0.2-0.5
ng/g (SI) and 0.005-0,1 ng/g (NCI)'; in fat (3-5 g sample) the
respective detection limits were approximately 2 ng/g (EI)
and 0.01 ng/g (NCI).
Firestone (1976) reported detection of 0.1 to 28 ppb of
total chlorodioxina (hexa-, hepta-, and octachlorodioxin) in
commercial gelatin. Samples after extraction and cleanup on
alumina and Florisil columns were examined by EC-GLC. The
presence of hexa-, hepta-, and octachlorodioxin and penta-,
hexa-, and heptachlorofuran in one of the samples (imported
from Mexico) was confirmed by GLC-MS. Photodechlorination was
used to confirm the presence of octachlorodioxin in some of
the samples *.
* '
The possible number of positional isomers of
chlorodioxins and chlorofurahs are shown in Table 7.18.
Aryl hydrocarbon hydroxylase activity (AHH) for dibenzo-p-
dioxins and dibenzofurans are shown in Tables 7.19 and
7.20 respectively.
TABLE 7.18
Chlorinated Dibenzodioxins and Dibenzofurans
Isomers and Sources
Possible Number of Positional Isomers
No. of Isomers
CI Substitution
Dioxin
Furan
Tetra-
Penta-
Hexa-
Hepta-
Octa-
Tri
Mono-
Di-
T
10
14
22
14
10
2
1
IT
"T
16
28
38
28
16
4
75
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7.2 Environmental Contamination and Exposure
7.2.1 Environmental Behavior of PCP and its Contaminants
7.2.1.1 Atmospheric Behavior
Most compounds have a measurable vapor pressure at
ambient temperatures. It is this characteristic of the
chemical that gives an indication of the propensity for the
substance to escape into the air. Vapor pressure alone is not
the determining factor in the rate of escape or volatilization
since other factors such as absorption, heat flux, air
movement/ i.e., the thickness of diffusion layer, and a number
of other factors are of equal importance (Hartley, 1969; Haque
and Freed, 1974; Plimmer, 1973). It is the rate of escape or
volatilization that is of interest in considering aerial
contamination and transport rather than vapor pressure, per
se. The rate of volatilization may be determined experi-
mentally, but, where constraints make this impractical the
rate of volatilization may be calculated using the vapor
pressure data by the following equation;
Q»1P
This equation gives an estimate of the rate of volatilization
in terms of g/cm2/sec when the material is vaporizing from
its own surface. However, when adsorbed on a solid surface or
within a matrix, the rate of volatilization is reduced by a
factor of 10-100 by adsorption forces. Where dealing with
compounds such as pentachlorophenol and its contaminants, a
conservative factor would be about 20 fold. In view of the
apparent strength of adsorption of these materials, this
factor is more likely to overestimate rate of volatilization
than underestimate.
Turning to the consideration of pentachlorophenol, we
observe that it has a vapor pressure of 1.6 x 10~4 mm Hg at
25°C and this would yield a vapor density of 2,3 x 10~9
g/cn when evaporating from its own surface. Following
adsorption on a solid surface,^the calculated rate of evapora-
tion would be 1.7 x 10 g/cm*"/sec.
M
2itKT
76
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IftBLS 7.19
Qibenzo-p-dToxins (3):
Approximate Activity of.Ccr.gar.er5 in Chick Erncryo Assay
for Induction of Aryl Kydrscaricn Hydroxy!ate(1)
(2) Apprex. Activity,
Compound . Sou res ' ¦ Relative to TCDO 1
1-Cl 0
2-CI b
1,3-Cl 0
1.6-CI-Q
1 ,9-ClfQ
2,3-Cl,0
2.7-ci;o
z,B-ap
1 ,2,3-Cl,0 B "
1 ,2,4-ClfO A "
2,3,7-0150 ' A,E,C 0-COT
1,2,3,4-Cl-O A,B Inactive
1,2,6,7-ClJ) B 0.CQ2
1,3,6,3-Cl^O - A, ¦ Inactive
1,3,7,3-CllD 8 0.1
2,3,7,3-Cl(TCDO) A.3.C.0.E 1.0
1.2.3.4.7-Cl.Q^ A . 0.1
1.2.3.7.8-Cl20 C 0,3
-1,2,4,7iS«Cl|0 C —
1,2,4,6,7,9-Clj.O A ,C 0.002
1,2,4,6,8,9-CtSo 8 ' —
1 ,2,3,5,7,9-CUD C 0.15
1,2,3,4,7,3-CUO A.C.O * 0.3
1 ,2,3,6,7,8-Cl-O C 0.25
1 ,2,3,7,3,5-ClgO " C ' .. . 0.2S
1,2,3,4,5,7,9-C1,D C 0.002
1,2,3.4,5,7,3-Cl jO C 0.15
1,2,3,4,5,7.3,2-ClgO A,S 0.002
2,3-Cl,,(Ul-UC)0- B Inactive
2,3,7,3-Cl^(l ,6- H)0 B 1.0
(1) Activity data provided Sy A. Poland; see also environmental. Heel.
Perspectives (1973) 5:245-251; J. Ora. Chen. (1974), 931-537; and
J. 3101, Che*. (197*7 251:4926-4545.
(2) (A) A.E. Pohland (See TTAf, Food Cham. (1972) 20:1093-1099); (b)
A.S. Kende (See pacer OSGii 130, manuscript in preparation, lo7th
Mat. Mtg. ACS, L.A., Ca1., Aoril 4, 1974); (C) A. Gray (See Tetra-
hedron Lsttar% (1575) ,'fo. 33; 2373-2975 and u. Ore. Chen. (1973) iU
2435-2^37; (0).0,2, McKinney, and (£) Dew Chemical Co. -
(3) 2,3,7,3-TCSO is assigned a relative activity of 1.0.
(4) Contains S3 of 1,2,3,4,7,3-ClgO impurity.
A
A
B
B,D
A'.E
A
Inactive
11
II
ii
11
rt
it
11
-------
TABLE 7.20
Difcenzofurans (F):
Approximate Activity*in Chick Embryo Assay for Induction of Aryl Hydrocarbon
Hydroxylase,*-
2 , . 3
Compound Source Apprcx. Activity Relative to TCSD
2,4-C12f D Inactive
2,8-Cl ? A,3
3,7-ci^ B
2,3,4-CIB 0.001
2.3.6-Cl^F 1 0.001
2.3.7-Cl^F B.C
2.3.8-0.^ B.C 0.001
2.3.9-Cl F C
2,4,6-Cl^F C
2,4,8-CljF 1 0.001
1,4,6,8-ci r r
1,2,7,8~C1*:f c
1.3.6.7-Cl r 1 Inactive
1.3.7.8—Cl F 1 0.02
2.3.6.7-Cl*F B 0.01
2.3.6.8-Cl> B,C 0.005
2,i,7,8-Cl^F 1,C 0.7
2.4.6.7-C1F S 0.01
2.4.6.8-Cl*F B,C Inactive
3,4,6,7-C1 .F B 0.01
4
1.2.3.6.7-Cl F B 0.2
1.2.3.7.8-ClgF 1 0.2
1,2,4,7,8-Cl^F C.
1,3,4,7,8-Cl^F C,D 0.005
2.3.4.6.7-Cl^F B 0.1
2.3.4.7.8-ClgF 8 0.7
2.3.4.5.7.8-Cl F B.S 0.2
2.3.4.7.8.9-ClgF B 0.3
1,2,3,4,6,7,S-C17? B 0.2
1,2,3,4,6,7,8,9-C1 F A,8 0.002
O
^Activity data provided by A. Poland; see also J, Biol. Chem. (19765
251, 4936-4946,
^ (A) A. B. Pohland: (B) A. S. Kende (See paper ORGN 130. manuscript in
preparation. 167th National Meeting, American Chemical Society, L. A,. Cal. ,
April 4. 1974): (C) A. ?. Gray (See J. Org. Chenn (1976) '41, 2423-2424}; (3)
I. H. Poraerantt; and (E) J. D. McKinney (in preparation); (F) S.W. Page (See
paper 0RG;i 63, manuscript in preparation. 172 nd Hational Meeting, ACS,
San Francisco, Cal, Aug. 20-Sept 3, 1976.3
3
2,3,7,8-TC0D is assigned a relative activity of 1.0.
73
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Table 7.21 presents the estimated.vapor density and
rate of evaporation'of chlorodioxins. The low vapor pressure
of the chlorodioxins coupled with the strong adsorption to
surfaces, as indicated by the high molar refraction and the
data of Kearney et al. (1972, 1973), lend credibility to the
values.
Table 7.21
Estimated Vapor Density3 and Rate
of Evaporation" (Q) of Chlorodioxins
Compound Vapor Density (g/cm3) Q (q/cra2/sec)
2,7—di 8.2 x 10-" 6.1 x 10*"
2,3,7,8-tetra 2.9 x 10"" 2.0 x 10""
penta 1.7 x 10~" 1.1 x 10
hexa 1.4 x 10 r± 8,4 x 10
*«/ aJLW X •
1.4 x 10-" 8,4 .. --
hepta 6.9 x 10"" 4.0 x 10""
octa 4.5 x 10~" 2,5 x 10""
4
(a) Above own surface, (b) from adsorbing surface.
13
According to Table 7.21, the rate of volatilization of
the chlorodioxins is very low. This low rate of evaporation
compared to pentachlorophenol could very rapidly explain the
findings of l^evin et al. (1976).
Table 7.22 presents similar data for the chlorinated
dibenzofurans. The data here indicate a slightly greater
vapor density and evaporative loss for the chloro-
dibenzofurans. This would be expected of compounds of
slightly lower molecular weight, higher vapor pressure, and
lower molar refraction'.
TABLE 7-22
Estimated Vapor Density3 and Rate of
Evaporation" (Q) of Chlorinated Dibenzofurans
Conoound Vapor Density (g.cra3) Q (g/ca^/sec)
2,4-di 8.2 x 10"" 6.8 x 10""
2,4,6-tri 5.2 x 10"" - 4.0 x 10""
2,3,7,8-tetra 3.0 x 10"" 2.1 x 10~"
1,4,6,8-tetra 3.7 x 10"" 2.7 x 10""
2,3,4,7,8-penta 1.9 x 10"" 1.3 x 10""
1,3,4,7,8-penta 2.2 x 10~" 1. 5x10""
octa 4.3 x 10"12 2.5 x 10"1J
(a) Above own surface, (b) from adsorbing surface.
79
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Although PCP has a relatively high vapor pressure (1.6 x
1Q~4 torr at 25°C and 3.1 x 10~3 torr at 50°C, the
temperature of a sunlit surface), there is evidence that it
may be slow to volatilize. However, its volatilization from
wood into an enclosed airspace is measurable, and the
atmosphere in a wood-treatment plant has been shown to contain
as much as 1.7 ug/m3 of PCP (Wyllie et al., 1975). PCP has
been detected in rainfall (Bevenue et al. , 1972}, but the
possibility remains that of this may have been due to its
presence on airborne particles rather than as atmospheric
vapor. Laboratory experiments indicate that PCP vapor is
stable to sunlight.
No evidence exists concerning the presence of dioxins or
dibenzofurans in air. The solubility and vapor pressure of
TCDD and OCDD are roughly similar to those of DDT, and DDT is
known to volatilize readily from soil and rapidly from water.
Neutral PCP impurities might logically be expected to behave
similarly, but their vapor should be stable to light.
7.2.1.2 Behavior in Soil
Three processes are of significance in soil. These are
adsorption, leaching and breakdown (Hamaker, 1975; Haque and
Freed, 1974). Adsorption occurs predominantly on the organic
matter (Hartley, 1969) and clay of soil, though the coarser
mineral particles also adsorb. Laboratory measurements that
have been shown to correlate well with adsorption include
molar refraction, latent heat of solution, and partition
coefficient. Based on this, one would expect that penta-
chlorophenol and its various contaminants would all be
relatively strongly adsorbed by soil.
A number of studies have been performed on the soil
behavior of pentachlorophenol. PCP is adsorbed to a moderate
degree under acidic conditions (as neutral molecules) but
moves quite readily in ionized form (under neutral or alkaline
conditions) (Kuwatsuka, 1972). Adsorption is greatest in a
soil in the pH range of 4.6-5.1, with very little adsorption
above pH 6.8 (Choi and Amoine, 1974). Microbial degradation
is relatively rapid, especially in wet soil where a variety of
tetra-, tri-, and dichlorophenols are formed; meta-chlorines
are the most stable (Ide et al., 1972). In aerated soil,
oxidation ahd methylation to pentachloroaonisole and 2,3,5,6-
tetrachlorol,4-dimethoxybenzene represent major routes of
degradation. Similarly, Kearney et al. (1973) and others
indicate a strong adsorption of 2,3,7,8-tetrachloro-
dibenzodioxin and octachlorodioxin (Arsenault, 1976).
Neither pentachlorophenol (ievenue and Seckmen, 1967;
Arsenault, 1976; Kearney et al., 1973) nor the dioxins have
been found to leach readily in soil, largely because of the
strong adsorption.
80
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The breakdown of pentachlorophenol and chlorodioxins in
soil have been incompletely studied. In the case of penta-
chlorophenol, it is-known that the breakdown is fairly rapid
(5 to 8 weeks in a moist soil at rates up to 20 lbs/acre).
Kearney et al. (1972, 1973) report a half-life of approxi-
mately one year for 2,3,7,8-tetrachlorodibenzo-p-dioxin in
soil,* the number of species of microorganisms attacking the
chemical appears limited (Matsumura and Benezet,.1973).
The fate of PCP and its impurities in or on treated wood
is not known, but practical experiments indicate that PCP
remains fungicidally effective for years (Arsenault, 1976).
PCP conceivably could generate OCDD in sunlight, but the usual
presence of hydrocarbon solvents would tend to promote
eventual dioxin photolysis on the wood surface. The burning
of PCP-treated wood or sawdust generates OCDD which sub-
sequently volatilizes, but the proportion is small in com-
parison to that already present in the wood (Crosby et al.,
1973; Stehl et al., 1973; Jensen and Renberg, 1973). (There
is a report, .presently discounted, that TCDD forms similarly
from organic matter containing trichlorophenol derivatives
(Buu-Hoi et al., 1971), but attempts to repeat the observation
have failed.)
7.2.1.3 Behavior in Aquatic Systems
7.2.1.3;1 Physical Behavior
The transport and persistence of PCP and sodium PCP in
aquatic systems has been extensively studied, particularly
where these chemicals had been used as a molluscicide (Strufe,
1968). Here it has been found that the material is rapidly
adsorbed on suspended particulates. Where there is a heavy
load of sediment in the water, the concentration of PCP or
sodium PCP is rapidly reduced in the aqueous phase and the
material settles to the bottom with these particles. PCP,
both as a free phenol and as a sodium salt, has been found to
undergo quite rapid degradation in water, both from sunlight
and anaerobic processes in the bottom mud.
Little information is available on behavior and fate of
the chlorodioxins and the chlorodibenzofurans in aquatic
systems, but it would seem correct to infer that with their
greater propensity for adsorption they would even more rapidly
and tightly bind to sediment than PCP. Since the biological
activity of pentachlorophenol has been shown to be markedly
reduced by the adsorption (Strufe, 1968), it would be presumed
that the same would hold true for the dioxins and dibenzo-
furans.
7,2.1.3.2 Breakdown in Aquatic Systems
In dilute aqueous solutions exposed to sunlight, PCP or
its salts undergo the replacement of ring chlorines by
hydroxyl groups described above. The resulting tetrachloro-
hydroquinone and tetrachlorocatechol are readily oxidized by
air to quinones which in turn are dechlorinated. If the
original PCP solution is sufficiently concentrated (as in the
ai
-------
case of a rice-paddy), the tetrachlorodiphenols can react with
the quinones to give a variety of nontoxic minor products.
However, under most circumstances, the quinone solution is
rapidly degraded to .dichloromaleic acid which itself is
converted to small fragments within a few days (Wong, 1977).
Considering the similarity between the vapor pressures
and solubilities of TCDD or OCDD and DDT, one might expect
more rapid volatilization of dioxins from water than from
soil. As mentioned, dioxins in water appear stable to light
due, perhaps, to their insolubility. In view of their high
degree of adsorption to particulate matter, the amount in
solution would be expected to be low (Matsumura and Senezet,
1973; Isensee and Jones, 197S).
7.2.2 Occupational Use and Exposure
Pentachlorophenol, both as a free phenol and as a sodium
salt, has been used as a wood preservative, an herbicide, a
fungicide, and a molluscicide. Use as a wood preservative in
recent years has consumed many times more pentachlorophenol than
all of the other uses. In fact, the use of pentachlorophenol or
sodium pentachlorophenate as an herbicide or a fungicide has
markedly declined in recent years as other chemicals have
replaced them.
In the United States pentachlorophenol, in an appropriate
solvent, has been the principal form used in wood preservation.
There are limited uses of the sodium pentachlorophenate for
prevention of the development of "blue mold." However, in some
countries, e.g., Indonesia, sodium pentachlorophenate is the
principal form in which this preservative is used.
There are two principal methods by which pentachlorophenol
may be applied for wood preservation (Arsenault, 1976),
pressure treatment or direct application of a solution of penta-
chlorophenol by painting, dipping or spraying. For the most
part the last three methods are employed by the individual while
the pressure treatment is used by commercial treatment plants.
Another commercial treatment is the thermal process (hot and
cold bath/submersion) which is used to introduce PCF into wood
(Ochrymowych, 1978).
In the pressure treatment with pentachlorohenol, the
phenol, in appropriate solvent, is applied to the pole or lumber
in a pressure retort at somewhat elevated temperatures. The
pressure treatment may be preceeded by a vacuum to increase
penetration, and it may be followed by a flash vacuum to reduce
surface deposits. Occupational exposure of humans, in this case,
may occur during preparation of the treatment solution or when
the retort is opened following treatment and the system is still
hot. Relatively lower levels of exposure would be expected in
handling the treated wood. The greatest exposure comes to the
worker in the immediate area of the treatment operation, whether
by dip, spray, or pressure treatment. In most of these
instances unless there is direct contact with the treatment
mixture or treated materials, the principal route of exposure
appears to be respiratory. This is in contrast to the
experience in Indonesia where the worker handles the freshly
dipped lumber or in herbicide treatment where there may be
direct dermal exposure.
82
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7.2.3 Environmental Transport and Exposure
pentachlorophenol has been found in a number of
different environmental samples (Kutz et al. , 1976), e.g.,
house dust, air, water, and in the urine (Sevenue et al.,
1972) of presumably non-exposed humans. This would appear
to indicate a rather high environmental mobility for penta-
chlorophenol. However, it must be remembered that
pentachlorophenol may be generated in chlorination of water
and that there is a residual background found upon analyses
of soil that gives analytical results, similar to PC P.'
However, based on the properties of pentachlorophenol,
namely that of vapor pressure and rate of volatilization,
measurable quantities would be expected to escape into the
air either from the chemical's own surface or from poorly
adsorbing surfaces to which it had been applied. But based
on pentachlorophenol's propensity for adsorption, one would
expect that a substantial amount of this vaporized material
would be found adsorbed to particulates in air. Another
route of transport to air would be the erosion of
contaminated dust particles*
On the other hand, the chlorodioxins and chlorodi-
benzofurans that occur in pentachlorophenol, having much
lower rates of volatilization, would not be expected to be
found as frequently in air samples. Again, because of the
propensity for adsorption and the low water solubility
(about 3 ppt for OCDD? Arsenault, 1976) one would not
expect to find a great deal of these materials in water. As
indicated earlier, the relative vapor pressures and rate of
evaporation of pentachlorophenol, chlorodioxins and
dibenzofurans would perhaps account for the findings of the
Swedish workers (Levin et al., 1976). Here it appeared
that the ratio of chlorodioxins and chlorodibenzofurans to
pentachlorophenol in wood increased appreciably over the
ratio found in the original treatment solution, it* seems •
that a reasonable explanation would be the probable greater
loss of pentachlorophenol through vaporization from the
sawdust in contrast to the other two types of chemicals.
Though pentachlorophenol and its contaminants are
probably transported by air and water (probably in the
adsorbed state), their biological activity is probably much
reduced by adsorption, thus attenuating the effect of
exposure, it has been found, for example, that penta-
chlorophenol adsorbed on sediment found in water had low
activity so far as control of snails is concerned.(Strufe,
1968). it is likely that the adsorptions of the chloro-
dioxins and chlorodi benzofurans also result in a reduction
of their biological availability.
83
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Breakdown ig another factor in reducing the concen-
tration and biological effects on these chemicals in
transport.
7.2.4 Food and Feed
PCP is a powerful herbicide, and its intentional use
around food crops would be expected to be negligible.
However, PCP is used as a desiccant on seed alfalfa and seed
clover, and sodium PCP is used in dilute aqueous solution
as a postharvest fungicidal dip. These are considered as
non-food uses, and no tolerance has been established,
although feeding treated forage or threshings to livestock
is not permitted in the United States.
Measurement of total diet residues (FDA Market Basket
Survey) has shown occasional PCP contamination (for example,
nine of 30 composite samples showed 0.01-0.0 2 ppm of PCP in
1972-3; two dairy products, one legume vegetable, and six of
sugar) (Johnson and Manske, 1976). OCDD and HCDD have not
been reported in food, although Firestone (197 6) reported the
presence of dioxins in commercial and "edible" packages of
gelatin. The presence of dioxins (chick edema factors) in
food grade oleic acid and oleic acid derivatives, e.g.,
glyceryl monooleate and a food emulsifier, prompted PDA to
issue a food additive regulation in 1960 (Firestone, 1973).
Chlorinated anisoles, originating in henhouse litter, have
been detected in chicken,meat (0.02-0.08 ppm) and have caused
a musty taste (Curtis et al. , 1972). PCP was reported to
occur at low ppb levels in fish caught in open water not
expected to contain appreciable levels of PCP (Zitko et al.,
1974).
7.2.5 Biological Uptake and Concentration
Higher plants do not absorb appreciable amounts of PCP
or TCDD from soil (Miller and Aboul-Ela, 1969; isensee and
Jones, 1971), and administration of these compounds directly
to leaves resulted in retention rather than translocation.
Algae, however, rapidly absorbed and concentrated TCDD about
10,000 fold from water (Isensee and Jones, 1975), although
they metabolized rather than concentrated PCP (Lu and
Metealf , 1975).
Rodents excreted PCP partly unchanged, partly as
glucosonide conjugate, and partly as tetrachlorohydro-
quinone and its conjugates (Jakobson and Yllner, 1971;
Ahlborg et al., 1974). Tetrachlorohydroquinone also was
detected in the urine of human workers occupationally
84
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exposed to PCP (Ahlborg et al., 1974). However, the rhesus
monkey excreted PCP more slowly, and apparently only as
free PCP, with a half-life of about 40 hours in the male
and 90 hours in the female (Braun and Sauerhoff, 1976).
There appear to be no data on organ accumulation of PCP
during chronic exposure, but recovery of pep and its
conjugates from urine and feces certainly is not quanti-
tative; for example, about 11% of a 10 rag/kg dose of PCP
was still retained by the monkey after 3S0 hours (1% in
liver, 71 in intestines, and 3% in other organs) (Braun and
Sauerhoff, 197S).
Animals in a model aquatic ecosystem concentrated PCP
as much as 300-fold during 48 hours of continuous exposure
(Lu and Metcalf, 1975), although up to 74% of the applied
dose was metabolized in that period. Fish accumulated the
most PCP after 120 hours of exposure to 0.1 ppra of PCP.
Fish had concentrated it 1000-fold, primarily in the gall-
bladder; return to clean water caused an initially rapid
clearance, mostly in conjugated form. Eventually up to 30%
of the original PCP body burden was retained (Kobayashi and
Akitalee, 197S). • .
Surprisingly, no data were available on the biocon-
centration of dioxins or dibenzofurans in higher animals
during chronic exposure. After a single oral dose of
5 0 ug/kg, the rat cleared TCDD with a half-life of 17 + 6
days (Piper et al., 1973). attention was primarily in the
liver and secondarily in the fat; the liver still contained
471 of the initial dose after three days and 11% after 21
days. Body burden of TCDD was only determined to 21 days,
at which time it still represented 401 of.initial dose;
there is no indication of what terminal residue eventually
might exist, if any. No metabolism of dioxins was evident.
Bioconcentration of TCDD in aquatic model ecosystems
was reported by Hatsumura and Senezet (1973) and isensee
and Jones (1975). Bioconcentration was proportional to the
amount of TCDD in the water; the bioconcentration factor of
approximately 104 in the species included and was rather
independent of the aqueous concentration. Attempts to
detect TCDD and other dioxins in samples from terminal
predators in the environment (gull eggs, eagle fat, and
sea-lion blubber) were unsuccessful, although the
analytical sensitivity was limited to the ppb range
(Woolson et al., 1973; Bowes et al. , 1973).
85
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while the potential exists for limited bioconcentration
PCP from food and the environment, its rather effective
metabolism by higher and lower animals suggests that the
effect may not be pronounced. On the other hand, TCDD shows
a bioconcentration potential (10 ) roughly similar to
that of the more inert chlorinated hydrocarbons (10 ).
7.2.6 Sources of exposure
Table 7.23 lists major registered uses of PCP.
From these, it is possible to determine a variety of
potential sources of occupational exposure (Table 7.24), but
in only a few instances (primarily in wood treatment
industries) has the exposure of workers been analyzed
(Klemmer, 1972f Ahlborg et al., 1974; and Wyllie et al.,
1975, are typical).
The widespread use of PCP in these applications
likewise provides increasing opportunities for incidental
exposure of the public to PCP and its impurities in the
home, business, and outdoor environment. Table 7,25 lists
a few of the more obvious possibilities. Such instances as
the detection of ppb levels of PCP in rainfall over a
remote island (Bevenue et al., 1972), in freshwater and
marine fish caught in areas remote from direct PCP dis-
charge (Zitko et al., 1974), and in the urine of random
samples of human populations not exposed occupationally
suggests a continual low-level background of environmental
PCP which requires further investigation.
Table 7.23
Major Registered Uses of PCP
Herbicide and desiccant for forage seed crops
Insecticide for beehives, seed flats, greenhouse use.
Microbiostat for commercial and industrial water cooling
Postharvest wash for fruit
Microbiocide for burlap, canvas, cotton, rope, and twine
Microbiocide for leather
Microbiocide and insecticide for wood treatment
Preservative for oil- and water-based paint
Slime control for pulp and paper
Microbiocide for petroleum drilling mud and flood water
Fumigant for shipping-van interiors
Preservative for hardboard and particle board
Herbicide for non-food vegetation control
86
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Table 7.24
Some Potential Sources of Occupational Exposure
to PCP and PCP Impurities
Manufacture and shipping of industrial chlorophenols
Sawmills
Wood-treatment plants
Carpentry and other lumber and wood working
Termite control
Agricultural pesticide application
Greenhouses
Industrial cooling towers and evaporative condensers
Treatment and handling of burlap, canvas, rope, leather
Paper manufacture
Petroleum drilling
Paint manufacture and use
Telephone and electrical line work
Table 7.25
Some Potential Sources of Incidental Exposure
to PCP and PCP Impurities
Smoke from sawmills and burning scrap lumber
sawdust (fuel, floor covering, particle board, etc.)
Vapor from treated lumber and plywood
Home treatment of lumber for termite control
Burlap, canvas, and rope
Leather products •
Paper products
Contact with paint and painted surfaces
Uses of utility and structural poles and railroad ties
ornamental wood-chips
Dairy products, sugar products, and fish
87
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96
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8. APPENDIX D
8.1 Age.nda of April 3-4, 1978 Meeting of
EHAC 100
. 8.2 Testimony of Interested Parties
8.2.1 Mr. Dennis Lindsay (AWPI)... 103
8.2.2 Mr. Dennis Lindsay (VMI) 10?
8.2.3 Mr. Sober t Arsenault (Koppers) 109
8.2.4 Dr. Gary A. van Gelder.. 129
8.2.5 Mr. Fred Shelton ( Reichhold) 140
8.2.6 Dr. Robert L. Johnson (Dow).................. 153
8.3 Comments of Interested Parties
8.3.1 Mr. Paul E. des Rosters (EPA).. 158
8.3.2 Dr. Gary A. van. Gelder. 161
8.3.3 Dr. Robert L. Johnson (Dow) 165
97
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8.1 Agenda of Environmental Health Advisory Committee
Meeting of April 3-4, 1978.
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FINAL
U.S. ENVIRONMENTAL PROTECTION AGENCY
SCIENCE ADVISORY 30ARD
ENVIRONMENTAL HEALTH ADVISORY COMMITTEE
Conference Room A (Room 1112}
Crystal Hall Building No. 2
Arlington, Virginia
April 3-4, 1978
AGENDA
Monday, April 3, 1973
9:00 a.m. 1. Introductions and Opening Remarks Dr. Whittenberger
2- Draft Report of Study Group on Fentachlorophenol
Contaminants iDra.ft dated March 1 978)
- Introductory Remarks Dr. Murphy
9:30 a.m. 3. Statements by Members of the Public
- Mr. Dennis Lindsay, Chairman, PCP Committee
American Wood Preservers Institute
- Mr. Robert Arssnault, Director, New Product Development
Koppers Company
- Mr. Dennis Lindsay, Technical Services
Vulcan Materials Company
- Dr. Gary A, van Gelder, Veterinary Toxicologist,
College of Veterinary Medicine
University of Missouri, Columbia, Missouri
- Mr, Fred She!ton, Vice President, Science and Technology
Reichhold Chemicals
- Dr. Robert L. Johnson, Senior Research Analyst
Dow Chemical Company
11:00 a.m. ***BREAK**»
100
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¦ENVIRONMENTAL HEALTH ADVISORY COMMITTEE
April 3-4, 1978
AGENDA
(Continued)
April 3, 1978
11:15 a.m. 4. Comments and Discussion
by Members of Committee and Study Group Dr. Whittenberger
12:30 p.m. ***LUNCH***
1:30 p.m. 5. Comments and Discussion (Cont'd) and
Development of Committee Recommendations
3:00 p.m. 6. Informational Items
- Publication of
"Noise - A Health Problem"
- Status of Benzene Assessment Reports
3:30 p.m. 7. Concluding Remarks
***RECESS***
Dr. Whittenberger
Mr. Marrazzo
Dr. Saz
Dr. Whittenberger
Agenda Notes:
Dr. James L. Whittenberger, Professor of Physiology, James Stevens Simmons
Professor of Public Health, School of Public Health, Harvard University,
Boston, Massachusetts
Dr. Sheldon D. Murphy, Professor of Toxicology, Department of Pharmacology,
University of Texas Medical School at Houston, Houston, Texas
Mr. Rudy Marrazzo, Science Advisor, Office of Noise Abatement and Control,
U.S. Environmental Protection Agency, Washington, D. C.
Dr. Arthur K. Saz, Criteria Development and,Special Studies Division,
Office of Research and Development, U.S. Environmental Protection
Agency, Washington, D. C.
101
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8.2 Testimony of Interested Parties
102 *
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8.2.1 SAB Meeting - April 3, 1978
Statement as AWPI Committee Chairman
My name is Dennis Lindsay. I am employed by Vulcan
Materials Company, a pentachlorophenol producer. The remarks
I wish to make now are on the behalf of the American Wood
Preservers' Institute, also known as AWPI. Approximately three
years ago the wood preserving industry organized an Environmental
Programs Task Group within the AWPI, a pre-existing trade associa-
tion. The purpose and goal of the task group was and still is
to make possible the survival of the wood preserving industry
during this time of extensive governmental regulation. We monitor
the governmental regulatory agencies and comment when appropriate
upon proposed regulation. We frequently offer our assistance
in helping the agencies understand what it is they are attempting
to regulate. Our task group chairman appoints subcomaitties and
assigns to them various responsibilities.
I am Chairman of EPTG subcommittee #6, on pentachlorophenol
which was formed about two years ago with the primary purpose
being to defend penta during the anticipated RPAR process and
eventually get it reregistered under FIFRA.
Our subcommittee appeared before your study group on penta
contaminants at a meeting they held 13 months ago today. We
made comments and supplied information which I trust was somewhat
useful to them. Your study group has worked diligently as
evidenced by their draft report. It is by far the most
103
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comprehensive document to date and does an excellent job of
explaining the many facets of this complex problem.
Our subcommittee has also been very active during these
past 13 months, both as a group and as individual companies.
I wish to point out some of our activities and inform you of
certain facts.
First of all I wish to call to your attention the fact
that we, as penta producers, are one less in number than we
were a year ago. In the fall of 1970, when the U.S. Department
of Agriculture first expressed concern about the presence of
chloro-dioxins in some "economic poisons", that now missing
producer was the greatest among us. Their production and sales
^exceeded that of any other producer.
Thirteen months ago, I reported to your study committee
that we had been negotiating with the Pacific Bio-Medical Research
Center at the University of Hawaii concerning the retrieval and
statistical analysis of data generated in a long term project
known as the Community Studies on Pesticides. This study deals
c e t n & (
with chronic/\exposure to technical penta. We 'did fund that project.
We had hoped for an earlier report; however, it is due within
the next two or three months. We will make it available to
your study group and would hope that they at least consider the
report before writing their final draft and recommendations.
This committee has also made possible the generation of
other data relevant to the charge of your study group. Most of
the work done during the past year by Dr. Gary Van Gelder,
University of Missouri, concerning Michigan dairy herds was funded
134
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by this committee. It was largely Dr. Van Gelder's work which
led the hearing officer, Dr. Gilbert H. Wise, D.V.H. to conclude:
"The evidence, while not removing all possibility of
hazard, does not support a finding of any measurable
magnitude of risk or likelihood of harm to the human
food chain from exposure of food animals to CDD in
technical penta." (Page 16 of hearing officer's report).
I have attached a copy of Dr. Wise's full report and findings
for your information. The underlining and notations are my own.
Next, I would like to call your attention to the current
draft report. Under III, Section '2, "Toxicology of Chlorinated
Dioxins and Dibenzofurans" ,* page 5, the last sentence states,
"Controlled dosing experiments, recently initiated,
may help answer questions raised by the Michigan field
studies concerning the pharmacokinetics and toxicity
of PC? and its contaminants in cattle." •
It is hoped that that report, when completed, would also
be considered by your study- group prior to their reaching a
conclusion and recommendation.
In addition, we are aware of a study by Dr. Firestone in
which he fed technical penta to lactating cows, amy information
relevant to this problem should be considered prior to a final
report by this committee.
Our committee is currently considering the funding of a
180-day calf feeding study using varying doses of different kinds
of pentachlorophenol which would be done by Dr. Van Gelder.
105
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We are presently waiting upon the results of the Firestone
and Moore studies to help us decide what questions remain
unanswered.
At the request of AWPt, the American Wood Preservers'
Association, AWPA, the standards writing organization for our
industry, has appointed a special committee to establish
standards for treating wood intended for use in housing food
producing animals. My point is to show you that we are attempting
to act responsibly in dealing with these problems.
I
3/28/78
-------
-5A3 Meeting - April 3, 1978
'Statement as- VMC -Representative
Gentlemen, I am changing hats now. The remarks I will
make from here on are as a representative of Vulcan Materials
Company,
I would first like to direct your attention to the draft
report, I, page 4, The last sentence of the top paragraph reads
as follows:
"Of course, the production of this more purified
product entails increased production costs, and. some
representatives of Industry felt this would result
in a product which may be more difficult to handle."
That statement is not strong enough, I am convinced that
this would result in a product which is more difficult to handle.
I know of three separate cases where it was attempted to use
Dowicide EC-7 in conventional hulk handling systems. All were
considered failures in the eyes of the customer, and one resulted
in considerable damage to the equipment.
Dow has apparently acknowledged this fact, since they
recently announced that they will now produce penta only in the
block form. That action has caused a large number of smaller
consumers of penta who have been Dow customers to come to the
other producers for a source. They (the smaller consumers)
cannot afford to purchase the block dissolving equipment.
Vulcan introduced bulk handling of penta ten years ago, and
we believe it to be unequaled in convenience, flexibility and
107
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reducing exposure to plant: personnel. Blocks may be a
useful manner of "handling penta, but blocks or bulk handling
simply will not serve the purpose of everyone in the industry.
Thirteen months ago our greatest concern with penta was
that of its contaminants. Today we hear concern expressed over
fetotoxieity, teratogenicity and even mutagenicity. In the
face of these concerns, it is difficult for a producer to justify
the capital expenditure in purification facilities for a product
with an environmentally doubtful future. One producer has ceased
production; and while environmental considerations were not the
underlying reasons, you can be sure that the uncertain future
for this product helped tip the scale in their decision-making
process.
I would like to propose what I believe is a common sense
solution to this problem. It is not a new idea. Others have
proposed it before, but in my opinion, it has merit.
After studying the draft report of your study group, I
conclude that sufficient scientific evidence upon which to base
a decision is lacking. Further, since technical penta has been
used for 40 years with only minor and controllable incidents,
I believe that this study group should direct their attention
to outlining the testing which would enable thera to make a
decision. Such testing might be accomplished on a cooperative
basis by the chemical producers. In this way the wood treaters
would be spared the cost of different handling equipment until
such time as it was necessary, if at all.
3/30/73
108
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Fswtst Pfoflucts Clvi#ion, Kocwfs Company, Inc.
Pittsburgh. PA 1S219. Telephone 412-390X000 227-2460
8.2.3
Robart D. A/Mnawlt
SSSZo***,wmm Architectural and
Architectural and
Construction Materials
April 13, 1978
Mr. Ernst Linde
Scientist Administrator
Science Advisory Board, A-101
Environmental Protection Agency
Washington, D. C. 20460
Dear Mr. Linde:
Attached is the written statement of essentially what I said at the
SAB Meeting,
Sincerely yours,
Robert D. A ra enautt
RDA/ma
enclosures
109
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Testimony to the EPA Science Advisory Board
Environmental Health Advisory Committee on Pentachlorophenoi
April 3, 1978
My name is Robert D. Arsenault. I am Manager of Product Development,
Forest Products Group, Koppers Company, Inc. I was formerly associated
with Monsanto Company, Paper & Wood Chemicals Group, as Market
Manager for pentachlo rophenoi and as such I had considerable working
knowledge of pentachlorophenoi chemistry and use in wood preservation.
Koppers Company uses considerable quantities of FCF in its wood treating
facilities and in formulating blended products for mill work, sapstain control
and other uses. In addition, Koppers sells PCF as a broker, formerly for
Monsanto and now for Reichhold and Vulcan.
I appreciate the opportunity to speak to the,Environmental Health Advisory
Committee today. I will restrict my comments to the draft report of the
Study Group on FCP Contaminants. I will first make some general com-
ments followed by specific commmts,
On the whole I feel that the study group has done an excellent job in reviewing
the current knowledge on FCP contaminants. Their conclusions concerning
the potential hazards are especially noteworthy, but these conclusions are
inconsistent with the bottom line conclusion.
For example, on page 1-5 the statement reads, "there is really very little
data on the environmental persistence and transport of the dioxin and dibenzo-
furan contaminants of pentachlo rophenoi". On page 1-6 the paper reads,
"The toxicological information necessary to make the evaluation of relative
hazard of purified versus standard commercial FCP is also deficient.
Pentachlo rophenoi itself is a toxic chemical in its own right. " On page 1-7
the paper reads, "This finding of low, but detectable, levels of chlorinated
dioxins in tissues of these animals is a matter of public health concern,
however, the biological significance of this finding is not presently known. "
And, "There is insufficient information concerning the identity and dosage
of dioxins involved to allow these observations in man to be useful in a
quantitative assessment of the relative hazard of purified PCF versus com-
mercial products containing dioxin contaminants. There are no data that
permit an estimate of the relative susceptibility of humans to systemic
effects of the dioxins and related contaminants of FCP. " "As yet, there is
no quantitative information which permits a comparison of the toxicity of
dioxin to humans versus other animals. "
110
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-2-
All these statements reinforce our consistent opinion that there are no
laio-wn significant hazards related to the current levels of impurities in
PCPj ind there are no data to set any target level judged to be "safe".
Yet, these conclusions were the result of a review of all known data an
hazards. No such review was made of the costs associated with gaining
these unstated "benefits" from removing the impurities; yet, the state-
ment is made an page 1-4, "Of coarse, the production of this more
purified product entails increased production costs and some represen-
tatives of industry felt this would result in a product which may be more
difficult to handle". A thorough study of the "costs" would have shown
that not only are they huge, but.the costs would include an increase in
exposure to PCP due to the product being more dusty. Also, the costs
would include disposal problems with dioxin still bottoms and difficulty
in using the purer grade hi some industry solvents such as Koppers
Cellon process.
Despite all the above mentioned lack of information, the Study Group wrote
conclusion 10 which simply states that since technology is available to clean
up PCP, "it would seem prudent" to do so. This statemmt seems to us to
be unjustified, though it is politically expedient.
On pages n-7 and V-3-35 acknowledgement is made that some of the PCP
in' the eariraamat may come from generation of PCP by chlorination of
water or creation by natural processes. However, the implication is that
PCP in the environment, found in urine of non-exposed humans, and in
tissue comes from exposure to treated wood in the environment.
One of the problems that has arisen is that pentaehlorophenol in the environ-
ment seems to be ubiquitous. It is found in samples takoi from the environ-
ment, from animals, and from humans. For. example, the March 1st issue
of Pesticide St Toxic Chemicals News reports that the "EnvirnnmmtaL
protection Agency's national human monitoring program has found in the
400 samples of human urine analyzed that nearly 85% of the samples show
'quantifiable amounts of pentaehlorophenol1, a constituent of many wood
preservatives and a contact herbicide". Also, the June 30, 1976 issue of
Pesticide Chemical News contained an article that stated, "hexachloroben-
zene residues have beai found in 75% of mother's milk samples and 95% of
human adipose tissue samples collected in the U.S. by the EPA". Attached
is a copy of the entire text of this article. It also states that HCB contami-
nation of meat is increasing and breast fed infants, in a worst case situation,
could be exposed to HCB levels approaching those demonstrating adverse
effects in laboratory animals.
Ill
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-3-
Tying these two findings together in order to show that PCF and HCB are
interrelated one would only have to prove that pentachlo rophenol La a metab-
olite of hexachlorobenzene, or vice-versa. Since pentachlorophenol is 113 ed
in small quant it ies as a wood preservative compared to hexachlo robenzene
production in the chemical industry, one would have to agree that pentachloro-
phenol could be a metabolite of hexachlorobenzene in humans, if shown in
laboratory animals, to fact, it was shown in monkeys that hexachlorobeazene
metabolized to pentachlo rophenol. I am attaching a copy of a paper by Yang,
et al entitled, "Chromatographic Methods for the Analysis of Hexachloroben-
zene and Poss ible Metabolites in Monkey Fecal Samples".
Another paper by Engst, et al, "The Metabolism of Hexachlorobenzene in
Rats1', confirmed earlier findings by Mabendale in 1975 that pentachlo ro-
phenol was a metabolite of hexachlorobenzene in animals. I am also
attaching a copy of a paper by Rourke, et al entitled, "Identification of
Hexachlorobenzene as a Contaminant in Laboratory Plastic Wash Bottles",
which references three papers by Yang, et al on the metabolism of hexa-
chlorobenzene in Rhesus monkeys. I have given you a copy of the paper by
Renner entitled, "2, 4, 5-trtchlo rophenol, A New Urinary Metabolite of
Hexachlorobenzene".
Now how does the hexachlorobenzene get in the environment? To answer
that question I am enclosing a copy of a paper written for the Hazardous
Waste Management Division of EPA entitled, "Sources, Characteristics,
and Treatment and Disposal of Industrial Waste Containing Hexachloro-
benzene". According to the paper there are 23,665 tons per year of
hexachlorobenzene containing waste materials from chlorinated solvent
production alone plus 2,650 tons of hexachlorobenzene from chlorinated
solvents which were presumably removed from the chlorinated solvents
before the sale of the solvents. It is also known that many of the chlori-
nated solvents used for dry cleaning contained traces of hexachlorobenzene
and this could be another reason why humans are exposed to hexachloro-
benzene everywhere.
Another paper which was sent to us from the Office of Toxic Substances
entitled, "Hexachlorobenzene, A Man Made Pollutant", is attached for
your information.
It is apparent also that this is not a one-way proposition. Pentachloro-
phenol could conceivably degrade to hexachlorobenzene under certain
conditions. Dr. Donald Crosby in his paper to the EPA Science Advisory
Board, "Reactions arid Environmental Fate of Pentachlorophenol and its
112
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-4-
Impuritles", stated, "the original pyrolytic conversion of a POP salt to
OCDD was accompanied by a large portion of hexachlorobenzene, sug-
gested to arise from decomposition of decachlorodiphenyl, but this has
not been confirmed". Hexachlorobenzene also appears to be a byproduct
of UV light degradation of pentachlorophenol on the surface of wood* It
is my impress ion that hexachlorobenzene contamination of the environ-
ment is caused from the hexachlorobenzene impurities in chlorinated
chemicals as well as the over 26 million ton3 per year of HCB containing
waste which are dumped.
Also attached are two articles which appeared in J* Environ. Scu Health
in 1976, both covering another source of penta in the environment. The
use of lindane as an insecticide on lettuce and endives resulted in the
lindane to convert to trichlorophenol, tetrachloropheaol, pentachlorophenol,
and conjugates of tetra and pentachlorophenols. Non-polar compounds,
including hexachlorobenzene were also farmed. In the top soil was also
some penta. While the article calls these breakdown products metabolites
from the crop,' I think it more likely that they are UV light breakdown
products*
The other article covers the metabolism of lindane in rats« Pentachloro-
phenol is shown to be one of the metabolites. Other metabolites include
2,3,4, 6-tetrachlorophenol, 2, 3, 5,6-tetrachlorophenol, and 2,4,6-tri-
chlorophenol. Minor metabolites were gamma 2, 3,4, 5, 6-pentachloro-
cyclohexene and its metabolite, tetrachlorocyclohexanol*
This work also shows other chemicals which have penta as a metabolite*
They are pentachlorobenzene and 2, 3, 4, 5, 6-pentachiorocyclohexene-(2)«
ol-(l) and gamma 2,3,4,5,6 pentachlorocyclohexene.
It Is beginning to look like there are many ways for penta to end up in
the food chain, both as metabolites and a3 b teak down products of other
commonly used pesticides, including hexachlorobenzene and lindane.
We at Koppers feel so strongly about this issue of .pentachlorophenol
being a universal contaminant "caused by use in wood preservation" that
I asked R* S. Detrick of Koppers to presait a paper which appeared in
the Forest Products Journal in 1977* Attached is a copy of the paper*
It refers to many of the items which I have already discussed, but in
summary it shows that pentachlorophenol in the ppb level can be caused
from other factors than pentachlorophenol exposure.
There is another area of concern which I feel must be dealt with in the
Report. Photolysis of PCF can create OCDD and hexachlorobenzene in
113
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-5-
the environment. Since both of these contaminants are already present
in technical PCP, we question why take them out if they are only going to
form again from sunlight. However, they also rapidly break down in the
same sunlight.
The paper on page 11-8 states that PCP photodegrades in water and various
solvents. This is covered again briefly on pages V-3-17, V-3-19, V-3-20,
V-3-22, and V-3-32. However, on page V-3-22 the Report states that
organic, hydrogen-donating solvent must be present for photolysis of
dioxins or dibenzofuran to occur. This is not true. We have demonstrated
repeatedly that photolysis and rapid degradation occurs when dioxins are
present on cellulose substrate without solvent. We have extensive infor-
mation to CPA with a letter to Mr, Edwin Johnson dated June I, 19?? on
the degradation of PCP and OCDD by sunlight and artificial UV light. None
of these data are referenced in. this report,
1 am attaching a copy of that June 1st letter and also a copy of a letter
written to Dr. Donald Is lib as part of the Michigan Hearing Record. These
documents show that both technical PCP and EC-? PCP reach the same
maximum of OCDD level in micrograms per unit surface area after one
day irradiation by UV light. This maximum was then depleted as the OCDD
photodegraded and there is no difference in the rate of buildup or the rate
of breakdown between commercial FCP and EC-7 PCP. The OCDD con-
centration on the surface reached 3060 ppm on the basis of initial PCP
concentration regardless whether the initial PCP started with commercial
PCP (1600 ppm OCDD) or EC-7 PCP (60 ppm OCDD).
Hexachlorobenzene also is a degradation byproduct of photolysis of PCP.
However, HCB is also a contaminant of PCP. In fact, we found a sample
of EC-7 PCP contained approximately four times the HCB level (170 ppm)
as Monsanto's PCP (45 ppm). In wipe tests of wood utility poles exposed
to sunlight for less than one week, poles treated with EC-7 PCP in oil had
approximately ten times the level of HCB on the surface of the poles as
expected based on the amount of PCP present. When compared to poles
treated with commercial PCP in oil ifter three years exposure in Ohio
(different oil), the EC-7 treated poles had about four times the level of
HCB on the surface as the commercial PCP treated poles. While these
levels are not judged to be an environmental hazard (levels of 0.001 to
0.02 ug/in. HCB), they do indicate that there is no benefit from the
environmental standpoint of reducing the contaminants in PCP.
We are continuing our work on photolysis of PCP, OCDD, and HCB using
wood as a substrate. As more information is generated, we are finding
that UV light degradation eliminates these products from the environment.
114
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Therefore, although the grade of PCF makes ao difference in quantitative
amount of impurities formed, in reality the impurities are not a hazard,
whether in the PCF initially or formed from TJV light.
115
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June 1, 1977
Mr. Edwin L. Johnson
Deputy Assistant Administrator
I Or Pesticide Programs
Environmental Protection Agency
Washington, D. C. 20460
Dear Mr. John a on;
In the pA at wf have submitted info rmst ion to you on the en viron mental
fate of pmtach to rophenol {PC P) Including information on degradation of
PCP In Boll and the degradation of octachlorodibenzo- p-dloxin (OCDD)
in soil. Thia was a part of the package which was submitted by Ron
Dreer to the Science Advisory Board Ad Hoc Panel studying the dioxin
question.
We understand that the Science Advisory Board will shortly be completing
their report and recommendation*. One part of the Draft copy of the
report, written by Dr. Cros by, referred to pentachlorophenoxlde-lon
undergoing cyclical Ion to OCDD In water, and also photodegradation of
OCDD by ultraviolet (UV) light in the presence of a hydrogen donor such
aa alcohol. Dr. C ro»by w rot c that, "the rate of photo-reduction ia
Inversely proportional to the degree of chlorination indicating that the
lower chlorinated dioxins degrade faster than the higher chlorinated
dioxins, He further wrote that, "PCP could conceivably generate OCDD
in iunllRht, but the usual presence of hydrocarbon solvents would tend
to promote eventual dioxin photolysis on the wood surface".
A» part of our continuing program of environmental and health studies
with wood preservatives, we have been investigating the photochemistry
of pentachloroplw nol and the contained dioxins. Thus far, this work
supports the statements made by Dr. Crosby, and the penults emphasize
that dioxins that may be generated from PC F Irradiation on the surface
of the wood are (hemp rives degraded, A hydrogen donor solvent, however
is not n.ecessary. Celluloslc material can act aa the hydrogen donor.
116
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Mr. F'lwln L. Johnson
Page 2
June I, 1977
From An environmental point of view the surface of the treated wood Is
Important because It constitute* Art avenue of exposure to man and the
environment. In order to s Imulitf the surface of the wood without having
interactions such as bleeding, variability, and analytical difficulty, we
have done most of our work with filter paper Impregnated with a solution
of PCP orOCDD.
We have conducted several experiments exposing technical PCP, purified
PCP. Dowicide EC-7 PCP, and OCDD on filter paper and technical PCP
and Dowicide EC-7 PCP on wood, with and without oil present, in artifi-
cial UV li(»ht and In sunlight. Our experiments are continuing, but we
have preliminary results that we feel are meaningful even though we have
not yet completed these studies.
Working with filter paper, our studies show that when PCP Is exposed to
UV light, photodegradatlon occurs and OCDD I# one of the products formed.
Continued exposure to UV light degrades the OCDD. These chemical
reactions occur whether the PCP being exposed to UV light la of the EC-7
grade or the technical grade. What surprised us In our studies, however,
was that regardlenH of the original OCDD content of the PCP. the ultimate
level to which the OCDD builds up is about the same.
The EC-7 fample we used contained 13 ppm of OCDD. The commercial
PCP sample contained 1,466 ppm of OCDD. When 15 mg of EC-7 grade
PCP was irradiated for two days, the dioxin level on the filter paper rose
from the initial 0- 2 ug to 5H ug of OCDD. When 15 mg of commercial PCP
was Irradiated, the dioxin level rose from the Initial 22 ug to 64 ug. The
EC-7 grade TCP generated 58 ug in the same time that commercial PCP
generated 42 uj:, and both gradeo of PCP developed approximately the
same level of OCDD. Once a critical level of OCDD was reached* the
OCDD photodegraded to lower levels.
After seven days only 3To of the original PCP remained and the OCDD
level had dropped about 33^ front the peak value. After ten days the
OCDD level had dropped to 8bout 50% of the peak value.
In our te«l.-v a larrje. part of, the TCP was lost due to volatilization rather
than photolynls. Working without UV light, but keeping all other condi-
tions constant, 52% Of a 7. 5 mg sample volatilized In three days' exposure#
Similar studies h*ve not been conducted an yet on OCDD. However, Inas-
much as OCDD has a vapor pressure less than 1 /800 that of PCP, it is
-------
Mr. id win L. John n On
J'ngc \
June 1. 1977
assumed that fl Iftnificant Ions by volat 11 Izot lou dors not occur. V."e would
expect hip.her chlorinated dlo*in« to degrade on the surface by UV light
rather than vaporize 'into the environment.
Our work with PCP treated wood pol03 han not reached the point today
that wc can prove conclun Ively that dioxins are formed from the PCP
on the surface of v/ood that in exposed to sunlight. V/c believe, however,
that such In the case. The work docs Indicate that there is a breakdowa
of dloxino that are originally present or which may be farmed oa the sur-
face of the wood.
Wipe teats conducted on three commercial PCP/Celion treated poles
which were in place for three years in California, show lower PCP and
OCDP concent rat ions on the a uon y south ilde of the pole than on the north
shaded aide. The PCP content on the south side of these poles averaged
0. 34 ug/sq, in. and on the north side averaged 2. 08 ug/sq. in. The
corresponding OCDD levels were 0,010 ug/sq, in. on the south side aad
0. 024 ug/sq. in. on the north side. The lower OCDD content on the south
side of the pole aa compared to the north side reflects the effect of UV
light on OCDD. W
-------
Mr, I >Kvlii L,, Juiihntin
June 1, 1977
Co Hon polos treated with the technical r .1 d r of PC P after 15 weeks*
exposure to the nun In Pennsylvania. Whrther Iheoe numbers reflect
results from bleediug, PCP loss or sunlight generation is unconfirmed
We feel that these results support the conclusions drawn from the
laboratory teats that (I) FC-7 grade PCP on a cellulose substrate
exposed to UV lipht photodegrstdes to OCDD, reaching the same OCDD
concentration level as technical grade PCP exposed under the same
conditions, and {Z) after reaching some critical level, the OCDD con-
centration decreases due to photodegradatIon-
It Is Important to note thnt we have not found any tetrachlorodibeaxo-p-
dloxln formed, due to phatolynis of PCP or OCDD, either in the
laboratory or field studies. Much of the work reported here are the
preliminary results in & continuing study.
We will keep you informed as new Information is generated. We will
appreciate the opportunity to visit with you to discuss the results of
our work In more detail.
Sincerely yours.
Robert D. Arsenault
RDA/ms
bcc; R, 1%. Sp.ilv.
1), T„
I). G, Tlall.ihan
119
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" '* • / - *r. t «,)UU«
mppms
July 20, 1977
Mr. Donald R. Islib
Chief Deputy 01 rector
Michigan Dept. of Agriculture
Louis Cass Bldg.
P. 0. Box 30017
Lansing, Michigan 40909
Subject: Effect of UV Light on
Pentachlorophenol (PCP)
Dear Mr. Isl1b:
At the Public Hearing on Proposed Regulation No. 637 on "ay 26, 1977, our
Mr. R. D. Arsenault mentioned that studies by Koppers Company had shown
that pentachlorophenol deposited on cellulosic.filter paper and exposed
to UV light was decomposed and one of the products of decomposition was
octachlorodibenzodioxin (0CD0) which in turn was also decomposed by the
UV light. At the continuation of the hearing on July 12, the validity of
the Koppers data was questioned on the basis that the artificial light
used by Koppers was substantially different from sunlight. The purpose
of this letter is to provide you with additional Information and comments
on these subjects.
Even though pentachlorophenol is toxic in its own right, much of the
discussion of risks before the hearing board has focused on the chloro-
diben2odioxins that are impurities in comnercial grades of pentachloro-
phenol. Octachlorodibenzodioxin (0C00) is the most prevalent chloro-
dibenzodioxin in commercial grades of pentachlorrphenol and i analysis
is subject to fewer uncertainties. Therefore, much of the following
discussion will focus on octachlorodibenzodioxin (0CD0). Tetrachlorodi-
benzodioxin (TCDD) was not detected as a degradation product of either
0CDD or pentachlorophenol. Hexa- and heptachlorodibenzodioxins were
detected, but not quantified.
Octa- and tetrachlorodibenzodioxins (OCDD and TC0D) deposited on filter
paper are readily degraded by UV light from both sunlight and artificial
light sources. Experimental data are summarized in the attached tables
I and II. These tables include long and short wavelength intensities of
the artificial light source and Pittsburgh sunlight and art shown to be
similar. The calculated velocity constants, assuming first order reactions,
are shown in Table III. The experimental procedure by which these data were
obtained is also attached.
120
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Mr. Donald K. !slib
July 20, 1977
2.
Pentachlorophenol (PCP) (both conmercial grade and Oow EC-7 gride) deposited
on filter paper is readily degraded by UV light. Experiments were confined
to artificial light, because this light source was considered to be a
reasonable facsimile of sunlight, 1t is uniform from hour to hour while
sunlight is not, and the degradation of pentachlorophenol by sunlight had
already been demonstrated by other Investigators.
The attached paper entitled "Weathering and Stabilization of Polyolefins" by
J. A. Melchore (I&EC Product Research & Development, Vol.1, Mo. 4 pp 232-235
(1962) describes the artificial light source used in our work. The wave-
lengths of light in sunlight and the artificial light are shown in Figure 1.
Both sources emit light at wavelengths below 350 mw which 1s the wavelength
below which pentachlorophenol (PCP) absorbes UV light. Pentachlorophenol
(PCP) absorbes UV light strongly at wavelengths below about 310 my.
Presumably, these are the wavelengths that provide the energy for the
observed degradation of PCP.
Experimental data for the UV degradation of pentachlorophenol (PCP)
obtained in recent weeks are summarized in Table IV and V, for conmercial
grade and EC-7 grade PCP, respectively. Starting at 7500 yg PCP, about
the same concentration on the filter paper that would be used for the
treatment of wood, more than 90S of the PCP had degraded in seven days.
In both cases, OCDD was produced as a degradation product at a peak value
of 23 uf OCOD regardless of the initial concentration of OCDO in the PCP.
The same data are shown in Tables VI and VII, In which the OCDO on the UV
exposed paper is expressed in parts per million (ppm) of the initial
quantity of PCP that was applied to the paper. On this basis, the OCDD
concentration reached 3050 ppm in both cases.
In assessing the risks of exposure of either humans or animals to treated
wood, chemicals on the surface of the wood should be the principal concern,
not the chemicals embedded in the internal structure of the wood, from
this point of view, the foregoing experiments on filter paper strongly
suggest that exposure of either humans or animals to either commercial
grade or EC-7 grade of Pentachlorophenol would not be significantly
different.
Yours truly,
P., S. Detrick, Manager
Environmental Health and Safety Section
KSD:mjt
Attachments
tec: f-r. y, ArsswiH
»'»*, D. I,.
121
-------
EFFECT OF UV LIGHT O.'i PLHTACMLOfiOPHCNCL (1W
am smcTgo crmcbM^wminr^
1. Experimental Procedure
Standards of GCDD and 1,2,3,4-TCDO were obtained from Analabs, and the
2,3,7,8-TCDO from D. Firestone of the FDA. All dicxins were used without
further purification. All stock solutions were prepared in reagent
grade benzene, and stored in aluminum foil covered bottles In the dark.
All work concerning the TCOD was done on the 1,2,3,4-TCDO Isomer unless
noted,
Dioxins to be irradiated by UV were applied in benzene solutions via a
2 cc pipet onto a 2-inch by 5-inch strip of Whatman No, 42 ashless filter
paper. The weight of a strip of filter paper was 0,72 gram, and the
concentrations of the OCDO were calculated to be in the same ratio as
they exist on a typical penta-treated pole.
The UV degradation rates of OCDO and TCOD in various sample systems
were determined in both sunlight and artiflcally produced UV light. The
description and operation of the artificial UV exposure system is
discussed by Melchore,3 The UV radiation was measured at the surface
of the samples by an U1tra-V1olet Products UV Meter at both short and
long wavelengths. The average Intensities for the unit were 1.02 milli-
watts/cm for the short wavelength (254 nm peak), and 0.63 mwatts/cm
for the long wavelength (365 nm peak) detector*
The dioxins were recovered from the filter paper by cutting the paper Into
small strips and placing them in a small bottle along with a 25 cc
aliquot of benzene. The samples were shaken on a wrist action shaker
for 30 minutes, and the benzene solution was analyzed by a gas chromato-
graphic technique.
Gas chromatographic analyses (GC) were carried out on a Hewlett-Packard
instrument (Model 5701A) using a V x 1/4" glass column packed with 10%
0V-1Q1 on 60/80-mesh Chrom Q, a si lane-treated diatomaceous earth support.
Programmed temperature gas chromatography was used for the analysis of
all samples containing OCDO. Samples containing only TCDD were analyzed
Isothermally at 25Q^C. The temperature program consisted of holding
at 250°C for 8 minutes, raising the temperature to 2C0°C at Scc/min.
and holding at that temperature for an additional 8 minutes. Under
these conditions the TC00 eluted at 4,4 minutes and the 0CD0 at 17.0
minutes. A Ni63 electron capture detector was used because of its
sensitivity to halocenated compounds. The carrier was a 90/10
mixture of argon/methane, and its flow rate was 40 cc per minute. Samples
were analyzed quantitatively for either TCOD or OCOD by using band area
measurements (the height x width at half-height method) and absolute
standards.
3, "Weathering and Stabilization of PolyolefinsMel chore, J.A.,
I&SX Product Research and Development. Vol. 1_ Mo. 4, pp 232-235,
December, 1962.
-------
2. Cloan-up Procedures
a. Monsanto Method No, 70-20
This method provided by Monsanto is designed to remove from the sample
phenolic compounds which might Interfere with the analysis of the
various chlarodioxirrs. In this method, the sample, which has been
dissolved in benzene, is extracted three times with 20-cc portions of
52 NIOH, and backwashed twice with 20-cc portions of distilled water
containing about 0.2 gram NaCl. This benzene solution is then passed
through clean cotton in the tip of the separatory funnel. This benzene
solution is either analyzed directly or further purified by the alumina
column described below.
b. Alumina "Mini" Columns
The "mini" columns were prepared from 5 nro I.D. glass tubing which was
drawn to a fine tip. A small plug of glass wool was inserted, and the
column filled with Alcoa F-20 alumina heated for 16 hours at 400QC. The
height of the alumina was approximately 200 nun. A 5-cc aliquot of the
sample solution was placed on the column. Since some of the sample
solution was absorbed on the column, additional benzene was added until
exactly 5 cc was eluted from the column.. This was done by placing the tip
of the column into a 5-cc volumetric flask and filling it to the mark as
the benzene solution eluted from the column.
3. Recovery of QCDO and TCOD front Filter Paper Strips
Standard solutions of OCDD and TCDO, were applied to the filter paper
strips and recovered as previously described. The recovery was determined
for various periods of time. These included: (a) immediately after the
benzene had evaporated, (b) after 18 hours in the dark, and (c) after
67 hours in the dark.. The results show that the recovery of OCOO was
at least 95% with or without oil; the recovery of TCDD averaged 9235
with or without oil.
4. Recovery of QCDD from Alumina "Hint" Columns
Since the alumina "mini" columns were used to clean up the wood extracts,
the recovery of the OCDO was determined to insure that no OCDD was being
adsorbed by the columns. A 5-cc aliquot of an OCDO standard, treated
as previously described, gave 100S recovery.
5. Degradation Rates of OCDO and TCDD by Artificial UV light
Standards of OCDD, 1,2,3,4-TCDD, and 2,3,7,8-TCPD were applied to filter
paper strips and exposed to artificial t»V liqht for varying periods of
time. The data which is shown in Table t can be summarized as follows:
a) the degradation of TCDD is faster than OCDD, b) the degradation of
OCDD is faster in systems containing oil (P-9 or Nujol) than in systems
not containina oil, c) the degradation of OCDD is faster in systems containing
Nujol than systems containing P-9 oil, and d) the degradation of 2,3,7,8-TCDD
is faster than that of 1,2.3,4-TCDO. The UV degradation of both OCDO
and TCDD on cellulose appears to occur at a faster rate than in solution.1
1. "Photo Decomposition of Chlorinated Dibenzo-p-Dioxins," Plimmer, J. R.,
and Wool son, E, A., Science, August 1971.
'123
-------
i.
6. De<;rari.>ticn Pa,Lvs o f 1 'i bD and ICfr b/ S'lM l f-.ihi:
Standards of OCQO, with an without: oil, and TCDO were applied to filter
paper strips and exposed to sunlight for varying periods of time. The
8-hour and 16-hour exposure tests were run rw«r a period of 2 to 3 days,
and were stored in a dark cupboard ovenii'jht. ihu UV intensity during
exposure was measured quite frequently because of the extreme variation that
was observed. The internity data was intc-yrated over the exposure time
to measure total exposure. The degradation date which can be seen in Table IV
showed the same trends observed for the samples exposed to artificial UV
light, except that the r.jtas in sunlight were slower than those observed in
the artificial light. The first order velocity constants were calculated
for all samples to further substantiate the observations noted above and
can be seen in Table III.
124
-------
Table 1
Degradation of UCDD ;md TCDD by Artificial UV Limits
Exposure Intensity
, Exposure (rnw.TCts/cin3)
Dloxin Oil (hra ¦) Lcng Wavplcnnth Short VJavelengch . Z Remaining
OCDD Nona 1 0.63 1.02 94
2 1.2*5 2.04 88
h 2.52 4.08 85
6 J. 78 6.12 77
16 tO.t 16.3 60
67 42.1 68.3 33
TCDD None 1 0.63 1.02 86
2 1.26 2.04 81
4 2.52 4.08 69
6 3.78 6.12 58
16 10.1 16.3 20
TCDD1/ None 4 2-52 4.08 - 38
8 5-04 ,8.16 28
16 10.1 16.3 6
OCDD Nujol 6 3.78. 6.12 2
1.6 10. t " 16.3 <0.5
P-9 6 7 42.1 68.3 8
1/ This TCDD is the-2,3,7,8 isomer.
125
-------
Tdhle II
Dcpr,nig lion of QftUQ atul ICDU |>y :'a;.'ital >uti I IjJiJC
Dioxin
OJ1
Exposure Intensity
Exposure (mwarts/cm")
(hrs .) Long Wavr length Shore Wave length
X Remaining
OCDD
None
5.5
8
16
2 .26
3.86
6,83
4.19
6.78
12.1
89
91
83
QCDD
F-9
j
8.8
16
2.26
3 .86
6.88
4.19
6.78
12.1
47
47
34
OCDD
Mu jo 1
3
16
2.26
.86
.88
.19
,78
12.1
48
42
18
TCDD
None
5.5
8.8
16
26
86
88
U
6 ,
12,
19
78
1
82
77
57
Table III
Velocity Constants for the Decomposition
of OCDD and TCDD
r
Dioxin UV Stmrcc Oil Velocity CrmgMnt, Urs."1
OCDD
Art i flrial
-
.002*
2 ,3,7,8-TCDD
Art if icial
-
.140*
OCDD
Art If icial
Ken i»
.039
1,2 ,3,4-TCDD
Art if icial ,
K?r.2
. 100
2,3,7,8-TCDD
Artificial
Knuc
.215
OCDD
Sunl if,lit
i.'.-n 2
.012
OCDD
Sun I ight
?-9
.081
OCDD
SunlIght
Nu j o I
.108
1,2,3,4-TCDD
Sunt iglit
Nona
.035
'These reaction velocity constants v*'ce cJtlcul.-.t-nl h/ t'u» Mathematics Greu?
from ilai.1 presented in the paper "Hioto D<.compos it ion j f Ch lor ina Cud
Dibenjo-p-Diox insFHutuor, J. R. .md U'.njlson, F,. A., which appeared in the
August 1971 issue o i Science- Rate studies we ce done in methanol so lut ions •
-------
T<]bli' IV t
Effect of UV light on
Commercial PBntachlorophenol (PCP)
on Filter Paper
(7.5 rag PCP)
. Exposure OCOO PCP
Time Found Remaining
Days n •
0 12 7500
1 23 2540
2 23 1800
3 19 1350
7 15 450
14 7.8 150
Table V
< -
Effect of UV Light on'
EC-7 Pentachlorophenol (PCP)
on Filter Paper
(7.5 mg PCP)
Exposure OCOD PCP
Time Found Remaining
Days uq ug
0 0,45 7500
1 23 2100
2 23 1420
3 21 1350
7 18 600
14 8,5 180
127
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Table VI
Effect of UV Light on
CoiTiTiefcial Pentachlorophenol (PCP)
on Filter Paper
QCDD Relative to Initial PCP
Exposure
Time
Days
0
1
2
3
7
14
QCOO as
ppm of starting
PCP
1600
3060
3060
2530
Z000
1040
Table VII
Effect of UV Light on
EC-7 Pentachlorophgnol (PCP)
on Filter Paper
QCDD Relative to Initial PCP
Exposure QCDD as
Time ppm of starting
Days PCP
0 60
1 3060
2 3060
3 2500
7 2400
14 1130
128
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March 24, 1978
TO: Environmental Health Advisory Committee
Science Advisory Board
U.S. EPA
Washington, D.C. 20460
FROM: 6. A, Van Gelder
Veterinary Toxicologist
College of Veterinary Medicine
University of Missouri
Columbia, Missouri 65201
Telephone 314-882-7011
RE: Draft Report on Pentachlorophenol
Introduction:
Ouring the past year I have served as a consultant to FDA, the
American Wood Preserver's Institute, Reichhold Chemical Company and
Vulcan Materials Company in matters relating to pentachlorophenol
and animal health. My reports have been made a matter of public
record.
THIS STATEMENT WAS PREPARED AT MY OWN INITIATIVE AND EXPENSE.
IT REPRESENTS MY PERSONAL OPINIONS IN THIS MATTER AND NOT NECESSARILY
THOSE OF ANY OTHER INDIVIDUAL Oft ORGANIZATION.
In the interest of your and my time this statement will be brief.
In summarizing complex issues there is a risk of being incomplete or
misunderstood. If any of the committee have questions please feel free
to call or write. A copy of a letter I wrote earlier is attached as an
appendix. This discusses in more detail some of the animal health
aspects.
Background:
1} I have visited most of the farms, Including those in Michigan,
in which pentachlorophenol related health problems were alleged.
2} I have conducted limited studies with pentachlorophenol and related
concentrated contaminants.
3) I have reviewed the available chronic rodent studies with penta-
chlorophenol including inhouse reports submitted as part of the
Michigan hearings.
'4) I set through and heard all testimony at all the Michigan Penta-
chlorophenol Hearings except for the one day Dow Hearing on the proposed
rule. '
5) I reviewed all material available under freedom of information
in the files of the Michigan Department of Agriculture related
to the alleged pentachlorophenol related herd health problems.
129
-------
Page 2
6) I have studied in detail the medical and diagnostic records related
to the herds in question.
Opinions and Conclusions:
1) The statement on page 111-2-4 which in part states . . dioxins in
tissues from a dairy herd in Michigan in which there were undiagnosed
health problems of chronic duration.", is not an accurate statement of
the facts in this case. Serious communication and decision making
process related problems existed within the diverse group of people
handling this herd. In fact, a number of diagnoses were made. The
problem was one of poor corrwunication. To the best of my knowledge
not a single person involved in that case had all of the information
in front of him. Investigator A was not aware of what investigator B
had found previously. The regulatory people acted without a
careful review and understanding of the situations on the several
farms. Politics played a larger role than science. The problems
existing on the Lemunyon farm based ori information in the Michigan
Department of Agriculture files Included;
a) fatty cow syndrome related 'to feeding of high energy ration
in excess of milk production.
b) a random culturing of cows showed a 50« incidence of infectious
mastitis, including bacteria that are more res is tent to usual
treatment.
c) infectious diseases in the calves of a type that are associated
with severe early calf losses.
d) a serious ventilation problem in the barn.
e) at times a lack of adequate bedding that contributed to the
mastitis problem.
A complete serious study of the multiple herd health findings in
the Lemunyon herd does not support the statement of "undiagnosed health
problems." Some of the problems went unmanaged, others received
partial attention.
The second part of the statement that needs amplification is . .
problems of chronic duration." The problems were persistent in that
mastitis, calf losses and cow losses continued over a two year period.
However, this does not mean that individual cows were sick for extended
periods. In fact, a careful review of the history shows that cows
became ill during the 21 day post-calving period, loss body condition and
in many cases died. This is generally recognized as part of the fatty
cow syndrome.
Continuing calf losses due to infectious diarrhea and respiratory
diseases in calves maintained in a totally unventilated, unheated calf
room are not unexpected.
It is my opinion that the allegation of undiagnosed health problems
should be deleted from the draft report. There is no need to perpetuate
this unfounded statement any further than has already been done.
130
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Page 3
The problems in the lemunyori herd do not provide acceptable
scientific data on which decisions related to potential adverse health
effects of pentachlorophenol can be based. In my opinion, the Lemunyon
herd represents a pentachlorophenol and dioxin chemical residue problem
and not a toxicologic problem.
2) As an example of the decision making process occurring at the time,
it is pointed out that one of the herds included in the pentachlorophenol
related quarantine had blood penta levels reported as 2 parts per billion.
This is consistent with the fact they were not being housed in a penta
treated facility.
3) Two toxicologists have estimated the daily penta exposure in the
Lemunyon cattle. One estimate was 0.12 mg/kg and my estimate was 0.3 mg/kg.
Both levels are less than the no significant effect levels in long term
rodent feeding studies with technical or purified pentachlorophenol.
* *
No one has shown by experimental studies or by calculations that
there is any reason to believe that the levels of exposure occurring in the
cattle could account for death or even Illness.
4) , In my opinion, the principle source of dioxin exposure for the Lemunyon
cattle was the sludge residue on the 2x6's used to construct the sides
of the feedbunk. I have been in numerous penta treated pole bams and
wood eating is something you just do not see with cattle. It did not
occur even in the herd that was not being fed an adequate diet.
The sludge was present as dry residue on the wood that could be
scrapped off with a knife. The residue was pretty much gone from both
sides of the feedbunk by February 1977.
5} The data in the table at the bottom of page III-2-4 means next to
nothing to a toxicologist. What the toxicologist wants to know is:
a) what were the levels?
b) what were the recoveries for-the method and,
c) what was the repeatability?
If the levels of HxCDD were 10-60 ppt then it should be so stated.
Few readers of this report are likely to have access to the actual data
unless it is included.
6) Page II1-2-5 refers to my work on this problem. The pertinent
findings were:
a) injections of extracts of the surface residue did not affect
the health of mice at doses estimated to be equivalent to the
cattle consuming all of the material in 1-2 days.
b) Extracts of the residue did not cause skin lesions when
injected subcutaneously in albino rabbits.
c) Guinea pigs fed finely ground wood obtained from the Lemunyon
barn were unaffected during the 64 day exposure to wood,
solvent, penta and whatever else was in the wood. Exposure
was at a level comparable to the cattle eating the barn in
180 days.
-------
Page 4
7) I am incompletes^ quoted cn page 111-2-5 where the statement
". . . Van Gelder concluded . , . that the PCP contaminants in the treated
wood were less toxic than PCP itself." Certainly, HxCDD is more toxic
than penta. But when one is exposed to technical penta, for each gram
of material there is much more penta present than HxCDD. My position
has been and continues to be that if-one eats technical pentachlorophenol
the level of penta exposure will kill you several times over before the
HxCDD exposure gets to a significant level.
8) Regulations and standards are needed relative to where treated wood
should and should not be used and also specifications should be
developed on the type of treatment and surface characteristics that are
acceptable for various end uses,
9) I am unconvinced that low non-phenolic pentachlorophenol solves any
significant actual real world problems. I follow the arguement on a
theoretical basis; but on a realistic basis the hazard to people and
animals is greater for pentachlorophenol than- for the contaminants when
considered from the viewpoint of relative exposures.
10) One must keep in mind that reported laboratory studies with technical
pentachlorophenol do,shed light on the relative toxicity of the contaminants.
Statements like "minimal focal hepatocellular degeneration" in rats
fed 30 mg/kg technical pentachlorophenol for 90 days is hardly alarming.
11) Considerations of chloroacne in industrial workers is a mixed bag.
Most of these people are also exposed to other chemicals, some including
TCDO. A process of producing low non-phenolic penta from technical
penta does not eliminate the Industrial exposure. Workers are still
needed to operate, clean and maintain the technical penta manufacturing
equipment. In addition, individuals involved in the distillation of
technical penta to produce the low non-phenolic product are also
potentially exposed. Arguements based on industrial considerations must
include full consideration of the entire process.
12) The overall hazard of accumulating concentrated penta related
contaminants in barrels, tanks or flasks for later off-line incineration
or other form of disposal needs to be weighed against the low magnitude
of problems generated by technical pentachlorophenol manufacture and
usage over the past 40 years. One judgement error in handling a barrel of
contaminants could have great environmental and/or health* impact.
132
-------
College of Veterinary Medicine
Veterinary Anatomy—Physiology
Veterinary Scierica
Columbia. Missouri o520t
Telephon# (314) 382-701J
Or. B. A. Schwets
Research Manager
Toxicology Research Laboratory
Health & Environmental Research
1603 Building '
Dow Chemical U.S.A.
Midland, Michigan 48640 *
Bear 3am:
Thank you for your letter of December 8. I certainly agree that
coraunications am needed in this entire natter. Unfortunately,
your latter catches re at a rather busy tine. Consequently I will not
be able to generate a detailed assessment of the Michigan PCP~01ox1n
situation with cross references to testimony and laboratory reports.
A complete description of my appraisal and analyses of the Michigan
dairy hard health situation would require a minimum of 5G pagas.
1} Statistical Analysis;
As i stated In our October 13 meeting, I quite agree that Dunnett 1s
an appropriate test for comparing treatment rseans against a ccirrcon control
group. (Gannett, J. An. Stat. Assoc. 3Q: 1035-1121, 1955). fly
point is that Dunnett should also be used on the data fron the first
study. See Steel and Torrie (1960) pages 10>-112 for a discussion
of the various multiple comparison tests and their relative sensitivity.
1 disagree that the Dunnetts t would have detected mora differences
than a blanket application of student t tests. If you rake 73 comparisons
at tii* 5* level, 4 of then by chance alone will appear significant.
Dunnetts 1s a mors conservative test. Dunnetts will discover rare "real"
d1fferencas in your data, that 1s differences due to treateent as
compared to differences due to treatment ana chance.
My concern 1s not that you would declare EC-7 similar to 95/5 on the
basis of your analyses, but rather that by using the multiple "t" tests
on "the Dow-7, 95/5 data you would ba led Into declaring differences
which nay be due to chance. Whether or not you or your laanasanent
makes those decisions 1s your business. I hardly think decisions costing
millions of dollars based on less than appropriate available statistical
procedures Is an academic matter. I do not know 1f the results would
change if you used Dunnett on the original data. You will have to run
the analysis to find out. Check m to saa If I am wrong, but if you use
the multiple t test on the EC-7, 83 day data, X believe you.would find
0 Q
UNIVERSITY OF MISSOURI-COLUMBIA
December 13, 1977
133
-------
Van Gelder
Page 2
December 13, 1977
that 1 mg/kg has a statistically significant effect cn absolute liver
weight. In other words, multiple t finds differences that Ounnetts
more conservative test which takes into consideration the number of
treat-nent levels keeps the investigator fron declaring significantly
different.
My other points regarding the 83 and 2 year studies not addressed
in your summary are Included hare. There ara 2 biological changes occurrino
in the Dow-7 groups that do not fit the overall response pattern. The
first 1s ths depression 1n RSC (and coupled PCY, Hb) at 30 no/kg.
This effect at the high dose (1/4 - 1/5 the acute LOeq) has been found
by others and not found by others. Since it is a relatively small change
and occurs at such a hiah dose it can be descrffaad as interesting but
not very exciting.
The otrier affect was the change in albumin levels with Dcw-7. My question
was v/Siy you did not fallow that up 1n the EC-7 studies? Since the
EC-7 studies do not include this measure one cannot say much about it.
The other responses fit a comon pattern although there are differences
1n dose-response. But my point is that before one can completely
compare the results one would like to see the d3ta analysed with a
uniformly applied netted.
Z) Com,r.iin1 cation:
It 1s my opinion that had MDA parsonnol been ccrtmunlcatinn with each
other and with ths MSU faculty a lot of the presant situation would have
been avoided. For example, 1t was very clear front my first visit to
Michigan In February, 1977, that the KDA-HSU people were r.ot comum'catini
1n a 2-way manner. One person would say the problem was XYZ and another
would later say 1t was ABC. Consequently, rey first report recommended
"I think all those Involved should reconsider the evidence upon which
they are r.aklng various decisions. !!y concern 1s that we not chasa
after something which nay turn out to be present but only as a
secondary or tertiary factor and not related to the cause of the
problem. Those parties involved are encouraged to go back and review
the information upon which they are making decisions to ensure that each
decision is being nade on cold, hard facts and not on isolated connents
or observations." My report also pointed out "there also stems to be a
number of different Ideas araoung the people who have been Involved 1n
the problems associated with this farm (lemunyon). I am not sure who
1s responsible to try and pull all these people together with all the
information that each one has and present some kind of debate or discussion
as to what the prablar.(s) really 1s(are). Further"as a start it would
$esm appropriate for someone to obtain or prepare a detailed history as
to when the death losses occurred, how long the cows were in the bam
before dying, when did deaths occur relative to calving and what
diagnostic services were actually conducted cn each of the animals that
died."
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Van Gelder
Page 3
December 13, 1977
3) Regarding the Herd Health Problems in Michigan:
You need to decide whether you are going to be 1n or out on this ratter.
In the past, Dow has maintained the posture of "non-lnvolve-nent". If
now you want to get Involved then please do your homework. Read all the
transcripts, study the laboratory reports, go to the farms, look at
the cattle, look at the management, get a herd history, look at the
entire picture. .
Furthermore, separate out the conditions on the various farms, each one
was different in one aspect or another. I did not Intend to leave
the Impression that the only problem on the lemunyon farm was Fat Cow
disease. He had other problems as well. Certainly all of these
disease problem can Interact. The diagnosis of fatty cm* was not nine,
it was made by Or. Coy 1n a letter to Le*tinyon on August 24, 1976,
and by Phase III team In i report on October 27, 1976, and by Or. Davis
1n a visit to the farm 1n Hay 1975, at which tine he necropsies a cow
that had just died. The other piece of Information to consider is the
herd history. The problem as defined by HDA occurred during the early
post partus period which 1s a VI part of the fatty cow syndrcrce. Your"
summary table on body weight changes 1s confused because ycu did not
separate acute from chronic effects 1n the fatty cow syndrome. Reread
the paper by Morrow, p. 1626 - "'.Tien recovery from the fat ccv syndrome
does occur there is frequently a delay In the onset of post nartusi
estrus and conception due to retained fetal rerr.branes and metritis,
and a narked loss In weight 1n severe!y affected cows".
By way of explanation one needs to soft sore things out 1n this conplex
situation. First, one rarely finds only one problem present in a herd
health situation with dairy cattle. One often finds a number of
problems Including mastitis, metritis, some foot/joint problems
especially with cattle on concrete 24 hours/day and compounded by deficient
bedding, sor.e calf problems and some nutritional problems. If I left
the impression that the only problem was fatty cow than I was too brief
in my comments since my findings' in this matter from the very beginning
have identified a nusiber of problems.
One must also sort out the clinical workups and necropsies done on
animals submitted live versus those done on animals dying on the farm.
The diagnosis of fatty cow was based on animals necropsled at the
farm. The clinical workup reported by Dr. Ellis et a] was on chronically
111, live cows submitted to the University
I also seriously question the purported observation of "general
debilitation" in the Michigan dairy cattle. I observed the cattle
on the lemunyon farm as well as four other involved farms. Even in
Lemunyon's case one could not say there was a general debilitation. The
herd I saw In February was 1n average condition. There were sone thin
135
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Van Gelder
Page 4
December 13, 1977
cows as well as some very fat cows. They were bright, alert, active.
Tha alleged chloracne simply was not present. The few skin lesions I
observed on the dorsal neck were typical of skin rubbing lesions seen
in cattle that have an opportunity to rub the top board on the manger.
In tiis casa of Lemunyon, this was a 2x6 with tongue down. The tongue
was worn smooth. To conclude that chloracna was present without
substanting histopathology 1s unwarranted 1n my opinion. Consequently,
since I have personally observed the cattle, looking specifically for
significant skin lesions and not finding them I must conclude that they
did not exist. I do not know who actually trade such a diagnosis. The
discussions I attended alluded to open abscesses or bleeding skin ulcers
on the legs. .Again, I did not see these when I examined the cattle.
What I did see were some hemotcmas on the legs which often result fron
cattle getting banged around against free stalls and other comers
or protrusions. On occasion these become infected, abscess and ulcsrata.
You .?.1ght be interested 1n noting that sctr.e Michigan farmers were
blaming tha her.:oto*as on PSB's as they stood and talked to you while
leaning an a sharp ended pipe jutting out 1n the main alley way!
The herd in the worst shape was the Dale H1ce herd 1n which he had
been quarantined for unsanitary conditions because of a dejp accusation
Of manure and several dead cows being found in the barn by the milk
Inspector. Hardly a usual situation. He was quite frankly, by his own
admission, not providing adequate care for tha cows. Consequently,
he lost his r:11 k market, then ran out of feed, was broke and
could r.ot buy feed, and nis cattle, as per the Michigan Veterinary
Diagnostic Laboratory report of February 22, 1977, suffer-sd frcr.
malnutrition secondary to poor quality feed; suppurative mastitis.
I saw the Hies herd in Karen, they "were uniformly thin, but alert and
active. They ware receiving a tninl'ial amount of hay as their total diet.
Anyone wanting mora Information on the management and operation of this
farm can obtain access to other resorts 1n f'DA files under the Michigan
sunshi.ie lav/. I have read them and as a result concur with the opinion
of Dr. Davis, MDA that the problems on the Hice farm were caused by factors
other than PC? or dioxins. If cattle are being fed a grossly inadequate diet
one does not need to look under rocks to determine the cause for loss
of body flesh.
The diagnoses of mastitis and calf viruses were made by HDA or HSU
veterinarians. The remarkable conclusion 1s that the mastitis was
claimed to be caused by bacteria which were allegedly cleared up by
antibiotics but cell counts persisted. This conclusion was reached
In the Hcht of 1) there is nothing concrete in the record that any cows
were cultered after treatment to see 1f 1n fact the infection was
eliminated.' This in the light of a 50% Infection rate that included not
only strep, but also staph. A background staph problem 1s mora difficult
to eliminate than the strep and furthermore, a background staph problem
may beccce more severe when the strep infection is cleared up.
136
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Van C-elder
Page 5
December 13» 1977
A great deal was being made about 1 prune suppression based on this
mastitis situation. One must seriously question such an Implication
based on the above workup. The other factors not accounted for In the
workup as testified to Included lack of evidence that milking equipment
was, in fact, chicked to make sure 1t was In proper working condition,
the stage of lactation was not considered in the evaluation of cell counts
and other stress factors such as bedding were either Ignored or not
considered.
Other information cn the Lemunyon herd v?as obtained which shewed that cow
death losses were occurring primarily in the period of 21 days post partuw.
This fits the fatty ccw syndrome. This coupled with the feeding pattern
and radical changes in diet, to advice given Mr. Lemunyon to feed dry
cows separately from 1actating cows plus the HQA diagnosis of fatty cow
syndrcrce cannot be ignored.
If one reads the paper of itorrow one finds that narked loss of weight
is seen in severely affected cattle. What one needs to differentiate is
pre-partum condition frost post partum condition. Consequently, the
initial recommendation to HQA was to pet a good herd history. This
was never done by f'DA to the bast of my knowledge. Others have
done nore in this area.
A similar restraint 1s warranted 1n the Interpretation of clinical
pathology data. Are the samples from acutely 111 cows? Chronic cows?
Cows with systemic infections? These are Important Factors because
fatty ccw syndronie is not a simple pathologic condition.
Regarding your coranent about white blood cell counts the following Is
offered. Cows have W3C counts ranging from 7-10,000 with agsd dairy
cows having counts as lew as 5,000. Cattle normally have (approxlnata)
25-3CS neutrophils, 50-65^ lymphocytes, 53 monocytes and 2-3'"' eosinophils.
If you look at the blood, picture for the 13 Lewunyon cows obtained by MSU
1n March, 1977 you will find two cows with elevated WSC counts both of
which have greatly increased neutrophil counts- which Indicates an
active Infectious process. The renalnino cows have WSC counts
within published normal ranges. Furthermore, If one looks closely at
the chlorodioxin itwune suppression data one gats a picture of Isrrone
suppression coupled with a decrease 1n absolute lymphocyte counts. If
you carefully analyze the-Lewunyon blood data you will find that absolute
lymphocyte counts are within normal ranges with the exception of the
two cows with a. left shift Indicating an active Infection.
The above ccrroents hold for the blood picture on the other farms as 1
remember then. It has bsen some tine since I carefully studied those.
• Consequently, I do not know what data your siumary table is referring to
when it makes the sumraary statement of "WBC count Barked!y Increased".
13'7
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Van Gelder
Page 6
December 13, 1977
Dr. Coy mentioned an eosinophelia in six cows. I would guess you ware
as surprised as I was when he did not follow that up with a diagnostic
check for internal parasites. You may recall the response frcrn Dr. Wise
the hearing officer.
As an asiou we also found a marked eosinophelia In the Htce cattle we
necropsled. The Intestinal parasitic lesions fit the usual pattern.
1 would suggest a bottom line along this avenue. Both Dew toxicologlsts
and myself have estimated the POP dose for lemunyon's cows to be 0.12-0.3
mg/kg per day. Your group analyzed the lumber and as I Interpret the
results the dioxin levels found Indicate a typical technical PCP. Based
on all your studies on PCP and on all the literature do you really
think there 1s any purceptlble risk to the health of a cow with 10 ppt
HxCOO or 1.4 ppb HxCQD 1n liver 1n light of the published work on
larger TCQi) liver residues in rats at levels claimed to be no effect?
I appreciate the fact one can always say "We do not know because we
have not tested it", but as a toxicologist one often uses his total data
base in making interpretations subject to experimental verification.
I feel rruch rare confidant about accepting the HDA diagnosis of fatty
cow, mastitis and viral infections and questioning the totally unsubstantiated
diagnosis of chloracne than I would be by accepting the cnloracne diagnoses
and rejecting the other diagnoses ruce by HDA. At least I know HDA
veterinarians have seen the other conditions on numerous occasions.
I aouLt if they ever saw ciiloracne or ever heard of it before. Add staph
to your list of causes of infectious mastitis. It 1s an important
consideration in view of the way the situation was handled.
Also, differentiate between the acute phase of fatty cov; and the chronic
sequalea. Cows may take one entire lactation to recover. If appropriate
management changes are net made then the syndrone can be r.ore severs
In the second and third lactations.
Dr. Davis's primary reservation with the fatty cow diagnosis as the prlrary
factor was because ha had not seen such large death losses previously. Yet MS'J
has published on such a high mortality. More racent studies out of
Tennessee support the finding of high morbidity and high mortality with
this disease.
T am a little bit confused by your reference to the gross and histcpath data
on the various PCP studies as being the primary concern. In the production
grade study of November 1971, on page 10 of the report it 1s stated
"Gross examination it necropsy revealed no compound related chancres.
Mlninal focal hepatocellular degeneration and necrosis were observed upon
microscopic examination of 11 vers from rats contained on diets containing
the top dosage level of sample S822A; these changes were not observed
1n rats maintained on a diet containing 95/5 which provided a similar dosage
of PCP." In view of the apparent minimal nature of the changes at a
dally dose equivalent to 1/4 - 1/5 the acute LDrq one can also cor.e to the
conclusion that there 1s not much of a hazard associated with low level
(fractions of rag's) exposure to technical PCP.
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Van Gelder
Page 7
Decernber 13, 1977
I quite agree with the findings of Dr. Wise that sensible use restrictions
and use guidelines will do more to reduce the hazard associated with PCP.
Alone that line has Dow ccroe up with a recommendation on the use of EC-7
to treat feed bunks?
I quite agree with your statement "also because the dioxin content of PCP
could be reduced, v/e have consistently recoroended that the nonphenolic
content of PCP be reduced, etc.". If I was a corporate manager and had
just Invested a million dollars In a thermal oxidizer(incinerator} and
saw an opportunity to get dual use by cleaning up 2,4,5-T and PCP
at the semi time, I would do 1,t also. It 1s a neat marketing manuver.
Unfortunately, the toxicologic picture is less clear because of the
difference in opinion on the actual hazard associated with technical
penta. Is Dow aware of any problems encountered in livestock related
to the non-phenolic content in Dowic1de-7? Or did that product have a
clean use record for 30 years except for the obvious occasional misuse?
*
Sincerely yours.
Gary A, Van Gelder, D.V.M., Ph.D.
Professor and Chairman
GAVG:nc
cc: Dennis Lindsay
139
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5.2.5
REICHHOLD CHEMICALS, INC
Creative. Chtimi-sbry . . .Ijait-r jlarbnc.r in !P.roqrx±ss
O&i• t C I BU11DING, WMI1I PIAINS, M. T 10 to 1
April 18, 1978
Dr. Sheldon D. Murphy
Professor of Toxicology
Department of Pharmacology
University of Texas Medical School at Houston
P.O. Box 20708
Houston, Texas 77025
Dear Dr. Murphy;
SCIENCE ADVISORY BOARD '
ENVIRONMENTAL HEALTH ADVISORY COMMITTEE
Ad Hoc Study Group on Pentachlorophenol Contaminants
""Ibraft Report — Public Hearing April 3, 197S
The purpose of this communication is to amplify. Reichhol
-------
Dr. SheJdon D. Murphy
April IS, 1978
Page 2
2. Incineration. It has been suggested in the report that technology to
dispose of these waste streams exists — presumably this means by
incineration. Construction of a suitable incinerator designed to handle
this highly toxic chlorinated maierial, as the principal material to be
incinerated, is a very expensive and difficult proposition. Experts advise
us that these highly chlorinated refractory materials require temperatures
in the order of 1200°C to assure complete conversion to HC1, CO- and
H_Q. Because of the presence of HC1 and other corrosive by-proaucts,
the materials of construction are critical and expensive. Operating costs
to achieve and hold the necessary temperatures are high.
To the best of our knowledge, there is no licensed incinerator in operation
that will- accept these materials for incineration. Therefore, we must
conclude that the technology is not available to satisfactorily dispose of
these waste streams with the confidence that the chlorinated materials
will be completely destroyed. We are aware of work performed by various
departments of government which have addressed this problem. Reichhold
strongly suggests that before the assumption is made that technology is
available to safely dispose of the hazardous waste streams created by
removing and concentrating the contaminants in PCP, that the Technology
Assessment Pollution Control Advisory Committee of the Science Advi-
sory Board be requested to review this entire question. The secretary of
this Committee is Lloyd Taylor.
We have applied substantial resources to the investigation of the chlorination of
phenol without the formation of chlorodioxins and have, as a result of this
study, substantially reduced the ehiorodioxin and dibenzofuran content. This
reduction yields a technical grade PCP with a total dioxin content in the range
of 1200 ppm.
The ideal solution would be to produce pentachlorophenol without co-producing
any toxic contaminants. The technology to do this is not known. We believe
that the years of experience with technical grade pentachlorophenol has
indicated that it is far better to widely distribute a less than no effect
concentration of the contaminants than to have them separated and exist in one
highly concentrated stream at several widely dispersed manufacturing sites.
These highly concentrated streams would be subject to possible catastrophic
error in handling which would result in a major hazard to the immediate
surroundings. The handling and disposing of these highly toxic waste materials
is subject to all of the hazards of transportation — broken pipelines, leaking
drums, derailed rail cars, etc.
If they are ultimately conveyed safely to an incinerator, then the safe operation
of the incinerator is of paramount importance. The incinerator must be
constantly monitored or the contaminants will merely be made airborne and
dispersed over a substantial area in more than toxic effect concentrations. An
improperly operated incinerator could contaminate large areas of land and
create an incident of the magnitude comparable to1 that which occurred at
141
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Dr. Sheldon D. Murphy
April 18, 1978
Page 3
Seveso, Italy. We feel that the question of safe disposal of the highly
contaminated waste streams created by removing the impurities from technical
grade PCP must be thoroughly addressed by experts before industry is forced to
create a dangerous waste for which there is currently no acceptable means of
disposal.
We would appreciate your communicating this addendum of our testimony to the
Committee members for consideration.
Again, thank you for the opportunity to appear before your Committee. We
deeply appreciate the many hours of concentrated effort that the members
applied in bringing the facts to light regarding pentachlorophenol.
Very truly yours,
REICHHOLD CHEMICALS, INC
F. J. Shelton
Vice President
Science <5c Technology Worldwide
FJS;cm
142
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TESTIMONY ON PENTACHLOROPHENOL TO THE
SCIENCE ADVISORY BOARD ENVIRONMENTAL HEALTH
ADVISORY COMMITTEE
April 3, 197S
My name is Frederic 3. Sheiton. I am Vice President, Science &
Technology Worldwide, for. Reichhoid Chemicals, toe. Reichhold is one of the three
major manufacturers of pentachlorophertol in the United States, and as such has a
direct interest in all phases of regulatory activity concerning PC P. Other
manufacturers include Vulcan Materials Company and Dow Chemical Company.
Reichhold is appearing here today in response to a letter dated March m, 1978,
advising of a two-day meeting of the Environmental Health Advisory Committee of the
Science Advisory Board. Since the principal purpose oL this meeting was to consider
and discuss the draft report of the committee's study group on pentachlorophenol
contaminants, Reichhold requested time during the meeting of the Environmental
Health Advisory, Committee to present comments on the draft report. Reichhold
thanks the Environmental Health Advisory Committee for this opportunity.
As background, Reichhold has manufactured commercial grade penta-
chiorophenol (PCP) since 1955, and since the beginning of production has been deeply
concerned about the health and safety aspects of PCP, both in regard to the general
public, to the environment, and to its employees. PCP, and the contaminants which
are present as the result of manufacture, have been a subject of study at Reichhold
since manufacturing was commenced. Through the years, Reichhold has sponsored and
participated in several scientific investigations into the chemical makeup of
commercial grade PCP and has conducted a number of toxicological studies designed
143
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to assess the safety o! commercial grade PCP, As a result of the work which
Reichhold has conducted, the company is not aware of any studies or reports which
support the premise that commercial grade PCP containing trace quantities of
contaminants, including chlorodibenzo-p-dioxins (CDD's) and chlorodibenzofurans
(CDFs), present any significant hazard to man and the environment when properly
used. The results of these studies and investigations have been presented to the
Federal EPA as well as to various state regulatory bodies.
Reichhold conducts physical examinations on each of its production
employees oh an annual basis, and more often if the man requests. No unusual physical
conditions have ever been reported for these men. Reichhold field personnel have had
more than twenty years of contact with its PCP users and are unaware of any human
or animal health problems attributable to properly used PCP. PCP finds commercai
use in the wood treating and preservation industries because of its toxic properties. It
must be handled and treated with respect because of its innate toxicity. The handling
and treatment afforded PCP and PCP containing products, because of the toxicity of
PCP itself, is sufficient to protect the users, and others who come into contact with
PCP treated wood, from any hazards due to the chlorodioxins contained in the product.
In the early 1950's, PCP was used and recommended for a broad spectrum
of pesticide uses. In most of these uses, PCP was applied from a solution prepared by
dissolving the PCP in a petroleum distillate. If a water solution was required, the
alkali salt of PCP was prepared by reacting the PCP with aqueous sodium or potassium
hydroxide. Early uses of PCP included ail phases of wood preservation and protection,
both against microorganisms and insect attack. The preservation of water based paints
and adhesives, and the preservations of textiles and cordage, as well as weed control,
were also significant uses of PCP. In addition, PCP was used in red mite control in
144
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poultry houses. Reichhold felt that many of these historical uses of PCP presented the
possibility of excess user exposure to the irritational and toxicological properties of
PCP itself. Although Reichhold has had a large number of registrations covering a
wide variety of PCP uses, it currently maintains a registration for the use of PCP for
manufacturing purposes (wood preservation) only. Reichhold"s PCP is sold to
commercial wood treaters and is used in the industrial treatment of wood by a variety
%
of processes. We believe that commercial grade PCP, as manufactured by Reichhold
and others, does not pose undue hazard to man, livestock and the environment, when
properly used.
We would like to now comment specifically on several portions of the
draft report of the Ad" Hoc Study Group on pentachlorophenol contaminants, dated
March 197S. On page 1-8, under Item 3, Conclusions« paragraph 1, Reichhold confirms
that it has not detected any TCOD (2,3,7,S-tetrachJoro
-------
that these changes would have on the workers involved.
A number of alternative methods for producing various grades of PCP
have been proposed. Some of these processes present the possibility of increased
worker exposure to PCP and/or PCP contaminants because of the characteristics of
the final PCP produced. Reichhold has examined its process for the production of
PCP, as well as the handling characteristics of its finished product, and feels that
presently it cannot suggest a reasonable alternate to its PCP product. Reichhold urges
that before any action is taken, that all aspects of the production and utilization of
any new PCP product be thoroughly examined. We feel that particular emphasis should
be placed upon the physical characteristics of the final PCP product, as well as the
creation and disposal of any waste or by-products caused by its production.
On page I'10, paragraph 9, Reichhold certainly agrees that certain uses of
PCP be objectively examined and that regulation be considered to reduce those
applications of PCP treated wood which may come in contact with humans or animals,
or food products. However, as we have repeatedly stated, we believe that there is an
absolute need for PCP treated wood for use in and around farm buildings and
structures where degradation by microbial attack from soil:, and other materials is
critical.
Paragraph 10, on the same page, states that certain technology has been
disclosed which is designed to reduce the levels of CDD's and CDF's in PCP through
distillation of technical PCP. However, we do not totally agree with the statement,
"It would seem prudent to control the contaminants to the extent possible by best
manufacturing practice." We would like to emphasize that consideration must be given
to the question of trade-off of occupational hazards. Reichhold feels that there are
significant 'occupational hazards associated with the use and handling of the PCP
146
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products which it has seen on the market which are claimed to have reduced levels of
CDD*s and CDF's. Reichhold, furthermore, is very concerned about the concentration
of COD'S and COPs in waste streams generated by the distillation process used for the
cleanup of the technical PC P. The economic impact evaluation would have to take
into consideration the distillation process and cleanup of PCP as well as the
incineration of the waste stream generated. It would also have to take Into account
the automation of the process which would then minimize exposure to the waste
stream. The commercial process used by Reichhold to produce PCP does not produce a
concentrated waste stream containing CDD's and CDPs. We urge the Science
Advisory Board Environmental Health Advisory Committee to very seriously consider
this possible route of exposure to concentrated CDD's and COPs streams produced in a
PCP distillation process when considering possible hazard trade-offs.
Continuing, on page 11-3, a chart is given exemplifying the composition of
a purified grade of PCP, labeled Dowcide EC-7. It is noted that only certain
chlorinated CDD's are listed, namely the octachloro, the heptachloro and hexachloro
dibenzo-par a-dioxins. However, on referring to Section V-3, page 52, Appendix No.
it is indicated that the possible number of CDD's are listed as being 75 in number. The
hexa, hepta and octa CDD's would account for approximately 13 of the possible 75.
This would appear to leave 61 additional CDD's which could be present since it has
been established that no 2,3,7,8-tetrachlorodibenzo-para-dioxin has been detected in
any domestic grade of PCP commercially available today. Since the purpose of this Ad
Hoc Study Group is to examine and report on all of the CDD contaminants in PCP, we
feel that comment is needed relative to the presence or absence of one or more of
these other possible CDD's. We feel that the study should be thorough and complete
before any regulatory action is taken. It would be extremely disruptive to the industry
147
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if considerable sums of money and technical development were expended to reduce
p
certain CDD's only to learn at some later date that certain remaining CDD's were
present at levels which were then determined to be environmentally undesirable. It is
Reichhold's position that prior to any regulatory action mandating a reduction in
chlorodioxins, that consideration should be given to all of the chlorodioxins which
might be present.
*•
On page II!—1, the report states that octochlorodibenzo-para-dioxin, or
OCDD, has shown little toxicity. Reichhold would like to point out that the
commercial technical grade of PCP which it manufactures, as well as material
manufactured by other companies, contains as the major CDD contaminant, OCDD,
Typically, the amount of OCDD present is on the order of five to seven times greater
than the amount of hepta and hexa CDD's.
On page III-3, one reference was cited which detailed an experiment pro-
ducing chloracne in rabbit ears. This test indicated that commercial samples of PCP
have produced chloracne in the rabbit ear bioassay tests wherein purified PCP did not
produce chloracne. Reichhold conducted similar tests at IBR-US Laboratories, in
Miamisvilie, Ohio. The results of these tests indicated that no significant differences
could be discerned in the results obtained using either commercial, analytical or
purified commercial grades of PCP. The results obtained from one material were
comparable to results obtained with another. This information was submitted to the
Science Advisory Board Ad Hoc Group, and the results of this tests have not been
included in this report.
On page III-9, paragraph k, reference is made to work done by Kimbrough
in 1972. Reichhold has reviewed all referenced articles authored by Renate
Kimbrough, dated 1972 and has not seen any report implicating technical grade PCP in
148
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causing teratogenic effects in women. We suggest that this reference be verified.
On page 111-12, Conclusion ft, Reichhold agrees that all commercial grades,
technical and purified, of PCP contain quantifiable amounts of CDD's; however, we are
not convinced, nor are we aware of any studies which conclusively demonstrate that
the concentrations of CDD's present in technical PCP are sufficient to»ha biologically
ac*t¥e. While it cjught be proven academically that by isolating certain chlorodioxins
and conducting laboratory biological- studies with them, effects might he noted,
Reichhold feels that these results are not applicable to the real world situation
wherein man or animals do not come in contact with sufficient quantities of these
mPmbm tS '
materials to produce harm. Reichhold?do 03 net fael that tho total .picturo-m»ffllvlng
possible harm to^an or tha enxiranmont fram-tha-propw usa of technical gfade PCP
pr-ga""m ¦¦¦ ¦¦ ¦ • I that regulatory action totally banning
PCP, or requiring PCP to have certain levels of CDD's is not indicated.
On page III-2-4, reference is made to a study done at the National Insti-
tute of Environmental Health Sciences which consisted of analyzing tissues taken from
a dairy herd in Michigan for CDD's. The impression given by the information provided
on page lII-2-ft, would lead one to conclude that significant quantities of CDD's were ~
discovered in the animal tissues and that they could be linked to the undiagnosed
health problem in this dairy herd in Michigan. We would like to point out that the level
of CDD's reported in these tissues ranged as follows?
HexaCDD .01 ppb to 1.3 ppb
HeptaCDD . .03 ppb to 12 ppb
Octa CDD .23 ppb to ppb
Investigation by a team of highly qualified toxicologists, dairy herd
specialists, and wood treatment specialists, of the entire Michigan dairy herd incident
149
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allegedly connected with PCP exposure, has resulted in a number of papers being
published which define and describe the herd health problems in these Michigan dairy
herds. As a result of this work, it was concluded that these dairy herd problems were
not related to exposure to PCP or CDD contaminants. All of these data and reports
have been previously submitted to the National Institute of Environmental Health
Sciences, Environmental Protection Agency, as well as to the Food and Drug
Administration, and to the Ad Hoc Study Group on pentachlorophenol contaminants.
In addition, the Michigan Department of Agriculture conducted a
hearing on the application of Reichhold for reinstatement of its state PCP registration
which was summarily suspended during the dairy herd incident. Dr. Gilbert H. Wise,
DVM, the hearing officer appointed by the Department concluded, after the week-long
hearing, that the cancelled registrations should be reinstated. Dr. Wise, in an 18-page
decision, found in part as follows:
"No evidence was developed showing that wood preser-
vative formulations containing penta have presented demon-
strable risk to the food chain through exposure of food
animals to CDD (chlorodioxins) in penta.
"The evidence, while not removing ail possibility of
hazard, does not support a finding of any measurable
magnitude of risk or liklihood of harm to the human food
chain from exposure of food animals to CDD in technical
penta."
On page IV-5, a hypothesis has been put forth which suggests that chlorin-
ated dioxoins, chlorinated dibenzofurans, polychlorinated biphenyis, polybrominated
biphenyls, and chlorinated azoxy benzenes should be considered as a class from the
ISO
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toxicoiogical standpoint. Reichhold disagrees with this premise because it has been
repeatiy demonstrated that specific members of a class of compounds may have vastly
different biological activities. One needs only to review the work done in the drug
industry to realize that it is dependent upon these variations in activity, relative to
structure, to produce drugs which minimize pain and suffering. We think it would be
extremely risky and unsupportable to regulate various individual readily identifiable
¦»
chemical compounds as a class rather than as individuals. .
There are numerous reports that PCP has been found in many parts of the
environment, including in man and animals. It has generally been assumed that this
PCP has been coming from the wide-spread commercial use of PCP as a wood
preservative or pesticide. !t should be noted that it has been reported that PCP may
*
be formed as a metabolite from animals and microorganisms. Furthermore, it is re-
ported that PCP may be formed in the environment from other chemicals such as
hexachlorobenzene and LINDANE and from the chiorination of drinking water.
The source' of CDD's in the environment is not exclusively from PCP.
Other chemicals such as hexachlorophehe and polychlorinated biphenyls also contribute
COO's. Other widely used pesticides such as 2,4,3-T are recognized as containing
CDD's.
PCP has a number of registered uses for which there are reasonable
alternatives. Reichhold would urge consideration of these registered uses of PCP and
that an effort be made to determine where proven alternative materials are available.
Perhaps this concern over a wide-spread use of PCP can be more easily regulated by
restricting the registered uses of PCP to those for which there is no reasonable
alternative, such as for wood preservation.
On the whole, Reichhold applauds the work which has gone into the pre-
151
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paration of this draft report. We feel that much effort has been made to factually
evaluate and report on the data and literature which is available! however, we would
appreciate consideration of the points which we have raised today.
Again, thank you for this opportunity to appear here today.
152
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.2.6 Testimony of Dr. Robert I. Johnson
•The Dow Chemical*"Company' s "position with respect to the non-
phenolic impurities in PC? has been and continues to be:
1. that pentachlorophenol containing such impurities above
certain levels manifests'enhanced toxicolegical responses
as demonstrated by laboratory test animal -experiments.
2. that these non-phenolic impurities should be minimized by
the manufacture and use of a PCP containing the least
amount of these impurities technically possible.
3. that it would not be possible to assess adequately the hazard
of the many individual non-phenolic: impurities in PC?.
. Therefore, it was logical and prudent to reduce these impuri-
ties to the lowest possible level for commercial PC? and,
thereby minimize the risk to the producer, the users, and
the environment.
4. that readily identified adaptable technology is available
to separate the non-phenolic impurities from PC? and that
disposal of such impurities can be dealt with at the pro-
ducing site where acknowledged risk can be minimized.
5. that a pentachlorophenol can be manufactured in commercial
quantities that mimics chemically pure PCP in both acute
and subchronic toxicological studies. With the urging of
the EPA and at reasonable expense to Dow, such a commercial
- facility has been constructed and is being operated.
The ad hoc committee draft report represents a significant and
worthwhile- effort to compile all the available information per-
tinent to the presence' of non-phenolic impurities "in technical
- PC?. The report is thorough in pointing out that:
153
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1. Suitable analytical methods for the specific dioxin and
furan isomers present in technical PCP are lacking.
2. There are very little data on the environmental persistence
and transport of the dioxin and furan contaminants of PCP.
3. The comparative chronic toxicological information on purified
versus standard commercial PCP is limited. (Sab-chronic
studies have revealed toxicological differences between
these two grades cf PC?, especially la the liver.)
4. There are virtually no data on the chronic toxicity of the
non-phenolic contaminants of PCP.
5. The biological significance of the finding of low, but
detectable, levels of chlorinated diaxins in tissues of
farm animals is not presently known.
6. There is insufficient information on occupational exposure
of man to these PCP contaminants by manufacturers or users
to allow quantitative assessment of the relative hazard of
f
purified PCP versus conaaercial products containing dioxin
contaminants.
These information deficiencies are used in the draft report to
explain why an ultimatum to the wood treating industry to manu-
facture and use cnly purified grades of pentachlorophenol cannot
be issued.
154
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On'the other hand, the draft report, without exception, describes
the constant concern associated with the.presence of the non-
phenolic impurities in PC?, For example:
1. The toxicity of the polychlorinated dibenzodioxins and
. dibenzofurans is recognized,
2. The recent reports of induction of neoplasms by TCDD raise •
the specter that the polychlorinated dibenzodicxin contami-
nants in PC? may also have this potential,
3. The finding of low- but detectable levels of chlorinated
dicxins in tissues of farm animals is a matter of public
health concern.
4. Reports of occupational exposure to chlorinated dibenzo-
dicxins, which resulted in adverse health effects in aan,
were mentioned.
All these references and comments clearly indicate the relevency
of conclusion, No. 10, which reads in part,
"Tzchnology JU now availubZz which covutd maA.ki.dly
Kzdu.cz tht IzvzZi o£ dJ.bin.zodiox.-Ln and dibznzo&ufi.an
contaminant* [In PC?! . It Mould 6 zzm pnudznt,
thz\z^0A.z, to contJioZ the, contaminant* to the. zxtznt
poi&iblz by bz4t manufacturing pxactict".
155
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The PCP producers were initially urged by federal regulatory
agencies to reduce the non-phenolic impurities content in 1971,
and again advised to proceed in that direction ir. 1973. It is
now 1973,* specific timing as to when all commercial ?c? should
be of a purified grade, or the specific reasons as to why a
purified PC? grade is no longer necessary, is urgently needed.
The original charge to the ad hoc committee was to comment, to
the extent possible, on the potential hazard to humans which
can be attributed to registered uses of PC? and the extent that
this ha2ard may be mitigated by the use of the commercial pro-
cess which results in lower levels c£ the contaminants of
interest. We urge that this charge be completely satisfied as
soon as possible in a less ambiguous manner and without
encumbrances of economic constraints which have created ambigui
in the present conclusions.
156
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8.3' COMMENTS OF INTERESTED PARTIES
157
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KAY
ft
8.3.1
SUBJECT;
TO ;
FROM :
Comments on EPA Science Advisory Board Environmental Health
Advisory Committee Meeting; Pentachlorophenol Contaminants
(April 3, 1978)
Ernst Linde, Executive Secretary, Science Advisory Board (RD-673)
Paul E. des Rosier If^Senlov Staff Engineer, Industrial and
Extractive Division (RD-681)
I believe it is important that the Science Advisory Board (SAB)
be made aware of certain facts in order that ail aspects of the
pentachlorophenol (PC?) contaminants issue are addressed correctly.
As you krow, I was present during the "session held on
Monday, April 3, 1978, during which time current producers of PCP,
namely, Dow Chemical Company, Reichhold Chemicals, aod Vulcan
Materials Company presented their respective statements to the
SAB Environmental Health Advisory Committee. I am considered an
Agency expert on the treatment and control of organochlorine
chemicals, have in-depth experience with military defoliants
dating back to 1967, and as a result, am thoroughly familiar with
disposal/detoxification methods for Herbicide Orange and its teratogenic
artifact, tecrachlarodibenzo-p-dioxin (TCDD).
In this respect, I was a member of the EPA Herbicide Orange
Disposition Advisory Panel to the U, S. Air Force/Defense Supply
Agency, provided technical consultation to the State of Missouri
Department of Health concerning the Verona, HO TCDD episode, and was
Interviewed by the British Broadcasting Corporation regarding the
Seveso Icaeaa plant TCDD incident in Italy.
In retrospect, I was particularly impressed at the meeting by
the perception of Dr. Van Gelder, a veterinarian, who in his
testimony, alluded to the fact that disposal of concentrated
quantities of PCP contaminants might prove to be more of a problem
than maintaining the status quo.
At this time, I wish to delineate some pertinent historical
facts relating to significant dioxia-type incidents:.
(1) 2.3 million gallons (24 million lbs) of Herbicide Orange
with approximately 2 tag/kg TCDD (about 49 lbs) could not be disposed
of by incineration either in Illinois Otonsanto's Sauget facility)
or in Texas (Rollins contract facility), or by land assimilation
158
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in Utah or in Oregon.
(2) Chemical detoxification of Herbicide Orange vzs proposed co
the U. S. Air Force by the Veisicoi Chemical Corporation, which entailed
deesterification via alkaline hydrolysis/solvent extraction/UV-photo-
chemical decomposition/reformulation; however,, Veisicoi withdrew its
proposal. Agent Chemical Incorporated was selected by the Air Force
to demonstrate at pilot scale, an activated coconut charcoal method
for "stoichiometric" selective removal of TCDD from Herbicide Orange;
however, disposal of spent charcoal cartridges containing hlzh concen-
trations of TCDD presented a significantly greater environmental risk,
and the project was officially curtailed.
(3) The M/T Vuleanua incinerator ship was employed to combust
Herbicide Orange at sea some 200 miles southwest of Johnston Island
in the South Pacific. Incineration of the defoliant was accomplished
at 12S0-1450°C with a dwell/retention time of 1.3 second, at a cost
exceeding $3 million. Subsequent to the successful incineration,
the M/T Vulcauus has been unable to obtain recertification because
of contamination of the ship's storage tanks/deck with aiaiscule
amounts of TCDD (ppt).
(A) There also exists today in Verona, MO, approximately 4600
gallons of highly contaminated (300-350 ppm TCDD) chlorinated still
bottoms from previous hexachlorophene manufacture. Systex Agribusiness,
the present owners of the industrial site, and Che Stace of Missouri
have been unable to secure an environmentally acceptable method for
the ultimate disposition of the waste residue.
(5) Presently, for every 5000 Ibs/hr of FCP manufactured,
approximately 10 percent or 500 lbs/hr of still bottom residues
are produced, which may contain, at varying concentrations: octa-,
hepta-, hexa- chlorodibenzodioxins and chlorodibenzofurans, tetra~
chlorophenol, trichlorophenol, chlorophenoxyphenols, hydroxydiphenyl
ethers, hexachlorobenzene, chlorinated biphenyIs, chlorinated polymers,
etc. This residue production would be equivalent to roughly a 2000
tons/year quantity requiring disposal.
"to
Specifications for the first at-sea incineration of Shell Chemical
Company organochlorine waste residues by the M/T Vulcanus were based
on Mississippi State University Prof. 8. J. Stojanovic's muffle
furnace data obtained with analytical grade TCDD.wHe found TCDD
completely combusted between 980-1000°C.
From the foregoing, it becomes obvious that public awareness and
anxiety play important roles as to how, when, where, and by which
method a "dioxin" contaminated material/waste is to be treated.
159
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Should the SAB Environmental Health Advisory Committee recommend that
technical grade FCP be purified to reduce contaminant levels to less
than 0.1 percent, then EPA is faced with a predicament - the question
of trade-off of occupational hazards.
There is no doubt that it is technically feasible, although at a
higher cost, to produce commercially purified grade PC? that can meet
reasonable regulatory constraints relative to chlorinated dioxins and
dibenzorurans. Furthermore, I have doubt concerning Dow's contention
that it possesses incineration capability to "destroy" the waste
residues therefrom. Nevertheless, the Dow case is unique - the Midland,
MI facility represents probably the largest integrated petrochemical
complex in the U. S, and large volumes of waste residues are admixed
with relatively small volumes of PC? wastes, the latter essentially
losing its identity through volumetric dilution before incineration
commences.
Such is not the case with Reichhold and Vulcan, however. Special
incinerators would have to be designed, parts ordered, constructed,
and subsequently evaluated, prior to application for an operating
permit. Such a permit request would undoubtedly require a public
hearing because "dioxins" are present in the wastes. Based on my
experience, I can assure you that the resulting permit requirements
will be severely restrictive (e.g., exhaustive monitoring, operational
constraints, etc.) and quite possibly could eliminate land-based
incineration as a technology option. (Since both Reichhold and
Vulcan would solicit strong guarantees from EPA that, once equipment
was on order, they would indeed be allowed to proceed with full-scale
construction and be able to operate the incineration units without
undue harassment from environmental groups. Naturally, EPA would be
in no position, legally or otherwise, to honor such requests.)
In my opinion, there are but four alternatives available for
consideration by the SAB regarding this matter:
(1) At-sea incineration aboard a vessel similar to the JI/T
Vulcanus.
(2) Privately owned/contractor operated incineration facility
(e.g., Marquardt's high efficiency SUE incineration unit.)
(3) la-process change/process modification (i.e., catalyst
substitution) to minimize dioxin/dibenzofuran byproduct
production - to include analysis of feedstock (phenol)
quality.
(4) Encouragement of accelerated R&D into incorporation of PCP
waste residues as feedstocks to cement kilns.
All options could be explored should the SAB desire.
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8.3.2
College of Veterinary Medicine
Veterinary Anatomy—Physio log>
UNIVERSITY OF MISSOURI-COLUMBIA
Corfumbta. Missouri £S20~
Taiepnom (3K) 332-ror
April 24, 1973
Mr. Ernst Unde
Executive Secretary
Environmental Health Advisory Committee
Science Advisory Board A-101
Washington, D.C. 20460
Dear Mr. Linde:
Enclosed are 20 copies of a report containing my additional conments
on the draft report on pentachlorophenol contaminants.
Please distribute these to the proper persons.
Sincerely yours,
Gary A. Van Gelder, D.V.M., Ph.D.
Veterinary Toxicologist
GAYG:nc
161
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April 15, 1978
Part II (part I dated
3/24/73)
TO; Mr. Ernst Linde
FROM; Dr. Gary Van Gelder
RE: Corrments on Draft Report on Pentachlorophenol
The following additional comments are made relative to the draft report.
1) The charge to the committee was to assess the hazard to humans due
to contaminants In pentachlorophenol. Other than industrial
chloracne resulting in all probability from exposures to mixtures
of various "Chemicals the document fails to document any significant
human health hazard that has resulted from 40 years of use and
exposure. This statement is made with the acknowledged exception
of reported instances of gross negligence or intentional ingestion
resulting in illness and death.
The report fails to clearly elucidate the point that the present
methods of producing low non-phenolic content PCP will still
possess the presently alleged chloracne hazard since the starting
reactions are similar for both processes. The report implies
that obtaining concentrates of the contaminants is less hazardous
than working with very diluted concentrations. The above implication
is made in the report without any evidence that there was any
attempt to assess the risk involved. Additionally, comments made
at the hearing clearly demonstrated the lack of unanimous agreement
among waste disposal specialists on the reliability of incineration.
Critical issues are;
a) frequency of stack monitoring
b) levels of detection
c) location of stack relative to wind direction and population
d) presence of fail/safe devices
Without such information and risk assessment data, how can a
responsible decision be made to move from technology A to technology
B, especially when technology A has not been shown to be associated
with any significant, isolatable problem? Risk assessment involves
more than simply saying since process B exists we should use it.
2) Page 1-7 of the report refers to dioxins being found in milk from
Michigan cattle but no data are presented. The report later refers
to dioxins in liver and fat. This point needs clarification.
3) Page 111-14» Table II - The data are summarized in such a way as to
ignore dose. An important part of risk assessment is consideration of
dose and evaluation of dose-response patterns.
162
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In one sense the draft report begins to pull together the available
information. The next steps are evaluation and interpretation.
In my opinion, the last steps remain as uncompleted tasks for the
coranittee.
4) Page 111-9 - states "technical grade PCP has been implicated in
causing teratogenic effects in women - Kimbrough, 1972." The
report by Kimbrough does not make this statement. Stillbirths with
PCB's are reported.
5) Page II1-9 - The Larsen study cited is inadequate to address the
question of placental transfer. Based on information presented
it is likely that placenta/fetal PCP levels are comparable to
maternal blood levels.
6) Statistical methods used to evaluate the various 90-720 day studies
are not consistent. See my letter to Dr. Schwetz of Dow Chemical
which was attached to my comments dated March 24.
7) While I appreciate the conments of several members of the committee
that their concern is not animal health, I need to point out that
there are people in the public sector who, based on their understanding
of coirments made by members of this committee believe that low level
exposures to technical PCP kills cows. I am satisfied with the
progress being made to resolve that misconception.
8) The remaining issue is one of safety/hazard evaluation. It is
amazing that an EPA sponsored committee was not provided or did not
review the results of studies sponsored by EPA to evaluate the human
health effects of PCP. Why this body of information has been ignored
is unexplainable.
One cannot prove safety for any product or process, what one does
is evaluate toxicity and assess risk (hazard). Consequently,
studies done where technical PCP was fed to animals provide information
on the toxicity of the PCP related contaminants.
Furthernwre, evaluation of worker related health problems or the
lack of problems are also important items to consider in risk assessment.
9) My principle concern in this entire matter has been based on a
broad view of the entire situation. First, PCP is an economic
poison. Fortunately, it's toxicologic characteristics are such that
it does not present i large hazard. But PCP residues have been
found in food products of animal origin. To the extent -that those
residues can be reduced or eliminated without causing a major
economic effect 1s a worthwhile goal. Additionally, PCP constitutes
only 5% of what is put into wood to preserve it. The toxicity and
residue characteristics of the other 95% of the material has not
been determined. What is found as residues are generally those things
that excite an electron capture detector.
These considerations plus my own observations of over use and
unnecessary use of PCP treated wood in places that facilitate
animal exposure leads me to a broad based recommendation that addresses
163
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the entire-problem. Namely, the need to develop sensible use
restrictions to reduce animal exposure. The casual rubbing
against a post or occasional lick of a post is of no concern to
me. The issue is one of feed bunks, bunker silos and use of
treated wood in above grade, dry locations. The concern expressed
in item 10 below is also a part of my decision information base.
10) I have reason to believe that the level of dioxin formation on the
surface of treated wood exposed to light is higher than that felt .to
occur as expressed in the committee discussion. It is of sufficient
concern that Dow has conducted and has expressed thnir intent to
conduct additional studies in this regard.
164
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8 3 3
DOW CHEMICAL U.S.A.
May 9, 1978 p. q. box im7
2040 OOW CENTER
M1CHAN0. MICHIGAN 43640
Mr. Ernst Linde
Executive secretary
Environmental Health Advisory Committee
Science Advisory Board
U. S. Environmental Protection Agency
Washington, D. C. 20460
Dear Mr. Lindes
Attached is the requested description of the general procedures
utilized by Dow Chemical U.S.A. to contain and destroy the con-
taminants resulting from the production of DOWICIDE* EC-7
Antimicrobial grade of pentachlorophenol. We believe this is
the kind of additional information that was needed by the
Environmental Health Advisory Committee Study Group on Penta-
chlorophenol Contaminants to assure itself that these impurities
can be feasibly handled.
As Dow has repeatedly stated, we contend that disposal of the
toxic impurities inherent to commercial pentachlorophenol
should be dealt with at the producing site where acknowledged
risk would be minimized. The fact that we produce and market
a grade of pentachlorophenol with significantly reduced non-
phenolic impurity content supports this position.
We have included 10 copies of the requested information. If
additional copies are required for distribution, for example,
to members of the Environmental Health Advisory Committee,
please do not hesitate to let us know.
Very truly yours,
Robert Ii. Johnson
Designed Products Department
Technical Service & Development
517/636-1524
mbh
attach. ¦
~Trademark of The Dow Chemical Company
AN 0#»t*AT1Na UNTT OP TMi DOW CHCMlCAt. COMPANY
-------
DISPOSAL OP PENTACHLOROPHENOL IMPURITIES
Dow Chemical U.S.A.
The product known as DOWICIDE* SC-7 Antimicrobial grade of
pentachlorophenol (PCP) differs in chemical assay from the
older form of PC?. Numerous publications describe the com-
mercial process utilized in the U.S. to make PC?. As noted
in these publications, the process reaction mixture is main-
tained as a liquid (approximately 10"C above the product
melting point); no solvent is used or required. The commer-
cial process utilizes final chloriaation and the necessary
temperatures to produce a product with a pentachlorophenol
content in the range of about 85-90%. These production con-
ditions also result in the formation of the various contaminants
found in PCP.
The finished reaction mixture, in the Dow process, is distilled
to yield a grade of which meets the imposed specifications
for DOWICIDE EC-7. A copy of the DOWICIDE EC-7 technical
bulletin, which describes the composition, is attached.
The still bottoms resulting from this additional PCP processing
contain the non-phenolic contaminants identified as chlorinated
dibenzo-p-dioxins and chlorinated dibenzofurans. Other materials
included in the still bottom residue, or tars, are the chloro-
phenoxyphenols, chlorodiphenyl ethers, and even a percentage of
higher phenols such as pentachlorophenol itself.
These tars are handled, stored and transported to the Dow
tar burner in closed systems. Eye protection, rubber gloves
and protective clothing are routinely used by all personnel
~Trademark of The Dew Chemical Company
166
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involved in these operations. A rigorous industrial hygiene
and health monitoring program is and has been in'effect for
these personnel. Anytime that work on contaminated equipment
is needed, extreme protective measures are taken including
full rubber suits and self-contained breathing apparatus.
Normal operating conditions in the tar burner are maintained
to achieve a minimum 1,8-second residence time at temperatures
of 900-1000'C. The temperature is continuously monitored with
approoriete warning alarms and shut.-off devices. Combustion
gases go through a three-stage scrubbing system, before discharge
to the atmosphere. The scrubber water is - treated in the waste
water treatment plant before recycle and/or discharge to the ,
Tittabawassee River.
5/9/78
167
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technical data
DOWICIDE EC-7 ANTIMICROBIAL
GENERAL
DOWICIDE EC-7 Antimicrobial is Daw's designation for pentachloro-
phenol, p-uxified grade. This antimicrobial is designed to comple-
ment DOWICIDE 7 Antimicrobial in all industrial uses that require
the control of bacteria and fungi, particularly in the of
wood preservation.
PHYSICAL PROPERTIES
(These are laboratory or literature-data typical-of the product
and are not-to be considered as,, or confused with, specifications.)
STRUCTURE 0H
CI
Formula .....
Molecular Weight
Flash Point, °F ...... .
Fire Point, "F
Specific Gravity, 25/25*C .
. C-C1-0H
None
None
1.9
2§6.1
Solubility, appro*, g/100 g solvent at 25°C
Acetone
Methanol
Ethanol (F30) .
Isopropanol
Diacetone Alcohol
DOWAHOL TPM Glycol Ether ........
Ethylene Glycol
Methylene Chloride . .
o-Xylene
Turpentine
52
175
125
80
145
115
12
7
18
7
NOTICE; TYui xnformatiort i* in goexi faith, boi no wanamv, m*omwm or moimo, ;* given
nor ri tfwiltim from »n» Bjwm ovtrmO ft* Th» Oo«. Csmcany or aw ommr» to Da nlmrrma.
THE DOW CHEMICAL COMPANY
DESIGNED PRODUCTS DEPARTMENT • MIDLAND. MICHIGAN 48640
-------
DOWICIDE EC-7 ANTIMICROBIAL
Page 2
PRODUCT DESCRIPTION
DOWICIDE EC-7 Antimicrobial has. the following composition:
Active ingredients . ....... 100%
Pentachlorophenol ........ 88%
2,3,4,6-Tetrachlorophenol ......... 12%
Chlorinated Dioxins
Octachlorodibenzo-p-dioxin 30 ppm, max.
Hexachlorodibenzo-p-dioxins 1 ppm, max.
Description ....... Off-white to
light yellow
prills*
EPA Reg.. No. 464-431
PACKAGES
Prilled and pelleted forma of DOWICIDE EC-7 Ant4microbial are
sold in multiwall paper bags having a net weight of 50 pounds#
in fiber drums having a net weight of 300 pounds, in wire-bound
boxes having a net weight of 2500 pounds and in bulk to be
transported in tank tracks and rail ears. The block form is
sold in units having a net weigh't of 2000 pounds.
(Typical Laboratory Data)
% DOWICIDE EC-7
Test Organism for Inhibition
Trichoderaia virida, ATCC#8678 0.0025-0.005
Tgichcaeraff so., Madison 1-42 0.001-0.0025
Cerarocystls pilifera# ATCCS15457 ' .0.0005-0.001
golyaorUs :: la lip if e r ae, ATCCS11245 . < 0.0001
Suzocus^gc o1onifeg, ATCC g 6 2 27a "0.0001-0.00025
lensizes rrabea, Madison 617 0.0001-0.00025
Cerazocystis ips, ATCCI12860 0.001-0.002S
Siaetoialum glooosuia, ATCCf6205 0.0001-0.00025
Aspergillus"ftiger, ATCC?6275 0.001-0,0025
i
Bacillus cereus var. mycoides, ATCC#1177i 0.0005-0.001
3aciXlis subtills, ATCC#S473: 0.005-0.01
Escherichia colXT ATCCI11229 • 0.025-0.05
Pseuqosionas aeruginosa, ATCC315442 0.1-0.25
Enterobacter aerogenes, ATCC513043 0.05-0.1
Screpcornyces gnseus, ATCCS10137 0.0005-0^001
Flavooacteriun arborescens, ATCC$4358 0.00025-0.0005
Formulators- may be required to develop their own efficacy data as
well as use and precautionary labeling based on the represented
properties and intended-uses of their finished femulations, and
in accordance with all pertinent laws and regulations.
159
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DCWICIDE EC-7 ANTIMICROBIAL
Page 3
HEALTH HAZARDS
DCWICIDE EC-7 Antimicrobial is capable of causing' conjunctival
redness, iritis, and slight corneal injury. Prompt flushing of
contaminated eves will lessen the degree of injury. A single,
prolonged skin contact with, the product may cause slight redness
and swelling. Repeated, prolonged contact nay result in a chemi-
cal burn. DCWICIDE EC-7 is not absorbed through the skin in
acutely toxic amounts. However, the product, in solution, say
be absorbed through the skin in acutely toxic amounts depending-
upon the solvent and the concentration of DCWICIDE EC-7. Dusts
may be irritating to the nose and throat.
PRECAUTIONS FOR SAFE HANDLING
Safety gaggles should be worn to protect the eyes when DOWICIDE
EC-7 Antimicrobial is handled.
Protective clothing should be worn when skin contact with DOWICIDE
EC-7 is anticipated. Work clothes should be changed at regular
intervals and when gross contamination occurs. Grossly contami-
nated clothing, shoes or gloves should not be reused until they
have been thoroughly cleaned.
Any exposure to obviously dusty atmospheres will require the use
of a dust respirator approved by the U.S. Bureau of "Mines for use
with toxic dusts.
FIRST AID MEASURES
Sye Contact - Contaminated eyes should be flushed with plenty of
wa^er :or at least 15 ainutes. Medical attention should be obtained
promptly.
Skin Contact - Contaminated skin should be washed with soap and
plenty of water. Any irritation that develops should receive
medical attention.
Inhalation - Anyone experiencing any noticeable ill effects from
breaking the dusts of the product should be removed to fresh air.
Medical attention should be obtained.
170
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