Pentachlorophenol (EHC 71, 1987)

INTERNATIONAL PROGRAMME ON CHEMICAL SAFETY

ENVIRONMENTAL HEALTH CRITERIA 71

PENTACHLOROPHENOL

This report contains the collective views of an international group of
experts and does not necessarily represent the decisions or the stated
policy of the United Nations Environment Programme, the International
Labour Organisation, or the World Health Organization.

Published under the joint sponsorship of
the United Nations Environment Programme,
the International Labour Organisation,
and the World Health Organization

World Health Orgnization
Geneva, 1987

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CONTENTS

ENVIRONMENTAL HEALTH CRITERIA FOR PENTACHLOROPHENOL

1. SUMMARY

1.1. Identity, physical and chemical properties, analytical
methods
1.2. Sources of human and environmental exposure
1.3. Environmental transport, distribution, and transformation
1.4. Environmental levels and human exposure
1.5. Effects on organisms in the environment
1.6. Kinetics and metabolism
1.7. Effects on experimental animals and in vitro test systems
1.8. Effects on man

2. IDENTITY, PHYSICAL AND CHEMICAL PROPERTIES, ANALYTICAL METHODS

2.1. Identity
2.1.1. Pentachlorophenol (PCP)
2.1.2. Sodium pentachlorphenate (Na-PCP)
2.1.3. Pentachlorophenyl laurate
2.2. Impurities in pentachlorophenol
2.2.1. Formation of PCDDs and PCDFs during thermal
decomposition
2.3. Physical, chemical, and organoleptic properties
2.4. Conversion factors
2.5. Analytical methods
2.5.1. Sampling methods
2.5.2. Analytical methods

3. SOURCES OF HUMAN AND ENVIRONMENTAL EXPOSURE

3.1. Natural occurrence
3.2. Man-made sources
3.2.1. Industrial production
3.2.1.1 Manufacturing processes
3.2.1.2 Emissions during production
3.2.1.3 Disposal of production wastes
3.2.1.4 Production levels
3.3. Uses
3.3.1. Commercial use
3.3.2. Agricultural use
3.3.3. Domestic use
3.3.4. Use for control of vectors
3.3.5. Formulations

4. ENVIRONMENTAL TRANSPORT, DISTRIBUTION, AND TRANSFORMATION

4.1. Transport and distribution between media
4.1.1. Volatilization
4.1.2. Adsorption
4.1.3. Leaching
4.2. Biotransformation
4.2.1. Abiotic degradation

4.2.2. Microbial degradation
4.2.2.1 Aquatic degradation
4.2.2.2 Degradation in soil
4.3. Degradation by plants
4.4. Ultimate fate following use
4.4.1. General aspects
4.4.2. Disposal of waste water
4.4.3. Incineration of wastes

5. ENVIRONMENTAL LEVELS ANS HUMAN EXPOSURE

5.1. Environmental levels
5.1.1. Air
5.1.2. Water and sediments
5.1.3. Soil
5.1.4. Aquatic and terrestrial organisms
5.1.4.1 Aquatic organisms
5.1.4.2 Terrestrial organisms
5.1.5. Drinking-water and food
5.1.6. Consumer products
5.1.7. Treated wood
5.2. Occupational exposure
5.3. General population exposure
5.4. Human monitoring data

6. KINETICS AND METABOLISM

6.1. Absorption
6.1.1. Animal studies
6.1.2. Human studies
6.2. Distribution
6.2.1. Animal studies
6.2.2. Human studies
6.3. Metabolic transformation
6.3.1. Animal studies
6.3.2. Human studies
6.4. Elimination and excretion
6.4.1. Animal studies
6.4.2. Human studies
6.5. Retention and turnover
6.5.1. Animal studies
6.5.2. Human studies
6.6. Reaction with body components

7. EFFECTS ON ORGANISMS IN THE ENVIRONMENT

7.1. Microorganisms
7.2. Aquatic organisms
7.2.1. Plants
7.2.2. Invertebrates
7.2.3. Vertebrates
7.3. Terrestrial organisms
7.3.1. Plants
7.3.2. Animals

7.4. Population and ecosystem effects
7.5. Biotransformation, bioaccumulation, and
biomagnification
7.5.1. Aquatic organisms
7.5.2. Terrestrial organisms

8. EFFECTS ON EXPERIMENTAL ANIMALS AND IN VITRO TEST SYSTEMS

8.1. Acute toxicity
8.2. Short-term toxicity
8.2.1. Pure or purified PCP
8.2.2. Technical grade PCP
8.2.3. Comparative studies
8.3. Long-term toxicity
8.4. Effects on reproduction and fetal development
8.5. Mutagenicity
8.6. Carcinogenicity
8.7. Other studies
8.8. Contaminants affecting toxicity
8.8.1. Octachlorodibenzodioxin (OCDD)
8.8.2. Heptachlorodibenzodioxin (H₇CDD)
8.8.3. Hexachlorodibenzodioxin (H₆CDD)
8.8.4. Polychlorinated dibenzofurans (PCDFs)
8.8.5. Polychlorodiphenyl ethers (PCDPEs)
8.8.6. Other microcontaminants
8.9. Mechanism of toxicity

9. EFFECTS ON MAN

9.1. Acute toxicity - poisoning incidents
9.2. Effects of short- and long-term exposures
9.2.1. Occupational exposure
9.2.1.1 Skin and mucous membranes
9.2.1.2 Liver and kidney
9.2.1.3 Blood and haemopoetic system
9.2.1.4 Nervous system
9.2.1.5 Immunological system
9.2.1.6 Reproduction
9.2.1.7 Cytogenetic effects
9.2.1.8 Carcinogenicity
9.2.1.9 Other systems
9.2.2. General population exposure

10. EVALUATION OF HUMAN HEALTH RISKS AND EFFECTS ON THE ENVIRONMENT

10.1. Evaluation of human health risks
10.1.1. Occupational exposure
10.1.1.1 Exposure levels and routes
10.1.1.2 Toxic effects
10.1.1.3 Risk evaluation
10.1.2. Non-occupational exposure
10.1.2.1 Exposure levels and routes
10.1.2.2 Risk evaluation
10.1.3. General population exposure
10.1.3.1 Exposure levels and routes

10.1.3.2 Risk evaluation
10.2. Evaluation of effects on the environment
10.3. Conclusions

11. RECOMMENDATIONS

11.1. Environmental contamination and human exposure
11.2. Future research
11.2.1. Human exposure and effects
11.2.2. Effects on experimental animals and in vitro test
systems
11.2.3. Effects on the ecosystem

12. PREVIOUS EVALUATIONS BY INTERNATIONAL BODIES

REFERENCES

WHO TASK GROUP ON PENTACHLOROPHENOL

Members

Dr U.G. Ahlborg, Unit of Toxicology, National Institute of
Environmental Medicine, Stockholm, Sweden

Dr R.C. Dougherty, Department of Chemistry, Florida State
University, Tallahassee, Florida, USA

Dr H.H. Dieter, Federal Health Office, Institute for Water, Soil,
and Air Hygiene, Berlin (West)

Dr A.H. El Sabae, Pesticide Division, Facultry of Agriculture,
University of Alexandria, Alexandria, Egypt^a

Dr A. Furtado Rahde, Ministry of Public Health, Porto Alegre,
Brazil

Dr S. Gupta, Department of Zoology, Faculty of Basic Sciences,
Punjab Agricultural University, Ludhiana, Punjab, India^a

Dr L.V. Martson, All Union Scientific Research Institute of the
Hygiene and Toxicology of Pesticides, Polymers, and
Plastics, Kiev, USSR^a

Dr U.G. Oleru, Department of Community Health, College of Medicine,
University of Lagos, Lagos, Nigeria

Dr Shou-Zheng Xue, Toxicology Programme, School of Public Health,
Shanghai Medical University, Shanghai, China

Observers

Dr F.F. Hertel, Fraunhofer Institute for Toxicology and
Aerosol Research, Hanover, Federal Republic of Germany

Dr E. Kramer (European Chemical Industry Ecology and Toxicology
Centre), Dynamit Nobel A.G., Cologne, Federal Republic of
Germany

Dr D. Streelman (International Group of National Associations of
Agrochemical Manufacturers), Agricultural Chemicals Registration
and Regulatory Affairs, Philadelphia, Pennsylvania, USA

Mr G. Ozanne (European Chemical Industry Ecology and Toxicology
Centre), Rhone Poulenc DSE/TOX, Neuilly-sur-Seine, France

Mr V. Quarg, Federal Ministry for Environment, Nature Conservation
and Nuclear Safety, Bonn, Federal Republic of Germany

---------------------------------------------------------------------------
^a Invited but unable to attend.

Observers (contd)

Dr U. Schlottmann, Chemical Safety, Federal Ministry for
Environment, Nature Conservation and Nuclear Safety, Bonn,
Federal Republic of Germany

Dr M. Sonneborn, Federal Health Office, Berlin (West)

Dr W. Stober, Fraunhofer Institute for Toxicology and Aerosol
Research, Hanover, Federal Republic of Germany

Secretariat

Dr K.W. Jager, International Programme on Chemical Safety, World
Health Organization, Geneva, Switzerland (Secretary)

Mrs B. Bender, International Register for Potentially Toxic
Chemicals, Geneva, Switzerland

Dr A. Gilman, Industrial Chemicals and Product Safety Section,
Health Protection Branch, Department of National Health and
Welfare, Tunney's Pasture, Ottawa, Ontario, Canada (Temporary
Adviser) (Rapporteur)

Dr L. Ivanova-Chemishankska, Institute of Hygiene and Occupational
Health, Medical Academy, Sofia, Bulgaria (Temporary Adviser)

Dr E. Johnson, Unit of Analytical Epidemiology, International
Agency for Research on Cancer, Lyons, France

Dr G. Rosner, Fraunhofer Institute for Toxicology and Aerosol
Research, Hanover, Federal Republic of Germany (Rapporteur)

Dr G.J. Van Esch, Bilthoven, Netherlands (Temporary Adviser)

NOTE TO READERS OF THE CRITERIA DOCUMENTS

Every effort has been made to present information in the
criteria documents as accurately as possible without unduly
delaying their publication. In the interest of all users of the
environmental health criteria documents, readers are kindly
requested to communicate any errors that may have occurred to the
Manager of the International Programme on Chemical Safety, World
Health Organization, Geneva, Switzerland, in order that they may be
included in corrigenda, which will appear in subsequent volumes.

* * *

A detailed data profile and a legal file can be obtained from
the International Register of Potentially Toxic Chemicals, Palais
des Nations, 1211 Geneva 10, Switzerland (Telephone no. 988400 -
985850).

ENVIRONMENTAL HEALTH CRITERIA FOR PENTACHLOROPHENOL

A WHO Task Group on Environmental Health Criteria for
Pentachlorophenol met at the Fraunhofer Institute for Toxicology
and Aerosol Research, Hanover, Federal Republic of Germany from 20
to 24 October, 1986. Dr W. Stöber opened the meeting and welcomed
the members on behalf of the host Institute, and Dr U. Schlottmann
spoke on behalf of the Federal Government, who sponsored the
meeting. Dr K.W. Jager addressed the meeting on behalf of the
three co-operating organizations of the IPCS (UNEP/ILO/WHO). The
Task Group reviewed and revised the draft criteria document and
made an evaluation of the risks for human health and the
environment from exposure to pentachlorophenol.

The drafts of this document were prepared by DR G. ROSNER of
the Fraunhofer Institute for Toxicology and Aerosol Research,
Hanover, Federal Republic of Germany, and DR A. GILMAN of the
Health Protection Branch, Ottawa, Canada.

The efforts of all who helped in the preparation and
finalization of the document are gratefully acknowledged.

* * *

Partial financial support for the publication of this criteria
document was kindly provided by the United States Department of
Health and Human Services, through a contract from the National
Institute of Environmental Health Sciences, Research Triangle Park,
North Carolina, USA - a WHO Collaborating Centre for Environmental
Health Effects. The United Kingdom Department of Health and Social
Security generously supported the costs of printing.

1. SUMMARY

1.1. Identity, Physical and Chemical Properties, Analytical Methods

Pure pentachlorophenol (PCP) consists of light tan to white,
needlelike crystals and is relatively volatile. It is soluble in
most organic solvents, but practically insoluble in water at the
slightly acidic pH generated by its dissociation (pKa 4.7).
However, its salts, such as sodium pentachlorophenate (Na-PCP),
are readily soluble in water. At the approximately neutral pH of
most natural waters, PCP is more than 99% ionized.

Apart from other chlorophenols, unpurified technical PCP
contains several microcontaminants, particularly polychlorinated
dibenzo- p-dioxins (PCDDs) and polychlorinated dibenzofurans
(PCDFs), of which H₆CDD is the most relevant congener
toxicologically. 2,3,7,8-T₄CDD has only once been confirmed in
commercial PCP samples (0.25 - 1.1 µg/kg). Depending on the
thermolytic conditions, thermal decomposition of PCP or Na-PCP may
yield significant amounts of PCDDs and PCDFs. The use and the
uncontrolled incineration of technical grade PCP is one of the most
important sources of PCDDs and PCDFs in the environment.

Most of the analytical methods used today involve acidification
of the sample to convert PCP to its non-ionized form, extraction
into an organic solvent, possible cleaning by back-extraction into
a basic solution, and determination by gas chromatography with
electron-capture detector (GC-EC) or other chromatographic methods
as ester or ether derivatives (e.g., acetyl-PCP). Depending on
sampling procedures and matrices, detection limits as low as
0.05 µg/m³ in air or 0.01 µg/litre in water can be achieved.

1.2. Sources of Human and Environmental Exposure

PCP is mainly produced by the stepwise chlorination of phenols
in the presence of catalysts. Until 1984, Na-PCP was partly
synthesized by means of the alkaline hydrolysis of
hexachlorobenzene, but it is now produced by dissolving PCP flakes
in sodium hydroxide solution.

World production of PCP is estimated to be of the order of
30 000 tonnes per year. Because of their broad pesticidal efficiency
spectrum and low cost, PCP and its salts have been used as
algicides, bactericides, fungicides, herbicides, insecticides, and
molluscicides with a variety of applications in the industrial,
agricultural, and domestic fields. However, in recent years, most
developed countries have restricted the use of PCP, especially for
agricultural and domestic applications.

PCP is mainly used as a wood preservative, particularly on a
commercial scale. The domestic use of PCP is of minor importance
in the overall PCP market, but has been of particular concern
because of possible health hazards associated with the indoor
application of wood preservatives containing PCP.

1.3. Environmental Transport, Distribution, and Transformation

The relatively high volatility of PCP and the water solubility
of its ionized form have led to widespread contamination of the
environment with this compound. Depending on the solvent,
temperature, pH, and type of wood, up to 80% of PCP may evaporate
from treated wood within 12 months.

The adsorption and leaching behaviour of PCP varies from soil
to soil. Adsorption of PCP decreases with rising pH and so PCP is
most mobile in mineral soils, and least mobile in acidic clay and
sandy soils.

Solid or water-dissolved PCP can be photolysed by sunlight
within a few days, yielding aromatic (lower chlorinated phenols,
etc.) and nonaromatic fragments, as well as hydrogen chloride (HCl)
and carbon dioxide (CO₂). Traces of PCDDs, mainly OCDD are formed
photochemically on irradiation of Na-PCP in aqueous solution.

PCP degrading microorganisms have been isolated from waters and
soils. High organic matter and moisture content, median
temperatures, and high pH enhance microbial breakdown in soil
(half-life = 7 - 14 days). Low oxygen conditions are generally
unfavourable for the biodegradation of PCP, allowing it to persist
in soil (half-life = 10 - 70 days under flooded conditions), water
(half-life = 80 - 192 days in anaerobic water), and sediments (10%
decomposition within 5 weeks to almost no degradation). Several
studies have proved that PCP can be degraded by activated sludge.
However, in full-scale treatment plants the treatment efficiency is
often reduced.

Numerous metabolites have been identified resulting from the
methylation, acetylation, dechlorination, or hydroxylation of PCP.
Of the possible metabolites, at least tetrachlorocatechol seems to
be relatively persistent. However, there is a lack of data
concerning the fate of the intermediate products of both the
abiotic and biotic degradation of PCP.

1.4. Environmental Levels and Human Exposure

The ubiquitous occurrence of PCP is indicated by its detection,
even in ambient air of mountain rural areas (0.25 - 0.93 ng/m³). In
urban areas, PCP levels of 5.7 - 7.8 ng/m³ have been detected.

While elevated PCP concentrations can be found in groundwater
(3 - 23 µg/litre) and surface water (0.07 - 31.9 µg/litre) within
wood-treatment areas, the PCP level of surface waters is usually in
the range of 0.1 - 1.0 µg/litre, with maximum values of up to 11
µg/litre. PCP concentrations in the mg/litre range can be
encountered near industrial discharges.

Sediments of water bodies generally contain much higher levels
of PCP than the overlying waters. Soil samples from PCP or
pesticide plants contain around 100 µg PCP/kg (dry weight); heavily
contaminated soil (up to 45.6 mg PCP/kg) can be found in the
vicinity of wood-treatment areas.

Residues of PCP in the aquatic invertebrate and vertebrate
fauna are in the low µg/kg range (wet weight). Very high levels
(up to 6400 µg/kg) are found in fish from waters that are
contaminated with wood preservatives, while sediment-dwelling
organisms, such as clams, show PCP levels of up to 133 000 µg/kg.
Fish kills result in PCP residues in fish of between 10 and
30 mg/kg.

After agricultural PCP application, birds can be highly
contaminated (47 mg/kg wet weight in liver). Exposure of farm
animals to PCP-treated wood shavings used as litter causes a musty
taint of the flesh as a result of contamination with
pentachloroanisole, a metabolite of PCP biodecomposition. PCP
levels ranging from not detectable to 8571 µg/kg have been found in
the muscle tissue of wild birds.

The general population is exposed to PCP through the ingestion
of drinking-water (0.01 - 0.1 µg/litre) and food (up to 40 µg/kg in
composite food samples). Apart from the daily dietary intake (0.1
- 6 µg/person per day) resulting from direct food contamination
with PCP, continuous exposure to hexachlorobenzene and related
compounds in food, which are biotransformed to PCP, may be another
important source.

In addition, because of its widespread use, the general
population can be exposed to PCP in treated items such as textiles,
leather, and paper products, and above all, through inhalation of
indoor air contaminated with PCP. Generally, PCP concentrations of
up to about 30 µg/m³ can be expected, for up to the first month,
after indoor treatment of large surfaces; considerably higher
levels (up to 160 µg/m³) cannot be excluded under unfavourable
conditions. In the long term, values of between 1 and 10 µg/m³ are
typical PCP concentrations after extensive treatments, though
higher levels, up to 25 µg/m³, have been found in rooms treated one
to several years earlier. For comparison, PCP indoor air levels in
untreated houses are generally below 0.1 µg/m³.

According to the usage pattern, the main sources of
occupational exposure to PCP are the treatment of lumber in
sawmills and treatment plants, and exposure to treated wood during
carpentry and other wood-working activities. Most of the reported
air concentrations at the work-place are below the TWA MAC value of
500 µg/m³ that has been established by several countries.
Occupational exposure to PCP mainly occurs via inhalation and
dermal exposure.

Since the PCP concentrations in the sources (air, food) do not
directly indicate the actual PCP intake by the different routes,
extrapolation from urine residue data has been used to estimate
human total body exposure. Mean or median urine-PCP levels range
around 10 µg/litre for the general population without known
exposure, around 40 µg/litre for non-occupationally exposed
persons, and around 1000 µg/litre for occupationally exposed
people.

The ranges of urine levels observed in exposed and unexposed
persons overlap considerably. This overlap probably occurs because
occupational exposure does not necessarily involve high loading,
while non-occupationally exposed people may, in some instances, be
exposed to PCP at levels encountered at the work-place.

1.5. Effects on Organisms in the Environment

As a result of its biocidal properties, PCP negatively affects
non-target organisms in soil and water at relatively low
concentrations. Algae appear to be the most sensitive aquatic
organisms; as little as 1 µg/litre can cause significant inhibition
of the most sensitive algal species. Less sensitive species show
EC₅₀ values of around 1 mg/litre.

Most aquatic invertebrates (annelids, molluscs, crustacea) and
vertebrates (fish) are affected by PCP concentrations below 1
mg/litre in acute toxicity tests. Generally, reproductive and
juvenile stages are the most sensitive, with LC₅₀ values as low as
0.01 mg/litre for fish larvae. Low levels of dissolved oxygen, low
pH, and high temperature increase the toxic effects of PCP.
Concentrations causing sublethal effects on fish are in the low
µg/litre range. As PCP contamination in many surface waters is in
this range, population and community effects cannot be ruled out.
This is also indicated by the substantial alterations in the
community structure of model ecosystems that are induced by PCP.

PCP is accumulated by aquatic organisms. Fresh-water fish show
bioconcentration factors of up to 1000 compared to < 100 in marine
fish. The portion of PCP taken up, either through the surrounding
water or along the food chain, is probably species specific.

PCP taken up by terrestrial plants remains in the roots and is
partly metabolized.

1.6. Kinetics and Metabolism

PCP is readily absorbed through the intact skin and respiratory
and gastrointestinal tracts, and distributed in the tissues.
Highest levels are observed in liver and kidney, and lower levels
are found in body fat, brain, and muscle tissue. There is only a
slight tendency to bioaccumulate, and so relatively low PCP
concentrations are found in tissues. In rodent species,
detoxication occurs through the oxidative conversion of PCP to
tetrachlorohydroquinone, to a small extent also to
trichlorohydroquinone, as well as through conjugation with
glucuronic acid. In rhesus monkeys, no specific metabolites have
been detected. In man, metabolism of PCP to
tetrachlorohydroquinone seems to occur only to a small extent.

Rats, mice, and monkeys excrete PCP and their metabolites,
either free or conjugated with glucuronic acid, mainly in urine
(rodents, 62 - 83%; monkeys, 45 - 75%) and to a lesser extent with
the faeces (rodents, 4 - 34%; monkeys, 4 - 17%). The
pharmacokinetic profile following single doses depends on the

species and possibly on the sex of the test animals. Rats and mice
eliminate PCP rapidly, with a half-life of 6 - 27 h. The kinetics
in rats follow a biphasic elimination scheme with a comparatively
slow second elimination phase (half-life, 33 - 374 h), perhaps
because extensive enterohepatic circulation retains PCP in the
liver. Retention may also be the result of plasma-protein binding
of PCP, which seems to become stronger at lower PCP concentrations.

In rats, 90% of an applied single oral dose is excreted by day
3 with small amounts still remaining in the liver (0.3%) and kidney
(0.05%) after 9 days. On the other hand, monkeys show a much
slower elimination rate (half-life, 41 - 92 h), apparently because
they do not metabolize PCP; even 15 days after oral application of
a single dose (10 mg/kg bodyweight), about 11% of the total dose
remained in the body, particularly in the intestines and liver.

The elimination kinetics of PCP in human beings are a
controversial subject. A study on 4 male volunteers ingesting a
single oral dose of water-soluble Na-PCP at 0.1 mg/kg body weight
showed a rapid elimination of PCP both in urine (half-life, 33 h)
and plasma (30 h). Within 168 h, 74% of the dose was excreted in
urine as free PCP and 12% as its glucuronide, while about 4% was
eliminated in the faeces. In contrast to this study, the
application of oral doses of between 0.016 and 0.31 mg PCP/kg body
weight in 40% ethanol revealed a substantially slower PCP
excretion rate, with elimination half-lives of 16 days (plasma) and
18 - 20 days (urine). These low elimination rates have been
ascribed to the high protein binding tendency of PCP.

Some animal data indicate that there may be long-term
accumulation and storage of small amounts of PCP in human beings.
The fact that urine- or blood-PCP levels do not completely
disappear in some occupationally exposed people, even after a long
absence of exposure, seems to confirm this, though the
biotransformation of hexachlorobenzene and related compounds
provides an alternative explanation of this phenomenon. However,
there is a lack of data concerning the long-term fate of low PCP
levels in animals as well as in man. Furthermore, no data are
available on the accumulation and effects of microcontaminants
taken up by people together with PCP.

1.7. Effects on Experimental Animals and In Vitro Test Systems

In the main, mammalian studies have been relatively consistent
in their demonstration of the effects of exposure to PCP. In rats,
lethal doses induce an increased respiratory rate, a marked rise in
temperature, tremors, and a loss of righting reflex. Asphyxial
spasms and cessation of breathing occur soon before cardiac arrest,
which is in turn followed by a rapid, intense rigor mortis.

PCP is highly toxic, regardless of the route, length, and
frequency of exposure. Oral LD₅₀ values for a variety of species
range between 27 and 205 mg/kg body weight according to the
different solvent vehicles and grades of PCP. There is limited

evidence that the most dangerous route of exposure to PCP is
through the air.

PCP is also an irritant for exposed epithelial tissue,
especially the mucosal tissues of the eyes, nose, and throat. Other
localized acute effects include swelling, skin damage, and hair
loss, as well as flushed skin areas where PCP affects surface blood
vessels. Exposure to technical formulations of PCP may produce
chloracne. Comparative studies indicate that this is a response to
microcontaminants, principally PCDDs, present in the commercial
product. The parent molecule appears responsible for immediate
acute effects, including irritation and the uncoupling of oxidative
phosphorylation with a resultant elevated temperature.

Short- and long-term studies indicate that purified PCP has a
fairly limited range of effects in test organisms, primarily rats.
Exposure to fairly high concentrations of PCP may reduce growth
rates and serum-thyroid hormone levels, and increase liver weights
and/or the activity of some liver enzymes. In contrast, technical
formulations of PCP usually at much lower concentrations can
decrease growth rates, increase the weights of liver, lungs,
kidneys, and adrenals, increase the activity of a number of liver
enzymes, interfere with porphyrin metabolism, alter haematological
and biochemical parameters and interfere with renal function.
Apparently microcontaminants are the principal active moities in
the nonacute toxicity of commercial PCP.

PCP is fetotoxic, delaying the development of rat embryos and
reducing litter size, neonatal body weight, neonatal survival, and
the growth of weanlings. The no-observed-adverse-effect-level
(NOAEL) for technical PCP is a maternal dose of 5 mg/kg body weight
per day during organogenesis. The NOAEL for purified PCP is lower.
In one study, it was reported that purified PCP was slightly more
embryo/fetotoxic than technical PCP, presumably because
contaminants induced enzymes that detoxified the parent compound.

PCP is not considered teratogenic, though, in one instance,
birth defects arose as an indirect result of maternal hyperthermia.
The NOAEL in rat reproduction studies is 3 mg/kg body weight per
day. This value is remarkably close to the NOAEL mentioned in the
previous paragraph, but there are no corroborating studies in other
mammalian species.

PCP has also proved immunotoxic to mice, rats, chickens, and
cattle; at least part of this effect is caused by the parent
molecule.

Neurotoxic effects have also been reported, but the possibility
that these are due to microcontaminants has not been excluded.

PCP is not considered carcinogenic for rats. Mutagenicity
studies support this conclusion in as much as pure PCP has not been
found to be highly mutagenic. Its carcinogenicity remains
questionable because of shortcomings in these studies. The
presence of at least one carcinogenic microcontaminant (H₆CDD)

suggests that the potential for technical PCP to cause cancer in
laboratory animals cannot be completely ruled out.

Note: Since the publication of this monograph in 1987, however, the
results of adequate carcinogenicity studies with commercial-grade
pentachlorophenol have been published. The conclusions of these studies
are indicated in the addendum to 8.6 Carcinogenicity.

1.8. Effects on Man

The effects of PCP on man are very similar to those reported in
experimental animals. Human data have been obtained primarily from
accidental exposures and from the work-place. Unfortunately, there
are few precise estimates of exposure, hence dose-response
relationships are difficult to establish in human beings.

It is clear that the use of PCP may pose a significant hazard
with regard to specific aspects of the health of workers employed
in the production or use of PCP. Chloracne, skin rashes,
respiratory diseases, neurological changes, headaches, nausea, and
weakness have been documented in workers at numerous production and
manufacturing sites. Similar symptoms have been reported in some
inhabitants of houses treated internally with PCP. Acute
intoxications leading to hyperpyrexia and death have been clearly
associated with exposure to the chlorophenol molecule itself,
whereas chloracne appears to be an effect of the PCDD and PCDF
microcontaminants. Changes in industrial practice have resulted
in fewer high-dosage, acute exposures, but deaths due to
occupational overexposure to PCP are still being reported.

Studies designed to examine biochemical changes in wood-workers
exposed to high levels of PCP for extended periods have failed to
indicate statistically significant effects on major organs, neural
tissues, blood elements, the immune system, or reproductive
capacity. However, many of these studies were based on small
sample sizes; hence, analyses of trends indicating effects on liver
enzymes, kidney function, T-cell suppression, nerve conduction
velocity, etc., have not been statistically significant. Others
have been non-specific in the search for signs of intoxication in
large groups of workers. However, there are mounting indications
that long-term exposure to relatively high levels of PCP leading to
blood-plasma concentrations as high as 4 ppm is likely to cause
borderline effects on some physiological processes. Some of these
effects, especially those involving the liver and the immune
system, may be caused, in whole or in part, by the
microcontaminants of these chlorophenols, especially H₆CDD.

Several epidemiological studies from Sweden and the USA have
indicated that occupational exposure to mixtures of chlorophenols
is associated with increased incidences of soft tissue sarcomas,
nasal and nasopharyngeal cancers, and lymphomas. In contrast,
surveys from Finland and New Zealand have not detected such
relationships. The major deficiency in all of these studies
appears to be a lack of specific exposure data.

There are no conclusive reports of increased incidences of
cancers in workers exposed specifically to PCP; however, there have
not been any carefully conducted studies of a suitably exposed

occupational group large enough to provide the necessary
statistical power to identify an increase in cancer mortality.
Furthermore, there are few occupational groups that have been
exposed to a single chemical, such as PCP. Finally, the various
levels of microcontaminants in different formulations make
inferences to PCP in general difficult.

Persons non-occupationally exposed to technical PCP in rooms
complained about relatively unspecific symptoms (headache, fatigue,
hair loss, tonsillitis, etc.); a causative connection with PCP
could not be proved or disproved.

2. IDENTITY, PHYSICAL AND CHEMICAL PROPERTIES, ANALYTICAL METHODS

Pentachlorophenol (PCP) and its salt, sodium pentachlorophenate
(Na-PCP), are the most important forms of pentachlorophenol in
terms of production and use. Other derivatives such as the
potassium salt, K-PCP, and the lauric acid ester, L-PCP are of
minor importance. Reflecting this minor role, few data on the
physical and chemical properties of K-PCP and L-PCP are reported in
the literature. Hence, this section primarly concerns PCP and its
sodium salt.

2.1. Identity

2.1.1. Pentachlorophenol (PCP)

Molecular formula: C₆HCl₅O

CAS chemical name: Pentachlorophenol

Common synonyms: chlorophen; PCP; penchlorol; penta;
pentachlorofenol; pentachlorofenolo;
pentachlorphenol; 2,3,4,5,6-
pentachlorophenol

Common trade names: Acutox; Chem-Penta; Chem-Tol; Cryptogil
ol; Dowicide 7; Dowicide EC-7; Dow
Pentachlorophenol DP-2 Antimicrobial;
Durotox; EP 30; Fungifen; Fungol; Glazd
Penta; Grundier Arbezol; Lauxtol; Lauxtol
A; Liroprem; Moosuran; NCI-C 54933; NCI-C
55378; NCI-C 56655; Pentacon; Penta-Kil;
Pentasol; Penwar; Peratox; Permacide;
Permagard; Permasan; Permatox; Priltox;
Permite; Santophen; Santophen 20;
Sinituho; Term-i-Trol; Thompson's Wood
Fix; Weedone; Witophen P

CAS registry number: 87-86-5

2.1.2. Sodium pentachlorphenate (Na-PCP)

Molecular formula: C₆Cl₅ONa
C₆Cl₅ONa x H₂O (as monohydrate)

Common synonyms: penta-ate; pentachlorophenate sodium;
pentachlorophenol, sodium salt;
pentachlorophenoxy sodium; pentaphenate;
phenol, pentachloro-, sodium derivative
monohydrate; sodium PCP; sodium
pentachlorophenate; sodium
pentachlorophenolate; sodium
pentachlorophenoxide

Common trade names: Albapin; Cryptogil Na; Dow Dormant
Fungicide; Dowicide G-St; Dowicide G;
Napclor-G; Santobrite; Weed-beads;
Xylophene Na; Witophen N

CAS registry number: 131-52-2 (Na-PCP);
27735-64-4 (Na-PCP monohydrate)

2.1.3. Pentachlorophenyl laurate

The molecular formula of pentachlorophenyl laurate is
C₆Cl₅OCOR; R is the fatty acid moiety, which consists of a mixture
of fatty acids ranging in carbon chain length from C₆ to C₂₀, the
predominant fatty acid being lauric acid (C₁₂) (Cirelli, 1978b).

2.2. Impurities in Pentachlorophenol

Technical PCP has been shown to contain a large number of
impurities, depending on the manufacturing method (section 3.2.1).
These consist of other chlorophenols, particularly isomeric
tetrachlorophenols, and several microcontaminants, mainly
polychlorodibenzodioxins (PCDDs), polychlorodibenzofurans (PCDFs),
polychlorodiphenyl ethers, polychlorophenoxyphenols, chlorinated
cyclohexenons and cyclohexadienons, hexachlorobenzene, and
polychlorinated biphenyls (PCBs). Table 1 presents analyses of PCP
formulations taken from several publications. According to Crosby
et al. (1981), the quality of PCP is depends on the source and date
of manufacture. Furthermore, analytical results may be extremely
variable, particularly with regard to earlier results, which should
be considered with caution. Jensen & Renberg (1972) detected
chlorinated 2-hydroxydiphenyl ethers, which obviously may transform
to dioxins during gas chromatography, thus giving a false
indication of a higher level of PCDDs. Unlike these "predioxins",
other isomers are not direct precursors of dioxins, and are
labelled "isopredioxins".

Table 1. Impurities (mg/kg PCP) in different technical PCP products
---------------------------------------------------------------------------------------------------
Component Specification, producer, PCP content (%)
Tech- Tech- Tech- Techni- Techni- Techni- Technical^f
nical^a nical^b nical^b,e cal^c,g,h cal^d,i cal^e
Monsanto Dow Dow Dow Dow Dyn. Nobel Rhône-Poulenc
(84.6%) (88.4%) (98%) (90.4%) (ns)^j (87%) (86%)
---------------------------------------------------------------------------------------------------
Phenols
Tetrachloro- 30 000 44 000 2700 10 4000 ns 50 000 70 000
Trichloro- ns < 1000 500 < 1000 ns 20 ns
Higher chlorinated ns 62 000 5000 ns ns ns 70 000
phenoxyphenols

Dibenzo-p-dioxins
Tetrachloro- < 0.1 < 0.05 < 0.05 < 0.05 < 0.2^k < 0.001 < 0.01
Pentachloro- < 0.1 ns ns ns < 0.2 ns ns
Hexachloro- 8 4 < 0.5 1 9 3.5 5
Heptachloro- 520 125 < 0.5 6.5 235 130 150
Octachloro- 1380 2500 < 1.0 15 250 600 600

Dibenzofurans
Tetrachloro- < 4 ns ns ns < 0.2 ns ns
Pentachloro- 40 ns ns ns < 0.2 0.2 ns
Hexachloro- 90 30 < 0.5 3.4 39 10 ns
Heptachloro- 400 80 < 0.5 1.8 280 60 ns
Octachloro- 260 80 < 0.5 < 1.0 230 150 ns

Hexachlorobenzene ns ns ns 400 ns ns ns
---------------------------------------------------------------------------------------------------
^a From: Goldstein et al. (1977).
^b From: Schwetz et al. (1974).
^c From: Schwetz et al. (1978).
^d From: Buser (1975).
^e From: Umweltbundesamt (1985).
^f From: Anon (1983b).
^g Purified.
^h Dowicide EC-7.
ⁱ Dowicide 7.
^j ns = not specified.
^k < = below detection limit.
In Fig. 1, the structures and numbering system for the
polychlorinated dibenzodioxins (PCDDs) and dibenzofurans (PCDFs)
are illustrated.

Since the toxicity of PCDDs and PCDFs depends not only on the
number but also on the position of chlorine substituents, a precise
characterisation of PCP impurities is essential. The presence of
highly toxic 2,3,7,8-tetrachlorodibenzo- p-dioxin (2,3,7,8-T₄CDD)
has only been confirmed once in commercial PCP samples. In the
course of a collaborative survey, one out of five laboratories
detected 2,3,7,8-T₄CDD in technical PCP and Na-PCP samples at
concentrations of 250 - 260 and 890 - 1100 ng/kg, respectively
(Umweltbundesamt, 1985). Buser & Bosshardt (1976) found detectable
amounts of T₄CDD (0.05 - 0.23 mg/kg) in some samples of different
technical PCP products, but on re-analysis were unable to confirm
the compound's identity. In other cases, T₄CDD has not been
identified at detection limits of 0.2 - 0.001 mg/kg (Table 1).

The higher polychlorinated dibenzodioxins and dibenzofurans
are more characteristic of PCP formulations (Table 1).
Hexachlorodibenzo- p-dioxin (H₆CDD), which is also considered
highly toxic and carcinogenic (section 8), was found at levels of
0.03 - 35 mg/kg (Firestone et al., 1972), 9 - 27 mg/kg (Johnson et
al., 1973), and < 0.03 - 10 mg/kg (Buser & Bosshardt, 1976).
According to Fielder et al. (1982), the 1,2,3,6,7,9-, 1,2,3,6,8,9-,
1,2,3,6,7,8-, and 1,2,3,7,8,9-isomers of H₆CDD have been detected
in technical PCP. The 1,2,3,6,7,8and 1,2,3,7,8,9-H₆CDDs
predominated in commercial samples of technical PCP (Dowicide 7)
and Na-PCP. Octachloro-dibenzo- p-dioxin (OCDD) is present in
relatively high amounts in unpurified technical PCP (Table 1).

Recently, the identification of 2-bromo-3,4,5,6-
tetrachlorophenol as a major contaminant in three commercial PCP
samples (ca. 0.1%) has been reported. This manufacturing by-
product has probably not been detected in other analyses because it
is not resolved from the PCP peak by traditional chromatographic
methods (Timmons et al., 1984).

2.2.1. Formation of PCDDs and PCDFs during thermal decomposition

The thermal decomposition of PCP or Na-PCP yields significant
amounts of PCDDs and PCDFs, depending on the thermolytic
conditions. For pure PCP, dimerization of PCP has been suggested
as an underlying reaction process; in technical PCP, additional
reactions, i.e., dechlorination of higher chlorinated PCDDs and
cyclization of predioxins are involved in forming various and
different PCDD isomers (Rappe et al., 1978b).

Pyrolysis of alkali metal salts of PCP at temperatures above
300 °C results in the condensation of two molecules to produce
OCDD. PCP itself forms traces of OCDD only on prolonged heating in
bulk and at temperatures above 200 °C (Sandermann et al., 1957;
Langer et al., 1973; Stehl et al., 1973).

Although present in original technical PCP products, a number
of PCDDs, other than OCDD, are generated during thermal
decomposition (290 - 310 °C) in the absence of oxygen (Table 2)
(Buser, 1982).

Table 2. PCDDs (mg/kg PCP) in the
pyrolysate of technical PCP and Na-PCP^a
--------------------------------------
PCP Na-PCP
--------------------------------------
2,3,7,8-T₄CDD -^b -^c
1,2,3,7,8,9-H₆CDD 53 2.1
1,2,3,6,7,8-H₆CDD 66 0.95
Total H₆CDD 455 10.5
H₇CDD 5200 65
OCDD 15 000 200
--------------------------------------
^a From: Buser (1982).
^b Detection limit (1 mg/kg).
^c Detection limit (0.25 mg/kg).

2.3. Physical, Chemical, and Organoleptic Properties

Pure pentachlorophenol consists of light tan to white,
needlelike crystals. It has a pungent odour when heated (Windholz,
1976). Its vapour pressure suggests that it is relatively
volatile, even at ambient temperatures. Since PCP is practically
insoluble in water at the slightly acidic pH generated by its
dissociation, readily water-soluble salts such as Na-PCP are used
as substitutes, where appropriate.

Na-PCP is non-volatile; its sharp PCP odour results from slight
hydrolysis (Crosby et al., 1981). Technical PCP consists of
brownish flakes or brownish oiled, dustless flakes, coated with a
mixture of benzoin polyisopropyl and pine oil. Technical Na-PCP
consists of cream-coloured beads (Anon., 1983a,b). Technically
pure L-PCP consists of a brown oil that is insoluble in water and
alcohols, and soluble in non-polar solvents, oils, fats, waxes, and
plasticizers (Cirelli, 1978b).

PCP is non-inflammable and non-corrosive in its unmixed state,
whereas a solution in oil causes deterioration of rubber (Mercier,
1981).

Because of the electron withdrawal by the ring chlorines, PCP
behaves as an acid, yielding water-soluble salts such as sodium
pentachlorophenate. Due to nucleophilic reactions of the hydroxyl
group, PCP can form esters with organic and inorganic acids and
ethers with alkylating agents, such as methyl iodide and
diazomethane (Crosby et al., 1981). This property has been used
for analytical purposes (section 2.5.2).

PCP may exist in two forms: the anionic phenolate, at neutral
to alkaline pH, and the undissociated phenol at acidic pH. At pH
2.7, PCP is only 1% ionized; at pH 6.7, it is 99% ionized (Crosby
et al., 1981). Other relevant properties of pure PCP and Na-PCP
are shown in Table 3.

PCDDs and PCDFs may also be formed during the combustion of
materials treated with either purified or technical PCP. Smoke from
birch leaves impregnated with purified Na-PCP and burnt on an open
fire showed considerably increased amounts of PCDDs compared with
the original sample (Table 4). The mass fragmentograms revealed 14
of the 22 possible T₄CDD isomers with 1,3,6,8- and 1,3,7,9-T₄CDD as
the main and 2,3,7,8- T₄CDD as minor isomers. The formation of
PCDFs, including small amounts of 2,3,7,8-T₄CDF, during either
combustion or micropyrolysis (280 °C, 30 min) was only observed in
technical PCP samples; purified Na-PCP was negative in this respect
(Rappe et al., 1978b).

Table 3. Physical, chemical, and organoleptic properties of PCP
and Na-PCP
------------------------------------------------------------------
PCP Na-PCP
------------------------------------------------------------------
Boiling point^a 310 °C (decomposition)

Relative molecular mass^b 266.4 288.3
306.3
(monohydrate)

Melting point^a 191 °C

Density (d₄²² in g/ml)^b 1.987 2

Vapour pressure kPa (mmHg)
at 20 °C^c 2 x 10^-6 (1.5 x 10^-5)
at 19 °C^d 6.7 x 10^-7 (5 x 10^-6)

Saturation vapour density 220
(µg/m³) (20 °C)^c

Steam volatility^e 0.167
(g/100 g water vapour)
(100 °C)
------------------------------------------------------------------

Table 3 (contd.)
------------------------------------------------------------------
PCP Na-PCP
------------------------------------------------------------------
Solubility in fat 213
(g/kg) (37 °C)^f

n-Octanol/water partition 4.84 (pH 1.2);
coefficient (log P)^g 3.56 (pH 6.5);
3.32 (pH 7.2);
3.86 (pH 13.5)

pKa (25 °C)^e 4.7

Solubility in water:
(g/litre)^e,h,i
0 °C, pH 5 0.005
20 °C, pH 5 0.014
30 °C, pH 5 0.020
20 °C, pH 7 2
20 °C, pH 8 8
20 °C, pH 10 15 > 200
25 °C 330

Solubility in organic
solvents (g/100 g)
(25 °C)^b:
acetone 50 35
benzene 15 insoluble
ethanol (95%) 120 65
ethylene glycol 11 40
isopropanol 85 25
methanol 180 25

Odour threshold 1.6 (in water)
(mg/litre)^j:

Olfactory threshold 0.03 (in water)
(mg/litre)^j:
------------------------------------------------------------------
^a From: IRPTC (1983).
^b From: Cirelli (1978b).
^c From: Zimmerli (1982).
^d From: Dobbs & Grant (1980).
^e From: Crosby et al. (1981).
^f From: Rippen (1984).
^g From: Kaiser & Valdmanis (1982).
^h From: Gunther et al. (1968).
ⁱ From: Bundesamt für Umweltschutz (1982).
^j From: Dietz & Traud (1978a).

Jansson et al. (1978) observed a very wide range of PCDD
concentrations in the smoke from burning wood chips impregnated
with a technical PCP formulation (Table 4). The formation of PCDDs
was favoured by temperatures below 500 °C, oxygen deficit, and
lower gas-retention time. The results given in Table 4 are
corrected for the very low background values obtained by burning
untreated wood chips.

When technical PCP was burnt in a quartz reactor (600 °C, 10
min), Lahaniatis et al. (1985) identified the following thermolytic
products: pentachlorobenzene, hexachlorobenzene, octachlorostyrole,
octachloronaphthaline, decachlorobiphenyl, H₆CDF, OCDF, and OCDD.
2,3,7,8-T₄CDD was not detected at a detection limit of 1 mg/kg PCP.

Olie et al. (1983) found only slightly higher levels of PCDDs
and PCDFs in the fly ash of burned new wood treated with PCP
compared with painted wood, which was more than 60 years old.
However, because data were missing on PCDD/PCDF levels in the
original samples and on the conditions of burning, meaningful
interpretation of these results is not possible.

2.4. Conversion Factors

1 ppm = 10.9 mg PCP/m³ (25 °C, 101.3 kPa)
1 mg PCP/m³ = 0.09 ppm

Table 4. Amount of PCDDs in the original sample and in
the smoke from combusted materials treated with purified
Na-PCP or technical PCP
----------------------------------------------------------
Birch leaves^a Wood chips^b
(mg PCDDs/kg Na-PCP (mg PCDDs/kg PCP
(purified)) (technical))
Original Smoke^c Original Smoke^c,d
sample sample
----------------------------------------------------------
T₄CDD < 0.02 5.2 nd^e < 4.7 - 47
P₅CDD < 0.03 14 nd < 1.2 - 419
H₆CDD < 0.03 56 7 < 9.3 - 93
H₇CDD 0.3 172 93 < 4.7 - 279
OCDD 0.9 710 186 < 0.9 - 442
----------------------------------------------------------
^a Adapted from: Rappe et al. (1978b).
^b Adapted from: Jansson et al. (1978).
^c Smoke trapped on charcoal filter.
^d Depending on combustion conditions.
^e nd = not determined.

2.5. Analytical Methods

A number of methods have been used to determine PCP in a
variety of media. The earlier procedures were reviewed by Bevenue
& Beckman (1967). They were mostly based on colour reactions,
which are not very specific and relatively insensitive. For
several years, more sophisticated devices have been available to
analysts, of which gas chromatography has become the method of
choice (Table 5).

Table 5. Analytical methods for the determination of PCP
---------------------------------------------------------------------------------------------------------
Medium Sampling method Analytical method Detec- Detection Reco- Reference
tion limit very
---------------------------------------------------------------------------------------------------------
Air

Air- Impinger collection Derivatization with diazo- EC^a 0.22 mg/m³ ns^c Hoben et al.
aerosol with KOH; hexane methane; purification in (1976a)
extraction chromatoflex Florisil
column; GC^d analysis

Air Filter and bubbler HPLC^e analysis; column: UV₂₅₄^b 0.27 mg/m³ 95.3- NIOSH
collection; ethylene µ Bondapack C₁₈; mobile 100.9% (1978)
glycol extraction phase: methanol/water

Air Bubbler collection; Derivatization with acetyl EC 0.05 µg/m³ ns Dahms &
absorption in K₂CO₃ chloride; GC analysis Metzner
solution; hexane (1979)
extraction

Air Adsorption on to GC analysis EC 0.5 µg/m³ ns Zimmerli &
filter papers Zimmermann
impregnated with (1979)
adsorbant extraction
concentration in ether

Air Impinger collection; HPLC analysis; column: UV₂₂₅ 0.5 µg/m³ ns Woiwode et
absorption in K₂CO₃- Lichrosorb C₁₈; mobile al. (1980)
solution; benzene phase: methanol
extraction

Air Air from wood samples GC analysis EC ns 89.7- Warren et
in reactor tube ads- (< 1.5 99.9% al. (1982)
orbed on silica gel; µg/m³)
desorption with benzene

Air Impinger collection; Derivatization with acetic EC ns ns Kauppinen &
absorption in anhydride in presence of Lindroos
toluene pyridine; GC analysis (1985)
---------------------------------------------------------------------------------------------------------

Blood Benzene extraction Derivatization with diazo- EC 20 µg/litre 87- Bevenue et
(human) from acidified methane; GC analysis 100% al. (1968)
solution

Blood, Ethyl ether extrac- No derivatization; GC anal- EC-³H 0.1 ng 90- Barthel et
urine, tion from acidified ysis; column: 3% diethylene EC-⁶³Ni 0.02 ng 100% al. (1969)
tissue solution; NaOH ex- glycol succinate + 2% H₃PO₄;
(human) traction; benzene confirmation by MS and TLC
extraction

Organic Hexane/isopropanol Der. with acetic anhydride EC ns 81-91% Rudling
tissues extraction from in presence of pyridine; (1970)
acidified sample; GC analysis
borax extraction

Urine Ethyl ether extrac- Derivatization with diazo- EC 10 µg/litre 92- Shafik et
(rat) tion from acidified ethane; GC analysis 98% al. (1973)
solution

Adipose NaOH extraction; Derivatization with diazo- EC 5 µg/kg 75% Shafik
tissue diethyl ether methane; GC analysis (1973)
(human) extraction from
acidified solution

Urine, Acidic hydrolysis No derivatization; negative MS^f 1 ng 90% Dougherty &
seminal (urine); hexane/2- chemical ionization (NCI) Piotrowska
fluid propanol or hexane/ mass spectrometry; internal (1976a;b)
(human) ether extraction from standard: p-chlorobenzophenone
acidified solution

Tissue, Hexane or benzene Derivatization with diazo- EC 20 µg/kg 91.4- Hoben et al.
plasma, extraction ethane (urine) or diazo- 95.3% (1976a)
urine methane; purification in
(rat) chromatoflex Florisil column;
GC analysis
---------------------------------------------------------------------------------------------------------

Table 5. (contd.)
---------------------------------------------------------------------------------------------------------
Medium Sampling method Analytical method Detec- Detection Reco- Reference
tion limit very
---------------------------------------------------------------------------------------------------------
Tissues Acetone extraction (a) TLC^g analysis on silica Radio- ns ns Glickman et
(fish) gel UV₂₅₄; mobile phase: active al. (1977)
methylene chloride

Acetone extraction (b) Derivatization with MS ns ns Glickman et
methyl iodide and K₂CO₃; al. (1977)
GC analysis

Urine Hexane extraction Derivatization with acetyl EC 10 µg/litre ns Dahms &
(human) from acidified chloride in the presence of Metzner
solution pyridine; GC analysis (1979)

Urine Benzene extraction Derivatization with diazo- EC 1 µg/litre 93.2- Edgerton
(human, from acidified methane; separation of 97.2% et al.
rat) solution methylated phenols in acid (1979)
alumina column; GC analysis;
GC-MS confirmation

Plasma Benzene extraction Derivatization with acetic EC 50 µg/litre 91- Eben et
(human) anhydride; GC analysis 102% al. (1981)

Urine Acidic or enzymatic Derivatization with acetic EC 20 µg/litre 77- Eben et
(human) hydrolysis; ethyl anhydride; GC analysis 98% al. (1981)
ether extraction;
benzene extraction

Tissues, Diethyl ether (ethyl Purification on Hypersil- UV₂₁₆ 1 µg/kg 62- Mundy &
serum, acetate-hexane) cartridge; mobile phase: 108% Machin
egg extraction from NaOH methanol; HPLC analysis (1981)
yolk/ (hydrochloric acid)
white solution; concentra-
tion by evaporation
---------------------------------------------------------------------------------------------------------

Table 5. (contd.)
---------------------------------------------------------------------------------------------------------
Medium Sampling method Analytical method Detec- Detection Reco- Reference
tion limit very
---------------------------------------------------------------------------------------------------------
Urine Acidic hydrolysis; HPLC analysis; column: Sphe- UV₃₁₃ 10 µg/litre 102% Drummond
(human) distillation; methy- risorb-ODS; mobile phase: et al.
lene chloride ex- acetonitrile; internal stan- (1982)
traction from acidi- dard: 3,5-dichloro-2,3,6-
fied solution; tribromophenol (DTP)
evaporation and
redistillation in
acetonitrile

Urine Acidic hydrolysis; LC analysis; column: Spheri- UV₂₅₄ 0.1 83.3± Pekari &
(human) hexane/isopropanol sorb-ODS; mobile phase: µmol/litre 3.7% Antero
extraction; evap- methanol (27 µg/litre) (1982)
oration and redis-
tillation in methanol

Urine Acidic hydrolysis; Derivatization with acetic SIM-MS^h 1 nmol/litre ns Harge-
(human) int.standard (4,6- or propionic anhydride; (0.27 sheimer &
dibromo- o-cresol) GC analysis µg/litre) Coutts
added; methylene (1983)
chloride extraction

Food

Milk Benzene extraction; Derivatization with acetic EC 5 µg/litre 80- Erney
(bovine) extraction with anhydride; GC analysis 87.2% (1978)
K₂CO₃ solution

Milk Sulfuric acid Purification in BioSil EC 10 - 15 80% Lamparski
(bovine) digestion; hexane A-column; derivatization µg/litre et al.
extraction with diazomethane; GC (1978)
analysis

Carrots, Soxhlet extraction Derivatization with diazo- EC 0.2 µg/kg 80- Bruns &
potatoes (carrots) or blending ethane; purification in 108% Currie
with acidified Florisil-column; GC (1980)
acetone analysis
---------------------------------------------------------------------------------------------------------

Table 5. (contd.)
---------------------------------------------------------------------------------------------------------
Medium Sampling method Analytical method Detec- Detection Reco- Reference
tion limit very
---------------------------------------------------------------------------------------------------------
Canned Methylene chloride Derivatization with diazo- EC ns 92- Heikes &
food and extraction from methane; purification in (< 0.3 103% Griffitt
jar lids acidified solution; Florisil-column; GC analysis µg/kg) (1980)
clean-up by gel perme-
ation chromatography

Edible Alkaline hydrolysis; Direct GC analysis on DEGS/ EC 5 - 10 µg/kg 83- Stijve
gelatins iso-octane extraction phosphoric acid column; con- 108% (1981)
from acidified firmation by GC analysis of
solution acetate derivative

Plant Maceration with acidi- Derivatization with diazo- EC ns 94.2% Fuchs-
mater- fied acetone; methane; purification in bichler
ials chloroform extr.; Florisil-column; GC analysis (1982)
cleanup by automated
gel chromatography

Mush- Steam distillation (a) Derivatization with ace- EC 0.5 µg/kg 92% Schönhaber
rooms from acidified sample; tic anhydride GC analysis fresh weight et al.
dichloromethane (b) HPLC analysis; column: UV₂₂₀ 0.5 µg/kg (1982)
extraction LiChrosorb RP-8; mobile
phase: methanol/ o-phos-
phoric acid

Soil

Soil NaOH extraction; Derivatization with diazo- EC 0.1 - 1 > 97% Renberg
clean-up by ion methane; GC analysis µg/kg (1974)
exchanger

Soil Nielsen-Kryger steam Direct GC analysis on fused EC ns 58- Narang et
distillation from silica SE 54 column 95% al. (1983)
acidified soil;
toluene-methylene
chloride extraction
---------------------------------------------------------------------------------------------------------

Raw and Petroleum ether TLC analysis on Al₂O₃ Colori- 0.5 µg/litre 75- Zigler &
treated extraction from plates; mobile phase: metric 100% Phillips
water acidified sample; (a) benzene;(b) NaOH/acetone; (1967)
evaporation; chromogenic agent: AgNO₃/2-
drying; evaporation phenoxyethanol

Natural, Benzene extraction Derivatization with acetic EC 0.01 84- Chau &
waste and K₂CO₃-solution anhydride; hexane extrac- µg/litre 93% Coburn
water tion; GC analysis (1974)

River Hexane/ethyl ether Derivatization with boron MS 0.01 ns Matsumoto
water extraction; ethyl trifluoride methanol and µg/litre et al.
acetate extraction trimethylsilyl; GC analysis (1977)
from acidified
solution

Surface Toluene extraction; Derivatization with acetic EC 0.01 85% Wegman &
water extraction with anhydride; petroleum ether µg/litre Hofstee
K₂CO₃-solution extraction; GC analysis (1979)

Waste Chloroform extraction Direct HPLC analysis of UV₂₅₄ 10 µg/litre ns Ervin &
water from acidified sample; chloroform extract; column: McGinnis
rotary evaporation silica gel; mobile phase: (1980)
cyclohexane-acetic acid and
other solvents

Surface Diethyl ether Direct HPLC analysis UV₂₁₅ 20 µg/litre > 80% Ivanov &
water extraction; evapor- Magee
ation; dissolution in (1980)
methanol-petroleum

Surface Chloroform extraction Direct analysis in double Absorp- 5 - 10 92- Carr et
water from acidified beam UV spectrophotometer tion µg/litre 102% al. (1982)
sample;NaOH extraction (320 nm)
---------------------------------------------------------------------------------------------------------

Table 5. (contd.)
---------------------------------------------------------------------------------------------------------
Medium Sampling method Analytical method Detec- Detection Reco- Reference
tion limit very
---------------------------------------------------------------------------------------------------------
Surface Concentration by GC analysis (no deriviti- EC 0.01 95 ± Rübelt et
water extraction, ads- zation); column: Carbowax µg/litre 3% al. (1982)
orption, rotary 20 M plus phosphoric acid;
evaporation confirmation by MS

Surface, Addition of Na₂HPO₄ Extraction and derivitzation EC 1 ng/litre 98- Abrahams-
waste, buffer solution by adding hexane containing 100% son & Xie
drinking-(for acid waste water internal standard (2,6-dibro- (1983)
water pH adjustment to 7 mophenol) and acetic anhy-
with NaOH dride directly to sample;
GC analysis

Water Samples prepared from HPLC analysis with isocratic UV₂₈₀ 21 ng ns Buckman et
stock solutions in elution of various substitu- al. (1984)
acetonitrile ted phenols

Wood

Wood Chloroform extraction TLC analysis on silica gel UV 0.06 µg ns Henshaw et
from wood shavings plates; developing solvent: al. (1975)
cyclohexane-acetone-paraffin

Wood- Soxhlet extraction Derivatization with diazo- EC ns 30-70% Levin &
dust with ether ether; methane; GC analysis Nilsson
evaporation; dissol- (1977)
ution in acetone;
TLC separation;
hexane elution

Lumber Pulverization of wood HPLC analysis; column: Sphe- UV₂₃₀ 0.1 µg/cm² ns Daniels &
(sur- sample; extraction risorb-ODS; mobile phase: Swan
face with acetonitrile water-acetonitrile-acetic (1979)
treated) containing internal acid
standard; ultrasonic
bath
---------------------------------------------------------------------------------------------------------

Table 5. (contd.)
---------------------------------------------------------------------------------------------------------
Medium Sampling method Analytical method Detec- Detection Reco- Reference
tion limit very
---------------------------------------------------------------------------------------------------------
Sawdust, Extr. with acetic TLC analysis; different sol- Colour 2 mg/kg ns Ting &
wood- acid-methanol; evap- vent systems; sprayed with reaction Quick
shavings oration; conversion tetrabase reagent (1980)
to chloranil in warm
nitric acid

Various materials

Toy Soxhlet extraction Direct GC analysis; confirm- FIDⁱ 1 - 4 mg 70- von
paints with acetone; concen- ation by TLC analysis /litre 100% Langeveld
tration by evaporation (1975)

PCP Dioxane extraction HPLC analysis; column: Bon- UV₂₅₄ ns 97% Hayes
formula- dapakC₁₈; mobile phase: (1979)
tions methanol/PIC A (paired ion
chromatography A reagent)
and water/PIC A

Sedi- Homogenization; Derivatization: pyrolytic EC 0.5 - 25 92.8- Butte et
ment, toluene extraction ethylation with triethyl µg/kg 97.6% al.
clams from acidified sample sulfonium-iodide; GC anal- (1983)
containing 2,4,6- ysis; confirmation by MS
tribromophenol as
internal standard
---------------------------------------------------------------------------------------------------------

Table 5. (contd.)
---------------------------------------------------------------------------------------------------------
Medium Sampling method Analytical method Detec- Detection Reco- Reference
tion limit very
---------------------------------------------------------------------------------------------------------
Tallow Vortex mixing; auto- Derivatization with diazo- EC 1 µg/kg 80- Lee et
mated gel permeation methane; Florisil-column; 107% al.
chromatographic clean- GC analysis; confirmation (1984)
up; rotary evapora- with MS
tion; solution in
hexane

Indus- Hexane extraction Derivatization with penta- 0.1 pg ns Sha &
trial (for starch: after fluorobenzyl bromide; GC EC Duffield
starch, steam distillation) analysis and negative ion (1984)
surface chemical ionization MS MS
water (NICI-MS) analysis
---------------------------------------------------------------------------------------------------------
^a EC = electron-capture detector.
^b UV = ultraviolet.
^c ns = not specified.
^d GC = gas chromatography.
^e HPLC = high-performance liquid chromatography.
^f MS = mass spectrometry.
^g TLC = thin-layer chromatography.
^h SIM = selected ion monitoring.
ⁱ FID = flame ionization detector.
^j NICI = negative ion chemical ionization.
The determination of PCP is based on the distinctive properties
of this substance: steam distillation is possible because of its
volatility; its acidic behaviour is used in extracting it into a
base and in ion-exchange chromatography; the electro-positive ring
reinforces selective chromatographic adsorption and the absorption
of ultraviolet radiation; finally, the reactivity of PCP with
certain organic compounds to form esters, ethers, and coloured
derivatives is of great importance for its detection and
measurement (Crosby et al., 1981).

Most of the analytical methods used today involved
acidification of the sample to convert PCP to its non-ionized form,
extraction into an organic solvent, possible cleanup by back-
extraction into basic solution, and analysis by gas chromatography
or other chromatographic methods as ester or ether derivatives. In
the following section, the sampling and analytical methods is
described as reviewed mainly by Bevenue & Beckman (1967), Gebefuegi
et al. (1979), and Crosby et al. (1981). In addition, the more
recently published methods for PCP determination in various
matrices are summarized (Table 5).

2.5.1. Sampling methods

In principle, the sampling techniques summarized by Bevenue &
Beckman (1967) are still the methods of choice; more recent methods
are included in Table 5.

The first step in preparing a sample consisting of a solid
material is a thorough pulverization or homogenization in special
mills or blenders. Maceration of the sample in a blender with an
organic solvent is more rapid than Soxhlet extraction and similar
efficiencies can be achieved with both procedures (Bruns & Currie,
1980).

For cellulose materials, adhesives, agricultural commodities,
biological tissues, and water, an initial extraction with dilute
sodium hydroxide solution at room temperature for several hours,
followed by acidification and steam distillation may be preferable.
For samples that contain components strongly complexed with PCP,
such as soybean oil, treatment with hot concentrated sulfuric acid
is recommended prior to steam distillation. Liquid-liquid
partitioning or distillation of the filtered extract at the boiling
point of water may also be used to isolate PCP (Bevenue & Beckman,
1967).

When alkaline soil extracts are acidified, gel formation can
occur at pH values lower than 6, resulting in interference with the
extraction of PCP. According to Renberg (1974), proper separation
is possible if the acidic substances are bound, under alkaline
conditions, to an anion ion exchanger.

When analysing liquid materials, particularly urine samples,
the sample should first be hydrolysed by heating the acidified
urine to free the PCP moiety of its sulfate and glucuronide
conjugates (Edgerton & Moseman, 1979; Drummond et al., 1982; Butte,

1984). Enzymatic hydrolysis is questionable, because the metabolite
tetrachlorohydroquinone strongly inhibits the enzyme
beta-glucuronidase (Ahlborg et al., 1974).

For determining the PCP content of air several possible
sampling procedures are described by Gebefuegi et al. (1979)
including: absorption in liquids, such as potassium carbonate
(K₂CO₃) solution or ethylene glycol; adsorption on activated
charcoal or silica gel; freezing and condensing by sucking the air
through cooling traps; or derivatization by phenolate formation in
alkaline solution. By pumping high volumes of air through the
sample-collecting device, PCP is concentrated in the collector,
thus enhancing the detection limit.

Concentration is also required for other matrices with
relatively low PCP contents. For water samples, procedures used
involve the separation of PCP from the water by distillation,
sublimation, freeze-drying, adsorption, and extraction (Rübelt et
al., 1982). The extraction solvents, in turn, are concentrated by
distillation or evaporation.

Only a few investigators have used internal standards, adding
specific substances to the samples to check for completeness of
recovery during the extensive solvent extractions and manipulative
steps required. Drummond et al. (1982) used 3,5-dichloro-2,3,6-
tribromophenol, while Needham et al. (1981) incorporated 2,4,6-
tribromophenol, and Hargesheimer & Coutts (1983) spiked the samples
with 4,6-dibromo- o-cresol.

Most recovery data given in Table 5 were obtained by spiking
samples with known amounts of PCP and carrying them through the
entire analytical procedure. Ernst & Weber (1978a) used ¹⁴C-PCP
for this purpose. To check the efficiency of acetylation, Rudling
(1970) compared spiked samples with a pentachlorophenyl acetate
standard. According to NIOSH (1978), an appropriate correction
factor should be used if recovery of PCP in air samples is less
than 95%.

Using the analytical method of Erney (1978) (Table 5), Zimmerli
et al. (1980) found that only about 8% of "endogenous" PCP was
extractable from raw bovine milk, though 82.5% of known amounts of
PCP added had been recovered on average. A complete extraction was
only achieved by acid or alkaline pretreatment of the milk (cf.,
Lamparski et al., 1978) (Table 5), which probably releases the PCP
bound to proteins. Zimmerli et al. (1980) concluded from this
finding that recovery data may indicate values that do not
correspond to the true recovery.

2.5.2. Analytical methods

Earlier methods, which have been thoroughly reviewed by Bevenue
& Beckman (1967), were based on the formation of coloured
derivatives from the reaction of PCP with either nitric acid or 4-
aminoantipyrine. Other reagents commonly used in this respect are

p-nitraniline, sulfanilic acid, and 3-methyl-2-benzenethiazoline-
hydrazine (Koppe et al., 1977). As already mentioned, these
colorimetric or spectrometric methods are not very specific and
comparatively insensitive, and therefore only suitable for pure
solutions or for production and routine controls. They may be of
some importance in determining total phenolics, for example, in the
monitoring of levels of phenolics in surface and waste waters.
However, comparative studies, in which 45 laboratories within the
European Communities participated, revealed that photometric
procedures gave rather different results, depending on specific
laboratory conditions (Sonneborn, 1976; Rübelt et al., 1982).
According to Crosby et al. (1981), colorimetric or
spectrophotometric procedures achieve a sensitivity that is, at
best, in the low ppb-range (1:109).

Gas chromatography, particularly when combined with an
electron-capture detector, substantially lowers the detection
limits to the ppt-range (1:10¹¹ - 1:10¹²) and is therefore the
preferred method today. Very few investigators have applied direct
gas chromatography after the extraction procedures. To reduce peak
tailing, derivatization of PCP with appropriate compounds prior to
analysis is preferred. Diazomethane is most commonly used to
produce the methyl ether. As shown in Table 5, this method, which
is based on the work of Bevenue et al. (1966), has been used to
determine PCP in a variety of matrices including blood, urine,
fish, soil, and water. According to Crosby et al. (1981), it is
an official method for regulatory analysis in the USA. The
procedure for measuring PCP in blood and urine samples as
recommended by the National Institute for Occupational Safety and
Health (NIOSH), USA, is described by Eller (1984a,b).

Other alkyl ethers have been produced as derivatives of PCP,
including the ethyl, propyl, 1-butyl, isobutyl, amyl, and isoamyl-
PCP (Cranmer & Freal, 1970). Besides the potential health risk
incurred when using hazardous reagents such as diazomethane or
dimethyl sulfate, the alkylation method is subject to interferences
from other compounds with active H-atoms, e.g., carboxy acid
herbicides such as 2,4-dichloro-and 2,4,5-trichlorophenoxyacetic
acid (Chau & Coborn, 1974; Crosby et al., 1981). These drawbacks
are avoided by the acetylation of PCP with acetic anhydride to give
acetyl-PCP as reported by Rudling (1970), Chau & Coborn (1974), and
other research workers (Table 5).

Several techniques, other than gas chromatography, have been
used in connection with electron-capture detection. These include
thermal conductivity and microcoulometric detectors (Bevenue &
Beckman, 1967), thin-layer chromatography (TLC), gas chromatography
in connection with mass spectrometry (MS), and high-performance
liquid chromatography (HPLC) equipped with UV detectors. In
particular, the last two methods have become more and more
prevalent as reflected by Table 5. In many cases, mass
spectrometry has been used to confirm the identity of PCP peaks
determined by EC detectors. Dougherty & Piotrowska (1976a) and
Kuehl & Dougherty (1980) screened environmental and tissue samples
for PCP using negative chemical ionization (NCI) mass spectrometry.

This method provides a sensitivity of detection comparable to GC-
ECD analysis. Moreover, it can be used for compound
identification. Since both of these methods require an extensive
amount of pretreatment, a procedure had to be adopted for PCP
determination by which samples could be measured simply and
precisely, without the tedious extraction and formation of
derivatives needed for the other methods. High-performance liquid
chromatography offers these advantages, as using this method direct
determination of PCP is possible, giving peaks of constant height
and high resolution. Comparative GC-ECD and HPLC analyses of
mushrooms conducted by Schönhaber et al. (1982) resulted in similar
detection limits (Table 5).

Detection limits depend not only on the sensitivity of the
detection systems, but also, to a great extent, on the volume of
the sample. The detection limits given in Table 5 refer to the
smallest amounts of PCP detectable using the procedure and sample
size described by the authors. In many cases, it would be possible
to lower the detection limit by taking larger samples, particularly
in the case of gaseous and fluid matrices.

Analytical interferences may become a problem in PCP analysis
for residues, particularly at low measurement levels. Bevenue &
Ogata (1971) reported errors during the determination of PCP in the
picogram range, because of analytical-grade reagents such as sodium
hydroxide. Arsenault (1976) observed an apparent contamination of
samples with PCP from the general laboratory atmosphere. However,
measuring blank samples as controls and purifying reagents should
exclude false data. For example, Dietz & Traud (1978b) distilled
the extraction solvent diethyl ether to remove the antioxidant BHT
(2,6-di- tert-butyl-4-methyl-phenol). Similarly, the authors
recommended the distillation of dioxan prior to its use as
extraction solvent; otherwise, some volatile impurities could
interfere with the measurement of PCP.

Substances interfering during gas chromatography may cause more
of a problem. These include chloronaphthalenes, polychlorinated
biphenyls (PCBs), pesticides such as diuron, and p-methoxytetra-
chlorophenol. Arsenault (1976) therefore questioned the GC-ECD
method in the µg range. In a thorough study on phenolics in water
(Rübelt et al., 1982), derivatization was omitted because non-
specific reactions might occur in complex mixtures, e.g., in
polluted waters. The working group achieved best results in terms
of separation of chlorophenols with a column of 10% Carbowax 20 M
plus 2% phosphoric acid, the mobile phase being nitrogen enriched
with formic acid. The latter was found to prevent tailing
resulting from adsorption of chlorophenols on the packing material
of the column. For quantitative analysis with an unequivocal
identification, it has been recommended that after gas
chromatographic separation the carrier gas should be split and
conducted to both an electron capture detector (ECD), and a flame
ionization detector (FID), as well as to a mass spectrometer (MS).

3. SOURCES OF HUMAN AND ENVIRONMENTAL EXPOSURE

3.1. Natural Occurrence

Arsenault (1976) hypothesized the existence of a natural
background level of PCP or analytically similar compounds. He
suggested this on the basis that paramethoxytetrachlorophenol, a
metabolite of a fungus, could interfere with the GC-EC analysis of
PCP, because of its similar molecular size, shape, and retention
time. The hypothesis of a natural background level of PCP has not
been examined further. Unsuccessful attempts to produce higher
chlorophenols by enzymatic conversion (Siuda, 1980) suggest that
sources of environmental PCP are exclusively related to human
activities.

3.2. Man-Made Sources

3.2.1. Industrial production

3.2.1.1 Manufacturing processes

PCP was first synthesized by Merz & Weith (1872) using a
similar preparation method to that currently used during commercial
production (Prager et al., 1923). The use of PCP as a wood
preservative started in the late 1930s (Doedens, 1964).

PCP is produced by one of two methods: direct chlorination of
phenols and hydrolysis of hexachlorobenzene. The direct
chlorination is carried out in two steps. First, liquid phenol,
chlorophenol, or a polychlorophenol is bubbled with chlorine gas at
30 - 40 °C to produce 2,4,6-trichlorophenol, which is then
converted to PCP by further chlorination at progressively higher
temperatures in the presence of catalysts (aluminum, antimony,
their chlorides, and others). The second method involves an
alkaline hydrolysis of hexachlorobenzene (HCB) in methanol and
dihydric alcohols, in water and mixtures of different solvents in
an autoclave at 130 - 170 °C (Melnikov, 1971). In the Federal
Republic of Germany, PCP is synthesized by means of stepwise
chlorination of phenols. Na-PCP was produced until 1984 using
hexachlorobenzene hydrolysis; now, it is produced by dissolving PCP
flakes in sodium hydroxide solution (BUA, 1986). In the USA, the
general reaction used is the chlorination of phenols (Crosby et
al., 1981).

In addition to the formation of PCP, numerous by-products are
generated, as reflected by analytical profiles in Table 1. The
chlorination procedure yields a technical product that usually
contains a considerable amount of tetrachlorophenols (4 - 12%) due
to incomplete chlorination reactions. The formation of
microcontaminants is favoured by elevated temperatures and
pressure. With both manufacturing methods, toxic by-products, such
as chlorinated ethers, dibenzofurans, and dibenzo- p-dioxins, are
formed. In addition, the alkaline HCB hydrolysis method can result
in the presence of hexachlorobenzene in the resulting PCP (Jensen
& Renberg, 1973; Plimmer, 1973; Firestone, 1977; Jones, 1981).

3.2.1.2 Emissions during production

Some data are available concerning the loss of phenolic and
nonphenolic compounds into the environment during the normal
production of PCP or Na-PCP (Umweltbundesamt, 1985). The following
air emission concentrations (mg/m³) and mass flow values (g/h) were
reported: PCP 0.7 mg/m³, 9 g/h; tetrachlorophenols 0.2 mg/m³, 0.8
g/h; trichlorophenols 0.02 mg/m³, 0.04 g/h; hexachlorobenzene 23.9
mg/m³, 12 g/h; pentachlorobenzene 2 mg/m³, 15.5 g/h;
tetrachlorobenzene 2.8 mg/m³, 66.5 g/h; OCDD 0.05 mg/m³, 0.04 g/h;
OCDF 0.02 mg/m³, 0.002 g/h.

The annual air emission values resulting from the production
of approximately 2000 tonnes of PCP or Na-PCP, respectively, per
annum are given in Table 6.

Table 6. Air emissions of phenolic and non-phenolic
compounds during production (maximum values)^a
------------------------------------------------------
Annual air emissions (kg/year)
during production of:
2000 tonnes 2000 tonnes
PCP/year Na-PCP/year
------------------------------------------------------
PCP 18 65
Other chlorophenols 9 5
Hexachlorobenzene - 105
Other chlorobenzenes 1 700
OCDD 0.2 0.2
------------------------------------------------------
^a Adapted from: BUA (1986).

While no waste water occurs during the production of PCP, the
annual loss of various compounds resulting from Na-PCP production
into the waste water was as follows: PCP, 60 kg; OCDD, 0.34 g;
H₇CDDs, 0.1 g; H₆CDDs, 0.001 g; OCDF, 0.1 g; H₇CDFs, 0.026 g;
H₆CDFs, 0.002 g (BUA, 1986).

3.2.1.3 Disposal of production wastes

The volume of contaminated waste water generated during the
production of Na-PCP is small, because manufacturers and regulatory
agencies have emphasized efficient process design (Jones, 1981).

During the production of approximately 2000 tonnes PCP/year,
about 8 tonnes of washing methanol, 4 tonnes of activated charcoal,
and 2 tonnes of other wastes occur. These wastes, as well as the
filtration sludge resulting from Na-PCP production, contain
considerable amounts of hazardous chemicals (Table 7). They are
generally disposed of by either storage in underground disposal
sites (filtration sludge) or incineration at temperatures above
1200 °C (BUA, 1986).

Table 7. Phenolic and non-phenolic compounds in the combined
wastes (PCP production) and filtration sludge (Na-PCP production)
---------------------------------------------------------------
Compound Combined wastes Filtration sludge
(kg/year) (kg/year)
---------------------------------------------------------------
PCP 1350 900
Other chlorophenols 0.7 ns^b
Hexachlorobenzene ns 6000
Decachlorobiphenyl ns 3400
Decachlorophenoxybenzene ns 44
OCDD (OCDF) 0.98 0.67 (0.67)
H₇CDDs (H₇CDFs) 0.13 0.17 (0.045)
H₆CDDs (H₆CDFs) 0.013 0.092 (0.015)
P₅CDDs (P₅CDFs) 0.003 x 10^-3 0.016 (0.005)
T₄CDDs (T₄CDFs) 0.002 x 10^-3 0.007 (0.001)
2,3,7,8-T₄CDD ns 0.001
---------------------------------------------------------------
^a Adapted from: BUA (1986).
^b ns = not specified.

US EPA (1985) proposed that wastes from the production and
manufacturing use of PCP should be classifed as acutely hazardous
wastes, on the basis of the presence of substantial concentrations
of the carcinogenic congener H₆CDD and the chronic toxicity
potential of PCP itself.

3.2.1.4 Production levels

No precise estimates can be made of the total world production
of PCP and Na-PCP. According to the data profile of IRPTC (1983),
90 000 tonnes of PCP per year are produced globally. The Economist
Intelligence Unit (1981) estimated world production to be of the
order of 50 000 - 60 000 tonnes per year, based on the North
American and European Community output. However, the production
figures presented in Table 8 indicate a total production of only
30 000 tonnes per year. The production, foreign trade, and
consumption figures given in this summary table can give only a
rough idea of the true PCP market. Recent restrictions on the use
of PCP (section 3.3), a decline in the forestry industry, and the
increasing use of alternative means of wood preservation have
probably reduced the demand for PCP over the last few years.

The major PCP producers operating in 1980 are shown in Table 9
together with the plant locations and their capacities. Some
additional factories exist in which PCP is mixed or formulated to
yield special end-use products. There are also chemical producers
who sell pure, analytical grade PCP, but do not produce PCP for
technical purposes. The Monsanto Company, which had a capacity of
11.8 kilotonnes in the USA, stopped PCP production in their plant
at Sauget, Illinois, in 1978 (Jones, 1981). Dow Chemical closed
down its manufacturing plant at Midland, Michigan in October 1980
(Jones, 1984). Similarly, the only PCP producing plant in the
United Kingdom, also operated by the Monsanto Company, was closed
down in the same year (Economist Intelligence Unit, 1981), while

Reichhold Chemicals Inc., at Tacoma, Washington, USA ceased PCP
production in 1985. In the Federal Republic of Germany, the
production of PCP and Na-PCP was stopped in 1986.

3.3. Uses

The main advantages of PCP and its derivatives are that they
are effective biocides and soluble in oil (PCP) or water (Na-PCP).
Few pesticides show a similarly broad efficiency spectrum at low
cost. Therefore, PCP and its salts have a variety of applications
in industry, agriculture, and in domestic fields, where they have
been used as algicides, bactericides, fungicides, herbicides,
insecticides, and molluscicides.

3.3.1. Commercial use

In Table 10, the major registered commercial uses of PCP are
broken down for the United Kingdom and the USA. Although PCP and
its derivatives have many uses, by far the major application is
wood preservation. Cirelli (1978a), Hoos (1978), and Jones (1981)
have reported on commercial use patterns in North America. In the
USA, about 80% of PCP is used for commercial wood treatment, 6% is
in use for slime control in pulp and paper production, and 3%
accounts for non-industrial purposes, such as weed control, fence-
post treatment and paint preservation (Crosby et al., 1981);
however, the last two cases imply wood treatment as well. The
remaining 11% is converted to Na-PCP, which in turn is partly used
for wood preservation, mainly sapstain control in waterborne
conditions, e.g., for treating pressboard. Overall, some 95 - 98%
of American PCP production is used directly or indirectly in wood
treatment (Economist Intelligence Unit, 1981).

Table 8. Production, foreign trade, and consumption of PCP and Na-PCP (tonnes per year)
according to data available from government authorities and producers
--------------------------------------------------------------------------------------------------
Belgium/ France^a Germany, Italy^a Nether- United Canada^c USA^d
Luxemburg^a Federal lands^a Kingdom^a
Republic of^b (year (year (year
(year na)^e 1979 1979 1984 na)^e na)^e na)^e 1981 1977
--------------------------------------------------------------------------------------------------
Production
PCP 0 1700 2450 1550 0 0 0 1700 20 349
Na-PCP 0 2800 2100 1750 0 0 0 70

Imports
PCP 150- insigni- 0 0 250 - 30 - na 500 na
Na-PCP 160 ficant 300 0 280 40 na 0 na

Exports
PCP 0 300- 1950 1360 0 0 300 600 approxi-
Na-PCP 0 700 2150 1710 0 0 0 mately
200^f

Consumption
PCP approxi- 1000 500 190 250- 30- 500 1536 na
Na-PCP mately 2500 250 40 280 40 32 na
150
--------------------------------------------------------------------------------------------------
^a From: Economist Intelligence Unit (1981).
^b From: BUA (1986).
^c From: Jones (1984).
^d From: Jones (1981).
^e na = not available.
^f Approximately 1% of domestic sales.
Table 9. Pentachlorophenol producers and their capacities in 1980
--------------------------------------------------------------------
Producer Country Plant Capacity
Location (tonnes)
(total PCP)
--------------------------------------------------------------------
Uniroyal Chemical,^a Canada Clover Bar, 1800
Division of Uniroyal, Ltd Alta

Rhône-Poulenc^b France Pont-de-Claix 4500

Dynamit Nobel^b Germany, Rheinfelden 4000
Federal
Republic of

Dow Chemical, USA^a USA Midland, 13 500
Michigan
--------------------------------------------------------------------

Table 9 (contd.)
--------------------------------------------------------------------
Producer Country Plant Capacity
Location (tonnes)
(total PCP)
--------------------------------------------------------------------

Reichhold Chemicals^a USA Tacoma, 8100
Inc. Washington

Vulcan Material^a USA Wichita, 9000
Company Chemical Division Kansas
--------------------------------------------------------------------
^a From: Jones (1981).
^b From: Economist Intelligence Unit (1981).

Data from Canada and the Federal Republic of Germany confirm
the main use of PCP as a wood preservative. In Canada, about 95%
of the PCP is used for this purpose (Jones, 1981). Approximately
61% of the volume of PCP used in the Federal Republic of Germany in
1983 was used for wood preservation, while considerable amounts of
PCP were used by the textile (13%), leather (5%), mineral oil (6%),
and glue (6%) industries, respectively (Angerer, 1984). No PCP was
used in the paint or pulp industry whereas, in 1974, as much as 3%
or 7%, respectively, were used in these branches. PCP used on
textiles is usually in the form of the PCP ester rather than PCP or
Na-PCP.

Pentachlorophenyl laurate (L-PCP) was developed especially for
application on fabrics (Hueck & LaBrijn, 1960; Bevenue & Beckman,
1967). The estimates of L-PCP use in the United Kingdom in Table
10 are based on a publication from the year 1974 (HMSO, 1974).
According to an unpublished note submitted to the IPCS by Catomance
Limited, Hertfordshire, the sole manufacturer of pentachlorophenyl
laurate in the United Kingdom, the usage pattern in the United
Kingdom has not changed following the cessation of production of
PCP in 1978. However, most of the PCP ester used there today is
said to be for domestic timber preservation; the use of L-PCP for
textile preservation is supposed to be mainly confined to tropical
or semi-tropical countries.

In the USSR, PCP is used for the preservation of commercial
timber, paints, varnishes, paper, textiles, ropes, and leather
(IRPTC, 1984).

Na-PCP is also used to inhibit algal and fungal growth in
cooling tower waters at electric generating plants (Hoos, 1978); in
1976, about 30% of the Na-PCP used in Canada was for this purpose
(Jones, 1981).

Table 10. Major commercial (non-agricultural) uses of PCP in the
United Kingdom and the USA^a
---------------------------------------------------------------------------
Use Active
ingredient
---------------------------------------------------------------------------
United Kingdom
Anti-mildew agent in the wool textile industry L-PCP, Na-PCP
Mothproofing carried out by dyers and cleaners L-PCP
Wood preservation PCP, L-PCP,
Na-PCP
Paint additives PCP
Antimicrobial (slimicide) agents in paper and board PCP
Antifungal agent in textiles other than wool (cotton,
Flax and jute fabric, ropes, cordage and tentage) L-PCP
Cable impregnation L-PCP
Anti-mildew agent in leather ns^b
Fungicide in adhesives Na-PCP
Bactericide in drilling fluids ns^b

USA
Microbiostat for commercial and industrial water cooling Na-PCP
Microbiocide for leather K-PCP, PCP
Microbiocide for burlap, canvas, cotton, rope, and twine PCP
Microbiocide and insecticide for wood treatment PCP, Na-PCP
Preservative for oil and water-based paint PCP
Slime control for pulp and paper PCP
Microbiocide for petroleum drilling mud and flood water PCP
Fumigant for shipping-van interiors PCP
Preservative for hardboard and particle-board PCP
---------------------------------------------------------------------------
^a From: Crosby et al. (1981).
^b ns = not specified.

Alterations in the use pattern have taken place during the last
few years as a result of the increased concern about the potential
health hazards from PCP and its impurities. In Japan, the
production of PCP was 14.5 kilotonnes in 1966 and 3.3 kilotonnes in
1971, after which production ceased entirely (IARC, 1979a). In the
Federal Republic of Germany, 3300 tonnes of total PCP were produced
in the year 1984, of which 93% was exported, leaving 230 tonnes for
use in the country (BUA, 1986). Nine years earlier (1974), 4100
tonnes of PCP were produced, 60% of which were exported; in 1979,
84% of the 4503 tonnes produced were sold abroad (Angerer, 1984).
These figures indicate a drastic decrease in the consumption of PCP
in the Federal Republic of Germany during the last few years. In
Canada, the Federal Republic of Germany, and Sweden, where PCP had
been heavily used as a slime control agent in the paper mills, the
use of chlorinated phenols for this purpose was prohibited in
recent years as a consequence of the discharges, which had toxic
effects on the aquatic environment. In Sweden, all use of PCP was
banned in 1977 (Ahlborg & Thunberg, 1980; Jones, 1981). The US
Environmental Protection Agency does not intend to prohibit the use

of PCP in oil-well water or in pulp and paper mills, provided that
impermeable gloves are worn during application and that the H₆CDD
content will be reduced to 1 ppm (US EPA, 1984b). Similarly, the
use of PCP (including its salts) for wood protection has not been
cancelled in the USA. However, the US EPA (1984a) intends to
establish certain changes in the terms and conditions of
registration.

3.3.2. Agricultural use

Significant quantities of PCP were previously used in a number
of agricultural applications. These resembled industrial uses in
that most were to prevent wood decay, in farm buildings, fences,
and storage facilities (Jones, 1981). However, PCP or its sodium
salt have also been used as a herbicide and dessicant for forage
seed crops, a herbicide for non-food vegetation control, a biocide
in the post-harvest washing of fruit, and as an insecticide for use
in beehives, seed plots, and greenhouses (Crosby et al., 1981).
PCP was formerly used as a herbicide in paddy and upland rice
fields, particularly in Japan (Kobayashi, 1978; Crosby et al.,
1981). In addition, PCP and Na-PCP have been approved for a number
of applications in the food industry, such as biocides in packaging
materials and glues (Table 11).

In the USSR, PCP is applied as a nonselective herbicide and as
a desiccant on cotton plants. At least 10 days should lapse
following cotton plant treatment (IRPTC, 1984).

Table 11. Other uses of PCP and its salts as a potential
source of food contamination^a
-------------------------------------------------------------
Use Specific compound
-------------------------------------------------------------
Slime control on paper and paperboard K-PCP, Na-PCP
Preservative in can-end cement Na-PCP
Defoaming agents Na-PCP
Paper contacting aqueous and fatty food Na-PCP
Animal glue for containers Na-PCP
Sealing gaskets for containers K-PCP, Na-PCP
Preservative for wood products PCP, Na-PCP
Preservative in coatings Na-PCP
Rubber antioxidant Na-PCP
Preservative for ammonium alginate Na-PCP
-------------------------------------------------------------
^a Adapted from: Firestone (1973).

Recently, regulations to limit or even ban some uses of PCP
have been established in a number of countries. The Canadian
government suspended agricultural applications of PCP and Na-PCP in
mushroom culture, above-ground interior woodwork of farm buildings,
and as herbicides and soil sterilants (Jones, 1984). Japan
restricted herbicidal use of PCP because of its high toxicity to
fish (Kobayashi, 1979; Crosby et al., 1981). The paper industry of
the Federal Republic of Germany and Sweden no longer use PCP in
packaging paper (Ahlborg & Thunberg, 1980; Angerer, 1984).

US EPA (1984b) proposed cancelling the registration of
pesticide products containing PCP as the active ingredient for non-
wood preservative uses, i.e., herbicidal and antimicrobial uses.
In addition, PCP-containing wood preservatives for home and farm
use must not be applied where there may be direct contact with
domestic animals or livestock or close contact with food or feed
(US EPA, 1984a).

3.3.3. Domestic use

The largely uncontrolled use of PCP by private individuals is
almost exclusively related to the treatment of wood, both outdoors
and indoors. PCP is the main active ingredient in certain wood
preservatives for home use, and is added to products such as stains
and paints. Although this category of products plays only a minor
role in the overall PCP market, it has been of particular concern,
since cases of apparent PCP intoxication after indoor application
in private homes have been reported (section 5). As a consequence
of such incidents, the use of PCP for the preservation of interior
timber has been banned in Canada (Jones, 1981) and the Netherlands
(Economist Intelligence Unit, 1981). Since 1986, the use of PCP as
a biocide for indoor application has been forbidden in the Federal
Republic of Germany by government regulatory action (FRG, 1986).
Furthermore, there is a gentlemen's agreement between the
government and industry to suspend the use of PCP in wood
preservatives in general (BUA, 1986). The US EPA (1984a) intends
to limit the use of PCP-containing wood preservatives in interiors
to certain support structures. This is also true for the indoor
use of PCP-treated wood. The sale and use of PCP is restricted to
certified applicators. Thus, the domestic use of PCP is not as
significant as it was some years ago.

Other reported applications of PCP include health-care products
and disinfectants for use in the home, farms, and hospitals. PCP
may also be contained in dental-care products (Jones, 1981),
bactericidal soaps, laundry products, and medical products for the
skin (Crosby et al., 1981).

3.3.4. Use for control of vectors

The application of Na-PCP to control vectors of pathogens has
been of some relevance in tropical and subtropical areas. Na-PCP
has been used as a herbicide to control Salvinia sp., a host plant
of Mansonia mosquitos, which transmit the elephantiasis-causing
filarias to man (Chow et al., 1955).

Na-PCP has also been used for control of the intermediate snail
hosts of schistosomiasis (Berry et al., 1950; Toledo et al., 1976).
After World War II, Hunter et al. (1952) proposed Na-PCP as the
molluscicide of choice for use in Japan. In China, Na-PCP is still
in use for this purpose today (Xue, 1986)^a.
___________________________________________________________________
^a Personal communication to the Task Group on Pentachlorophenol.

3.3.5. Formulations

In the treatment of wood, PCP is usually administered as a 5%
solution in a mineral spirit solvent, such as No. 2 fuel oil or
kerosene (Cirelli, 1978a), or methylene chloride, isopropyl
alcohol, or methanol (Ingram et al., 1981a). Since PCP is not very
soluble in hydrocarbon solvents, and tends to migrate to, and
crystallize on, treated wood surfaces (a phenomenon known as
"blooming"), formulations may also contain co-solvents and anti-
blooming agents (David, 1985^a). Most commercial formulations also
contain other chlorophenols, mainly tetrachlorophenol (Nilsson et
al., 1978). The aim of such mixtures is to prevent blooming on
treated wood by lowering the melting point of the chlorophenols.
An aqueous solution of Na-PCP is used for commercial sapstain
control (Konasevich et al., 1983).

Chlorophenols may be combined with other active components such
as methylene bisthiocyanate and copper naphthenate in the
formulation of PCP pesticides (von Rümker et al., 1974).
Conversely, PCP is added to biocides, the primary active ingredient
of which is another compound; for example, sodium fluoride
formulations for wooden poles and posts may contain up to 10%
technical PCP (US EPA, 1973).

---------------------------------------------------------------------------
^a Personal communication, Catomance Ltd, Welwyn Garden City,
Hertfordshire, United Kingdom.

4. ENVIRONMENTAL TRANSPORT, DISTRIBUTION, AND TRANSFORMATION

4.1. Transport and Distribution Between Media

Several physical and chemical parameters affect the transport
and distribution of PCP in soil, water, and air. Volatilization
and adsorption are the major mechanisms; leaching and movements on
surfaces and in air are of minor importance (Jones, 1981).

4.1.1. Volatilization

Volatilization can be an important source of loss of PCP from
water and soil surfaces as well as from PCP-treated materials.
Dip- or brush-treating coniferous wood may lead to a 30 - 80% loss
of PCP, due to evaporation, within 12 months (Morgan & Purslow,
1973; Petrowitz, 1981).

Several factors influence the rate of volatilization of PCP
from wood. Ingram et al. (1981b) showed that certain solvents or
mixtures of solvents may either reduce or increase the
volatilization of PCP. Such solvents, as well as resins, are used
to achieve a timely release of PCP through solubilization and/or
occlusion, e.g., PCP evaporation was decreased by about 20%, when
15% of an alkyd resin was added to a wood preservative containing
5% PCP (Petrowitz, 1981). Temperature appeared to be the external
variable that had the greatest effect on volatilization; a rise in
temperature from 20 to 30 °C caused a 3- to 4-fold increase in
volatilization. Relative humidity and rate of air flow had only a
minor influence on PCP volatilization from wood. The loss of PCP
from pine-wood samples was half as much as that from spruce wood
samples after 21 days, apparently because pine is much more easily
impregnated than spruce. Thus, the depth of penetration of PCP in
wood, the species of wood, and the process of treatment appear to
be other external variables influencing diffusion and
volatilization. As an example, immersion of small blocks of pine
sapwood with a 5% PCP solution leads to a PCP loss of 20% after 6
months compared with only 4%, 9 months following double vacuum
treatment (Morgan & Purslow, 1973).

Evaporation is used for the disposal of PCP in waste water at
some wood-preserving plants (section 4.4). Extensive studies on
the volatilization of PCP from water or soil have not been carried
out, but Klöpffer et al. (1982) studied this process in an aqueous
solution in the absence