Information Regarding Pentachlorophenol
PENTACHLOROPHENOLEvidence for Carcinogenicity:
Evaluation: There is limited evidence in
humans for the carcinogenicity of combined exposures to polychlorophenols and
their sodium salts. ... There is sufficient evidence in experimental animals for
the carcinogenicity of pentachlorophenol.
Overall evaluation: Combined exposures to polychlorophenols or to their sodium
salts are possibly carcinogenic to humans (Group 2B). /Polychlorophenols &
sodium salts/
CLASSIFICATION: B2; probable human carcinogen
BASIS FOR CLASSIFICATION: The classification is based on inadequate human data
and sufficient evidence of carcinogenicity in animals: statistically significant
increases in the incidences of multiple biologically significant tumor types (hepatocellular
adenomas and carcinomas, adrenal medulla pheochromocytomas, and malignant
pheochromocytomas, and/or hemangiomas) in one or both sexes of B6C3F1 mice using
two different preparations of pentachlorophenol.
In addition, a high incidence of two uncommon tumors (adrenal medulla
pheochromocytomas and hemangiomas/hemangiosarcomas) was observed with both
preparations. The classification is supported by mutagenicity data, which
provides some indication that pentachlorophenol
has clastogenic potential. HUMAN CARCINOGENICITY DATA: Inadequate. ANIMAL
CARCINOGENICITY DATA: Sufficient.
A3: Confirmed animal carcinogen with unknown
relevance to humans.
Human Toxicity Excerpts:
INGESTION CAUSES INCR THEN DECR OF RESP, BLOOD
PRESSURE, URINARY OUTPUT; FEVER; INCR BOWEL ACTION; MOTOR WEAKNESS, COLLAPSE
WITH CONVULSIONS & DEATH. CAUSES LUNG, LIVER, KIDNEY DAMAGE; CONTACT
DERMATITIS. ... DUST CAUSES SNEEZING.
MOST IMPORTANT EFFECT OF PENTACHLOROPHENOL
INHALATION IS ACUTE POISONING CENTERING IN CIRCULATORY SYSTEM WITH ACCOMPANYING
HEART FAILURE. ... DUSTS ARE PARTICULARLY IRRITATING TO EYES & NOSE IN CONCN
GREATER THAN 1 MG/CU M. SOME IRRITATION OF NOSE MAY OCCUR AT 0.3 MG/CU M. ...
SURVIVORS OF ... INTOXICATION SUFFER ... VISUAL DAMAGE & ACUTE TYPE OF
SCOTOMA. OTHER DAMAGE INCL ACUTE INFLAMMATION OF CONJUNCTIVA &
CHARACTERISTICALLY SHAPED CORNEAL OPACITY, CORNEAL NUMBNESS & SLIGHT
MYDRIASIS.
Immersion of hands for 10 min in a 0.4% soln
caused pain and inflammation.
Dust and mist concn greater than 1.0 mg/cu m
resulted in painful irritation of upper respiratory tract in persons not
previously exposed to pentachlorophenol.
Violent sneezing and coughing accompanied exposure. Conditioned persons
tolerated concn up to 2.4 mg/cu m.
Chronic exposure in workers resulted in
elevated bilirubin and creatine phosphokinase. Higher prevalence of gamma
mobility c-reactive protein in sera.
Five cases of pentachlorophenol
poisoning, including 2 fatalities, occurred in two small wood preservative
plants ... fever ... severe hyperpyrexia ... increased anion gap and renal
insufficiency. ... Pentachlorophenol
may uncouple oxidative phosphorylation, resulting in a poisoning syndrome
characterized by hyperpyrexia, diaphoresis, tachycardia, tachypnea, abdominal
pain, nausea and even death.
Repeated exposure to commercial (technical
grade) pentachlorophenol preceded
aplastic anemia in four patients and pure red cell aplasia in two. Two patients
developed concomitant or subsequent Hodgkin's disease and acute leukemia ... .
Chromosome analyses were carried out on
peripheral lymphocytes from 22 male workers employed at a pentachlorophenol
producing factory. ... A small but significant increase in the frequency of
dicentrics and acentrics was observed. ...
Workers (3 women, 15 men) in a pentachlorophenol
processing factory, with a mean activity of processing pentachlorophenol
for 12 years were studied. ... Pentachlorophenol
levels in plasma ranged from 0.02-1.5 ug/l, median 0.25 ug/l, and in urine
13-1224 ug/l, median 112 ug/l or 11-2111 ug/g creatinine, median 111 ug/g
creatinine. ... Individual evaluation of the toxicological and
neurophysiological results gave /indications/ that in some cases decreased nerve
conduction velocity was caused by chronic exposure to pentachlorophenol.
A cytogenetic study was performed on 20
healthy workers exposed to pentachlorophenol
in concentrations ranging from 1.2 to 180 ug/cu m (maximum concentration at the
workplace is 500 ug/cu m) for 3 to 34 years. Pentachlorophenol
was determined in the blood plasma of all probands, yielding concentrations
between 23 and 775 ug/l (Biological Tolerance Value is 1000 ug/l). In vitro pentachlorophenol
up to 90 mg/l was added to phytohemagglutinin-stimulated lymphocytes of normal
healthydonors without any effect on sister chromatid exchange or chromosomal
aberrations, whereas a slow down of cell proliferation could be detected in the
presence of 60 mg pentachlorophenol/l.
A series of studies of chronically exposed
workers has been conducted in Hawaii. The first involved workers in wood
treatment plants & farmers or pest-control operators. Elevation of serum
enzyme levels, ie, serum glutamic-oxaloacetic transaminase, serum glutamic
pyruvic transaminase, & lactic dehydrogenase, & low-grade infections or
inflammations of the skin, eye, & respiratory tract were found in the
exposed groups. In a /separate/ study, plasma protein levels were found to be
elevated in exposed, as compared with unexposed, workers.
ALTHOUGH PENTACHLOROPHENOL
IS HIGHLY TOXIC IN ITS OWN RIGHT, SOME STUDIES SUGGEST THAT CONTAMINANTS MAY BE
RESPONSIBLE FOR /SRP: SOME OF THE POISONOUS POTENTIAL OF/ THE TECHNICAL GRADE.
COMPARISON OF EFFECTS OF TECHNICAL VERSUS PURIFIED PCP INDICATED THAT ONLY
TECHNICAL GRADE PRODUCED CHLORACNE, CHICK EDEMA, HEPATIC PORPHYRIA & INCR
RELATIVE LIVER WT. TECHNICAL GRADE WAS ALSO MUCH MORE ACTIVE AS LIVER ENZYME
INDUCER.
/NRC Safe Drinking Water Committee/ ... noted
that the toxicity of pentachlorophenol
is increased by impurities contained in the technical product. For example, the
No Observed Effect Level for pure pentachlorophenol
is 3 mg/kg/day; however, the No Observed Effect Level for technical pentachlorophenol
is 1 mg/kg/day, indicating increased toxicity due to impurities.
The general population is more susceptible
during hot weather.
Individuals emptying bags of prilled
(granular) or powder formulations of pentachlorophenol
and of sodium pentachlorophenol are at
an incr oncogenic risk.
SEVERAL AREAS IN PENTACHLORPHENOL
TOXICOLOGICAL PROFILE, SUCH AS CARCINOGENESIS & MUTAGENESIS, ARE NOT
COMPLETE. WITH REGARD TO OCCUPATIONAL EXPOSURES, PRECAUTIONS SHOULD BE TAKEN TO
AVOID DIRECT CONTACT & AIR LEVELS SHOULD BE KEPT WITHIN ACCEPTABLE LEVELS.
A case of a 33 yr old man who died following
occupational exposure to pentachlorophenol
is presented. Postmortem examination revealed cerebral edema and fatty
degeneration of the viscera.
A longitudinal study was performed to examine
whether chronic occupational exposure to pentachlorophenol
or its compounds causes measurable alterations in the conduction velocity in
peripheral nerves as an adverse effect. In total, the results of nerve
conduction velocity determinations in 1980 and 1984 in 10 subjects (7 men, 3
women) who had been exposed for an average of 16 years (range 4-24) were
available. The concentrations of pentachlorophenol
in the air at the workplace varied between 0.3 and 180 ug/cu m and were thus
below the maximum allowed concn (MAK value) of 500 ug/cu m. The biological
monitoring carried out showed the following results: pentachlorophenol
in the serum: 38-1270 ug/l; pentachlorophenol
in urine 8-1224 ug/l. Compared with the upper normal limits pentachlorophenol
in the serum 150 ug/l, pentachlorophenol
in the urine 60 ug/l), distinct internal exposure to pentachlorophenol
has resulted in some of the employees. Determinations of the nerve conduction
velocity of motor and sensory nerve fibers (ulnar, median, peroneal, and sural
nerve) were always in the normal range. A significant difference in the nerve
conduction velocity for the period 1980-4 could not be detected. In addition,
the correlation analyses did not show any hints of dose-effect relations. It is
concluded that occupational exposure to pentachlorophenol
over several years in the concentrations observed probably do not lead to any
adverse effects on the peripheral nervous system.
Three case reports of skin lesions associated
with exposure to pentachlorophenol in
wood preservatives were described. Since pentachlorophenol
and its sodium salt are commonly used in wood preservatives, paints, and
disinfectants due to their fungicidal, insecticidal, bactericidal, herbicidal,
and molluscicidal properties, exposure can occur in both occupational and
non-occupational settings. The cases described involved two males and one
female, all of whom were caucasian. Serum pentachlorophenol
levels were measured in each individual. In non-exposed individuals, normal
levels did not exceed 15 ug/l. The first case was that of a 41 year old man
diagonosed as having pemphigus vulgaris. Exposure was attributed to a bookcase
which had been treated with pentachlorophenol.
Serum levels of pentachlorophenol
varied from 10 to 47 ug/l in this patient, and clinical improvement was
associated with decreased serum levels. A 28 year old female also diagnosed as
having pemphigus vulgaris. Exposure in this case was ascribed to rafters in her
home which had been treated with pentachlorophenol.
Serum pentachlorophenol levels ranged
from 10.8 to 114 ug/l, and also tended to decline with periods of clinical
improvement. The third case was that of a 35 year old male who suffered from
urticaria. Exosure in this case occurred when the patient had treated wood
framework. Serum pentachlorophenol
levels varied from 20.9 to 96 ug/1 in this individual. The role of pentachlorophenol
in the pathogenesis of these cases is not understood. The ... possible
mechanisms could include direct toxic effects, photoreactivity, or induced
changes in epidermal immunology.
A 32 year old white male was seen at a
university dermatology clinic complaining of an acneform eruption of 6 months
duration. The patient was part owner of a firm that constructed piers for small
boat marinas. The lumber used was pretreated with pentachlorophenol.
Within about 9 months after beginning work, he noted a papular acneform eruption
that occurred over the entire body. The eruption was characterized by multiple,
small yellow/white papules. Areas most involved included the malar regions of
the face, post auricular area, the trunk, buttocks, thighs, and lower legs. Some
of papules were inflamed. A trephine punch biopsy of one of the papules showed a
small epithelial lined cystic structure that communicated with the surface. The
lining epithelium was composed of atrophic, but normal appearing, epidermis.
Contained within the cyst was keratin-like material. The condition was diagnosed
as chloracne. The patient's condition improved after 6 weeks oral treatment with
isoretinoin. The patient remained asymptomatic for the ensuing 2 years of
observation. The patient returned to work wearing appropriate protective
clothing. A sample of pentachlorophenol
used by the firm and samples of treated wood were analyzed for
octachlorodibenzodioxin. Samples from the surface of the lumber contained about
ten to 40 times the amount of octachlorodibenzodioxin as did the wood itself.
The undiluted pentachlorophenol
contained 1600 ppm octachlorodibenzodioxin. It was concluded the patient
developed chloracne after exposure to pentachlorophenol
treated lumber. The octachlorodibenzodioxin containing surface residue seemed to
be the major source of the intoxication.
... Liquid or solid causes smarting of skin
and first-degree burns on short exposure; may cause secondary burns on long
exposure.
The most important effect of pentachlorophenol
inhalation is acute poisoning centering in the circulatory system with
accompanying heart failure.
Industrial hygiene experience shows that pentachlorophenol
and its sodium salt are capable of inducing discomfort and local as well as
systemic effects. Dusts are particularly irritating to the eyes and nose in
concentrations greater than 1 mg/cu m. Some irritation of the nose may occur at
0.3 mg/cu m. Hardened workers can tolerate up to 2.4 mg/cu m. Pentachlorophenol
is highly poisonous with a wide range of acute action but no pronounced
cumulative properties.
The survivors of pentachlorophenol
intoxication suffer with impairments in autonomic function, circulation, visual
damage, and an acute type of scotoma. Other damage included acute inflammation
of the conjunctiva and characteristically shaped corneal opacity, corneal
numbness, and slight mydriasis. Other symptoms involve excessive sweating,
tachycardia, tachypnea, respiratory distress, hepatic enlargement, and metabolic
acidosis.
Symptoms of overexposure include an increase
followed by a decrease in respiration, blood pressure, and urinary output;
fever; increase in bowel action; motor weakness; and collapse with convulsions
and death.
Chlorophenols appear to be mildly hepatotoxic,
and studies in animals indicate that pentachlorophenol
may reduce humoral and cell-mediated immunity as well as act as a cocarcinogen.
/Chlorophenols/
Evaluation of lymphocyte phenotype
frequencies, functional responses, serum immunoglobulin levels, and
autoantibodies was completed for 38 individuals (ie, 10 families) who were
exposed to pentachlorophenol in
manufacturer treated log houses. Comparison of subjects with controls revealed
that the exposed individuals had activated T cells, autoimmunity, functional
immunosuppression, and B cell dysregulation. Autoimmunity was evidenced by
elevation of TA1 phenotype frequencies and a 21% incidence of anti-smooth muscle
antibody. Functional immunosuppression was evidenced by the significantly
reduced responses to all mitogens tested and to allogeneic lymphocytes in the
mixed lymphocyte culture test. There was a significant elevation of CD10, and an
18% increase or decrease in serum immunoglobulins was noted. A striking anomaly
was the enhanced natural killer activity found in exposed females but not in
males.
A mortality study was conducted in a cohort of
2283 plywood mill workers employed for at least one year between 1945 and 1955
in this industry. There were 570 deaths in this cohort, which was only 74% of
the number expected based on comparable US mortality figures. A statistically
nonsignificant excess of deaths was observed for lymphatic and hematopoietic
cancer excluding leukemia (standard mortality ratio (SRM)=156). The greatest
excess was for multiple myeloma (SRM=333). The excess mortality due to lymphatic
and hematopoietic cancer excluding leukemia was highest after 20 yr duration of
employment and latency. The workers were potentially exposed to formaldehyde,
but there were no deaths due to nasal cancer. A subcohort of 818 workers
involved in drying or gluing operations and exposed to formaldehyde and pentachlorophenol
was also studied. Based on small numbers, statistically nonsignificant increased
risks of death from Hodgkin's disease (SRM=333) and lymphosarcoma (SRM=250) were
observed. The authors recommend further surveillance of the plywood mill worker
cohort.
The occurrence of chloracne among pentachlorophenol
(PCP) workers was evaluated, and the risk of chloracne among workers who had
records of direct skin contact with PCP was assessed. The workers had been
employed at a facility which had produced PCP from 1938 through 1978. Of the 926
hourly workers in the study cohort, 666 had medical records available and were
employed in 1953 or later; 65 had a diagnosis of chloracne, of which 47 were
thought to be associated with PCP. The increase in duration of exposure did not
appear to be related to the increased risk of chloracne. Episodes of direct skin
contact with PCP were reported throughout the history of the facility. The
workers with independent records of direct skin exposure had overall a four fold
increase in the risk of developing chloracne compared with workers who did not
have records of direct skin contact. Eight of the 13 cases had only one episode
of direct skin contact with PCP prior to the diagnosis of chloracne, three cases
had two episodes, and two cases had three episodes. The interval between the
latest episode of direct skin contact and the diagnosis of chloracne for these
13 cases ranged from about 7 weeks to about 14 years. Four of the 13 cases
occurred within 6 months of contact, four occurred between 1 and 2 years after
the skin contact. Two occurred between 2 and 3 years after contact and three
occurred more than 10 years after exposure. The authors conclude that exposure
to PCP contaminated with hexachlorinated, heptachlorinated, and octachlorinated
dibenzo-p-dioxins and dibenzofurans was associated with the occurrence of
chloracne.
Pentachlorophenol
(PCP) and its sodium salt are frequently used in wood preservatives. Little is
known about the effects on man when being chronically exposed. Only vague skin
symptoms, such as rashes, acne and cutaneous infections were described. We
present two cases of pemphigus vulgaris with a known non-occupational chronic
PCP exposure. The clinical course and the titer of pemphigus antibodies roughly
correlate with the PCP levels in serum. In one case of chronic urticaria the
exacerbations also run parallel to the PCP serum levels and increased anti-skin
antibodies, without any manifestation of pemphigus vulgaris. The role of PCP as
one of the causes provoking pemphigus vulgaris and chronic urticaria with raised
anti-skin antibodies is discussed.
A cytogenetic study was performed on 20
healthy workers exposed to pentachlorophenol
(PCP) in concentrations ranging from 1.2 to 180 ug/cu m (Maximum Concentration
at the workplace is 500 ug/cu m) for 3 to 34 years. PCP was determined in the
blood plasma of all probands, yielding concentrations between 23 and 775 ug/l
(Biological Tolerance Value is 1000 ug/l). In vitro PCP up to 90 mg/l was added
to phytohaemagglutinin stimulated lymphocytes of normal healthy donors without
any effect on sister chromatid exchange (SCE) or chromosomal aberrations (CA),
whereas a slowdown of cell proliferation could be detected in the presence of 60
mg PCP/l. In vivo we neither observed a relation between PCP concentrations and
the number of SCE nor an increase of CA.
Aplastic anemia, pure red cell aplasia,
leukemia, lymphoma and other hematologic disorders have followed exposure to
products containing the pesticide pentachlorophenol
(PCP). Information in a 25-year compilation of documented case reports is
summarized, involving industrial and home exposure and accidental poisoning in a
nursery. The potential hematologic, mutagenic and carcinogenic effects of PCP
and its dioxin-dibenzofuran contaminants also are reviewed. Owing to widespread
contamination of the environment by PCP products, and latent periods of up to
several decades after exposure before these disorders become manifest
clinically, it is necessary to consider their etiologic or contributory role.
These issues continue to surface in toxic tort litigation relative to causation.
Pentachlorophenol
(PCP) is a substance whose widespread use, mainly in wood protection and pulp
and paper mills, has led to a substantial environmental contamination. This in
turn accounts for a significant exposure of the general human population, with
rather high exposure levels being attained in occupational settings.
Investigations on the genotoxic activity of PCP have given rise to divergent
results which would seem to make an evaluation difficult. By grouping them into
3 categories a somewhat clearer picture, allowing finally an (admittedly
tentative) assessment, can be obtained. PCP does seem to be at most a weak
inducer of DNA damage: it produces neither DNA-strand breaks nor clear
differential toxicity to bacteria in rec-assays in the absence of metabolic
activation. Also in SCE induction no increase can be observed in vivo, while PCP
is found marginally active in a single in vitro experiment. Metabolic
activation, however, leads to prophage induction and to DNA strand breaks in
human lymphocytes, presumably through the formation of oxygen radicals. A
possible further exception in this area might be the positive results in the
yeast recombination tests, although their inadequate reporting makes a full
evaluation difficult. PCP does not seem to induce gene (point) mutations, as
most bacterial assays, the Drosophila sex-linked recessive lethal test and in
vitro assays with mammalian cells did not demonstrate any effects. Marginally
positive results were obtained in the mammalian spot test in vivo and in one
bacterial test; the positive result in the yeast assay for cycloheximide
resistance is fraught somewhat with its questionable genetic basis. PCP does,
however, induce chromosomal aberrations in mammalian cells in vitro and in
lymphocytes of exposed persons in vivo. Those in vivo results that were unable
to provide evidence of chromosomal damage are hampered either by methodological
inadequacies or by too low exposure levels. The (rodent) metabolite
tetrachlorohydroquinone might be a real genotoxic agent, capable of binding to
DNA and producing DNA strand breaks; this activity is probably due to
semiquinone radical formation and partly mediated through active oxygen species.
Since this compound has not been tested in the common bacterial and mammalian
mutagenicity assays, the few ancillary results on this substance cannot be used
in a meaningful human risk assessment of PCP. Furthermore, this metabolite has
only been produced by human liver microsomes in vitro, but has not been detected
in exposed humans in vivo.
Urinary PCP was monitored in male volunteers
exposed to Fungifen solution which is
a readily accessible pharmaceutical product containing 1% of PCP as active
ingredient, and is recommended for the local treatment of interdigital mycoses.
PCP absorbed readily through the skin and its elimination was slow. After the
topical application of Fungifen,
maximumlevels of urine PCP ranged from 109 to 1290 ug/l. In a single case a peak
value of 3200 ug/l was measured. At the same time, PCP could be detected in the
saliva, too. Urinary preexposure levels (ranged around 10 ug/l) were reached
within 75 and 90 days, respectively. Maximum urinary levels represent exposures
corresponding to occupational ones, known from other studies. The toxicity of
PCP as well as the health risk of the Fungifen
use to the great masses of the people (including pregnant women and children)
are discussed.
Immune parameters were examined in 188
patients who were exposed for more than 6 mo to pentachlorophenol
containing pesticides. Blood levels of pentachlorophenol,
lymphocyte populations, in vitro responses to mitogenic and allogenic
stimulation, plasma neopterin levels, plasma cytokine and cytokine receptors
were determined. Impaired in vitro lymphocyte stimulation responses were
impaired in 65% of the patients. ... Impaired lymphocyte stimulation incr
significantly with levels of pentachlorophenol
that exceeded 10 ul/l (p<0.05). Patients who had high levels of pentachlorophenol
and abnormal lymphocyte stimulation also had incr proportions of blood monocytes
in blood (p<0.05), as well as incr IL-8 serum levels (p<0.02). Eleven
patients had abnormal mitogen stimulation experienced decr CD4/CD8 ratios of
< 1.0; 5 of these patients had decr CD4+ lymphocyte counts of <500/ul, and
3 patients had incr plasma neopterin of >15 nmol/l. ... This indicates that
incr levels of pentachlorophenol in
blood can lead to severe T lymphocyte dysfunction.
Excessively treated interior surfaces may be a
source of exposure sufficient to cause irritation of eyes, nose, and throat.
Skin, Eye and Respiratory Irritations:
Dust or vapor irritates skin. ...
Eye and skin irritant.
All chlorophenol ... dusts are ... irritating
to the respiratory tract. /Chlorophenols/
Dust and vapor of pentachlorophenol
are irritating to the eyes, causing lacrimation.
Medical Surveillance:
Whole Blood: Reference Ranges: Normal - Not
established; Exposed - Not established; Toxic - Not established. The assessment
of pentachlorophenol exposure can be
accomplished through measurement of free pentachlorophenol.
However, the reference ranges found in the literature were for pentachlorophenol
in serum or plasma, which appears to be the better specimen for analysis. Pentachlorophenol
exists primarily in the plasma, thus analysis of this specimen would be more
sensitive.
Serum or Plasma: The assessment of pentachlorophenol
exposure can be accomplished through measurement of free pentachlorophenol.
However, other compounds such as hexachlorobenzene and lindane may be
metabolized to pentachlorophenol in
the body, which can confound the identification of exposure. Hemolysis of the
blood specimen will have no effect on the analysis, since pentachlorophenol
is present in red cells in a negligible amount. Reference Ranges: Normal -
Background levels of up to 0.1 mg/l have been found in people in the general
population with no recognized exposure to pentachlorophenol;
Exposed - BEI (sampling time is end of shift, measured as free pentachlorophenol):
5 mg/l. Serum levels of pentachlorophenol
below 1.3 mg/l have not been associated with any adverse health effect. Pentachlorophenol
concentrations in serum/plasma that have been found to correlate with workplace
air concentrations are as follows: Pentachlorophenol
air levels 0.05 and 0.1 mg/cu m correlate to serum/plasma pentachlorophenol
levels (sampling time not fixed) of 1000 and 1700 ug/L, respectively; Toxic -
Serum levels of pentachlorophenol
ranging from 23 to 162 mg/L have been reported in cases of fatal overexposure.
Urine: The assessment of pentachlorophenol
exposure can be accomplished through measurement of total pentachlorophenol
(free and conjugated), which has been found to correlate well with air levels.
However, other compounds such as hexachlorobenzene and lindane may be
metabolized to pentachlorophenol in
the body, and may also cause elevated pentachlorophenol
levels. Exposure to these pesticides should be ruled out when evaluating urinary
levels. Reference Ranges: Normal - Average concentration approximately 0.063
mg/L, but has been found to be up to 0.100 mg/L in people with no recognized
exposure to pentachlorophenol; Exposed
- BEI (sampling time is prior to the last shift of workweek, measured as total pentachlorophenol):
2 mg/g creatinine. Pentachlorophenol
concentrations in urine that have been found to correlate with workplace air
concentrations are as follows: pentachlorophenol
air levels of 0.05 and 0.10 mg/cu m correlate to urine pentachlorophenol
levels (sampling time not fixed) of 300 and 600 ug/L, respectively; Toxic - Not
established.
Urine Albumin: Albuminuria has been shown to
be a specific marker of glomerular dysfunction. Tubular damage, however, can
also result in increased levels of albumin in the urine.
Urinary Beta-2-Microglobulin and/or Retinal
Binding Protein: Measurements for the presence of either of these low molecular
weight proteins are useful in detection of early impairment of proximal tubular
function. However, beta-2-microglobulin is unstable at urinary pH less than 6,
and may degrade in the bladder prior to collection and subsequent neutralization
of the urine sample. Measurement of retinal binding protein appears to be a
better marker for early tubular dysfunction due to its stability in the urine
subsequent to collection and analysis. However, retinal binding protein is
produced in the liver and not a constitutive protein of the kidney, so that its
presence in the kidney provides only indirect evidence of tubular damage.
Urinary Alpha () and Pi () Isoenzymes of
Glutathione S-Transferase: Radio-immunological and Elisa techniques have been
developed for quantitation of and isoenzymes of glutathione S-transferase, which
are constitutive proteins in the kidney. The isoenzyme is located only in the
proximal tubule, while the isoenzyme is located in the distal convoluted tubule,
the loop of Henle, and the collecting ducts of the kidney. Damage to epithelial
cell membranes can result in the increased excretion of these isoenzymes in the
urine. This test for assessing renal tubular damage appears to have many
advantages over other available tests, such as: (1) the and isoenzymes are
constitutive proteins in the kidney; (2) these isoenzymes are stable in the
urine, (3) the test is simple and reproducible; and (4) due to selective
localization of the isoenzymes, differential diagnosis of specific tubular
damage is possible. In addition, increased levels of these isoenzymes were seen
in patients previously exposed to nephrotoxicants where conventional tests for
kidney function were normal, indicating a high degree of sensitivity.
Urinary Enzyme N-acetylglucosaminidase: This
lysosomal enzyme has shown promise in assessment of subclinical nephrotoxic
injury. This enzyme is not normally filtered at the glomerulus due to its high
molecular weight. In the absence of glomerular injury, this enzyme will be
detected in the urine as a result of leakage or exocytosis from damaged,
stimulated, or exfoliated renal cells. The sensitivity of measurement for this
enzyme has not been thoroughly studied, but it's usefulness has shown some
promise. However, this enzyme is unstable at urinary ph greater than 8, which
could diminish the sensitivity of the measurement due to enzyme degradation.
Routine Urinalysis: Performing a routine
urinalysis including parameters such as specific gravity, glucose, and a
microscopic examination may be useful for assessing renal toxicity.
Biochemical Tests: Enzymes that reflect
cholestasis - alkaline phosphatase, 5'-nucleotidase, leucine aminopeptidase; ...
Enzymes that detect direct hepatic damage - aspartate aminotransferase, alanine
aminotransferase.
Clearance Tests: Indocyanine green; Antipyrine
test; Serum bile acids.
Respiratory Symptom Questionnaires:
Questionnaires have been published by the American Thoracic Society and the
British Medical Research Council. These questionnaires have been found to be
useful in identification of people with chronic bronchitis, however certain
pulmonary function tests such as FEV 1 have been found to be better predictors
of chronic airflow obstruction.
Chest Radiography: This test is widely used
for assessing pulmonary disease. Chest radiographs have been found to be useful
for detection of early lung cancer in asymptomatic people, especially for
detection of peripheral tumors such as adenocarcinomas. However, even though
OSHA mandates this test for exposure to some toxicants such as asbestos, there
are conflicting views on its efficacy in detection of pulmonary disease.
Pulmonary Function Tests: The tests that have
been found to be practical for population monitoring include: Spirometry and
expiratory flow-volume curves; Determination of lung volumes; Diffusing capacity
for carbon monoxide; Single-breath nitrogen washout; Inhalation challenge tests;
Serial measurements of peak expiratory flow; Exercise testing.
Sputum Cytology: Sputum cytology along with
chest radiographs have been the standard procedures for detecting early lung
cancer in asymptomatic patients. Sputum cytology has been found to be useful for
detection of central tumors, especially squamous carcinomas. For this test to be
effective, exfoliated respiratory mucosal cells must be present in the
expectorated specimen. Pooling of sputum collected over 2-3 days may enhance the
sensitivity of this test by increasing the yield of exfoliated cells in the
specimen.
Evaluation of Peripheral Neuropathy: Nerve
conduction study; Electromyography; Quantitative sensory testing; Thermography.
Evaluation of Central Nervous System Effects:
Evaluation of CNS effects can be performed through neuropsychological
assessment, which consists of a clinical interview and administration of
standardized personality and neuropsychological tests. The areas that the
neuropsychology test batteries focus on include the domains of memory and
attention; visuoperceptual, visual scanning, visuospatial, and visual memory;
and motor speed and reaction time. There is limited data on which components of
the test batteries are best indicators of early CNS effects.
Evaluation of Cranial Neuropathies: Evaluation
of cranial nerve damage, as evidenced by symptoms such as loss of balance,
visual function, smell, taste, or sensation on the face, can be accomplished
through a physical examination focusing on tests such as: Smell assessment -
standardized odor threshold and identification testing; Visual assessment
-standard acuity tests, visual field tests, contrast sensitivity, and color
vision measurements (vision assessment); Facial and Trigeminal Nerve assessment
- blink reflex (pontogram); Vestibular assessment - pure tone audiometry for
bone- and air-conducted sounds, threshold decay at 4 kHz, speech discrimination
and speech reception thresholds, tympanograms and acoustic thresholds,
electronystagmograms; Hearing assessment - audiometry testing.
PRECAUTIONS FOR "CARCINOGENS":
Whenever medical surveillance is indicated, in particular when exposure to a
carcinogen has occurred, ad hoc decisions should be taken concerning ... /cytogenetic
and/or other/ tests that might become useful or mandatory. /Chemical
Carcinogens/
Populations at Special Risk:
INDIVIDUALS SUFFERING FROM KIDNEY & LIVER
DISEASES ... SHOULD /BE PROTECTED FROM/ OCCUPATIONAL EXPOSURE.
Probable Routes of Human Exposure:
NIOSH's National Occupational Exposure Survey
(NOES) (1981-83) has statistically estimated that 22,107 workers, including
3,881 women, are exposed to pentachlorophenol
in the USA(1). The NIOSH survey indicates that major occupational exposure is to
workers in the electric services industry (wood preservative)(2). 25 wood
preservative factories avg 0.012 ppb(2). Elevated levels were found in workers'
urine and serum(2). Aerial spraying of farm crops gave rise to levels of pentachlorophenol
of 0.9 mg/cu m in the cockpit of the spray plane, 38 mg/cu m in the vicinity of
the signal man and 1-4 mg/cu m outside the treated field(3). At a sawmill in
Finland, urine from exposed workers contained pentachlorophenol
at concns from not detected to 15.9 ng/mg creatinine(4).
Major human exposure will be workers or other
people who handle or breathe air near wood that has been preserved with pentachlorophenol
and through consumption of food that contains the pesticide(SRC). General water
and air contamination are not likely sources of human exposure. Results of an
environmental partitioning model indicate that ingestion of food accounts for
99.9% of human exposure to pentachlorophenol(1,SRC).
Body Burden:
BLOOD: 15 ppb(1), 10-120 ppb in users of
PCP-contaminated water(2). Serum of 123 residents of PCP-treated log homes
ranged from 69-1340 ppb, 420 ppb mean, while 34 controls ranged from 15-75 ppb,
40 ppb(3). Serum levels in 25 occupationally-exposed workers in 5 workplaces
ranged from 26 to 84,900 ppb(3). Medium serum PCP levels in 4 of the workplaces
ranged from 83 to 490 ppb, while in the chemical packaging area of a chemical
plant it was 62,000 ppb(3). Avg serum concn (of pentachlorophenol)
of 7 workers continuously exposed to chlorophenols at 2 saw mills was 0.84-0.85
ppm(4). Concns of pentachlorophenol in
the blood serum and urine of workers involved either with the production of pentachlorophenol
or with the treatment of wood with pentachlorophenol
have been measured(5). Urine of workers responsible for lumber dipping, spraying
or brushing contained pentachlorophenol
at mean concns from 1.31 to 2.83 mg/l (blood serum mean=5.14 mg/l); urine from
an individual in the office at a lumber yard contained 0.06 mg/l pentachlorophenol
(blood serum mean=0.65 mg/l). Individuals involved with pentachlorophenol
production had mean blood serum and urine levels of 0.72-2.38 mg/l and 4.73
mg/l, respectively(5). Adipose tissue from 58 people (not occupationally
exposed) from southern and northern Finland contained pentachlorophenol
at a median concn of 0.002 ug/g residue fat; 75-81.8% of the samples were
positive(6). 84.6% of the liver samples were positive for pentachlorophenol
with a median concn of 0.004 ug/g(6).
HUMAN MILK: Bavaria, Germany - 0.03-2.83 ppb -
21 donors(1). Milk from 10 to 20 Swedish women, from 1972 to 1989, contained pentachlorophenol
at 0.0125 to 0.036 ug/g fat(8). URINE: 85% pos over 400 samples 6.3 ppb mean,
193 ppb max(2). Urine of 118 residents of PCP-treated log homes ranged from
1-340 ppb, 69 ppb mean, while 143 controls ranged from 1-7 ppb, mean 3.4 ppb(3).
All urine samples from 197 Arkansas children contained pentachlorophenol(4).
The median and max pentachlorophenol
concn was 14 and 240 ppb. SEMINAL FLUID: 20-70 ppb(2), 100-200 ppb(5). ADIPOSE
TISSUE: 250-500 ppb(5), 23 ppb(6). The mean levels of pentachlorophenol
in samples collected from the general population in Barcelona, Spain, in 1982-83
were 25 ng/ml (50 samples) in urine and 21.9 ng/ml (100 samples) in serum(7).
All 87 urine samples collected randomly in Saskatchewan, Canada, contained pentachlorophenol
at concns from 0.5 to 9.1 ng/mL (detection limit=0.2 ng/ml; avg=1.6 ng/ml and
median=1.3 ng/mL)(9). A second study of 38 urine samples from "normal,
healthy" humans living in Saskatchewan, Canada, reported pentachlorophenol
concns from 0.1 to 3.6 ng/ml with an avg concn of 0.9 ng/ml and a median concn
of 0.5 ng/ml(9).
Pentachlorophenol
was detected during hand wipe studies of 5 children living on 3 different farms;
concns ranged from 9 to 99 ng(1). The National Human Monitoring Program for
Pesticides, USEPA, has shown that ~85% of all human urine samples contain pentachlorophenol
at a mean of 0.0063 ppm and a max of 0.193 ppm(2). Avg concns of pentachlorophenol
in tissue samples obtained from 8 humans from western Oregon were as follows:
testis, 1.087 ppm; kidney, 0.953 ppm; prostate, 0.838 ppm; liver, 0.592 ppm;
omentum fat, 0.029 ppm; subcutaneous fat, 0.017 ppm; perinephric fat, 0.016
ppm(2).
A study of serum and urine pentachlorophenol
(87865) (PCP) concentrations in persons living in log homes and workers
occupationally exposed to PCP was conducted. The study group consisted of 35
persons exposed to PCP in six workplaces and 123 persons living in 45 homes
constructed of PCP treated logs. The comparisons consisted of 143 persons living
in conventional homes and not occupationally exposed to PCP. Urine and blood
samples were collected and analyzed for PCP. Among the comparisons, urine PCP
concentrations ranged from 1 to 17 ppb, mean 3.4 ppb. Serum samples from 34
comparisons ranged from 15 to 75 ppb, mean 40 ppb. In persons living in PCP
treated log homes, serum PCP concentrations ranged from 69 to 1340 ppb, mean 420
ppb. The serum PCP concentrations decreased with increasing age. Subjects in the
2 to 7 year old group had significantly higher serum PCP concentrations than
those over 15 years old. The serum PCP concentrations in children 2 to 15 years
old averaged 1.7 to 2.0 times that of their parents. Repeat blood samples taken
from ten persons residing in homes in which the logs were coated with a sealant
showed that sealing the logs resulted in decreased serum PCP concentrations.
Urine PCP concentrations ranged from 1 to 340 ppb, mean 69 ppb. When the urine
PCP concentrations were corrected for creatinine concentrations, they correlated
well with the serum PCP concentrations. Serum PCP concentrations in the PCP
workers ranged from 26 to 84900 ppb. The lowest concentrations occurred in
workers constructing homes from PCP treated logs and the highest in workers
exposed to PCP in chemical factories. Urine PCP concentrations in four workers
ranged from 2400 to 13800 ppb, mean 10000 ppb.
Average Daily Intake:
Pentachlorophenol
partitions mainly into soil (96.5%), and food chains, especially fruits,
vegetables and grains, account for 99.9% of human exposure to pentachlorophenol.
The long-term, avg daily intake of pentachlorophenol
is estimated to be 16 ug/day(1). Air intake (assume 0) - 0; Water intake (assume
0) - 0; Food intake - 0.014(2), 3.6(3), 16(4) ug(SRC).
Animal Toxicity Studies:
Evidence for Carcinogenicity:
Evaluation: There is limited evidence in
humans for the carcinogenicity of combined exposures to polychlorophenols and
their sodium salts. ... There is sufficient evidence in experimental animals for
the carcinogenicity of pentachlorophenol.
Overall evaluation: Combined exposures to polychlorophenols or to their sodium
salts are possibly carcinogenic to humans (Group 2B). /Polychlorophenols &
sodium salts/
CLASSIFICATION: B2; probable human carcinogen
BASIS FOR CLASSIFICATION: The classification is based on inadequate human data
and sufficient evidence of carcinogenicity in animals: statistically significant
increases in the incidences of multiple biologically significant tumor types (hepatocellular
adenomas and carcinomas, adrenal medulla pheochromocytomas, and malignant
pheochromocytomas, and/or hemangiomas) in one or both sexes of B6C3F1 mice using
two different preparations of pentachlorophenol.
In addition, a high incidence of two uncommon tumors (adrenal medulla
pheochromocytomas and hemangiomas/hemangiosarcomas) was observed with both
preparations. The classification is supported by mutagenicity data, which
provides some indication that pentachlorophenol
has clastogenic potential. HUMAN CARCINOGENICITY DATA: Inadequate. ANIMAL
CARCINOGENICITY DATA: Sufficient.
A3: Confirmed animal carcinogen with unknown
relevance to humans.
Non-Human Toxicity Excerpts:
TOXICITY OF PENTACHLOROPHENOL
TO SHEEP & CALVES HAS BEEN EXAMINED ... MIN ACUTE LETHAL DOSE RATE WAS FOUND
TO BE APPROX 120 & 140 MG/KG RESPECTIVELY IN THE 2 SPECIES. ... DEATH
OCCURRED IN 2 TO 14 HR. MOST PROMINENT CLINICAL SIGN WAS ACCELERATED BREATHING
... WHICH DISTINGUISHED DOSED ANIMALS FROM CONTROLS 1 TO 2 HR AFTER /ORAL/
DRENCHING. BADLY AFFECTED ANIMALS STOOD SWAYING, WITH HEAD LOWERED, PANTED
NOISILY, & MADE LITTLE ATTEMPT TO MOVE WHEN APPROACHED. SALIVATION WAS
OBSERVED IN CALVES & COAT FELT DAMP. RECOVERY FROM THIS STAGE ... WAS RAPID
& COMPLETE. IN FATAL CASES, COMPLETE COLLAPSE OCCURRED, ANIMALS LYING WITH
LEGS LIMP & PANTING VIGOROUSLY THROUGH OPEN MOUTH. ASPHYXIAL TREMORS, BUT NO
CONVULSIONS, SET IN JUST BEFORE DEATH.
POST MORTEM, ACUTELY POISONED SHEEP /FROM ORAL
DRENCHING/ SHOWED GENERALIZED CONGESTION. LYMPH NODES APPEARED ENLARGED &
EDEMATOUS. THERE WERE HEMORRHAGES IN EPICARDIUM & ALONG AORTA. LUNG SHOWED
ISOLATED AREAS OF COLLAPSE & GENERALIZED CONGESTION. BLOOD SPLASHES WERE
OCCASIONALLY SEEN ON DIAPHRAGM. STOMACH, INTESTINES, LIVER & KIDNEY
SOMETIMES SHOWED MILD CONGESTION. BLADDER INVARIABLY EMPTY.
PURIFIED & COMMERCIAL GRADES ... GIVEN
ORALLY TO /SPRAGUE-DAWLEY/ RATS AT DOSES RANGING FROM 5-10 MG/KG BODY WT/DAY AT
VARIOUS INTERVALS DURING DAYS 6-15 OF PREGNANCY. SIGNS OF EMBRYOTOXICITY &
FETOTOXICITY ... RESORPTIONS, SC EDEMA, DILATED URETERS & ANOMALIES OF
SKULL, RIBS, VERTEBRAE & STERNEBRAE WERE OBSERVED AT INCIDENCE WHICH INCR
WITH DOSE. EARLY ORGANOGENESIS ... MOST SENSITIVE PERIOD. NO-EFFECT ... LEVEL OF
COMMERCIAL GRADE WAS 5 MG/KG/BODY WT/DAY; PURIFIED PENTACHLOROPHENOL
GIVEN AT SAME ... LEVEL CAUSED ... SIGNIFICANT INCR IN INCIDENCE OF DELAYED
OSSIFICATION OF SKULL BONES BUT NO OTHER EFFECT ON ... DEVELOPMENT. INGESTION OF
3 MG/KG BODY WT/DAY OF COMMERICALLY AVAILABLE PURIFIED GRADE HAD NO EFFECT ON
REPRODUCTION, NEONATAL GROWTH, SURVIVAL OR DEVELOPMENT.
A single 60 mg/kg body wt oral dose of
purified pentachlorophenol was given
to pregnant Charles River CD strain rats on days 8, 9, 10, 11, 12, or 13 of
gestation. Treatment on days 9 or 10 had the greatest effect on fetotoxicity.
SIX GROUPS OF 27 MALE & ... FEMALE
WEANLING SPRAGUE-DAWLEY (SPARTAN SUBSTRAIN) RATS ... GIVEN LAB CHOW ...
CONTAINING PENTACHLOROPHENOL (SAMPLE
XD-9108.002: PENTACHLOROPHENOL 90.4%;
TETRACHLOROPHENOL 10.4%; TRICHLOROPHENOL LESS THAN 0.1%; HEPTA- &
OCTACHLORODIBENZO-P-DIOXINS ABOUT 21 MG/KG; HEXA- & HEPTACHLORODIBENZOFURANS
ABOUT 5.2 MG/KG; & HEXACHLOROBENZENE 400 MG/KG) TO PROVIDE ... LEVELS OF 0,
1, 3, 10 OR 30 MG PCP/KG BODY/DAY. PENTACHLOROPHENOL
WAS DISSOLVED IN ANISOLE & CONCN ... ADJUSTED ON A MONTHLY BASIS TO MAINTAIN
DESIGNATED DOSE LEVELS ... GROUPS OF 27 MALE & 27 FEMALE CONTROLS ...
RECEIVED LAB CHOW CONTAINING ANISOLE ONLY. FEMALE RATS WERE MAINTAINED ON TEST
DIETS FOR 24 MO, BUT THE MALE/S/ ... WERE TAKEN OFF ... AFTER 22 MO BECAUSE OF
HIGH MORTALITY ...THE TOTAL & INDIVIDUAL TUMOR INCIDENCES BY SITES, TIMES OF
APPEARANCE ... & AVG NUMBERS ... PER ANIMAL (PREDOMINANTLY BENIGN NEOPLASMS)
WERE NOT SIGNIFICANTLY DIFFERENT FROM THOSE OBSERVED IN CONTROL RATS. THE NUMBER
OF RATS WITH TUMORS/THOSE EXAM WERE, IN MALES: 11/27 (CONTROLS), 13/26 (1
MG/KG), 13/27 (3 MG/KG), 12/27 (10 MG/KG), 11/27 (30 MG/KG); IN FEMALES: 27/27
(CONTROLS), 26/27 (1 MG/KG), 25/27 (AT ALL OTHER DOSES).
GROUPS OF 18 MALE & ... FEMALE
(C57BL/6XC3H/ANF)F1 MICE & 18 MALE & FEMALE (C57BL/6XAKR)F1 MICE
RECEIVED ... DOWCIDE-7 (IMPURITIES UNSPECIFIED) ... /AT/ 46.4 MG/KG BODY WT IN
0.5% GELATIN AT 7 DAYS OF AGE BY STOMACH TUBE & SAME AMT (NOT ADJUSTED FOR
INCR BODY WT) DAILY UP TO 4 WK OF AGE; SUBSEQUENTLY, THE MICE WERE FED 130 MG/KG
/PPM/ DIET UNTIL ... 78 WK OF AGE AT WHICH TIME 16, 18, 17 & 16 MICE WERE
STILL ALIVE IN THE 4 GROUPS, RESPECTIVELY. TUMORS DEVELOPED IN 3/18, 4/18, 3/17
AND 2/18 MALE & FEMALE ... MICE; THESE INCIDENCES WERE NOT SIGNIFICANTLY
GREATER THAN IN 79-90 NECROPSIED MICE OF EACH SEX & STRAIN, WHICH HAD EITHER
BEEN UNTREATED OR HAD RECEIVED GELATIN ONLY.
GROUPS OF 18 MALE & 18 FEMALE
(C57BL/6XC3H/ANF)F1 MICE & 18 MALE & 18 FEMALE (C57BL/6XAKR)F1 MICE ...
GIVEN SINGLE SC INJECTIONS OF 46.4 MG/KG BODY WT ... (DOWCIDE-7; IMPURITIES
UNSPECIFIED) IN CORN OIL AT 28 DAYS OF AGE & WERE OBSERVED UP TO 78 WK OF
AGE, AT WHICH TIME 14, 18, 18 & 16 MICE IN THE 4 GROUPS, RESPECTIVELY WERE
STILL ALIVE. NEG CONTROL GROUPS CONSISTED OF ANIMALS THAT WERE EITHER UNTREATED
OR RECEIVED GELATIN, CORN OIL OR DIMETHYLSULFOXIDE & COMPRISED 141 MALES
& 154 FEMALES OF THE FIRST STRAIN AND 161 MALES & 157 FEMALES OF THE
SECOND STRAIN. THE INCIDENCES OF HEPATOMAS (4/17) IN MALES OF 1ST STRAIN WAS
SIGNIFICANTLY INCR ... OVER THAT IN CONTROLS (9/141).
Acute and chronic toxicity to saltwater
aquatic life occur at concentrations as low as 53 and 34 ug/l, respectively.
Twenty one day chronic mortality of Daphnia
magna was produced at 320 ug/l, but not at 180 ug/l.
IN FEEDING EXPT WITH DROSOPHILA MELANOGASTER,
7 MILLIMOLAR PENTACHLOROPHENOL FAILED
TO INDUCE SEX-LINKED RECESSIVE LETHALS IN MEIOTIC & POSTMEIOTIC STAGES OF
MALE GERM CELLS. IN LATERAL ROOTS OF VICIA FABA SEEDLINGS TREATED WITH 43.5-174
MG/L ... THERE WAS INCR IN FREQUENCY OF ABNORMAL CELL DIVISIONS (EG, STICKINESS
& LAGGING OF CHROMOSOMES & CHROMOSOME FRAGMENTATION); THESE
ABNORMALITIES WERE MORE FREQUENT DURING METAPHASE THAN IN EARLIER STAGES &,
IN GENERAL, INCR WITH INCR CONCN.
The no observable effect level for fetal
resorption in pregnant Sprague Dawley female rats was 5.8 mg/kg/day of
commercial grade pentachlorophenol and
15 mg/kg/day of purified pentachlorophenol.
Measurements were also taken on fetal body weight and crown rump length, both of
which decreased with increasing dose. The no observable effect level for these
parameters was 15 mg/kg/day for both commercial grade and purified pentachlorophenol.
Pregnant Syrian golden hamsters given daily
oral doses of pentachlorophenol
(unspecified purity) ranging from 1.25 to 20 mg/kg from days 5 to 10 of
gestation experienced an increase in fetal deaths & resorptions. The no
effect level was 2.5 mg/kg/day.
/Pentachlorophenol/
... (0, 5, 50, or 500 ppm) /was administered/ to Sprague-Dawley rats in the diet
beginning with the rats own weaning through the weaning of their pups. ...
Significant effects /were observed/ on the immune system (as indicated by
decreased antibody titers, decreased delayed hypersensitivity to oxazolone, and
increased peritoneal macrophage numbers) & reduced ethylnitrosourea-induced
transplacental carcinogenesis.
... Effects /were/ observed ... on the central
nervous system in rabbits after 60 days of exposure to subcutaneous doses of 5%,
10% & 25% of the minimum lethal dose (275 mg/kg body wt). Nervous system
lesions were seen in all dose groups. Neurochemical effects were observed in 30
male Wistar rats given 20 mg/l concn of technical grade pentachlorophenol
in drinking water for 3 to 14 wk. Thirty controls were also studied. ... The
main effects seen in the rat brain were transient biochemical effects ... .
In a 160 day study, cattle fed 20 mg/kg doses
of technical pentachlorophenol for 42
days, followed by 15 mg/kg/day for the remainder of the study, had decreased wt
gain, progressive anemia, & immune effects. Only minimal adverse effects
were observed after exposure to analytical grade pentachlorophenol.
PENTACHLOROPHENOL
WAS EMBRYOTOXIC & FETOTOXIC /TO SPRAGUE-DAWLEY RATS/ @ DOSES OF COMMERCIAL
& PURE PENTACHLOROPHENOL OF 15
MG/KG & ABOVE. ... DELAYED OSSIFICATION OF SKULL WAS OBSERVED AFTER
TREATMENT WITH PURE PENTACHLOROPHENOL.
ORAL ADMIN ... TO HAMSTERS ON DAYS 5-10 OF GESTATION PRODUCED FETAL DEATH
&/OR RESORPTIONS AT 5 MG/KG/DAY AND ABOVE.
PROVED NEGATIVE IN SEX-LINKED LEVEL TEST IN
DROSOPHILA ... .
The effects of pure and technical grade pentachlorophenol
on primary cultured rat hepatocytes were compared to determine if contaminants
of commercial preparations of pentachlorophenol
increased its toxicity. Hepatocytes isolated from adult Sprague-Dawley rats were
incubated with analytical /grade/ pentachlorophenol
of 99% purity, technical grade pentachlorophenol,
or its sodium salt, which contains only minor concentrations of technical
impurities. Monooxygenase activity was markedly induced by technical grade pentachlorophenol
in a concentration dependent pattern, with a maximum response of approximately
14 fold seen at concentrations of 30 to 50 micromoles. Monooxygenase induction
was much less marked after exposure to 50 micromoles sodium salt of technical pentachlorophenol,
only 2.7 fold, and was barely detectable after exposure to 50 micromoles 99%
purity pentachlorophenol. Phase II
metabolism of monooxygenase product was equally inhibited by pretreatment with
any of the pentachlorophenol
preparations. Cell membrane damage, assessed by leakage of LDH into the culture
medium, was also observed with all the pentachlorophenol
preparations tested. These results indicated that monooxygenase induction was
attributable to technical impurities, while cytotoxic effects were caused by the
pentachlorophenol itself.
The teratogenic activities of highly purified pentachlorophenol
and pentachloroanisole, administered in the diet of Sprague Dawley rats of both
sexes, at the rate of 4, 13 or 43 mg/kg and 4, 12 or 41 mg/kg/day, respectively,
for a period of 181 days, were investigated. Pregnant females treated with pentachlorophenol
ate more food than untreated controls. As compared to controls, dams treated
with the highest doses of both compounds had a lower body wt on day 0 of
gestation and gained less weight during their pregnancy. Animals treated with
the highest dose of pentachlorophenol
gained less weight during pregnancy than controls. Embryonic deaths were
recorded following treatment with pentachlorophenol
at the rate of 43 mg/kg/day, while lower doses of the compound induced dose
related reductions in body wt. At the rate of 13 mg/kg/day only, pentachlorophenol
reduced the crown to rump length and increased the skeletal alterations of the
fetus. Decreased numbers of corpora lutea and embryonic death were recorded
following the administration of pentachlorophenol
at the rate of 4 and 41 mg/kg/day. At the same dose pentachlorophenol
reduced the body wt and the crown to rump length of male fetuses, while their
female counterparts were not affected. Neither pentachlorophenol
nor pentachloroanisole affected the soft tissue of the animals. Results indicate
the pentachlorophenol is slightly more
toxic than pentachloroanisole in Sprague Dawley rats.
In a 7 day experiment, food conversion
efficiency (as g of growth/g of food eaten) in fry of largemouth bass was
significantly affected in a concentration-dependent fashion at concentration of pentachlorophenol
>10 ug/l; with exposure to increasing pentachlorophenol
concn >10 ug/l, there was a significant concentration-related reduction in
total length of largemouth bass at the end of a 57 day exposure. For the length
data, the threshold response value was 25.2 ug/l which was very close to that of
the food-coversion efficiency value (23.4 ug/l). When comparing pentachlorophenol
induced mortality, behavioral responses, length at the end of a long-term
exposure, and food-conversion efficiency, the latter two are the most sensitive
indicators of pentachlorophenol
effects on fish.
Rainbow trout were exposed for 4 or 8 days to
various types of toxicants, each applied to the test water at a high sublethal
concn. The activity of liver UDP-glucuronosyltransferase was assayed from the
submitochondrial fraction using p-nitrophenol as an aglycone. Activity of
UDP-glucuronosyltransferase was inhibited ... by pentachlorophenol,
a toxicant regularly found in effluents of the pulp and paper industry.
The induction of mutation of the hypoxanthine-guanine
phosphoribosyl transferase locus and cytotoxicities of 6 different chlorophenols
(2,4- and 2,6-dichlorophenol, 2,4,5- and 2,4,6-trichlorophenol,
2,3,4,6-tetrachlorophenol and pentachlorophenol)
were examined in V79 Chinese hamster cells without exogenous metabolic
activation. The chlorophenols were cytotoxic to V79 cells, but fail to produce
significant increases in the frequency of 6-thioguanine-resistant mutants.
Largemounth bass Micropterus salmoides were
reared over their first 8 weeks of free-swimming life in uncontaminated control
water or in water containing one of five concentrations of pentachlorophenol
ranging from 1.6 to 88 ug/l. Over the final 3 weeks of the study, fish reared in
concentrations of 67 and 88 ug pentachlorophenol/l
performed significantly fewer feeding acts (orientations, bites) and had a lower
rate of prey capture than did control fish. However, fish in high concentrations
spent significantly more time swimming than did control fish, which indicated
that exposure to pentachlorophenol
made them hyperactive. By inhibiting energy intake while inducing higher energy
expenditures, pentachlorophenol may
reduce survival of young largemouth bass over the winter.
The immunosuppressive effects produced by
exposure to technical grade pentachlorophenol
were compared with those produced by purified pentachlorophenol
both in vitro and in vivo in mice. Female B6C3F1 mice were administered daily
doses of 10, 30, or 100 mg/kg technical grade pentachlorophenol,
or corn oil via gastric intubation for 14 days. Animals were sacrificed the day
after the last dose, and antibody responses to multiple antigenic stimuli were
measured in spleen cell suspensions from the mice. There were no differences in
the antibody responses in the spleen cell suspensions from technical grade pentachlorophenol
or purified pentachlorophenol treated
animals as compared to controls. When mice were immunized with sheep
erythrocytes on day 10 or 11 of the 14 day exposure period, there was a dose
dependent suppression of the immunoglobulin-M antibody response to sheep
erythrocytes in spleen cells from mice treated with technical grade pentachlorophenol.
No changes were observed in the antibody responses of spleen cells from mice to
purified pentachlorophenol which were
immunized during exposure. When added directly to spleen cell cultures from
untreated mice, both technical grade pentachlorophenoland purified pentachlorophenol
suppressed the in vitro antibody responses and were cytotoxic to the spleen
cells. The in vitro antibody assay is of limited value in studying the mechanism
of immunosuppression by technical grade pentachlorophenol,
and that technical grade pentachlorophenol
induced immunosuppression cannot be attributed to a direct effect on
immunocompetent cells.
The effects of chronic dietary exposure to
technical grade pentachlorophenol on
humoral immune responses in mice were examined. Primary and secondary splenic
antibody responses to the T-dependent antigen, sheep red blood cells, were
examined in mice using the Hemolytic Antibody Isotope Release assay. To assess
the direct effects of technical grade pentachlorophenol
on B cells, the splenic plaque-forming cell response and serum antibody titers
to the T-independent antigen, dinitrophenyl Ficoll, were examined. Technical
grade pentachlorophenol exposure
altered the kinetics and the magnitude of the humoral antibody responses to
sheep red blood cells and dinitrophenyl Ficoll. Peak splenic antibody production
and serum antibody responses were dose-dependently suppressed by technical grade
pentachlorophenol exposure. IgM
responses appeared to be more sensitive to technical grade pentachlorophenol
induced suppression than the IgG response. Significant depresssion of the IgM
anti-sheep red blood cells splenic hemolytic antibody isotope release response
was apparent as early as 2 wk after initiation of technical grade pentachlorophenol
exposure and persisted for at least 8 wk after terminination of technical grade pentachlorophenol
feeding. Liver weight and serum lactate dehydrogenase and alanine
aminotransferase levels were significantly elevated during technical grade pentachlorophenol
exposure and returned to control levels after a 4-6 wk recovery period. The
immunotoxic effect of pentachlorphenol
on humoral immunity was observed only in animals exposed to technical grade pentachlorphenol
known to be contaminated with significant levels of other chlorinated phenols as
well as nonphenolic impurities including chlorinated dioxins, furans, and
diphenyl ethers. Animals exposed to analytical grade pentachlorophenol
did not exhibit depressed humoral immunity.
The rat embryo was shown to be most
susceptible to the toxic effect of pentachlorophenol
during the early phases of organogenesis.
/Mean oral/ LD50 for female mallards at age 3
mo was 380 mg/kg and for female pheasants at age 3-6 mo, 504 mg/kg./ Signs of
intoxication: Polydipsia and regurgitation (in mallards), tachypnea, wing
shivers or twitching, jerkiness, shakiness, ataxia, imbalance, tremors, and
spasms. Signs appeared as soon as 10 min and mortalities in mallards usually
occurred between 2 and 24 hr after treatment and in pheasants between 3 and 5
days after treatment. However, one pheasant died after about 3 hr and one died
between 10 and 12 days after treatment. Remission took up to 2 wk.
By means of controlled laboratory experiments
it was established that timber treatment fluids containing gamma
hexachlorocyclohexane and pentachlorophenol
and used according to manufacturers' recommendations rapidly cause the death of
pipistrelle bats roosting in contact with timber treated between six weeks and
14 months previously. The chemicals responsible are presumably ingested when the
bats groom their fur after they have been in contact with the treated timber.
Bats prevented from establishing such bodily contact took longer to die
indicating that absorption of the vapor phase of the tested chemicals also takes
place across the skin or respiratory epithelium. Acrylic resin reduces the
lethal effect when used as a sealant over wood treated with gamma-hexachlorocyclohexane
and pentachlorophenol, but
polyurethane varnish does not. It has also been established that no obvious harm
is caused to bats roosting for 16 to 22 weeks in contact with timber treated
with the synthetic pyrethroids permethrin, cypermethrin and deltamethrin at
concentrations which have previously proved effective for the control of wood
boring beetles. Similarly, no obvious harm is caused to bats roosting for 13
weeks in contact with timber treated with the fungicides borester 7 and zinc
octoate. However, greater mortality was recorded in bats housed in cages treated
with the fungicide tributyltin oxide than in control groups. It is clear from
these results that synthetic pyrethroids should replace gamma-hexachlorocylcohexane
for the treatment of wood boring beetles in bat roosts. A high priority should
be accorded to replacing pentachlorophenol
with a fungicide which is not toxic to bats.
The suitability of ejaculated bovine
spermatozoa as an in vitro model of the assessment of the cytotoxic potential of
chemicals was evaluated using several endpoints: swimming activity, adenine
nucleotide content, membrane integrity and oxygen consumption. A series of
chlorophenols inhibited sperm motion (motility and velocity) in a concentration
dependent manner. This could be determined quantitatively and reproducibly by
means of videomicrography and automatic computer image analysis. The sper
immobilizing potency increased with increasing chlorination and was positively
correlated with lipophilicity. Concentrations which reduced the percentage of
moving sperm to 50% of controls ranged from 43 muM for pentachlorophenol
to 1440 muM for 4-monochlorophenol. Determinations of adenine nucleotides and
percentages of viable cells revealed qualitative differences between the action
of pentachlorophenol and the lower
chlorinated phenols. While the latter decreased the total adenine nucleotide
contents and the percentage of unstained cells in parallel to motion inhibition,
no such changes occurred after exposure to immobilizing concentrations of pentachlorophenol.
Penta-, tetra-, and trichlorinated phenols stimulated cellular respiration,
indicating their uncouping activity, at concentrations lower than those
necessary for motion inhibition. The results indicate that bovine spermatozoa
may become a useful in vitro model for the toxicological evaluation of chemicals
providing quantitative as well as qualitative data.
The acute toxicity of a technical formulation
of pentachlorophenol and pure pentachlorophenol
to three age classes of Daphnia magna, and adult Daphnia pulex and Daphnia
galeata mendotae was determined by static toxicity tests. The influence of a
number of factors on toxicity of pentachlorophenol
was also examined. The 48 hr LC50 estimates for adult daphnids of the three
species exposed to pure pentachlorophenol
were 1.78, 4.59 and 0.51 mg/l, respectively, while those for the technical
formulation were 2.57, 3.66 and 0.33 mg/l, respectively. There was little
difference in toxicity between the technical and pure pentachlorophenol;
however, toxicity of both forms of pentachlorophenol
was influenced by duration of exposure, age (and/or size) and species of test
organism and pH of the test solution. Pentachlorophenol
caused a toxic response over a very narrow range of concentrations, with the
greatest response occurring immediately between 0 and 24 hr. Pure pentachlorophenol
was equally toxic to all age classes of Daphnia magna but susceptibility to
technical pentachlorophenol decreased
with maturation. Daphnia galeata mendotae was ten times more sensitive than
Daphnia pulex to pentachlorophenol.
Pure pentachlorophenol was
significantly more toxic to Daphnia magna at pH 5.5 than 7.0 with mean 48 hr
LC50 values of 0.082 and 1.78 mg pentachlorophenol/l,
respectively. At 12 deg C, the toxicity of both forms of pentachlorophenol
to Daphnia galeata mendoate and Daphnia pulex did not differ significantly from
that at 20 deg C; however, technical pentachlorophenol
was significantly more toxic to Daphnia magna at 12 deg C for an exposure
duration of 48 hr. There was no effect of test container size (100, 250, 600 and
1,000 ml) on the toxicity of pentachlorophenol
to Daphnia magna at 20 deg C with the lower pH of 5.5, suggesting that
adsorption to glassware was not a factor in availability of pentachlorophenol
to test organisms. Beaker size had no effect on the toxicity of pentachlorophenol
to Daphnia pulex at 20 deg C with test solutions having a pH of 7.0-8.0.
In this investigation the effects of
chlorophenols on rat liver mitochondrial respiratory parameters were determined
and compared to the toxicities of those compounds in a variety of biological
systems currently being used for toxicity testing. Mitochondrial fractions were
exposed to six concentrations of five different chlorophenols in a semiclosed, 2
ml reaction vessel. Respiratory parameters were measured polarographically with
an oxygen electrode and compared to control experiments. The toxicity of the
chlorophenols, as measured by the concentration reducing the respiratory control
ratio of the control to 50%, increased with increasing chloro substitution. The
concentrations reducing the respiratory control ratio of the control to 50%
ranged from 599 muM with 2 chlorophenol to 0.110 muM with pentachlorophenol.
The RCR50 concentrations for the five chlorophenols were compared to six
physicochemical parameters for the same chlorophenols; high degrees of
correlation between the the concentrations reducing the respiratory control
ratio of the control to 50% and the physicochemical parameters were found (r :
0.890). The highest correlation coefficient obtained was with the n-octanol/water
partition coefficient (r = 0.991), indicating that the ability of chlorophenols
to partition into the lipid mitochondrial membrane plays a significant role in
eliciting its toxic effects. The concentrations reducing the respiratory control
ratio of the control to 50% were also compared to nine currently existing
short-term toxicity tests. High degrees of correlation were obtained with
several of the tests, including algal, bacterial, and fish bioassays. This
suggests that the uncoupling of oxidative phosphorylation may be the major
mechanism by which chlorophenols cause toxicity to intact cells as well as more
complex organisms. The use of mitochondrial respiratory parameters appears to
offer a complementary approach as a short term toxicity test for this class of
compounds. Further development and testing with a variety of other toxicants is
suggested.
GF-Scale cells, a fibroblastic cell line
derived from the scale of golfish, were used for the determination of the
cytotoxicity of chlorophenols and the quantitative structure-activity
relationship studies. As the cytotoxicity end point, the amount of neutral red
retained by viable cells after exposure to chemicals was quantified. The
sequence of cytotoxicity based on the concentration of chemicals that reduced
uptake of neutral red by 50% was penta-chloro > 2,4,5-trichloro >
2,3,4-trichloro > 2,3,4,6-tetrachloro > 3,5-dichloro > 3,4-dichloro
> 2,4-dichloro > 2,5-dichloro > 2,3-dichloro > 2,4,6-trichloro >
3-chloro > 4-chloro > 2,6-chloro > phenol. The in vitro cytotoxicity of
these chemicals was found to be significantly correlated to their in vivo acute
toxicity to aquatic species, and the concentrations of chemicals that reduced
uptake of neutral red by 50% were correlated with six physiochemical parameters
of chlorophenols. N-Octanol/water partition coefficient gave the best
correlation in simple linear regression analysis, as is frequently stated in
toxicity studies with aquatic animals. Multiparametric linear regression
equations yielded improved correlation coefficients and predictive capabilities,
including the n-octanal/water partition coefficient and pKa. These results
suggest that in vitro fish cytotoxicity assays using the GF-Scale cell line are
useful for ecotoxicity screening of aquatic pollutants.
Effects of administration of equimolar doses
of hexachlorobenzene and its metabolites pentachlorophenol
and tetrachlorohydroquinone on serum thyroxine and triiodothyronine levels in
rats were studied. Furthermore, it was investigated whether the observed effects
were related to the serum levels of hexachlorobenzene or pentachlorophenol.
Rats received either corn oil (controls) or hexachlorobenzene, pentachlorophenol
or tetrachlorohydroquinone in a single equimolar intraperitoneal dose of 0.056
mmol/kg. Results indicated that hexachlorobenzene did not alter serum thyroxine
and triiodothyronine levels for a period up to 96 hr after dosing. In contrast, pentachlorophenol
and tetrachlorohydroquinone were both capable of reducing serum thyroxine levels
with a maximum effect between 6 and 24 hr after exposure.
Tetrachlorohydroquinone was more effective in repressing triiodothyronine than
thyroxine blood levels. Dose response experiments were carried out in order to
obtain insight into the sensitivity of the observed effects. Rats received
different doses of pentachlorophenol
or tetrachlorohydroquinone intraperitoneally. The reductions of thyroxine levels
by pentachlorophenol were inversely
related to serum pentachlorophenol
levels in exposed animals, based on the toxicokinetics and dose response
profiles. Furthermore, pentachlorophenol
serum levels after hexachlorobenzene administration appeared too low to cause an
effect. The results of this study indicate that not hexachlorobenzene itself,
but rather its metabolites pentachlorophenol
and tetrachlorohydroquinone may be involved in reduced serum thyroid hormone
levels after hexachlorobenzene administration.
Bluegill sunfish (Lepomis macrochirus),
exposed to a 22 day subchronic exposure of pentachlorophenol
at concentrations of approximately 20 and 75% of the 96 hr LC50, showed
significant reductions in food conversion efficiency measured during the last 10
days of exposure. Bluegills exposed to a 3 day acute spill mimicking exposure of
pentachlorophenol at a concentration
of approximately 100% of the 96 hr LC50 failed to show a significant reduction
in food conversion efficiency measured during the 10 days following exposure.
Bluegill sunfish exposed to pentachlorophenol
at continuous low level concentrations are at a greater risk for decreased
growth than those exposed to a more concentrated short term pulse of toxicant.
To evaluate the toxicities of 37 xenobiotics
detected in drinking water, primary cultures of rat hepatocytes were treated
with the xenobiotics at a concentration of 0.5 mM. The toxicities were assessed
by four cellular markers: leakage of intracellular lactate dehydrogenase
activity, glycogenolytic activity as a specific function of hepatocytes,
intracellular glutathione content, and observations of cytopathic effects. The
cytotoxic assay revealed that pesticides of xenobiotics used in the current
study were the most toxic at muM levels, that phenolic compounds had potent
toxicity for the cultured cells while benzoic compounds did not, and that 3
carbon compounds with substitution of hydrogen to bromine or chlorine at both
positions 1 and 3 were highly toxic. The order of hepatotoxicity on the basis of
IC50 was, 1,3-dichloro-2-propanone > pentachlorophenol
: 1,2-dibromo-3-chloro-propane > hepatachlor > 2,4,6-trichlorophenol :
2,4,6-tribromophenol. Since lag times were observed for the expression of
cytotoxicity by the pesticides, biotransformation appeared important for the
toxicity. Currently the concentration of pesticides is very low in the
environment, and therefore the possibility of causing an impact on human health
is low. However, the long lifetime and high lipophilicity of pesticides give
them the potential to become some of the greatest environmental toxicants.
The inhibition of methane production by
Methanosaeta concilii GP6, Methanospirillum hungatei GP1, Methanobacterium
espanolae GP9, and Methanobacterium bryantii during short term (6 hr) exposure
to eight benzene ring compounds was studied. The concentration that caused 50%
inhibition of the methane production rate was dependent on the species and the
toxicant. Pentachlorophenol was the
most toxic of the tested compounds, with an IC50 of less than 8 mg/liter for all
species except Methanospirillum hungatei. Abietic acid was the next most toxic
compound for all the species, with an IC50 in the range of 1,225 to 32,400
mg/liter. 3-Chlorobenzoate was substantially more toxic (IC50, 450 to 1,460
mg/liter) than benzoate. The inhibition by benzene, phenol, vanillic acid, and
toluene was intermediate to that of pentachlorophenol
and benzoate. Long term incubation (days) studies to determine effect on growth
indicated that all eight compounds were usually much more toxic than predicted
from the short term data. In these latter studies, there was generally a good
correlation in the observed inhibition as determined from growth and methane
production.
The toxicity of polychlorinated aromatic
compounds was studied. Polychlorinated aromatic compounds in corn oil were
administered to adult male and female albino mice, NMRJ strain, orally or by
intraperitoneal injection. The median lethal dose for pentachlorophenol
was 3.85 mg/mouse by the oral route and 1.75 mg/mouse by ip injection, for
pentachloroanisole the values were 9.50 and 8.40, for tetrachlorocatechol 9.50
and 4.80, for tetrachlorohydroquinone 11.0 and 0.85, and for
tetrachlororesorcinol the median lethal doses were 22.0 and 10.5 mg/mouse,
respectively. After oral administration, pentachlorophenol
was found to be the most toxic compound. After intraperitoneal administration,
tetrachlorohydroquinone was found to be the most toxic compound. The animals
that received 12 mg oral or ip single doses of tetrachlorodimethoxybenzenes did
not die. Oral or ip single doses of tetrachlorobenzenediol-diacetates also
produced no death. The groups of males dosed orally with tetrachlorohydroquinone,
those dosed with tetrachlororesorcinol-diacetate, and the groups of males and
females dosed intraperitoneally with tetrachlororesorcinol-diacetate showed a
slower growth in body weight than controls. Microscopic examination of spleen,
kidney, liver and lung tissue indicated unspecific bronchitis and inflammatory
reaction in the hilar fat tissue in liver and slight infiltrates of lymphoid
cells in some animals.
The effects of pure and technical grade pentachlorophenol
on primary cultured rat hepatocytes were compared to determine if contaminants
of commercial preparations of pentachlorophenol
increased its toxicity. Hepatocytes isolated from adult Sprague Dawley rats were
incubated with analytical pentachlorophenol
of 99 percent purity, technical grade pentachlorophenol,
or its sodium salt (technical grade pentachlorophenol
sodium salt), which contains only minor concentrations of technical impurities.
Monooxygenase activity was markedly induced by technical grade pentachlorophenol
in a concentration dependent pattern, with a maximum response of approximately
14 fold seen at concentrations of 30 to 50 micromoles. Monooxygenase induction
was much less marked after exposure to 50 micromoles technical grade pentachlorophenol
sodium salt, only 2.7 fold, and was barely detectable after exposure to 50
micromoles analytical pentachlorophenol.
Phase II metabolism of monooxygenase product was equally inhibited by
pretreatment with any of the pentachlorophenol
preparations. Cell membrane damage, assessed by leakage of lactate dehydrogenase
into the culture medium, was also observed with all the pentachlorophenol
preparations tested. These results indicated that monooxygenase induction was
attributable to technical impurities, while cytotoxic effects were caused by the
pentachlorophenol itself. The authors
conclude that the measurement of monooxygenase activity in cultured rat
hepatocytes may provide a method of detecting enzyme inducers as contaminants in
complex industrial chemicals.
A study was designed to define the activity
ranges of different chlorinated phenols in the series from monochlorophenol to pentachlorophenol
in bacteria; to define the effect of these compounds on growth and viability
parameters, correlating experimental findings with those obtained by enzymatic
activities; and to define the relationships between toxicity and some
physicochemical properties of these compounds. Escherichia coli was grown in the
presence of test agents and assayed for growth and dehydrogenase and beta-galactosidase
activities. Under these experimental conditions, the lag time to initiation of
acclimation of growing cultures to phenol was 3 hours, while for chlorinated
compounds it was about 2 hours longer. No effect of chlorine substituent number
or concentration was seen. Toxicities of phenol, monochlorophenols, and
polychlorophenols were differentiated by plotting specific growth rates,
normalized to controls, against different concentrations. The validity of
dehydrogenase activity in determining the toxicity of various phenol compounds
by discriminating among different compounds was also demonstrated. Specific
growth rate and dehydrogenase activity gave the best responses for quantitating
toxicity and were compared for each phenol compound. The relative toxicity
values showed that for both parameters the values obtained were lower than 10
for monochlorophenols and higher than 25 for polychlorinated phenols. A
dependence of toxicity on phenol ionization constants was also noted. The
authors conclude that use of specific growth rates and dehydrogenase activity in
Escherichia coli is valid for evaluation of chemical toxicities of halogenated
phenol compounds.
The acute oral median lethal dose of technical
grade pentachlorophenol was
investigated in developing Sprague Dawley rats from 10 to 134 days old. Signs of
acute toxicity included ataxia developing about 15 minutes after dosing,
followed by rapidly developing motor weakness, hyperpyrexia, and rapid breathing
about 25 minutes after dosing. Most deaths occurred either between 20 minutes
and 2 hours, or between 4 hours and 8 hours following dosing. Those animals who
recovered had little salivation, rectal temperatures only 1 to 3 degrees F above
normal, and began to recover after 8 hours. Rats who were 10 to 20 days of age
and not yet weaned and adult rats aged 70 to 134 days old formed the two most
susceptible groups, far more susceptible than were juveniles aged 25 to 50 days,
to the toxic effects of pentachlorophenol.
The LD50 increased 4.4 times from postnatal day ten to postnatal day 25,
plateaued from day 25 to 50, and decreased 2.8 times from day 50 to 134. The
physiological reasons for the developmental susceptibility as evidenced in this
study were not known. The authors suggest that functional changes in both the
kidney and liver may be contributing factors.
The effect of pentachlorophenol
on microsomal mixed function oxidases was studied in cattle. Four adult
lactating Holstein cattle were fed 0.2 mg/kg technical grade pentachlorophenol
for 75 to 84 days, followed by 2 mg/kg for 56 to 60 days. Twelve adult
nonlaboratory Holstein cattle were administered 0, 0.1, 1.0, or 10.0 mg/kg
purified pentachlorophenol for 95
days. The pentachlorophenol was
administered directly into the rumen by way of a permanent cannula. Fifteen male
calves were administered 1, 2, 10, or 20 mg/kg technical grade or purified pentachlorophenol
from 5 to 43 days of age. The animals were observed for clinical signs of
toxicity; they were killed at the end of the dosing period and the liver and
lungs were removed and weighed. Liver and lung microsomes were prepared and
assayed for benzo(a)pyrene-hydroxylase, ethoxycoumarin-O-deethylase,
hexobarbital-hydroxylase, ethylmorphine-N-demethylase, aminopyrine-N-demethylase,
cytochrome-P450(448), or cytochrome-b5. None of the adult cattle exhibited
clinical signs of toxicity. Liver and lung weights were significantly elevated
in cattle given technical grade pentachlorophenol.
Liver and lung benzo(a)pyrene-hydroxylase was significantly increased in these
animals. Purified pentachlorophenol
had no effect on any enzyme activities. Toxic effects such as growth impairment
and mortality were observed in calves fed 10 and 20 mg/kg pentachlorophenol.
Liver weights were significantly increased. No toxic effects were seen in calves
fed pure pentachlorophenol.
Cytochrome-P450(448) and cytochrome-b5 were significantly increased by 10 mg/kg
technical or pure pentachlorophenol.
Technical grade pentachlorophenol at 1
and 10 mg/kg induced benzo(a)pyrene-hydroxylase and ethoxycoumarin-O-deethylase.
The 10 mg/kg dose of purified pentachlorophenol
also stimulated these enzymes. The /results suggest/ that pentachlorophenol
induces organ enlargement and stimulates cytochrome-P450(448) and certain mixed
function oxidases. Benzo(a)pyrene-hydroxylase is the most inducible enzyme. The
effects observed with technical grade pentachlorophenol
are attributed to chlorinated dioxin and furan impurities. Newborn cattle are
more susceptible to the inducing properties of pentachlorophenol
and its impurities than adults.
The effects of phenol and pentachlorophenol
on axonal conduction and ganglionic transmission were studied in vitro.
Desheathed sciatic nerves from toads (Caudiverbera caudiverbera) were incubated
with up to 10 mM phenol, pentachlorophenol,
or procaine (as a reference compound) for 20 minutes. The extent of axonal
conduction block was determined by measuring the compound action potentials
evoked by supramaximal stimulation. Desheathed sciatic nerve preparations were
incubated with 0.3 to 3 mM pentachlorophenol
for 20 minutes, following which the preparations were placed in fresh medium.
Compound action potentials were measured for up to 60 minutes to assess the
reversibility of the block. Sheathed or desheathed nerve preparations were
incubated with 3 mM pentachlorophenol
at pHs 7.0 and 9.0 to assess the effect of pH on the axonal block. Phenol, pentachlorophenol,
and procaine induced axonal conduction block in a dose dependent manner. The
doses for causing a 50% block were phenol 6.30 mM, pentachlorophenol
1.00 mM, and procaine 2.00 mM. The block was irreversible. Shifting the pH of
the medium from 7.0 to 9.0 in the absence of pentachlorophenol
caused a nonsignificant axonal conduction block. When pentachlorophenol
was present the same pH change caused a significant decrease in the axonal
block. The eighth ganglia from the paravertebral chain of C-caudiverbera spinal
cords were incubated with 0.003 to 0.03 mM pentachlorophenol
at pH 7.0 and 9.0. In some experiments 0.1 mM 3,4-diaminopyridine was present.
The effects on synaptic transmission were assessed by measuring compound action
potentials as before. Pentachlorophenol
induced a synaptic transmission block that was dose dependent and irreversible.
The pentachlorophenol induced block at
pH 9.0 was significantly less than at pH 7.0. 3,4-Diaminopyridine antagonized
the effect of pentachlorophenol. The
authors conclude that pentachlorophenol,
procaine, and phenol are able to block axonal conduction in toad nerve fibers,
with PCP showing a much greater potency than procaine or phenol.
The effects of chlorophenols on the function
and viability of rat hepatocytes were studied in vitro. Primary hepatocytes
obtained from male Sprague Dawley rats were cultured and incubated with PCP,
2,3,4,5-tetrachlorophenol (TCP), 2,4,5-trichlorophenol (TrCP),
2,4-dichlorophenol (DCP), or 4-chlorophenol (chlorophenol) for 1 hr at concn of
0 to 1X10-3 M. The effects on phase I and phase II metabolism of
7-ethoxycoumarin (7EC) were assessed by determining the concentrations for
inhibiting 7-ethoxycoumarin-deethylase activity and depleting intracellular ATP
content by 50 percent. The cultures were assayed for leakage of lactate
dehydrogenase (LDH) into the medium. The EC50s for inhibiting phase I 7EC
metabolism were: PCP, 37.5 uM; TCP, 34.6 uM; TrCP, 36.4 uM; DCP, 87.8 uM; and
clorophenol, 215.2 uM. The corresponding EC50s for phase II 7EC metabolism were
6.5, 22.8, 22.0, 30.9, and 48.4 uM, respectively. The EC50s for depleting
cellular ATP were: PCP, 6.4 uM; TCP, 18.4 uM; TrCP, 25.9 uM; DCP, 185.8 uM; and
chlorophenol, 1334.1 uM. None of the compounds caused a significant leakage of
LDH into the medium. When compared with published values of their octanol/water
partition coefficients, the log of the EC50s were linearly correlated with the
log of their partition coefficients. The /results indicate/ that short term
exposure to chlorophenols severely disrupts the metabolic function of primary
cultured rat hepatocytes at concentrations that do not affect cell membrane
integrity. Primary cultures of rat hepatocytes are a suitable model for
evaluating the short term toxicity of chlorinated phenols in vitro.
Phenol and the 19 isomers of chlorophenol were
evaluated in the Microscreen Prophage Induction Assay to characterize the
genotoxicity of these agents. Seven of the isomers induced prophage lambda in
the presence of S9, with 2,3,4-trichlorophenol, 2,4,5-trichlorophenol, and
3,4,5-trichlorophenol being about ten times as potent as 2,3,6-trichlorophenol,
2,4,6-trichlorophenol, and pentachlorophenol.
Medium potency was demonstrated by 2,3,4,5-tetrachlorophenol. Structurally, the
more potent isomers had one or no chlorine atoms in the ortho position to the
hydroxyl group. The less potent isomers had two chlorine atoms ortho to the
hydroxyl group. None of the 20 compounds was mutagenic in Salmonella. However,
the prophage induction results agreed with earlier results that most of these
seven isomers were clastogenic, were associated with cancer and chromosomal
aberrations in humans, and were carcinogenic in rodents. The /results/ suggest
that the metabolism of the parent isomer to a chlorohydroquinone is an important
step in the genotoxicity of these isomers. This chlorohydroquinone can form a
chlorobenzosemiquinone in the presence of oxygen. Free radicals can then be
produced that can cause DNA strand breaks, resulting in prophage induction in
Escherichia coli or possibly the chromosomal aberrations associated with human
exposure to chlorophenols.
An investigation was conducted to examine the
competition of various chlorinated phenol congeners with the thyroxine (T4)
binding site of transthyretin (TTR). Specifically, attempts were made to
determine whether the T4 binding site of TTR could be occupied by hydroxylated
chlorinated aromatic compounds using chlorinated phenol congeners as model
compounds in a competition assay with (125)I labeled T4. 2,3-Dichlorobenzene,
3,4,3',4'-tetrachlorobiphenyl, 4-hydroxybiphenyl, and phenol were inefficient
competitors. The chlorinated phenols which were tested were all competitors for
the T4 binding site of TTR. The most effective competitor was pentachlorophenol
(PCP), following in decreasing order by trichlorophenols, dichlorophenols, and
monochlorophenols. When the chlorine was present in both ortho positions to the
hydroxyl group, the competitor was more efficient. The relative affinity of
binding of PCP to TTR was twice that of T4. PCP mainly decreased the affinity
constant while the binding capacity was not altered. This indicated a
competitive type of inhibition. PCP competed successfully with T4 sites on
albumin as well with a relative affinity of 0.25. The binding of T4 to thyroid
binding globulin was much less affected by PCP interference. /Results suggest/
that a specific interaction of chlorophenols exists with the T4 binding site of
TTR.
The effect of pentachlorophenol
(PCP) and its metabolite tetrachlorohydroquinone (TCH) were tested on growth,
RNA, protein and ribosome syntheses, and ribosome content in yeast cells. Cells
exposed to increasing concentrations of PCP show increasing inhibition to RNA
and ribosome synthesis, and to cell growth. TCH causes a delay of the growth of
the cell culture (prolongation of the lag phase) but does not cause inhibition.
After treatment with TCH the maximum of the RNA synthesis was retarded, but
subsequently reached nearly the same level as the untreated control cells. On
ribosome synthesis and ribosome content, treatment with increasing
concentrations of PCP, as well as of TCH, leads to a substantial decrease in
ribosomal synthesis and, finally, total inhibition. Parallel to this, the
content of free and membrane-bound ribosomes is diminished. PCP exhibits a
stronger effect than TCH. The protein synthesis is only slightly reduced after
treatment with PCP or TCH (with concentrations up to 20 ug/ml).
Rainbow trout were exposed for 4 or 8 days to
various types of toxicants, each applied to the test water at a high sublethal
concentration. The activity of liver UDP-glucuronosyltransferase (UDP-GT) was
assayed from the submitochondrial fraction using p-nitrophenol as an aglycone.
Activity of UDP-GT was inhibited by 2,4,6-trichlorophenol, pentachlorophenol
and dehydroabietic acid, all toxicants regularly found in effluents of the pulp
and paper industry. The heavy metals cadmium and zinc, the polychlorinated
biphenyl, Pyralene 3010, and chloroform did not affect UDP-GT activity. The
slimicide N-methyl-dithiocarbamate (Vapam) significantly increased the enzyme
activity.
It is shown that p-tetrachlorohydroquinone (TCH),
the metabolite of the environmental chemical pentachlorophenol
(PCP), is more toxic to cultured CHO cells than PCP, and that it causes DNA
single-strand breaks and/or alkali-labile sites at concentrations of 2-10
microgram/ml as demonstrated by the alkaline elution technique.
Chronictoxicity test procedures (static, with
renewal) were used to determine the chronic toxicity of sublethal concentrations
of a technical formulation of pentachlorophenol
(PCP) and pure pentachlorophenol to
Daphnia magna. Test organisms 48 + or - 12 h old were exposed for their entire
lifespan (ie, until death) to 0.01, 0.05, 0.1 and 0.5 mg technical PCP/L and
0.01, 0.087 and 0.1 mg pure PCP/L. Criteria used to assess chronic toxicity were
mean time to appearance of the primiparous instar in the brood chamber, mean
number of days to release of the first brood, mean number of broods produced per
female, mean brood size per female, mean number of reproductive days, mean
number of young produced per reproductive day per female and survivorship. Pentachlorophenol
differentially affected maturation and reproduction but not survivorship or
longevity. Mean number of broods produced per daphnid, length of the
reproductive period, longevity and survivorship were insensitive criteria
relative to mean time to appearance of the primiparous instar, time to release
of first brood, brood size, and number of young produced per daphnid per
reproductive day. Generally, there was little difference in toxicity of the
three concentrations of pure PCP, for they significantly reduced mean brood size
and rate of reproduction of young and significantly but differentially affected
maturation. Technical PCP, at the highest concentration of 0.5 mg/L,
significantly reduced mean brood size and the rate of production of young, and
significantly delayed both time to appearance of the primiparous instar and
release of the first brood. When differences in toxicity occurred, generally,
pure PCP was more toxic than comparable concentrations of technical PCP.
Although enhanced maturation was observed there was no compensatory
reproduction.
Chlorinated phenols represent a major
component of hazardous oily and wood-preserving wastes that are widely
distributed in chemical dumpsites throughout the United States. Pentachlorophenol
has been reported to be highly embryolethal and embryotoxic in rats. However,
data pertaining to the developmental toxicities of other important chlorophenols
are limited. In this study, the toxicities of phenol, chlorophenol homologues
and their isomers, selected phenyl acetates, anisoles, sodium phenates, and
tetrachlorobenzoquinones (a total of 38 chemicals) were evaluated using cultures
of Hydra attenuata. Developmental hazard index (A/D ratio) was determined for
selected test chemicals (ie, those chemicals which resulted in an early toxic
endpoint at the lowest whole-log concentration in the adult hydra assay). These
same chemicals were evaluated at equimolar concentration in postimplantation rat
whole embryo culture. Hydra attenuata and whole embryo culture studies
demonstrated a linear relationship between toxicity and the degree of chlorine
substitution with pentachlorophenol
> 2,3,4,5-tetrachlorophenol > 2,3,5-trichlorophenol >
3,5-dichlorophenol > 4-chlorophenol > phenol. The developmental hazard
index A/D ratios from the Hydra attenuata assay were approximately 1 for all of
the chemicals tested. Findings from the whole embryo culture assay indicated
similar results based on growth, gross morphology, and DNA and protein content
of embryos. The results obtained in the Hydra attenuata and whole embryo culture
assays suggest that the chlorinated phenols are not potent teratogens. The
combination of Hydra attenuata and whole embryo culture may facilitate the rapid
detection and ranking of hazardous chemicals associated with complex mixtures of
chemical wastes.
This study investigated impairment of
oxidative phosphorylation in mitochondria isolated from the liver of
hexachlorobenzene treated rats. Partial and reversible uncoupling of the
phosphorylative process was found in liver mitochondria from rats dosed with
hexachlorobenzene for 60 days. Pentachlorophenol,
endogenously formed by hexachlorobenzene metabolism was detected in the
mitochondria at a concn of 0.3-0.4 nmol/mg protein. Based on the effect of pentachlorophenol,
added in vitro at a similar concn to that found in vivo, it was concluded that
the uncoupling of oxidative phosphorylation under the experimental conditions
was almost completely due to the presence of pentachlorophenol.
This study investigated the extent of
impairment in function parameters of liver mitochondria from rats treated for 60
days with hexachlorobenzene. A constant amount of mitochondrial uncoupling was
found throughout the treatment period. At the same time a nearly constant amount
of pentachlorophenol was detected in
these mitochondria. In contrast, the level of mitochondrial porphyrins increased
progressively. There was good correlation between the concentration of
mitochondrial pentachlorophenol and
the degree of uncoupling of oxidative phosphorylation.
National Toxicology Program Studies:
Carcinogenicity bioassays were conducted
utilizing 0, 100, or 200 ppm technical grade pentachlorophenol
or 0, 100, 200, or 600 ppm (Dowicide EC-7, a technical grade formulation) fed to
groups of 50 male and 50 female /B6C3F1 mice. ... Under the conditions of these
two yr studies, there was clear evidence of carcinogenic activity for male
B6C3F1 mice fed diets containing technical grade pentachlorophenol,
as shown by increased incidences of adrenal medullary and hepatocellular
neoplasms. There was some evidence of carcinogenic activity for female B6C3F1
mice exposed to technical grade pentachlorophenol,
as shown by increased incidences of hemangiosarcomas and hepatocellular
carcinomas. /Also/, there was clear evidence of carcinogenic activity for male
B6C3F1 mice exposed to pentachlorophenol,
EC-7, as shown by increased incidences of adrenal medullary and hepatocellular
neoplasms. There was clear evidence of carcinogenic activity for female B6C3F1
mice exposed to pentachlorophenol,
EC-7, as shown by increased incidences of adrenal medullary and hepatocellular
neoplasms and hemangiosarcomas.
Non-Human Toxicity Values:
LD50 Rat male oral 146 mg/kg
LD50 Rat female oral 175 mg/kg
LD50 Rat oral 210 mg/kg
LD50 Rat dermal 96-330 mg/kg
Ecotoxicity Values:
LC50 Tubifex tubifex 286, 619, and 1294 ug/l/24
hr at pH values of 7.5, 8.5, and 9.5, respectively.
TLm Carassius auratus (goldfish) flow through
bioassay at 25 deg C/96 hr: 0.22 mg/l; 120 hr: 0.253 mg/l; 336 hr: 0.189 mg/l
TLm Lepomis macrochirus (bluegill) flow
through bioassay at 25 deg C 30 hr: 0.303 mg/l; 243 hr: 0.251 mg/l; 406 hr:
0.188 mg/l
LC50 Trout, flow through bioassay 48 hr: 0.25
mg/l; 96 hr: 0.23 mg/l; 10 day: 0.23 mg/l at 15 deg C
LC50 (Brachydanio rerio) Zebra fish, flow
through bioassay 48 hr: 1.24 mg/l; 96 hr: 1.13 mg/l; 10 days: 1.08 mg/l at 25
deg C
LC50 (Jordanella floridae) Flagfish, flow
through bioassay 48 hr: 1.82 mg/l; 96 hr: 1.74 mg/l; 10 d: 1.74 mg/l at 25 deg C
LC50 (Channa gachua) Freshwater fish, static
test (test solutions changed every 24 hr) 24 hr: 0.79 mg/l; 48 hr: 0.56 mg/l; 72
hr: 0.43 mg/l; 96 hr: 0.39 mg/l
LC50 Pimephales promelas (fathead minnows) 4
wk old, 0.222 + or - 0.021 mg/l/24 hr /Conditions of bioassay not specified/
LC50 Pimephales promelas (fathead minnows) 7
wk old, 24 hr: 0.245 + or - 0.039 mg/l; 96 hr: 0.230 + or - 0.03 mg/l
/Conditions of bioassay not specified/
LC50 Pimephales promelas (fathead minnows) 11
wk old, 24 hr: 0.232 + or - 0.052 mg/l; 96 hr: 0.222 + or - 0.3 mg/l.
/Conditions of bioassay not specified/
LC50 Pimephales promelas (fathead minnows) 14
wk old, 24 hr: 0.200 + or - 0.016 mg/l; 96 hr: 0.190 + or - 0.0 mg/l.
/Conditions of bioassay not specified/
LC50 Poecilia reteculata Guppy 0.38 ppm/24 hr
at pH 7.3 /Conditions of bioassay not specified/
LC50 ONCORHYNCHUS TSHAWYTSCHA (CHINOOK SALMON)
68 UG/L/96 HR AT 10 DEG C (95% CONFIDENCE LIMIT 48-95 UG/L) WT 1 G. STATIC
BIOASSAY WITHOUT AERATION, PH 7.2-7.5, WATER HARDNESS 40-50 MG/L AS CACO3 AND
ALKALINITY OF 30-35 MG/L.
LC50 SALMO GAIRDNERI (RAINBOW TROUT) 52 UG/L/96
HR AT 11 DEG C (95% CONFIDENCE LIMIT 48-56 UG/L) WT 1 G. STATIC BIOASSAY WITHOUT
AERATION, PH 7.2-7.5, WATER HARDNESS 40-50 MG/L AS CACO3 AND ALKALINITY OF 30-35
MG/L.
LC50 PIMEPHALES PROMELAS (FATHEAD MINNOW) 205
UG/L/96 HR AT 20 DEG C (95% CONFIDENCE LIMIT 179-234 UG/L) WT 1.1 G. STATIC
BIOASSAY WITHOUT AERATION, PH 7.2-7.5, WATER HARDNESS 40-50 MG/L AS CACO3 AND
ALKALINITY OF 30-35 MG/L.
LC50 ICTALURUS PUNCTATUS (CHANNEL CATFISH) 68
UG/L/96 HR AT 20 DEG C (95% CONFIDENCE LIMIT 58-80 UG/L) WT 0.8 G. STATIC
BIOASSAY WITHOUT AERATION, PH 7.2-7.5, WATER HARDNESS 40-50 MG/L AS CACO3 AND
ALKALINITY OF 30-35 MG/L.
LC50 LEPOMIS MACROCHIRUS (BLUEGILL) 32 UG/L/96
HR AT 15 DEG C (95% CONFIDENCE LIMIT 23-44 UG/L) WT 0.4 G. STATIC BIOASSAY
WITHOUT AERATION, PH 7.2-7.5, WATER HARDNESS 40-50 MG/L AS CACO3 AND ALKALINITY
OF 30-35 MG/L.
LC50 COLINUS VIRGINIANUS (BOBWHITE) 10 DAYS
OLD, ORAL (5-DAY DIET) APPROX 3400 PPM
LC50 COTURNIX JAPONICA (JAPANESE QUAIL) 20
DAYS OLD, ORAL (5-DAY DIET) 5204 PPM (95% CONFIDENCE LIMIT 4536-6034 PPM)
LC50 PHASIANUS COLCHICUS (RING-NECKED
PHEASANT) 16 DAYS OLD, ORAL (5-DAY DIET) 4331 PPM (95% CONFIDENCE LIMIT
3926-4787 PPM)
LC50 ANAS PLATYRHYNCHOS (MALLARD DUCKS) 10
DAYS OLD, ORAL (5-DAY DIET) APPROX 4500 PPM
EC50 Thalassia testudinum (seagrass) flow
through bioassay 0.74 ppm/40 hr
LC50 CYPRINODON VARIEGATUS (SHEEPHEAD MINNOWS)
1 DAY OLD, 329 UG/L/96 HR, STATIC TEST
LC50 CYPRINODON VARIEGATUS (SHEEPSHEAD
MINNOWS) 2 WK OLD, 392 UG/L/96 HR, STATIC TEST
LC50 CYPRINODON VARIEGATUS (SHEEPSHEAD
MINNOWS) 4 WK OLD, 240 UG/L/96 HR, STATIC TEST
LC50 (CYPRINODON VARIEGATUS) SHEEPSHEAD
MINNOWS, 6 WK OLD, 232 UG/L/96 HR, STATIC TEST
LC50 (LYMNAEA ACUMINATA) PULMONATE SNAILS,
STATIC BIOASSAY, 0.16 MG/L (95% CONFIDENCE LIMIT 0.138-0.186 MG/L)
LD50 Coturnix japonica (Japanese quail) oral
5139 ppm (95% confidence limit 4149-6365 ppm)
LC50 (Viviparus bengalensis) Freshwater pond
snails 0.840 mg/l/96 hr static bioassay
LD50 Mallard 3 mo female oral 380 mg/kg (mean)
LD50 Pheasant 3-6 mo female oral 504 mg/kg
(mean)
Metabolism/Pharmacokinetics:
Metabolism/Metabolites:
... MAJOR METABOLITE OF HCB /HEXACHLOROBENZENE/
... .
FOLLOWING SINGLE ORAL DOSE OF PENTACHLORO-(14)C-BENZENE
(0.5 MG/KG) TO RHESUS MONKEYS ... /7% WAS EXCRETED/ AS PENTACHLOROPHENOL
... IN URINE.
PENTACHLOROPHENOL
... IS DECHLORINATED IN VIVO & IN VITRO IN RAT TO TETRA- & TRI-CHLOROHYDROQUINONE
... DECHLORINATION IS MEDIATED BY LIVER-MICROSOMAL ENZYMES, & THEIR ACTIVITY
IS ENHANCED BY PRE-TREATMENT WITH SEVERAL WELL-KNOWN INDUCERS OF CYTOCHROME
P450. ... PHARMACOKINETIC STUDY OF SINGLE ORAL DOSAGE (0.1 MG/KG) ... IN HUMAN
SUBJECTS ... REVEALED NO METABOLITES WERE DETECTED APART FROM GLUCURONIDE OF PCP
(ABOUT 12%).
BACTERIAL ISOLATE, RELATED TO SAPROPHYTIC
CORYNEFORM BACTERIA, WAS ABLE TO METABOLIZE PENTACHLOROPHENOL
AS SOLE SOURCE OF CARBON & ENERGY. PENTACHLOROPHENOL
WAS RAPIDLY METABOLIZED TO CO2. IN CULTURES OF TRICHODERMA VIRGATUM, PENTACHLOROPHENOL
WAS METHYLATED TO FORM PENTACHLOROANISOLE. SIMILARLY, PENTACHLOROANISOLE WAS
FORMED FROM PENTACHLOROPHENOL BY
PENICILLIUM SP & CEPHALOASCUS FRAGRANS.
THE PROTOPORPHYRIN ENZYME PEROXIDASE, DETECTED
IN SNAILS, CATALYZED OXIDATION OF PENTACHLOROPHENOL
TO 2,2',3,3',5,5',6,6'-OCTACHLOROBIPHENYLQUINONE.
... MOST OF PENTACHLOROPHENOL
TRANSFERRED TO HEPATOPANCREAS /IN GOLDFISH/ WAS DETOXIFIED BY SULFATE
CONJUGATION OR BY DECOMPOSITION. EXCRETION ... WAS IN FORM OF CONJUGATE
IDENTIFIED AS PENTACHLOROPHENYLSULFATE.
The metabolism of pentachlorophenol
is generally similar in mammalian species. In rodents, more than 40% is excreted
in urine unchanged. The remainder is excreted as tetrachlorohydroquinone and
glucuronide conjugates of pentachlorophenol.
In limited studies of humans, pentachlorophenol,
tetrachlorohydroquinone, & pentachlorophenol
glucuronide have been found in urine. In vivo retention of pentachlorophenol
by lipid-containing tissues may be attributable to conjugation with fatty acids.
Unchanged pentachlorophenol
is excreted in the urine of rabbit, rat, mouse, and monkey. In addition to free pentachlorophenol,
rats excrete tetrachloro-p-hydroquinone and trichloro-p-hydroquinone. ... Both
metabolites as well as the parent cmpd are excreted free and as glucuronides.
The biotransformation of pentachlorophenol
in man and animals takes place by conjugation, hydrolytic dechlorination, and
reductive dechlorination. Further species dependent reactions are oxidation and
methylation. The reaction with glutathione results in the formation of
conjugates and cleavage of glycine and glutamate gives cysteine conjugates.
Acetylation of the amino group of the cysteinyl moiety in mammals gives
mercapturic acids. The metabolic pathways leading to dechlorinated derivatives
may be mediated by the reaction with glutathione as the presence of the
N-acetyl-S-(pentachlorophenyl)cysteine.
The metabolism of pentachlorophenol
and its covalent binding to protein and DNA were tested in the microsomes of
Wistar rats of both sexes pretreated with hexachlorobenzene, phenobarbital,
3-methylcholanthrene, or isosafrole. Pentachlorophenol
when incubated with microsomes, was converted into tetrachloro-1,2-hydroquinone
and tetrachloro-1,4-hydroquinone. Isosafrole increased the rate of conversion 7
times as compared to control microsomes, while hexachlorobenzene, pentachlorophenol
and 3-methylcholanthrene increased the rate of conversion 2 to 3 times. The fact
that pentachlorophenol and
hexachlorobenzene accounted for the production of tetrachloro-1,4-hydroquinone
and tetrachloro-1,2-hydroquinone in a ratio of about 2, as compared to a ratio
of about 1.3 for 3-methylcholanthrene and isosafrole, and the fact that this
ratio decreased with increasing concentrations of pentachlorophenol
in microsomes from hexachlorobenzene treated rats, were indicative of the
involvement of the various cytochrome p450 isoenzymes. The covalent binding of pentachlorophenol
to protein was inhibited by ascorbic acid, with a subsequent increase in the
production of tetrachlorohydroquinones. The rate of covalent protein binding was
constant, regardless of variation in the rate of conversion observed in the
mirosomes of rats treated with various inducers. DNA binding was conversion
dependent and was lower than protein binding. The addition of DNA did not affect
the formation of soluble metabolites.
The metabolism of pentachlorophenol
in animals and man was reviewed. Tetrachlorophenols,
2,3,5,6-tetrachloro-1,4-benzoquinone, 2,3,4-trichlorophenol,
2,3,5-trichloro-1,4-hydroquinone, and their glucuronide conjugates were found in
animals and man. Also identified were pentachlorophenylacetate,
pentachloroanisole, and pentachlorophenylsulfate. The biotransformation of pentachlorophenol
in man and animals takes place by conjugation, hydrolytic dechlorination, and
reductive dechlorination. Further species dependent reactions are oxidation and
methylation. The reaction with glutathione results in the formation of
conjugates and cleavage of glycine and glutamate gives cysteine conjugates.
Acetylation of the amino group of the cysteinyl moiety in mammals gives
mercapturic acids. The metabolic pathways leading to dechlorinated derivatives
may be mediated by the reaction with glutathione as the presence of the
N-acetyl-S-(pentachlorophenyl)cysteine would indicate. The results of metabolic
in vivo studies on hexachlorobenzene, pentachloronitrobenzene,
pentachlorobenzene, and pentachlorophenol
indicate that one pathway stems from hexachlorobenzene and
pentachloronitrobenzene via sulfur containing conjugates to thiophenolic
derivatives and to chlorinated benzenes, primarily to pentachlorobenzene.
Another pathway transforms pentachlorophenol
to less chlorinated phenols. The authors state that pentachlorophenol
is a metabolite of various environmental chemicals and is itself metabolized.
Therefore there is no direct relationship between the level of pentachlorophenol
in body fluids and the degree of exposure.
Absorption, Distribution & Excretion:
Rapid absorption of pentachlorophenol
has been reported in rodents, monkeys, & humans following oral, dermal, or
inhalation exposure. ... The major tissue deposits vary somewhat between
species. In humans whose deaths were not related to pentachlorophenol
exposure, the liver (containing pentachlorophenol
residues of 0.067 ug/g), kidney, brain, spleen, & fat (0.013 ug/g) appeared
to be major deposition sites. In the mouse, the gall bladder is a principal
storage site. In the rat, it is the kidney.
WHEN WORKER EXPOSURE TO PENTACHLOROPHENOL
AT WOOD TREATMENT PLANT WAS MEASURED OVER 5 MO PERIOD, SERUM & URINE LEVELS
... WERE 348.4 TO 3963 UG/L & 41.3 TO 760 UG/L, RESPECTIVELY. PENTACHLOROPHENOL
RESIDUES IN WORKPLACE AIR WERE IN THE RANGE OF 5.1 TO 15275.1 NG/CU M.
(14)C-PCP WAS ADMIN TO MICE BY SC OR IP
INJECTION. MOST OF THE ACTIVITY (72-83%) WAS EXCRETED IN URINE IN 4 DAYS; ABOUT
HALF, IN 24 HR; & ONLY TRACE (0.05%), IN EXPIRED AIR. HIGH ACTIVITY OBSERVED
IN GALLBLADDER & ITS CONTENTS, WALL OF STOMACH FUNDUS, CONTENTS OF GI TRACT
& LIVER.
ENTEROHEPATIC CIRCULATION OF PENTACHLOROPHENOL
OCCURS IN MONKEYS & MICE. IN RATS, IT IS FOUND MAINLY IN PLASMA PROTEIN;
LIVER & KIDNEY HAVE HIGHEST TISSUE CONCN. PLASMA HALF-LIVES AT 10 MG/KG BODY
WT DOSE WERE ABOUT 15 HR IN RATS & 78 HR IN MACACA MULATTA MONKEYS.
UNLESS RENAL & LIVER FUNCTIONS ARE
IMPAIRED, PENTACHLOROPHENOL IS RAPIDLY
ELIMINATED FROM BLOOD & TISSUES.
PENTACHLOROPHENOL
HAS BEEN DETECTED IN HUMAN BLOOD PLASMA AT LEVELS OF 15.69 TO 15.86 UG/L IN
HEMODIALYZED PATIENTS & 15.0 UG/L IN PERSONS USED AS CONTROL. IT ALSO HAS
BEEN DETECTED IN URINE, SEMINAL FLUID (20-70 UG/KG) & FINGERNAILS OF
NON-OCCUPATIONALLY EXPOSED INDIVIDUALS. PENTACHLOROPHENOL
WAS FOUND IN 85% OF 416-418 SAMPLES OF URINE COLLECTED FROM GENERAL POPULATION
... MAX LEVEL WAS 193 UG/L & MEAN LEVEL 6.3 UG/L. ... URINE SAMPLES TAKEN AT
25 FACTORIES USING PENTACHLOROPHENOL
... SHOWED THAT AVG WORKER'S EXPOSURE TO PENTACHLOROPHENOL
IN AIR WAS 0.013 MG/CU M, WITH MAX RANGE OF 0.004-1.000 MG/ CU M, & LEVEL IN
URINE RANGED FROM 0.12 TO 9.68 MG/L.
Small amounts have been shown to cross the
placenta.
Plasma and urinary pentachlorophenol
was measured in 209 workers who had occupational exposure to wood preservatives
containing this compound and 101 workers not exposed occupationally to pentachlorophenol.
Workers were examined for chloracne and blood concentrations of bilirubin,
gamma-glutamyltransferase, cholesterol and high-density lipoproteins were
determined. All the occupationally exposed groups showed evidence of pentachlorophenol
absorption; highest mean concentrations were found in timber treatment
operatives (6.0 mmol/l for plasma and 274 nmol/mmol of creatinine for urine).
Pentachlorophenol
was given orally to ... volunteers at single doses of 3.9, 4.5, 9, and 18.8 mg.
Daily urinary excretion of pentachlorophenol
and pentachlorophenol conjugated to
glucuronic acid was monitored using gas chromatography with electron capture
detection. Based on first order elimination kinetics an elimination half-life of
20 days was derived. To eliminate interference by the uncontrolled absorption of
pentachlorophenol from the environment
0.98 mg (13)C-pentachlorophenol was
taken by one of the volunteers. Pentachlorophenol
levels in urine and plasma were determined using mass spectrometry with negative
chemical ionization. An elimination half-life of 17 days was found in both urine
and blood. The collected data were used to calculate the clearance of pentachlorophenol:
a value of 0.07 m1/min was found. The long elimination half-life of pentachlorophenol
is explained by the low urinary clearance due to the high plasma protein binding
(> 96%) and the tubular reabsorption. The pH-dependency of the elimination of
pentachlorophenol was investigated,
and a distinct increase in the daily excretion was observed following
alkalinization by oral administration of sodium bicarbonate. In order to
elucidate the role of the enterohepatic circulation as a possible pool for pentachlorophenol
in humans, the bile of cholelithiasis patients with postoperative T-drainage was
investigated for pentachlorophenol and
compared with the corresponding urine and plasma levels, but no accumulation of pentachlorophenol
in the enterohepatic circulation could be observed. The daily elimination and
plasma levels of pentachlorophenol in
a group of individuals without a specific exposure were found to range from 10
to 48 ug/day and 19 to 36 ug/1, respectively.
Urine from 230 Finnish sawmill workers exposed
to a combination of 2,3,4,6-tetrachlorophenol (80%), 2,4,6-trichlorophenol
(10-20%), and pentachlorophenol (5%),
was analyzed for the sum of the three chemicals as chlorophenols. Samples were
collected at the end of the work shift. Workers were divided into the following
exposure groups according to work tasks: primarily skin exposure (n= 112),
primarily respiratory tract exposure (n= 34), and equal exposure by both routes
(n= 84). Air concentrations at the workplace and amount of time spent with skin
contact were not studied. There was no control group; values were compared to
the nonexposed Finnish population level of < 0.1 umol/l. Skin absorption was
the most effective route of exposure as reflected by urinary chlorophenol
concentrations. The median concentration in workers with skin absorption was 7.8
umol/l (range 0.1 to 210.9 umol/l) and was significantly different from that in
workers with the respiratory tract as the main route of exposure (median
concentration 0.9 umol/l; range 0.1 to 13.3 umol/l; p< 0.001) and from those
with both routes of equal importance (1.4 umol/l; range 0.1 to 47.8 umol/l;
p< 0.001). /Tri-, Tetra-, and Pentachlorophenols/
The compounds are readily absorbed from the
gastroenteric tract and from parenteral sites of injection. /Chlorophenols/
Plasma half-life in man is 30.2 + or - 4.0 hr.
Half-lives for elimination of pentachlorophenol
and pentachlorophenol-glucuronide from
the urine are 33.1 + or - 4.5 and 12.7 + or - 5.4 hr, respectively.
The dependence of bats in Britain on houses as
roosts may result in them being exposed to pesticides used in remedial timber
treatments. Pentachlorophenol and
permethrin are used as a fungicide and a insecticide for timber treatment,
respectively. The present study investigated toxicity and distribution in body
tissues of these two pesticides in pipistrelle bats. Four groups of nine to ten
bats were kept in separate outdoor flight enclosures and were provided with
roost boxes treated with either pentachlorophenol
only, permethrin, pentachlorophenol/permethrin
mixture or solvent only (control). At the start of the experiment, mean (:
standard error) pentachlorophenol and
permethrin concentrations on the surface of wooden blocks that had been treated
in the same way as roost boxes were 69.32 : 6.76 mg/g (n = 6) and 3.3 : 1.6 mg/g
(n = 3), respectively. All bats exposed to pentachlorophenol
and pentachlorophenol/permethrin
treated boxes died within 24 and 120 hr, respectively; nine out of the ten
controls survived the 32 day experimental period (p< 0.001; both groups
compared with control). Bats exposed to permethrin treated boxes survived as
well as controls. Mean (: standard error) carcass pentachlorophenol
concentration (excluding deposits on fur) of bats exposed to pentachlorophenol
and pentachlorophenol/permethrin
treated boxes was 13.11 : 2.52 ug/g body wt (n = 20). Pentachlorophenol
burdens on fur were positively correlated with total weight of Pentachlorophenol
in the carcass (p< 0.001). Pentachlorophenol
was present in fat depots, liver, kidney and the remainder of the body which,
despite containing low pentachlorophenol
concentrations, was the main pentachlorophenol
reservoir (66.4 : 5.0% of carcass pentachlorophenol
load; n = 20). Total pentachlorophenol
in the carcass was significantly correlated with lipid weight (p< 0.005).
Permethrin was not detectable in body washes and tissues of bats exposed to pentachlorophenol/permethrin
mixture or permet.
A pilot study was conducted to determine the
overall efficiency of transdermal penetration of pentachlorophenol
and tetrachlorophenol applied to human cadaver skin. Two commercially available
wood preservatives were tested, one diesel oil based and the other a water based
product. To simulate human exposure conditions at the workplace, small doses
were used. The objective was to document the portion of applied dose which
permeated the skin and to examine the effect of vehicle or formulation on the
relative and absolute absorption of the chlorinated compounds. The penetration
of the diesel oil preparations was 62% for pentachlorophenol
and 63% for tetrachlorophenol. In the case of the aqueous based preparation,
penetration was 16% for sodium-pentachlorophenate and 33% for sodium
tetrachlorophenate. The incomplete recovery of each compound may have been due
in part to the irreversible binding or unfavorable partitioning of the
chlorophenols which would be consistent with the lipophilic character of these
compounds.
The excretion and conjugation of chlorophenols
were studied in workers exposed to 2,4,6-tri-, 2,3,4,6-tetra-, and
pentachlorophenolates, the main components of the chlorophenolate product
manufactured by direct chlorination of phenol. The workers were exposed in two
different saw mills in which sodium chlorophenolate was used for treatment of
lumber during the warm season. Urine specimens were collected at the end of the
treatment season as well as at the start of a new treatment period in the
spring. Serum specimens were collected towards the end of the treatment period.
Total and unconjugated chlorophenols were analyzed with a GC method. The maximal
concentrations of urinary 2,4,6-tri-, 2,3,4,6-tetra- and pentachlorophenol
at the end of the lumber-treatment period were 1-11.8, 3.4-17.3, and 0.2-0.9
umol/l, respectively, and the average apparent half-times calculated using a one
compartment model were 18 hr, 4.3 days and 16 days, respectively. For
2,3,4,6-tetrachlorophenol, the data of some subjects showed a better fit with a
two compartment model; the corresponding half-times were 5.3 and 26 days. During
the continuous-exposure period the average serum levels of tetra- and pentachlorophenol
were rather similar before and after the working day: 2.79 + or - 1.78 umol/l
for tetrachlorophenol and 0.85 + or - 0.4 umol/l for pentachlorophenol.
Renal clearance values for tetra- and pentachlorophenol
were related to urine flow and indicated tubular reabsorption. At low
concentrations, sulfate conjugation was dominant. With increasing chlorophenol
concentrations the proportion of glucuronide conjugation was increased,
especially for pentachlorophenol.
1. Interspecies variability in the metabolism
of pentachlorophenol (PCP) was
investigated by exposing rainbow trout, fathead minnows, sheepshead minnow,
firemouth, and goldfish to water-borne (14)C-PCP for 64 hr. 2. The amounts of
metabolites in bile and exposure water were species-dependent; all of the
metabolites excreted into the water were sulfate conjugates while bile was
enriched in glucuronide conjugates. 3. Biliary excretion accounted for less than
30% of the total PCP metabolites. 4. Biliary metabolites alone were a poor
indication of the metabolites produced and of the major routes of elimination.
Biological Half-Life:
Absorbed by goldfish from water and rapidly
excreted as a sulfate conjugate. Biological half-life of approx 10 hr.
Biological half-life for excretion in the
Rhesus monkey was 41 and 92 hr in males and females, respectively.
Half-life for absorption in man following
ingestion of 1.0 mg/kg was 1.3 + or - 0.4 hr. Peak plasma concn of 0.248 mg/l
occurred at 4 hr.
In humans, urinary excretion half-lives
following chronic exposure are significantly longer than after single high-dose
exposure (20 days versus 10 hr).
PLASMA HALF-LIVES OF 10 MG/KG BODY WT DOSE
WERE ABOUT 15 HR IN RATS & 78 HR IN MACACA MULATTA MONKEYS.
Mechanism of Action:
CHLORINATED PHENOLS ... ARE VERY EFFECTIVE
(... IN VITRO) AS UNCOUPLERS OF OXIDATIVE PHOSPHORYLATION. THEY THUS PREVENT
INCORPORATION OF INORGANIC PHOSPHATE INTO ATP WITHOUT EFFECTING ELECTRON
TRANSPORT. AS A RESULT OF THIS ACTION, WHICH IS BELIEVED TO OCCUR @
MITOCHONDRIAL /MEMBRANE/, CELLS CONTINUE TO RESPIRE BUT SOON ARE DEPLETED OF ATP
NECESSARY FOR GROWTH. /CHLOROPHENOLS/
The chlorophenols ... act at the sites of
adenosine triphosphate production and decrease or block it without blocking the
electron transport chain. Thus the poisons uncouple phosphorylation from
oxidation. Free energy from the electron transport chain then converts to more
body heat. As body temp rises, heat-dissipating mechanisms are overcome and
metabolism is speeded. More adenosine diphosphate and other substrates
accumulate, and these substrates stimulate the electron transport chain further.
The electron transport chain responds by using up more and more available oxygen
(increasing oxygen demand) in an effort to produce adenosine triphosphate but
much of the free energy generated is liberated as still more body heat. Oxygen
demand quickly overcomes oxygen supply, and energy reserves become depleted. /Chlorophenols/
... PENTACHLOROPHENOL
... CAUSES /SIGNIFICANT/ UNCOUPLING OF OXIDATION & PHOSPHORYLATION CYCLES IN
TISSUES. THIS PRODUCES ... INCR BASAL METABOLIC RATE & MARKED TEMP INCR. IN
VITRO TESTS HAVE SHOWN THAT 1X10-6 TO 1X10-3 (OR GREATER) MOLAR CONCN ...
UNCOUPLE OXIDATIVE PHOSPHORYLATION, INHIBIT MITOCHONDRIAL & MYOSIN ADENOSINE
TRIPHOSPHATASE, INHIBIT GLYCOLYTIC PHOSPHORYLATION, INACTIVATE RESPIRATORY
ENZYMES & CAUSE GROSS DAMAGE TO MITOCHONDRIA.
Pentachlorophenol
induces microsomal enzymes. However, in vitro studies of rat liver microsomes
have shown that pentachlorophenol
inhibits microsomal detoxification enzymes by disturbing electron transport from
flavins to cytochromes.
... EFFECTIVE UNCOUPLER OF OXIDATIVE
PHOSPHORYLATION. ... AT LOW CONCN (10-5 M) PCP PREVENTS THE UPTAKE OF INORGANIC
PHOSPHATE ASSOCIATED WITH THE OXIDATION OF ALPHA-KETOGLUTARATE. IN
PHOSPHATE-DEFICIENT SYSTEMS, ALPHA-KETOGLUTARATE OXIDATION IS STIMULATED BY PENTACHLORPHENOL.
PENTACHLOROPHENOL GREATLY ENHANCES
LIBERATION OF INORG PHOSPHATE FROM ATP IN FRESH MITOCHONDRIAL PREPN, BUT ... NO
EFFECT UPON ATPASE PREPARED FROM DISINTEGRATED MITOCHONDRIA. ... SUGGEST/ED/
EFFECT OF PCP MAY BE ONE OF ALTERING PERMEABILITY OF MITOCHONDRIA RATHER THAN
DIRECT EFFECT ON ATPASE.
A study of magnesium(2+)-ATPase and sodium(+),
potassium(+)-ATPase from various tissues of the rat revealed very complex
reactions, suggesting that pentachlorophenol
uncouples oxidative phosphorylation at low concn and inhibits it at high concn
and that sodium(+), potassium(+)-ATPase is the locus of action of the poison.
The effects of sublethal doses of pentachlorophenol
on the membranes of mammalian cells in cultures were studied using electron spin
resonance and fluorescence depolarization techiques. Chinese hamster fibroblasts
(V79-S171-W1) were exposed to pentachlorophenol
at a concn of 282 micromoles/l for 24 hr. Plasma membrane isolated from pentachlorophenol
treated cells demonstrated a 50% increase in fluidity. Pentachlorophenol
apparently reduced the interchain hydrophobic forces contributing to bilayer
stability. Similar changes were noted for preparations of total cell membrane,
suggesting that the toxicant is highly mobile and can access intracellular
membranes and plasmalemma. Experiments indicated that pentachlorophenol
partitioned well into the bilayer and exhibited little, if any, amphipathic
orientation. Toxicant transfer from cell surface to internal membranes
apparently occurred through endocytosis and fusion of endocytotic vesicles with
internal membranes. The content of phospholipid phosphate per cell was decreased
by up to 50% following 24 hr treatments with pentachlorophenol.
However, no significant change was noted in fatty acid composition of the
membranes and only a very small change occurred in the sterol fatty acid ratio.
The /results/ concluded that fatty acids are not selectively depleted from the
membranes, and that the lipid bilayer is altered by phospholipase-C, which
cleaves the phospholipid headgroup to form 1,2-diacylglycerol. It is noted that
the extensive fluidization of membranes and the decline in phospholipid
phosphate are manifestations of sublethal damage.
Interactions:
The toxicity to Pseudomonas fluorescens was
greater when pentachlorophenol and
2,3,4,5-tetrachlorophenol were given sequentially than when pentachlorophenol
alone was given. The antioxidant butylated hydroxyanisole enhances the toxicity
of pentachlorophenol to Pseudomonas
fluorescens.
Hexachlorobenzene (HCB) at 1000 ppm and 99%
pure pentachlorophenol (PCP) at 500
ppm admin to female Wistar rats for up to 8 wk resulted in an increased
accumulation of pentachlorophenol in
the liver. Pentachlorophenol ...
accelerated the onset of hepatic porphyria by hexachlorobenzene.
Pretreatment with pentachlorophenol
inhibits the carcinogenic effect of hydroxyamine acids and the hepatoxicity of
N-hydroxy-2-acetylaminofluorene.
/Pentachlorophenol/
... enhances the transplacental carcinogenicity of ethylnitrosourea.
The organochlorine pesticide, pentachlorophenol,
a potent sulfotransferase inhibitor, reportedly reduces the binding of
2,6-dinitrotoluene, an industrial hepatocarcinogen to hepatic DNA by 95% after a
single ip injection. Activation of 2,6-dinitrotoluene to genotoxic metabolites
involves enzymes in both the liver and the intestinal flora. Since pentachlorophenol
also has bactericidal activity and induced hepatic mixed function oxidase
activity after longer treatment, the effect of pentachlorophenol
on intestinal enzyme and the biotransformation of 2,6-dinitrotoluene to
genotoxic metabolites was studied after 1, 2, 4, and 5 weeks of treatment. Male
Fischer 344 rats were dosed daily, by gavage, with either 20 mg/kg pentachlorophenol
or the peanut oil vehicle. After 1, 2, 4, and 5 wk, select control and treated
aniamls were injected orally with 75 mg/kg 2,6-dinitrotoluene and transferred to
metabolism cages, where urine was collected for 24 hr and tested for mutagenic
activity in the Ames Salmonella typhimurium reversion assay. At 2 and 4 wk, six
control and six treated animals were sacrificed and nitroreductase, azo
reductase, beta-glucuronidase, dechlorinase, and dehydrochlorinase activities
were analyzed in homogenates of the small intestine, large intestine, and cecum.
At 5 wk, hepatic DNA adduct formation was assayed by the (32)P postlabeling of
DNA. Results from this study indicated that pentachlorophenol
accelerated the biotransformation of 2,6-dinitrotoluene genotoxic metabolites
and potentiated the formation of 2,6-dinitrotoluene induced DNA adducts in the
liver. This is the first report of a chemical interaction leading to increased
DNA adduct formation and indicates that chemical interactions could be important
to risk assessment since they alter the relationship between exposure, dose, and
the effect of genotoxicants.
The aim of the present work was to explore the
possibility that pentachlorophenol
influences the behavior of the resting Na efflux in single muscle fibers from
the barnacle, Balanus nubilus. It is shown here that pentachlorophenol
causes a transitory rise in the sodium efflux in both unpoisoned and ouabain
poisoned fibers and that the response is dose dependent, the minimal effective
concentration in ouabain treated fibers being less than 1X10-6 M. The efficacy
of pentachlorophenol is significantly
greater than that of 2,3,4-trichlorophenol. 2,3-Dichlorophenol is ineffective.
This is also the case with phenol.
2,6-Dinitrotoluene (2,6-DNT) and pentachlorophenol
(PCP) are used for industrial purposes and are found in the environment as
hazardous contaminants. Because concurrent exposure to both compounds can occur,
it is of interest to determine if organochlorine compounds potentiate the effect
of nitroaromatic chemicals. CD-1 mice were treated with PCP (42.8 mg/kg) for 4
weeks. On weeks 1, 2, and 4 after the initial PCP dose, mice were treated p.o.
with 2,6-DNT (75 mg/kg) and 24 hr urines were collected. After concentration,
the urines were tested for their mutagenic activity in Salmonella typhimurium
strain TA98 without metabolic activation in a microsuspension bioassay. A
significant increase (P less than .05) in mutagenicity was observed in urines
from mice treated with 2,6-DNT alone and in combination with PCP. By week 4,
mice that received both 2,6-DNT and PCP excreted urine that was more mutagenic
than that from animals which received only 2,6-DNT. At weeks 2 and 4, mice were
sacrificed and intestinal enzyme activities (nitroreductase, azo reductase,
beta-glucuronidase, dechlorinase, and dehydrochlorinase) were quantitated. The
enhanced genotoxicity observed in urines from 2,6-DNT/PCP-treated mice coincided
with a decrease in nitroreductase and an increase in beta-glucuronidase
activities in the small intestine.
Pharmacology:
Interactions:
The toxicity to Pseudomonas fluorescens was
greater when pentachlorophenol and
2,3,4,5-tetrachlorophenol were given sequentially than when pentachlorophenol
alone was given. The antioxidant butylated hydroxyanisole enhances the toxicity
of pentachlorophenol to Pseudomonas
fluorescens.
Hexachlorobenzene (HCB) at 1000 ppm and 99%
pure pentachlorophenol (PCP) at 500
ppm admin to female Wistar rats for up to 8 wk resulted in an increased
accumulation of pentachlorophenol in
the liver. Pentachlorophenol ...
accelerated the onset of hepatic porphyria by hexachlorobenzene.
Pretreatment with pentachlorophenol
inhibits the carcinogenic effect of hydroxyamine acids and the hepatoxicity of
N-hydroxy-2-acetylaminofluorene.
/Pentachlorophenol/
... enhances the transplacental carcinogenicity of ethylnitrosourea.
The organochlorine pesticide, pentachlorophenol,
a potent sulfotransferase inhibitor, reportedly reduces the binding of
2,6-dinitrotoluene, an industrial hepatocarcinogen to hepatic DNA by 95% after a
single ip injection. Activation of 2,6-dinitrotoluene to genotoxic metabolites
involves enzymes in both the liver and the intestinal flora. Since pentachlorophenol
also has bactericidal activity and induced hepatic mixed function oxidase
activity after longer treatment, the effect of pentachlorophenol
on intestinal enzyme and the biotransformation of 2,6-dinitrotoluene to
genotoxic metabolites was studied after 1, 2, 4, and 5 weeks of treatment. Male
Fischer 344 rats were dosed daily, by gavage, with either 20 mg/kg pentachlorophenol
or the peanut oil vehicle. After 1, 2, 4, and 5 wk, select control and treated
aniamls were injected orally with 75 mg/kg 2,6-dinitrotoluene and transferred to
metabolism cages, where urine was collected for 24 hr and tested for mutagenic
activity in the Ames Salmonella typhimurium reversion assay. At 2 and 4 wk, six
control and six treated animals were sacrificed and nitroreductase, azo
reductase, beta-glucuronidase, dechlorinase, and dehydrochlorinase activities
were analyzed in homogenates of the small intestine, large intestine, and cecum.
At 5 wk, hepatic DNA adduct formation was assayed by the (32)P postlabeling of
DNA. Results from this study indicated that pentachlorophenol
accelerated the biotransformation of 2,6-dinitrotoluene genotoxic metabolites
and potentiated the formation of 2,6-dinitrotoluene induced DNA adducts in the
liver. This is the first report of a chemical interaction leading to increased
DNA adduct formation and indicates that chemical interactions could be important
to risk assessment since they alter the relationship between exposure, dose, and
the effect of genotoxicants.
The aim of the present work was to explore the
possibility that pentachlorophenol
influences the behavior of the resting Na efflux in single muscle fibers from
the barnacle, Balanus nubilus. It is shown here that pentachlorophenol
causes a transitory rise in the sodium efflux in both unpoisoned and ouabain
poisoned fibers and that the response is dose dependent, the minimal effective
concentration in ouabain treated fibers being less than 1X10-6 M. The efficacy
of pentachlorophenol is significantly
greater than that of 2,3,4-trichlorophenol. 2,3-Dichlorophenol is ineffective.
This is also the case with phenol.
2,6-Dinitrotoluene (2,6-DNT) and pentachlorophenol
(PCP) are used for industrial purposes and are found in the environment as
hazardous contaminants. Because concurrent exposure to both compounds can occur,
it is of interest to determine if organochlorine compounds potentiate the effect
of nitroaromatic chemicals. CD-1 mice were treated with PCP (42.8 mg/kg) for 4
weeks. On weeks 1, 2, and 4 after the initial PCP dose, mice were treated p.o.
with 2,6-DNT (75 mg/kg) and 24 hr urines were collected. After concentration,
the urines were tested for their mutagenic activity in Salmonella typhimurium
strain TA98 without metabolic activation in a microsuspension bioassay. A
significant increase (P less than .05) in mutagenicity was observed in urines
from mice treated with 2,6-DNT alone and in combination with PCP. By week 4,
mice that received both 2,6-DNT and PCP excreted urine that was more mutagenic
than that from animals which received only 2,6-DNT. At weeks 2 and 4, mice were
sacrificed and intestinal enzyme activities (nitroreductase, azo reductase,
beta-glucuronidase, dechlorinase, and dehydrochlorinase) were quantitated. The
enhanced genotoxicity observed in urines from 2,6-DNT/PCP-treated mice coincided
with a decrease in nitroreductase and an increase in beta-glucuronidase
activities in the small intestine.
Environmental Fate & Exposure:
Environmental Fate/Exposure Summary:
Pentachlorophenol's
production and use in the US as an industrial wood preservative for utility
poles, cross arms, and fenceposts, and other items, that consume about 97% of
its production, may result in its release to the environment through various
waste streams(SRC). If released to air, a vapor pressure of 0.00011 mm Hg at 25
deg C indicates pentachlorophenol will
exist in both the vapor and particulate phases in the ambient atmosphere.
Vapor-phase pentachlorophenol will be
degraded in the atmosphere by reaction with photochemically-produced hydroxyl
radicals; the half-life for this reaction in air is estimated to be 29 days. Pentachlorophenol
may also be degraded in the vapor phase by direct photolysis. Particulate-phase pentachlorophenol
will be physically removed from the atmosphere by wet and dry deposition. If
released to soil, the mobility of pentachlorophenol
(pKa of 4.70) is expected to be based upon the soil pH. In light and heavy loam
soils, Koc values for the total dissociated phenol was calculated to be 1250 and
1800, (classified as low mobility) respectively, while for the undissociated
species, the Koc is 25,000 (classified as immobile). 25 to 51% of the added pentachlorophenol
in terrestrial microcosms was detected in the air, suggesting that evaporation
from soil of the formulated pesticide does occur. Photolysis of the dissociated
form from moist soil surfaces may also occur with as much as 55% of added pentachlorophenol
photodegraded in a sandy clay loam soil in 14 days. Both aerobic and anaerobic
biodegradation rates are expected to be sensitive to the concn of pentachlorophenol
present in both soil and water. Max mineralization rates of 0.3 to 0.5 mg/kg-day
were reported for pentachlorophenol at
30 mg/kg soil with 82% of the added pentachlorophenol
recovered as CO2 in 7 months. Less than 2% of the added pentachlorophenol
was mineralized in 7 months when it was present at 100 mg/kg. Biodegradation has
been reported using a non-adapted river sediment, required a lag period of 11
days with complete degradation by day 17. A biodegradation rate of <5 ng/L-day
was reported for pentachlorophenol in
a variety of natural waters. If released into water, pentachlorophenol
is expected to adsorb to suspended solids and sediment in water based upon its
measured Koc values. Volatilization from water surfaces is not expected to be an
important fate process based on a field study of an artificial stream in which
<0.006% of the added pentachlorophenol
was lost by volatilization. BCF values from approximately 100 to 1000 indicate
that bioconcentration of pentachlorophenol
in aquatic organisms is high. Bioconcentration is expected to be pH dependent
with greater accumulation at lower pH values. Occupational exposure to pentachlorophenol
may occur via dermal contact, primarily in situations where workers use this
compound as a preservative or are in contact with treated wood products. The
general population will be exposed primarily from ingesting food contaminated
with pentachlorophenol. (SRC)
Probable Routes of Human Exposure:
NIOSH's National Occupational Exposure Survey
(NOES) (1981-83) has statistically estimated that 22,107 workers, including
3,881 women, are exposed to pentachlorophenol
in the USA(1). The NIOSH survey indicates that major occupational exposure is to
workers in the electric services industry (wood preservative)(2). 25 wood
preservative factories avg 0.012 ppb(2). Elevated levels were found in workers'
urine and serum(2). Aerial spraying of farm crops gave rise to levels of pentachlorophenol
of 0.9 mg/cu m in the cockpit of the spray plane, 38 mg/cu m in the vicinity of
the signal man and 1-4 mg/cu m outside the treated field(3). At a sawmill in
Finland, urine from exposed workers contained pentachlorophenol
at concns from not detected to 15.9 ng/mg creatinine(4).
Major human exposure will be workers or other
people who handle or breathe air near wood that has been preserved with pentachlorophenol
and through consumption of food that contains the pesticide(SRC). General water
and air contamination are not likely sources of human exposure. Results of an
environmental partitioning model indicate that ingestion of food accounts for
99.9% of human exposure to pentachlorophenol(1,SRC).
Body Burden:
BLOOD: 15 ppb(1), 10-120 ppb in users of
PCP-contaminated water(2). Serum of 123 residents of PCP-treated log homes
ranged from 69-1340 ppb, 420 ppb mean, while 34 controls ranged from 15-75 ppb,
40 ppb(3). Serum levels in 25 occupationally-exposed workers in 5 workplaces
ranged from 26 to 84,900 ppb(3). Medium serum PCP levels in 4 of the workplaces
ranged from 83 to 490 ppb, while in the chemical packaging area of a chemical
plant it was 62,000 ppb(3). Avg serum concn (of pentachlorophenol)
of 7 workers continuously exposed to chlorophenols at 2 saw mills was 0.84-0.85
ppm(4). Concns of pentachlorophenol in
the blood serum and urine of workers involved either with the production of pentachlorophenol
or with the treatment of wood with pentachlorophenol
have been measured(5). Urine of workers responsible for lumber dipping, spraying
or brushing contained pentachlorophenol
at mean concns from 1.31 to 2.83 mg/l (blood serum mean=5.14 mg/l); urine from
an individual in the office at a lumber yard contained 0.06 mg/l pentachlorophenol
(blood serum mean=0.65 mg/l). Individuals involved with pentachlorophenol
production had mean blood serum and urine levels of 0.72-2.38 mg/l and 4.73
mg/l, respectively(5). Adipose tissue from 58 people (not occupationally
exposed) from southern and northern Finland contained pentachlorophenol
at a median concn of 0.002 ug/g residue fat; 75-81.8% of the samples were
positive(6). 84.6% of the liver samples were positive for pentachlorophenol
with a median concn of 0.004 ug/g(6).
HUMAN MILK: Bavaria, Germany - 0.03-2.83 ppb -
21 donors(1). Milk from 10 to 20 Swedish women, from 1972 to 1989, contained pentachlorophenol
at 0.0125 to 0.036 ug/g fat(8). URINE: 85% pos over 400 samples 6.3 ppb mean,
193 ppb max(2). Urine of 118 residents of PCP-treated log homes ranged from
1-340 ppb, 69 ppb mean, while 143 controls ranged from 1-7 ppb, mean 3.4 ppb(3).
All urine samples from 197 Arkansas children contained pentachlorophenol(4).
The median and max pentachlorophenol
concn was 14 and 240 ppb. SEMINAL FLUID: 20-70 ppb(2), 100-200 ppb(5). ADIPOSE
TISSUE: 250-500 ppb(5), 23 ppb(6). The mean levels of pentachlorophenol
in samples collected from the general population in Barcelona, Spain, in 1982-83
were 25 ng/ml (50 samples) in urine and 21.9 ng/ml (100 samples) in serum(7).
All 87 urine samples collected randomly in Saskatchewan, Canada, contained pentachlorophenol
at concns from 0.5 to 9.1 ng/mL (detection limit=0.2 ng/ml; avg=1.6 ng/ml and
median=1.3 ng/mL)(9). A second study of 38 urine samples from "normal,
healthy" humans living in Saskatchewan, Canada, reported pentachlorophenol
concns from 0.1 to 3.6 ng/ml with an avg concn of 0.9 ng/ml and a median concn
of 0.5 ng/ml(9).
Pentachlorophenol
was detected during hand wipe studies of 5 children living on 3 different farms;
concns ranged from 9 to 99 ng(1). The National Human Monitoring Program for
Pesticides, USEPA, has shown that ~85% of all human urine samples contain pentachlorophenol
at a mean of 0.0063 ppm and a max of 0.193 ppm(2). Avg concns of pentachlorophenol
in tissue samples obtained from 8 humans from western Oregon were as follows:
testis, 1.087 ppm; kidney, 0.953 ppm; prostate, 0.838 ppm; liver, 0.592 ppm;
omentum fat, 0.029 ppm; subcutaneous fat, 0.017 ppm; perinephric fat, 0.016
ppm(2).
A study of serum and urine pentachlorophenol
(87865) (PCP) concentrations in persons living in log homes and workers
occupationally exposed to PCP was conducted. The study group consisted of 35
persons exposed to PCP in six workplaces and 123 persons living in 45 homes
constructed of PCP treated logs. The comparisons consisted of 143 persons living
in conventional homes and not occupationally exposed to PCP. Urine and blood
samples were collected and analyzed for PCP. Among the comparisons, urine PCP
concentrations ranged from 1 to 17 ppb, mean 3.4 ppb. Serum samples from 34
comparisons ranged from 15 to 75 ppb, mean 40 ppb. In persons living in PCP
treated log homes, serum PCP concentrations ranged from 69 to 1340 ppb, mean 420
ppb. The serum PCP concentrations decreased with increasing age. Subjects in the
2 to 7 year old group had significantly higher serum PCP concentrations than
those over 15 years old. The serum PCP concentrations in children 2 to 15 years
old averaged 1.7 to 2.0 times that of their parents. Repeat blood samples taken
from ten persons residing in homes in which the logs were coated with a sealant
showed that sealing the logs resulted in decreased serum PCP concentrations.
Urine PCP concentrations ranged from 1 to 340 ppb, mean 69 ppb. When the urine
PCP concentrations were corrected for creatinine concentrations, they correlated
well with the serum PCP concentrations. Serum PCP concentrations in the PCP
workers ranged from 26 to 84900 ppb. The lowest concentrations occurred in
workers constructing homes from PCP treated logs and the highest in workers
exposed to PCP in chemical factories. Urine PCP concentrations in four workers
ranged from 2400 to 13800 ppb, mean 10000 ppb.
Average Daily Intake:
Pentachlorophenol
partitions mainly into soil (96.5%), and food chains, especially fruits,
vegetables and grains, account for 99.9% of human exposure to pentachlorophenol.
The long-term, avg daily intake of pentachlorophenol
is estimated to be 16 ug/day(1). Air intake (assume 0) - 0; Water intake (assume
0) - 0; Food intake - 0.014(2), 3.6(3), 16(4) ug(SRC).
Natural Pollution Sources:
It has been suggested that pentachlorophenol
is a product of fungus metabolism(1).
Artificial Pollution Sources:
PENTACHLOROPHENOL
HAS BEEN DETECTED IN 9/65 COMMERCIAL SAMPLES OF PAINTS USED ON CHILDREN'S TOYS
AT LEVELS OF 100 TO 2700 MG/KG; & IN WOOD-SHAVING LITTER FROM CHICKEN HOUSES
AT LEVELS OF 0.6 TO 83 MG/KG (FRESH) & 0 TO 4.1 MG/KG (AFTER 8 WK).
Pentachlorophenol
has been detected in: (1) river water and effluent water from a chlorinated
biological sewage treatment plant; (2) the effluent waters from various
manufacturing and processing plants; (3) well water.
/Pentachlorophenol/
has ... been detected in: (1) sewage influent and effluent water of cities at
levels, of 1-5 ug/l; (2) a river, at levels of 0.1-0.7 ug/l; (3) rain- snow-,
and lake-water at levels of 2-284, 14 and 10 ng/l; (4) creek- water containing
industrial discharges at levels of 0.1-10 mg/l
After treatment of greenhouse soil with pentachlorophenol
at levels of 15 & 45 kg/ha, residues in the soil were 20.4 and 69.1 mg/kg,
respectively.
Pentachlorophenol's
production and use in the US as an industrial wood preservative for utility
poles, cross arms, and fenceposts, and other items that consume about 97% of its
production(1,2) may result in its release to the environment through various
waste streams(SRC). Other uses that may lead to its release include the
manufacture of sodium pentachlorophenolate (3) and minor uses as a fungicide,
bactericide, algicide, and herbicide for crops, leathers and textiles(1,2). Pentachlorophenol's
use on wood is "restricted" and its non-wood use is undergoing special
review by EPA(4).
Environmental Fate:
TERRESTRIAL FATE: Results of an environmental
partitioning model indicate that pentachlorophenol
partitions mainly in soil (96.5%)(1). Since pentachlorophenol
has a pKa value of 4.70(2), its adsorptivity will be strongly dependent on pH.
Based on a classification scheme(3), Koc values for the total dissociated phenol
of 1250 and 1800 for light and heavy loam soils, respectively, and 25,000 for
the undissociated species(4), indicate that pentachlorophenol
is expected to have low to no mobility in soil, depending on the pH(SRC). A
survey of 4 RCRA sites that contained wood-preserving plants with surface
impoundments indicated that all had some groundwater contamination extending
down 20 to 60 ft(5). Both aerobic and anaerobic biodegradation rates are
expected to be sensitive to the concn of pentachlorophenol
present in the soil(SRC). Max mineralization rates of 0.3 to 0.5 mg/kg-day were
reported for pentachlorophenol at 30
mg/kg soil with 82% of the added pentachlorophenol
recovered as CO2 in 7 months(6). Less than 2% of the added pentachlorophenol
was mineralized in 7 months when it was present at 100 mg/kg(6). Mineralization
of pentachlorophenol (initially at 30
mg/kg) in a pristine sandy loam soil did not occur while a pristine peaty soil
mineralized 13% of a 30 mg/kg spike of pentachlorophenol
in 4 months(6).
TERRESTRIAL FATE: Volatilization of pentachlorophenol
from moist soil surfaces is not expected to be important(1,SRC) given a Henry's
Law constant of 2.45X10-8 atm-cu m/mole(2). However, significant amounts
(25-51%) of pentachlorophenol in
terrestrial microcosms have been detected in the air(3-4), which suggests that
evaporation from soil of the formulated pesticide will be significant(5). Pentachlorophenol
is not expected to volatilize from dry soil surfaces based on a vapor pressure
of 1.1X10-4 mm Hg(6). Photolysis of the dissociated form on moist soil surfaces
may be a significant process(7). As much as 55% of added pentachlorophenol
was photodegraded in a sandy clay loam soil in 14 days with conditions present
to increase rates of evaporative flux(7).
AQUATIC FATE: Based on a classification
scheme(1), Koc values ranging from 1250 to 25,000, depending on the pH(2),
indicate that pentachlorophenol is
expected to adsorb to suspended solids and sediment in water(SRC). Adsorption is
expected to be greater under acidic conditions(3,SRC). Both aerobic and
anaerobic biodegradation rates are expected to be sensitive to the concn of pentachlorophenol
present in the water column(SRC). Aerobic biodegradation of pentachlorophenol,
using a non-adapted river sediment, required a lag period of 11 days with
complete degradation by day 17; intermediate products of 3,5-dichlorophenol,
3,4,5-trichlorophenol, 2,3,4,5-tetrachlorophenol were reported(4). Increasing
the concn of pentachlorophenol, from 1
to 10 mg/l, increased the time required for complete biodegradation(4). The rate
of pentachlorophenol mineralization in
the relatively unpolluted water of Long Island Sound and water from several
sites in the Hudson Estuary in summer was very low (<5 ng/l/day)(5). Pentachlorophenol
is not expected to volatilize from water surfaces(6,SRC) based on a Henry's Law
constant of 2.45X10-8 atm-cu m/mole(7). This agrees with a field study in an
artificial stream in which <0.006% of the added pentachlorophenol
was lost by volatilization(8).
AQUATIC FATE: Photolysis of the dissociated
form in water may be a significant process(1,2). In water at pH 7.3, 90%
degradation occurred in 10 hr with sunlight while at pH 3 (mostly the
undissociated form), 40% degradation occurred in 90 hr(2). Both the temperature
and pH are expected to influence the loss of pentachlorophenol
from water surfaces; at pH 5, the half-life is 328 hours (30 deg C) while at pH
6, the half-life is 3120 hours(3). According to a classification scheme(4), BCF
values from approximately 100 to 1000(5-8) indicate that bioconcentration of pentachlorophenol
in aquatic organisms is high(SRC). Bioconcentration is expected to be pH
dependent with greater bioconcentration at lower pH values(9).
ATMOSPHERIC FATE: According to a model of
gas/particle partitioning of semivolatile organic compounds in the
atmosphere(1), pentachlorophenol,
which has a vapor pressure of 1.1X10-4 mm Hg at 25 deg C(2), is expected to
exist in both the vapor and particulate phases in the ambient atmosphere.
Vapor-phase pentachlorophenol is
degraded in the atmosphere by reaction with photochemically-produced hydroxyl
radicals(SRC); the half-life for this reaction in air is estimated to be 29
days(3,SRC). In addition, vapor phase pentachlorophenol
may be directly photolysed. Particulate-phase pentachlorophenol
may be physically removed from the air by wet and dry deposition(SRC).
Environmental Biodegradation:
The acute toxicity of pentachlorophenol
(PCP) was determined at pH levels 4, 6, 9 to the midge, Chironomus riparius,
with the findings that PCP is of greatest toxicity at pH 4 and of least toxicity
at pH 9. This differential toxicity is attributable to variations in uptake
levels at the respective pH levels. At pH 4, PCP is fully protonated and
therefore highly lipophilic. The amount of [14C]PCP present in the midges at 24
hr is thus highest at pH 4. Conversely, at pH 9, the compound is completely
ionized. The reduction in lipophilicity at pH 9 decreases the ability of the
compound to penetrate into the midge, thereby decreasing the observed toxicity
of the compound.
The 2nd year of a 2-year study of the fate of pentachlorophenol
in outdoor artificial streams focused on details of microbial degradation by a
combination of in situ and laboratory measurements. Replicate streams were dosed
continuously at pentachlorophenol
concentrations of 0, 48, and 144 ug/l, respectively, for an 88 day period during
the summer of 1983. Pentachlorophenol
was degraded both aerobically and anaerobically. Aerobic degradation was more
rapid than anaerobic degradation. Mineralization of pentachlorophenol
was concommitant with pentachlorophenol
disappearance under aerobic conditions, but lagged behind loss of the parent
molecule under anaerobic conditions. Biodegradation in the streams, or in
specific stream compartments such as the sediment or water column, was
characterized by an adaptation period (3-5 weeks for the stream as a whole, and
reproducible from the previous year), which was inversely dependent on the
concentration of pentachlorophenol and
microbial biomass. The adaptation in the streams could be attributed to the time
necessary for selective enrichment of an initially low population of pentachlorophenol
degraders on surface compartments. The extent of biodegradation in the streams
(percent loss of initial concentration of pentachlorophenol)
increased with increasing pentachlorophenol
input, which was explicable by an increase in the pentachlorophenol
degrader population with increasing pentachlorophenol
concentration. The sediment zone most significant to overall pentachlorophenol
biodegradation was the top 0.5 to 1 cm layer as shown by pentachlorophenol
migration rates and depth profiles of degrader density within the sediment. Pentachlorophenol
profiles in sediment cores taken during and after the adaptation period for
degradation showed that diffusion of pentachlorophenol
into the sediment was rate limiting to degradation in this compartment.
Screening biodegradability tests give
conflicting results(1-7); pentachlorophenol
does biodegrade but may require several weeks for acclimation(3-7). Using an
acclimated pentachlorophenol-degrading
culture, half-lives of 85 (lag time of 27 hours) and 420 (lag time of 220 hours)
hours were reported for aerobic and anaerobic conditions, respectively(8). 1% of
the theoretical BOD was reached in 28 days during the Modified MITI test with pentachlorophenol
initially at 100 mg/l and using an activated sludge inoculum(9). Acclimation of
microbial communities to pentachlorophenol
appears to increase tolerance to pentachlorophenol
and/or select for pentachlorophenol-tolerant
microorganisms(10). Pentachlorophenol,
at an initial concn of 300-500 ug/l, had a half-life of 2.6 days using a sludge
inoculum(11). At this concn, no lag phase was seen(11).
Avg first-order rate constants of 0.006,
0.002, 0.005 per hour were measured for pentachlorophenol
at an initial concn of 5 ug/L, 10 ug/l and 10 mg/l, respectively, in a SCAS test
using synthetic sewage with a sludge retention time of 10 days(1). An avg
first-order rate constant of 0.021 per hour was measured for pentachlorophenol
at an initial concn of 10 ug/L in a SCAS test using domestic sewage with a
sludge retention time of 10 days(1). Avg first-order rate constants of 0.006 and
0.027 per hour were measured for pentachlorophenol
at an initial concn of 10 mg/l and 10 ug/l, respectively, in a SCAS test using
domestic sewage with a sludge retention time of 20 days(1). Pentachlorophenol,
initially present at 890 ug/l, was found at 0.39 ug/l in the effluent of an
activated sewage sludge treatment plant; dewatered sludge contained 0.16 mg/kg pentachlorophenol(2).
41 and 60% removal was reported for pentachlorophenol
in a trickling filter system (49 ug/l in secondary sludge) and during activated
sludge treatment (99 ug/l in secondary sludge), respectively(3). After 6 months
of operation, a lab-scale fixed film reactor was able to remove about 60% of the
initially added pentachlorophenol; if
glucose was added then removal reached 98%(4). Biodegradation of pentachlorophenol
stopped when the sludge retention time was <8 days(5). Laboratory scale
activated sludge reactors run under continuous flow conditions gave minimum and
max first-order rate constants for the removal of pentachlorophenol
of 0-2 and 1-24 per g/MLSS/day(6). Six municipal wastewater treatment plants
were monitored for their ability to remove pentachlorophenol;
0.46, 0.43 (influent, effluent concns); 0.75, 0.50; 0.76, 0.65; 0.73, 0.62;
0.67, 0.41; 0.51, 0.19, were reported for the six treatment plants(7).
Pentachlorophenol
was added to both non-adapted river sediment and to river sediment which had
been adapted to 2,4-dichlorophenol and 3,4-dichlorophenol (over a one year
period) and incubated under anaerobic conditions(1). A lag period of 11 days
with complete degradation by day 17 was reported for the non-adapted culture;
the lag period was 9 days with complete degradation by day 13 days for the
adapted culture(1). Intermediate products of 3,5-dichlorophenol,
3,4,5-trichlorophenol, 2,3,4,5-tetrachlorophenol were reported(1). Increasing
the concn of pentachlorophenol, from 1
to 10 mg/l, increased the time required for complete biodegradation. Complete
biodegradation at pH 7 and 8 required 13 and 3 days, respectively; only 20%
biodegradation was reported by day 19 for cultures incubated at pH 6(1). No
significant biodegradation of pentachlorophenol-contaminated
soil (4 to 7 mg/kg soil) was reported in the first 6 days of aerobic incubation;
over the next 12 days, an avg of 87% of the initial concn was lost with an avg
rate of degradation of 0.32 mg/kg-day during the first 19 days and 0.64
mg/kg-day for day 12 to 19(2). Anaerobic biodegradation of a pentachlorophenol-contaminated
soil resulted in an initial increase in pentachlorophenol
concns due to desorption; this was followed by a period of dechlorination giving
2,3,4,5- and 2,3,5,6-tetrachlorophenol as initial metabolites(2). Mineralization
of pentachlorophenol in contaminated
soil was measured at 30 mg/kg and 100 mg/kg soil; max rates of 0.3 to 0.5
mg/kg-day were reported for the lower concn with 82% of the added pentachlorophenol
recovered as CO2 in 7 months(3). Less than 2% of the added pentachlorophenol
was mineralized in 7 months when it was present at 100 mg/kg(3). Mineralization
of pentachlorophenol (initially at 30
mg/kg) in a pristine sandy loam soil did not occur while a pristine peaty soil
mineralized 13% of a 30 mg/kg spike of pentachlorophenol(3).
The order of pentachlorophenol
dechlorination in anaerobic sediment is ortho to produce
2,3,4,5-tetrachlorophenol, ortho to produce 3,4,5-trichlorophenol, meta to
produce 2,4-dichlorophenol, and para or ortho to produce 2-chlorophenol or
4-chlorophenol(4). Less than 0.2% of the initially added pentachlorophenol
was degraded to CO2 in 5 weeks following inoculation with pentachlorophenol-contaminated
soil(5).
Little biodegradation was noted in 40 days in
a river die-away study or in stream sediment(1). However, approximately 6%
biodegradation occurred in aerobic soil in 160 days(2) while no biodegradation
occurred in anaerobic soil(2). Other studies in soil have suggested greater
biodegradation under anaerobic conditions producing pentachloroanisole and tri-
and tetrachlorophenols(3-4). A study of biodegradation in estuarine sediment
indicated that pH (test conditions= pH 5, 6.5, 8, 9) and redox potential (test
conditions= -250, 0, +250, +500 MV) considerably affected degradation;
significant biodegradation (70%-35 days, 17 day lag period) was only noted at pH
6.5 and 8.0 at redox potential of +500 MV(5).
Half-life in soil is approximately weeks to
months(1-3). The main degradation products of pentachlorophenol
in soil are 2,3,7,8-tetrachlorophenol and CO2(4). In an artificial stream,
microbial degradation became significant after 3 weeks and accounted for 26-46%
removal(5). Pentachlorophenol
mineralization in the relatively unpolluted water of Long Island Sound and water
from several sites in the Hudson Estuary in summer was also very low (<5 ng/l
per day)(6). 3 and 5 ppm PCP were completely degraded in 38 and 57 days,
respectively, when incubated in Pennsylvania and Virginia unsaturated soils
taken at 4 and 4.5 m depths(7).
Environmental Abiotic Degradation:
Pentachlorophenol
does not appear to oxidize or hydrolyze under environmental conditions; however,
photolysis of the dissociated form in water may be an important process(1,2). Pentachlorophenol
has a pH-dependent absorption max of 303 nm(8). A measured half-life for the
photolysis of pentachlorophenyl has been reported to be 0.86 hrs(7). In water at
pH 7.3, 90% degradation occurred in 10 hr with sunlight while at pH 3 (mostly
undissociated form), 40% degradation occurred in 90 hr(2). Reported half-lives
for photodegradation of the dissociated form have included 0.2 hr (10 cm
deep)(1), 3.5 hr(2), 4.75 hr (300 cm deep)(1), and 10 days(3). Products of
photodegradation include 2,3-dichloromaleic acid, 2,3,5,6- and
2,3,4,6-tetrachlorophenol, tetrachlororesorcinol, tetrachlorocatechol, some
benzoquinones(2-3), and possibly dioxins(5). Photolysis in a solution of
H2O-CH3CN using 290 nm wavelengths and a pH of 12 produces the photoproduct
2-methyl-4,5,6,7-tetrachlorobenazole(6). Half-lives of 24 minutes, 30.9 minutes,
and 635 minutes were reported for aqueous solutions of pentachlorophenol
under direct sunlight, under a clear plastic sheet, and under a black plastic
sheet, respectively(9). As much as 55% of added pentachlorophenol
was photodegraded in a sandy clay loam soil in 14 days with conditions present
to increase rates of evaporative flux(9). Little loss of pentachlorophenol
was noted in dry soils or soils covered with black plastic. Photodegradation
rates are lower than aqueous rates due to the attenuation of light by natural
chromophores(9). A second-order rate constant of 9.36X10+7 per M-sec was
reported for the reaction of pentachlorophenol
with singlet oxygen(10).
The rate constant for the vapor-phase reaction
of pentachlorophenol with
photochemically-produced hydroxyl radicals has been estimated as 5.5X10-13 cu
cm/molecule-sec at 25 deg C(SRC) using a structure estimation method(1,SRC).
This corresponds to an atmospheric half-life of about 29 days at an atmospheric
concn of 5X10+5 hydroxyl radicals per cu cm(1,SRC).
Environmental Bioconcentration:
Pentachlorophenol
is expected to bioconcentrate because of its low water solubility(13). The
bioconcentration factor (BCF) is expected to be dependent upon the pH of the
water; pentachlorophenol has a pKa of
4.70(12) indicating that in most environmental waters, it will be mainly present
as the anion(SRC). BCF values varied from 2 at pH 10, to 56 at pH 7, to 132 at
pH 5.5 in goldfish(1). Levels of pentachlorophenol
in pike from an acidified lake (pH=5.2)varied from 2.05 to 8.72 ng/g fresh
weight (geometrical mean=3.95 ng/g) while concns in pike from non-acidified
lakes (pH~ 8) ranged from 1.50 to 3.21 ng/g fresh weight (geometrical
mean=2.19)(11). Other reported BCF values are 776 in fathead minnow(2); 251-5370
in rainbow trout(3-4); 5-50 in sheepshead minnows(5); 295 in mosquito fish(6);
708(8) and 977(7) in zebra fish; and 417 in golden orfe(8). According to a
classification scheme(14), these BCF values suggest the potential for
bioconcentration in aquatic organisms is generally high(SRC). The accumulation
increased with temperature in golden orfe and decreased with temperature in
zebra fish(8). BCF values of 39-198 and 45-224 were measured in an 8-week carp
study with pentachlorophenol concns of
30 and 3 ug/l, respectively(9). BCF values of 214 in Jordanella floridae and
380-1698 in Oryzias latipes were reported for pentachlorophenol(7).
A BCF value of 13 was measured in bluegill muscle in an 8-day study(10).
The BCF of pentachlorophenol
in humans was measured from daily intake of pentachlorophenol
and measured concn in different tissues, giving the following results: 5.7, 3.3,
1.4, 1.4, and 1.0 in liver, brain blood, spleen and adipose tissue
respectively(1). Calculation using a linear one compartment pharmacokinetic
model yielded similar results(2). Eichhornia crassipes, an aquatic plant, had
measured BCF values of 114 and 156 in leaves and roots, respectively(3). BCF
values of 10000 to 45000 were measured in zebra mussels(4). Freshwater mussel
Anodonta anatina and Pseudanodonta complanata, exposed to pentachlorophenol,
had wet-weight based BCF values of 80-120 and 61-85, respectively(5). Passive
uptake of pentachlorophenol was
reported in Chironomus riparius, a midge; uptake was greater when sediment was
present(6). A BCF value of 458 was measured in Chironomus riparius (midge)
exposed to pentachlorophenol at 9 ug/l
in a 16 hour static phase; a depuration rate was determined in a flow-through
system as 55 ml/g-hr(7).
Soil Adsorption/Mobility:
Pentachlorophenol
has a tendency to adsorb to soil and sediment; calculated Koc=1000(1), measured
sediment Koc=3,000-4,000(2). Adsorption of pentachlorophenol
to oxidized sediment is greater than to reduced sediment(2). Adsorption to soil
and sediment appears to be pH dependent, with stronger adsorption under acid
conditions(3). Approximately 15% of the dose in an artificial freshwater stream
adsorbed to sediments(4). An accidental spill in a lake resulted in pentachlorophenol
in the sediment(5). After a 180 day microcosm experiment using radioactive
substrate, 40 to 43% of the radioactivity was present in the sediments(6).
Since pentachlorophenol
has a pKa of 4.70(8), its adsorptivity will be strongly dependent on pH. The
Freundlich adsorption constant for 6 Dutch soils are (soil (% organic carbon,
pH) log KF, 1/N): humic sand (1.7%, 3.4) 2.2, 0.9; humic sand (2.2%, 4.9) 2.2,
0.9; humic-rich sand (3.2%, 4.7) 2.6, 1.0; peat (29.8%, 4.6) 3.3, 0.8; light
loam (0.9%, 7.5) 1.1, 0.9; heavy loam (1.7%, 7.1) 1.5, 0.8(1). For loam soil
where pH >pKa, significant contribution from the phenolate ion can be
expected. The Koc values for the total dissociated phenol was calculated to be
1250 and 1800 for light and heavy loam, respectively, while for the
undissociated species, the Koc is 25,000(1). Koc values of 2285 (pH 4.9), 4267
(pH 5.0), 6224 (pH 5.9), 3684 (pH 4.6), 121681 (pH 3.5), 121810 (pH 3.9), 97471
(pH 3.7), 1586 (pH 5.0), 4109 (pH 5.1), 4009 (pH 5.5), 123563 (pH 3.5) were
measured for pentachlorophenol(2).
According to a classification scheme(7), these Koc values indicate that pentachlorophenol
is expected to have slight to no mobility in soil where the pH is acidic(SRC).
The fraction of pentachlorophenol
which is sorbed decreases linearly with pH to a pH of 6; above pH 6, significant
adsorption of the anion again occurs, contributing as much as 20% of the total
adsorption effect at pH 8(3). K values for a Bjuv clay (12% organic C) and an
aquifer soil (0.02% organic C) were 433 and 86 at pH 3.0, respectively, and 167
and 50 at pH 6.5, respectively(3). K values for a bentonite clay of 72 and 34
were measured at pH 3.0 and 6.5, respectively(3). The nonionized form of pentachlorophenol
had a K value of 3.63 ml/g in a sandy aquifer material (0.13% organic C) (Koc=2792)(4).
K values measured at pH 7 for a Guishan sandy loam (organic C=1.4%) and a Shulin
clay loam (organic C=2.0%) were 2.56 (Koc=183) and 7.03 (Koc=352),
respectively(5). The Koc for pentachlorophenol
was measured for five soils (foc from 0.07 to 2.96%; 3 sands, 1 loamy sand, 1
loam)(6). At pH 4, 7, and 10, the Koc values ranged from 10091-40120 (avg=19675),
178-1956 (avg=651), and 126-942 (avg=501), respectively(6). These Koc values
indicate that pentachlorophenol, while
expected to have low to no mobility in acidic soils, has higher mobility when
soils are basic(SRC).
Koc values of 241 and 433 were measured for
the upper (pH=6.1; organic C=1.38%) and lower (pH=6.5; organic C=0.36%) horizon,
respectively, of a Menfro silt loam soil(1). The addition of humic acid to this
soil resulted in a linear increase in adsorption of pentachlorophenol(1).
In situ Koc values from 4.2 to 560 were measured in an aquifer (foc=0.007) at pH
values ranging from 7.2 to 8.5(2). K values of 10.367, 13.955, 0.463, and 26.883
were measured in a quartz, calcite, kaolinite, and montmorillonite suspension,
respectively; the ionized form of pentachlorophenol
was dominant in this study(3). Retardation factors of 4.7 and 1.0 were measured
for pentachlorophenol in a Eustis soil
(0.37% organic C) column with water and methanol, respectively, used as the
mobile phase(4). Kf values of 120 (Koc=3243), 125 (Koc=2049), 57 (Koc=703), and
714 (Koc=4577) cu dm/kg were measured for a sandy soil (organic C=3.7%), a sandy
soil (organic C=6.1%), an OECD artificial soil (organic C=8.1%), and a peaty
sand (organic C=15.6%), respectively(5). Koc values of 2727, 2647, 100, 52, 208,
and 115 were measured at pH 7 (foc=0.0066), pH 6.6 (foc=0.68), pH 5.3 (foc=0.012),
pH 6.4 (foc=0.0087), pH >10 (foc=0.039), and pH>10 (foc=0.039),
respectively, in column studies(2). In batch studies, Koc values of 718 and 597
were measured at pH>7 (foc=0.0039) and pH 7.5 (foc=0.034), respectively(2).
Kp values (as l/g suspended solids) were
determined for pentachlorophenol using
microbial biomass as the sorbent; values of 2.44, 0.98, 0.66, 0.44, and 0.35
were measured at pH values of 4, 5, 6, 7, and 8, respectively(1). Koc values of
5337, 6887, 1487, and 2087 were measured for natural dissolved organic matter at
<0.1 mg/l DOC (pH 5.4), natural dissolved organic matter at 15 mg/l DOC (pH
5.4), natural dissolved organic matter at <0.1 mg/l DOC (pH 6.1), and natural
dissolved organic matter at 15 mg/l DOC (pH 6.1), respectively, in an aquifer
sand column with groundwater as the mobile phase(2).
Volatilization from Water/Soil:
The low water solubility (14 ppm)(1) and
moderate vapor pressure (0.00011 torr at 20 deg C)(2) would suggest that
evaporation from water is not rapid, especially at natural pH values where pentachlorophenol
is present in the dissociated form (pKa=4.70)(2). The Henry's Law constant for pentachlorophenol
was measured as 2.45X10-8 atm-cu m/mole(3). This Henry's Law constant indicates
that pentachlorophenol is expected to
be essentially nonvolatile from water surfaces(4,SRC). This agrees with a field
study in an artificial stream in which <0.006% of the added pentachlorophenol
was lost by volatilization(5). Both the temperature and pH influence the loss of
pentachlorophenol from water surfaces;
at pH 5, the half-life is 328 hours (30 deg C) while at pH 6, the half-life is
3120 hours(6).
Pentachlorophenol's
Henry's Law constant(1) indicates that volatilization from moist soil surfaces
is not expected(2,SRC). However, significant amounts (25-51%) of pentachlorophenol
in terrestrial microcosms have been detected in the air(3-4), which suggests
that evaporation from soil of the formulated pesticide will be significant(5). Pentachlorophenol
is not expected to volatilize from dry soil surfaces based on a vapor pressure
of 1.1X10-4 mm Hg(6).
Environmental Water Concentrations:
GROUNDWATER: Germany - 6.9% occurrence(1). Pentachlorophenol
was detected in groundwater in monitoring program in California, Oregon and
Minnesota(2). In Minnesota 3% of wells monitored by the Agriculture Department
had detectable pentachlorophenol with
a max level of 0.64 ppb. In Oregon, 1.4% of tested wells contained pentachlorophenol
and the max concn was 0.12 ppb(2). Concns of pentachlorophenol
in groundwater were 1047 and 152 ppb at Havertown PCP site, Havertown, PA(3) and
Doepke disposal site, Holliday, KS, respectively(4). The leaking of pentachlorophenol
from a sawmill dip tank in British Columbia resulted in the contamination of a
shallow aquifer at peak concns of 20 to 63 mg/l; the nearby Okanagan River
received contaminated groundwater with a travel time of 47 days (for 122 m
distance)(5). Groundwater from Visalia, CA was heavily contaminated with pentachlorophenol(6).
At the Pensacola site, a former wood treatment plant in Florida resulted in the
contamination of an underlying aquifer with pentachlorophenol
at concns from 0.0 to 3.53(6). Pentachlorophenol
was detected at a max concn of 40 ug/l in the Biscayne aquifer study area(7). Pentachlorophenol
was detected in one groundwater supply site in Atlantic Canada at 11 ug/l(8).
Groundwater was contaminated with pentachlorophenol
(maximum concn=0.01% solution) from a wood treatment facility in Florence,
SC(9).
DRINKING WATER: Pentachlorophenol
was detected in drinking water at the following concns and locations: 0.04-0.28
ug/l, Corvallis, OR; 0.07 ug/l (mean of 108 samples from the National Organics
Monitoring Survey); and <1 to 800 ppb (avg of 227 ppb) in 7 water wells in
Oroville, CA(1).
SURFACE WATER: Netherlands - 5 rivers - 0.41
to 9.9 ppb(1,2) Japan - urban rivers 0.1 to 10 parts/trillion(3); Willamette R,
Oregon 0.1-0.7 ppb(4), Lake Erie 0-1.7 ppb(5). Pentachlorophenol
concns in the Weser River and estuary (0.05-0.5 ug/l; Germany), German Bight
(<0.002-0.026 ug/l), Ruhr River (<0.1-0.2 ug/l; Germany), River Rhine (0.1
ug/l; Cologne, Germany), Tama River (0.01-0.9 ug/l; Tokyo, Japan), Sumida River
(1-9 ug/l; Tokyo, Japan), River Rhine(in 1976 and 1977, mean=0.7, 1.1 ug/l,
respectively; The Netherlands), River Meuse, The Netherlands (in 1976 and 1977,
0.3, and 0.8 ug/l, respectively; The Netherlands), 124 sampling points in South
Africa(not detected to 0.85 ug/l), an estuary in Galveston Bay, Texas (not
detected to 0.01 ug/l), and in a pond in Mississippi (<1 to 82 ug/l;
contaminated by waste from pole-treatment facility)(6). Rivers and streams from
the Zagreb, Croatia area contained pentachlorophenol
at concns from 2 to 23 ng/l (N=10; median=2 ng/l)(7). Lakes in the Zagreb area
contained from <1 to 5 ng/l (N=13; median=<1 ng/l)(7). Water sampled along
a gradient from the Iggesund pulp mill, Sweden, contained pentachlorophenol
at 43 to 1080 ng/l, with the higher concn reported for a sampling point very
close to the source(8). An upstream location from a pulp mill contained pentachlorophenol
at 0.007 ug/l while downstream locations had concns from 0.019 to 0.049 ug/l(9).
SURFACE WATER: Pentachlorophenol
was reported at seven surface water supplies in a study of municipal water
supply sources in Atlantic Canada from 0.002 to 0.021 ug/l during one sampling
period(1). Pentachlorophenol was the
only halogenated phenolic compound found in more than 20% of the raw water
samples from 40 potable water treatment plants across Canada in the fall and
winter samples at levels up to 53 ng/l with mean values of 1.9 and 2.8 ng/l,
respectively(4). Pentachlorophenol was
detected in the Isipingo River and the Isipingo Estuary, Republic of South
Africa, at concns from 0.1 to 3.79 ug/l(2). Concns of pentachlorophenol
from 0.040 to 5.26 ug/l (higher concn from a sample close to the water intake
plant) were measured in Pyhaoja Brook, Finland; the water was apparently
affected by a sawmill operation(3).
SEAWATER: Germany 0.02-1.30 parts/trillion(1).
Four sites located in the Scheldt estuary in North West Belgium and South West
Netherlands had concns of 0.1, 0.18, and 0.02 ppb, respectively(3).
Effluent Concentrations:
Oregon cities sewage treatment plant effluent
1-4 ppb(1). Detected in the effluents of the following industries (industry -
max concn, ppb): auto and other laundries - 27, coal mining - 3, iron and steel
manufacturing - 25, leather tanning and finishing - 3100, electrical/electronic
components - 10, foundries - 140, photographic equipment/supplies - 350,
pharmaceutical manufacturing - 110, paint and ink formulation - 490, pulp and
paperboard mills - 1400, rubber processing - 10, steam electric power plants -
6.5, textile mills - 15, timber products processing - 8300(2). 4.6 ppb mean
concn reported for organic manufacturing/plastics(2). Waste from a municipal
compositions facility on Long Island, NY has a concentration range of 7-210
ppb(3). Effluent from a pulp and paper bleach plant, aerated lagoon, and treated
effluent discharging into a river on site contained concentrations of pentachlorophenol
of 3.1, 1.3 and 0.6 ppb, respectively(4). Primary-treated and municipal
wastewater from the Iona Island treatment plant in Vancouver, British Columbia,
Canada contained pentachlorophenol
concentrations ranging from 0.4-13.2 ppb(5).
Raw effluent from several wood-treatment
plants contained pentachlorophenol at
concns of 25 to 150 mg/l(1). Influent and effluent from a sewage plant in
Corvallis, OR contained pentachlorophenol
at 1-5 ppb and 1-4 ppb, respectively(1). Pentachlorophenol
was measured in the waste from the production of sodium pentachlorophenol
at 51 g/kg waste(2). Pentachlorophenol
was present in a treated pulp mill effluent from Finland at 0.3 ug/l(3). A
typical concn of pentachlorophenol in
sewage sludge was reported as 1 to 5 mg/kg dry weight(4). Bleachery effluents in
a pulp and paper mill using chlorine dioxide substitution at 60% and 100%
chlorine dioxide, contained pentachlorophenol
at 2 and 0.5 ug/l; secondary treated mill effluents using this procedure
contained pentachlorophenol at less
than 1 ug/l at both chlorine dioxide concns(5). Pentachlorophenol
was detected in both free and chemically bound residues in effluents from the
chlorine (3.01 and 6.09 ug/l, respectively) and alkali extraction (9.23 and 9.93
ug/l, respectively) phases of chlorobleaching of pine kraft pulp(6). Pentachlorophenol
was not detected in influent and effluent of a pulp mill treatment system and
was not detected in discharge water samples; however, it was detected in
biosludge samples at 6.06 and 12.1 ng/g for free and bound residues,
respectively(7).
Pentachlorophenol
was detected in 8 samples of leachate (median=0.06, mean=0.21, max=1.1 ug/l)
collected from municipal and industrial landfills in Finland(1). Samples from
yard waste composting facilities contained pentachlorophenol
at concns from not detected to 91 ng/g; samples collected from municipal solid
waste composting programs contained pentachlorophenol
from 73 to 430 ng/g; samples collected from a facility that composts municipal
solid waste with dewatered sewage sludge contained pentachlorophenol
from 190 to 960 ng/g(2).
Pyrolysis of low molecular weight polyvinyl
chloride, in order to determine the effect of incinerator operations, resulted
in the production of several compounds, including pentachlorophenol(1).
The 1990 Toxics Release Inventory reported that 12 tons of pentachlorophenol
were released to the air per year(2). During incineration of pulp and paper mill
biosludges in a pilot-scale circulating fluidized bed incineration plant, pentachlorophenol
was released in the flue gases at concns from 0.10 to 0.74 ug/normalized
cu-m(3). Flue gas from two sites at a municipal waste incineration plant, after
an electrostatic precipitator and after a wet scrubber, contained pentachlorophenol
at 0.5 and 0.4 ug/normalized cu-m, respectively(4). Flue gas from the stack of
the second combustion line at a hazardous waste incinerator in Biebesheim,
Germany, contained pentachlorophenol
at 0.68 and 0.34 ng/normalized cu m(5). Pentachlorophenol
was detected in waste samples collected following two municipal landfill fires
at concns from -0.1 to 0.38 ug/g dry weight(6). Flue or ventilation emissions
from a metal reclamation plant in Sweden contained pentachlorophenol
at 0.1, 0.4, 2.0, 0.1, and 0.2 ug/normalized cu m from the aluminum smelting,
car shredding, turnings drying, sink and float separation and ring crusher
processes(7).
Sediment/Soil Concentrations:
SEDIMENT: Mississippi R outlet 1.6 ppm near
spill(1), Bremerhaven, Germany 0.095-20 ppb(2), German rivers 0.2-8 ppb(3),
Portland, ME 9 coastal sites, all pos, 0.01-2.4 ppb(4). SOIL: Abandoned sawmill
site near a wood-preserving site in Finland - 390 ppm(5). Gas Works Parks,
Seattle, Wash - 0.052 ppm(6); Lipar landfill, Manutua, Township, Gloucester Co.,
NJ - 2033 ppb(7). At several freshwater and marine sites in British Columbia,
Canada, which received effluents from the wood-treatment industry, avg pentachlorophenol
levels in the sediments ranged from not detectable to 590 ug/kg, while the
corresponding range for the overlying waters was from not detectable to 7.3 ug/l(8).
Pentachlorophenol concns in sediments
upstream from the Kinleith pulp and paper mill ranged from 0.5 to 5.5 ng/g;
downstream concns ranged from 11 to 13 ng/g near to the mill and from 0.41 to
1.6 ng/g further downstream(9). Pentachlorophenol
was present in sediment collected from sediment traps placed both upstream and
downstream from a pulp mill; upstream concns ranged from 0.05 to 0.06 and
downstream concns from 0.04 to 0.06 ug/g dry matter(10). Sediment concns at the
same sampling locations contained pentachlorophenol
at 0.040 to 0.050 ug/g dry matter at upstream locations and from 0.060 to 0.110
ug/g dry matter at downstream locations(10). A marine sediment collected in a
harbor on the west coast of Norway contained pentachlorophenol
at unreported concns(11).
Soil samples from four sites near a pentachlorophenol-production
facility in Switzerland contained 25 to 140 ug/kg (dry weight) at depths of 0-10
cm and 33-184 ug/kg at 20-30 cm(1). Soil from Finnish sawmills was heavily
contaminated with up to 45.6 mg/kg at 0-5 cm depth near the treatment basin and
up to 0.14 mg/kg in the area for storing treated wood. The background level was
0.012 mg/kg. Avg pentachlorophenol
levels in soil samples at 2.5, 30.5, and 152.5 cm from poles treated with pentachlorophenol
were 658, 3.4, and 0.26 mg/kg, respectively(1). Concns of pentachlorophenol
ranged from 0.012 to 0.227 ug/g dry weight in the sediment of Pyhaoja Brook,
Finland; this stream has been apparently affected by the operation of a
sawmill(2). Sediment samples collected from 3 sites, the basin of a bleached
kraft mill effluent treatment lagoon, from a location in the effluent drain
midway between this basin and the effluent outfall point, and from a location
immediately downstream of the outfall point contained pentachlorophenol
at 1045, 173, and 160.0 ug of Cl/g dry weight(3).
Atmospheric Concentrations:
Pentachlorophenol
was detected in two air samples from a single location at a median concn of 1 ng/cu
m(1). Bolivia and Antwerp, Belgium 0.023-0.70 parts/trillion(2). Detected in
Hamburg, Germany - 0.67 parts/trillion(3).
INDOOR: An estimation of children's (age 6
months to 5 years) exposure to pentachlorophenol
by respiration and household dust in nine homes ranged from not detected-1.4 ug/day
and <0.01 to 0.33 ug/day, respectively(2). In a pilot EPA study of
non-occupational exposure to pesticides, nine households in an urban-suburban
area of Jacksonville, FL, an area of high pesticide use, were monitored(3). Pentachlorophenol
was detected indoors in two households and outdoors in one household.
Food Survey Values:
US daily intake - % pos (ug): 1971 - 0.6%
(0.03 ug), 1972-0, 1973 - 2.5% (0.7 ug), 1974 - 3.0% (0.8 ug), 1975 - 5.4% (2.0
ug), 1976 - 0.8% (1.0 ug)(1). Results from the US FDA's Adult Total Diet Study
in which the typical 14-day diet of a 16-19 yr male was collected throughout the
US from market basket composite samples in 12 food groups (Fiscal Year-average
intake (ug/kg body wt/day)) are: FY79 0.006, FY 80 0.040, FY 81/82 0.052(2). An
analogous study for infants and toddlers calculated that in FY 81/82, that daily
pentachlorophenol input per unit body
weight was 0.023 and 0.079 ug/kg, respectively(2). In the 1988 Total Diet Study,
the intake of pentachlorophenol in ug/kg
body wt/day was 0.0004, 0.0002, and 0.0003 for a 6-11 month old, 14-16 yr male,
and 60-65 yr female, respectively(3). For the FY 81/82 Adult Total Diet Survey,
27 cities were sampled. In FY 81/82, there were 48 positive samples out of the
27 composites from each of the 12 food groups containing pentachlorophenol
levels up to 0.024 ppm(2). The avg 70 kg man would have an avg intake of 3.62 ug/day(2).
The food groups that contained pentachlorophenol
are (class, avg concn number of positives): meat, fish and poultry, 0.0037 ppm
14 positives; grain and cereal products, 0.0048 ppm 12 positives; oils and fats,
0.0072 ppm 18 positives; and sugar and adjuncts, 0.0010 ppm, 4 positives(2).
Mean daily intake of pentachlorophenol
from 1984-1986, determined during the FDA's Total Diet Study, was reported as
0.0169. 0.0379, 0.0135, 0.0183, 0.0130, 0.0156, 0.0108, and 0.0127 ug/kg body
weight/day for a 6- 11 month old child, a 2 year old child, a 14-16 year old
female, a 14-16 year old male, a 25-30 year old female, a 25-30 year old male, a
60-65 year old female and a 60-65 year old male, respectively(4). Intake of pentachlorophenol
found in the Total Diet Study analyses for 1986 to 1991 were reported as 0.0009,
0.0014, 0.0005, 0.0008, and 0.0007 ug/kg body weight/day for a 6-11 month old
child, a 2 year old child, a 14-16 year old male and female, a 25-30 year old
female and a 60-65 year old male and female, and a 25-30 year old male,
respectively(5). In a 10 year Revised Market Basket Study from 1982 to 1991, pentachlorophenol
was detected 485 times in 128 different foods at an avg concn of 0.0073 ug/g(6).
Plant Concentrations:
Surface wax of pine needles in Sweden,
collected in 1984 to 1986, contained pentachlorophenol
at about 1 ng/g in downwind locations (from a 1983-1984 spraying program in the
former East Germany); upwind needle concns (considered background) were reported
as 0.48 ng/g(1). Surface wax of pine needles collected from a series of stations
in West Germany, Denmark, Norway, and Sweden contained pentachlorophenol
from 0.6 to 7.3 ng/g fresh weight(2). Pine needle samples collected from Regina,
Saskatoon, and Yellowgrass in Saskatchewan, Canada, contained pentachlorophenol
at an avg concn of 0.93 ng/g with a standard deviation of 0.49 ng/g
(concentration range of 0.42 to 2.08 ng/g)(3). Rice samples taken from fields
which had been exposed to the effluent of a kraft pulp and paper mill in
Vietnam, contained pentachlorophenol
at concns from not detected to 0.02 ug/kg dry weight(4). Rice samples taken from
a nearby field which had not received waste effluents from the mill contained pentachlorophenol
at concns from not detected to 0.04 ug/kg dry weight(4).
Fish/Seafood Concentrations:
Not detected in meat, fish and poultry in
market basket surveys(1). New Brunswick, Canada fish 0.5-4 ppb, White shark
liver - 10.8 ppb, (2). Wabash R, IN - composite fish samples - detected, not
quantified(3). Fish 0.35-59 ppm(4). Gulf of Mexico, TX - flounder, killifish,
shrimp, crab and squid 2.6-7.5 ppb(5).
Mussels obtained from Lake Vanaja in Finland
contained pentachlorophenol at 180 to
260 ng/g lipid weight; mussels collected from the River Kymijoki contained pentachlorophenol
at concns less than 20-24 ng/g lipid weight(1). Perch, caught along a gradient
outside two pulp mills at Norrsundet and Iggesund, contained pentachlorophenol
at concns from 140 to 920 ng/g bile (lower number represents fish caught 10 km
from the mill) and 30 to 840 ng/g bile (lower value for low exposure to effluent
material), respectively(2). In a second experiment at Iggesund, perch bile
contained from 56 to 1100 ng/g with larger concns reported for fish caught
closer to the pulp mill(2). Mountain whitefish collected below a pulp and paper
mill, then transferred upstream of the mill for eight days during a depuration
phase, contained pentachlorophenol at
concns from not detected to 0.1 ug/g in fish bile samples(3). Limited longnose
sucker fish samples and other mountain whitefish collected below the mill ranged
from not detected-0.20 and from not detected-1.0 ug/g fish bile,
respectively(3). Fillets from longnose sucker fish and mountain whitefish
collected immediately downstream from the paper mill during spring 1991
contained pentachlorophenol at concns
from not detected to 4.00 ug/g(3). Pentachlorophenol
was not detected in any collected fish in the fall 1991 sampling period(3). Bile
obtained from goldfish collected from a New Zealand hydrolake, which received a
bleached kraft mill discharge, contained pentachlorophenol
at concns of 0.24-1.23 and 3.94-8.22 ug/g dry weight for locations upstream of
the outfall and downstream of the discharge point, respectively(4). 9.1 km
downstream of the discharge point pentachlorophenol
concns in goldfish bile were 0.17 ug/g dry weight(4).
Animal Concentrations:
In Canada, 6.6% of 881 pork liver samples
contained pentachlorophenol at concns
>0.1 mg/kg, max concn=0.72 mg/kg(1). 2% of 51 beef liver samples contained pentachlorophenol
at concns >0.1 mg/kg, max concn=0.35 mg/kg. Only one sample out of 214
chicken and 68 turkey liver samples contained pentachlorophenol
at a concn >0.1 mg/kg(1). Birds 0.04-0.49 ppm, snails 36-8 ppm; dairy cattle
in pentachlorophenol treated barn
58-1136 ppb(2); bird eggs 0.36-0.51 ppb(3).
IN THE STATE OF MICHIGAN, HERDS OF DAIRY
CATTLE WERE CONTAMINATED WITH PENTACHLOROPHENOL
USED TO TREAT WOOD OF BARNS WHERE THEY WERE HOUSED & FROM FEED BINS TREATED
WITH PENTACHLOROPHENOL; THE
CONTAMINATING PENTACHLOROPHENOL WAS
SAID TO CONTAIN 1 TO 1000 MG/KG DIOXIN. PCP LEVELS IN 18 COWS RANGED FROM 58 TO
1136 UG/KG. PENTACHLOROPHENOL HAS BEEN
FOUND IN BLOOD OF 8 SUCH HERDS.
Milk Concentrations:
Not detected in milk in market basket
surveys(1).
1 SAMPLE OF MILK WAS FOUND TO CONTAIN 0.09
MG/KG.
Other Environmental Concentrations:
One of three new cotton T-shirt samples,
tested for the presence of pentachlorophenol,
contained this compound at 2000 ng/g (detection limit=10 ng/g)(1). Mean concns
of pentachlorophenol in samples from
nine homes were reported as 0.48 ug/sq m, 0.03 ug/sq m, 0.02 ug/sq m, 0.02 ug,
0.05 ug/cu m, 0.03 ug/g, 0.02 ug/g, and 0.02 ug/g for house dust, PUF roller
(carpet dust), investigator hand, child hand rinse, air, entryway soil, walkway
soil, and play area soil, respectively(2). Pentachlorophenol
was measured in raw wood (3 of 15 samples positive; 0.25 mg/kg max), wood
packings and pallets (3 of 39 samples positive; 0.90 mg/kg max), interior
decoration (21 of 30 samples positive; 11.6 mg/kg max), beams (4 of 22 samples
positive; 0.32 mg/kg max), windows (64 of 68 samples positive; 163.3 mg/kg max),
fences and stakes (13 of 14 samples positive; 0.70 mg/kg max), cable-drums (4 of
10 samples positive; 1.32 mg/kg max), and recycling chips (8 of 9 samples
positive; 4.43 mg/kg max)(3). 9 of 65 paints used in children's toys(1);
wood-shaving litter from a chicken house(4).
Environmental Standards & Regulations:
FIFRA Requirements:
Criteria of concern: oncogenicity,
mutagenicity, and teratogenicity. Action: In order to avoid concellation,
registrants must adhere to the terms and conditions of the Federal Register
notices for ... pentachlorophenol ...
. Application: Wood preservatives (wood uses only). References: 49 FR 28666 July
13, 1984; 51 FR 1334 January 10, 1986.
Criteria of concern: oncogenicity,
mutagenicity, and teratogenicity. Action: Cancelled, all products for pentachlorophenol
products used in paper mills in the wet end of the paper making process ...
Cancelled, any of the retained registrations for pentachlorophenol
uses in cooling towers, pulp paper mills, and oil wells ... . Application: Wood
preservatives (nonwood uses only). References: 50 FR 41943 October 16, 1985; 53
FR 5524 February 24, 1988; 53 FR 24787 June 30, 1988.
As the federal pesticide law FIFRA directs,
EPA is conducting a comprehensive review of older pesticides to consider their
health and environmental effects and make decisions about their future use.
Under this pesticide reregistration program, EPA examines health and safety data
for pesticide active ingredients initially registered before November 1, 1984,
and determines whether they are eligible for reregistration. In addition, all
pesticides must meet the new safety standard of the Food Quality Protection Act
of 1996. Pesticides for which EPA had not issued Registration Standards prior to
the effective date of FIFRA, as amended in 1988, were divided into three lists
based upon their potential for human exposure and other factors, with List B
containing pesticides of greater concern and List D pesticides of less concern. Pentachlorophenol
is found on List B. Case No: 2505; Pesticide type: insecticide, fungicide,
antimicrobial; Case Status: OPP is reviewing data from the pesticide's producers
regarding its human health and/or environmental effects, or OPP is determining
the pesticide's eligibility for reregistration and developing the Reregistration
Eligibility Decision (RED) document.; Active ingredient (AI): Pentachlorophenol;
Data Call-in (DCI) Date(s): 01/06/92, 08/04/88, 05/30/86; AI Status: The
producers of the pesticide has made commitments to conduct the studies and pay
the fees required for reregistration, and are meeting those commitments in a
timely manner.
Acceptable Daily Intakes:
EPA RfD= 0.03 mg/kg
CERCLA Reportable Quantities:
Persons in charge of vessels or facilities are
required to notify the National Response Center (NRC) immediately, when there is
a release of this designated hazardous substance, in an amount equal to or
greater than its reportable quantity of 10 lb or 4.54 kg. The toll free number
of the NRC is (800) 424-8802; In the Washington D.C. metropolitan area (202)
426-2675. The rule for determining when notification is required is stated in 40
CFR 302.4 (section IV. D.3.b).
RCRA Requirements:
D037; A solid waste containing pentachlorophenol
may or may not become characterized as a hazardous waste when subjected to the
Toxicity Characteristic Leaching Procedure listed in 40 CFR 261.24, and if so
characterized, must be managed as a hazardous waste.
F027; Discarded unused formulations containing
tri-, tetra-, or pentachlorophenol or
discarded unused formulations containing compounds derived from these
chlorophenols are classified as a hazardous waste from a nonspecific source and
must be managed according to Federal and/or State hazardous waste regulations.
Generators of small quantities of this waste may qualify for partial exclusion
from hazardous waste regulations (see 40 CFR 261.5).
Atmospheric Standards:
This action promulgates standards of
performance for equipment leaks of Volatile Organic Compounds (VOC) in the
Synthetic Organic Chemical Manufacturing Industry (SOCMI). The intended effect
of these standards is to require all newly constructed, modified, and
reconstructed SOCMI process units to use the best demonstrated system of
continuous emission reduction for equipment leaks of VOC, considering costs, non
air quality health and environmental impact and energy requirements.
Chlorophenols is produced, as an intermediate or final product, by process units
covered under this subpart. /Chlorophenols/
Listed as a hazardous air pollutant (HAP)
generally known or suspected to cause serious health problems. The Clean Air
Act, as amended in 1990, directs EPA to set standards requiring major sources to
sharply reduce routine emissions of toxic pollutants. EPA is required to
establish and phase in specific performance based standards for all air emission
sources that emit one or more of the listed pollutants. Pentachlorophenol
is included on this list.
Clean Water Act Requirements:
Toxic pollutant designated pursuant to section
307(a)(1) of the Clean Water Act and is subject to effluent limitations.
Designated as a hazardous substance under
section 311(b)(2)(A) of the Federal Water Pollution Control Act and further
regulated by the Clean Water Act Amendments of 1977 and 1978. These regulations
apply to discharges of this substance.
The criterion level for pentachlorophenol
in water is 30 ug/l.
Federal Drinking Water Standards:
EPA 1 ug/l
State Drinking Water Guidelines:
(AZ) ARIZONA 220 ug/l
(ME) MAINE 1 ug/l
(MN) MINNESOTA 3 ug/l
FDA Requirements:
Pentachlorophenol
is an indirect food additive for use only as a component of adhesives.
Chemical/Physical Properties:
Molecular Formula:
C6-H-Cl5-O
Molecular Weight:
266.34
Color/Form:
COLORLESS CRYSTALS (TECH; DARK GREY)
Colorless to light-brown flakes or crystals
White monoclinic, crystalline solid
Needle-like crystals
Colorless to white crystalline solid.
Odor:
PHENOLIC ODOR
VERY PUNGENT ODOR ONLY WHEN HOT
Benzene-like odor.
Taste:
Taste threshold of 30 ug/l.
Boiling Point:
309-310 DEG C (DECOMP)
Melting Point:
174 deg C (monohydrate); 191 deg C (anhydrous)
Corrosivity:
Noncorrosive in absence of moisture
Density/Specific Gravity:
1.978 AT 22 DEG C/4 DEG C
Dissociation Constants:
pKa= 4.70
Heat of Vaporization:
16,742.6 gcal/gmole
Octanol/Water Partition Coefficient:
log Kow= 5.12
Solubilities:
In water, 14 mg/l at 26.7 deg C.
SLIGHTLY SOL IN PETROLEUM ETHER
SOL IN MOST ORGANIC SOLVENTS; SLIGHTLY SOL IN
PARAFFINS
Sol in ether
Sol in dilute alkali, carbitol, cellosolve
2 g/100 g in carbon tetrachloride at 20 deg C
8.5 g/100 g in o-dichlorobenzene at 20 deg C
3.1 g/100 g in diesel oil @ 20 deg C
32 g/100 g in pine oil @ 20 deg C
1.5 g/100 g in Stoddard solvent @ 20 deg C
In acetone: 50 g/100 g @ 25 deg C
In benzene: 15 g/100 g @ 25 deg C
In diacetone alcohol: 190 g/100 g @ 25 deg C
In ethanol (95%): 120 g/100 g @ 25 deg C
In methanol: 180 g/100 g @ 25 deg C
In isopropanol: 85 g/100 g at 25 deg C
In ethylene glycol: 11 g/100 g @ 25 deg C
Water Solubility: 5 mg/l in water @ 0 deg C;
14 mg/l in water @ 20 deg C; 35 mg/l in water @ 50 deg C; 85 mg/l in water @ 70
deg C
Spectral Properties:
MAX ABSORPTION (ALCOHOL): 300.5 NM (LOG E=
3.4); 308 NM (LOG E= 3.4); SADTLER REFERENCE NUMBER: 279 (IR, PRISM); 96 (IR,
GRATING)
Intense mass spectral peaks: 266 m/z (100%),
268 m/z (70%), 264 m/z (68%), 165 m/z (54%)
IR: 3657 (Coblentz Society Spectral
Collection)
UV: 112 (Sadtler Research Laboratories
Spectral Collection)
MASS: 1889 (National Bureau of Standards EPA-NIH
Mass Spectra Data Base, NSRDS-NBS-63)
Intense mass spectral peaks: 200 m/z, 228 m/z
Infrared (prism(279)); grating (96),
ultraviolet (112) and nuclear magnetic resonance (proton (39667); C-13 (26001))
spectral data have been reported.
Vapor Density:
9.20 (air= 1)
Vapor Pressure:
0.00011 mm Hg at 25 deg C
Other Chemical/Physical Properties:
DENSITY OF SATURATED AIR: 1.0000011 (AIR= 1);
PERCENT IN SATURATED AIR: 0.0000145% BY VOLUME AT 20 DEG C; 1 MG/L IS EQUIVALENT
TO 91.9 PPM & 1 PPM IS EQUIVALENT TO 0.01088 MG/L AT 25 DEG C
Henry's Law constant = 2.45X10-8 atm-cu m/mole
Chemical Safety & Handling:
DOT Emergency Guidelines:
Health: TOXIC, inhalation, ingestion, or skin
contact with material may cause severe injury or death. Contact with molten
substance may cause severe burns to skin and eyes. Avoid any skin contact.
Effects of contact or inhalation may be delayed. Fire may produce irritating,
corrosive and/or toxic gases. Runoff from fire control or dilution water may be
corrosive and/or toxic and cause pollution.
Fire or explosion: Non-combustible, substance
itself does not burn but may decompose upon heating to produce corrosive and/or
toxic fumes. Some are oxidizers and may ignite combustibles (wood, paper, oil,
clothing, etc.). Contact with metals may evolve flammable hydrogen gas.
Containers may explode when heated.
Public safety: CALL Emergency Response
Telephone Number. ... Isolate spill or leak area immediately for at least 25 to
50 meters (80 to 160 feet) in all directions. Keep unauthorized personnel away.
Stay upwind. Keep out of low areas. Ventilate enclosed areas.
Protective clothing: Wear positive pressure
self-contained breathing apparatus (SCBA). Wear chemical protective clothing
which is specifically recommended by the manufacturer. It may provide little or
no thermal protection. Structural firefighters' protective clothing provides
limited protection in fire situations ONLY, it is not effective in spill
situations.
Evacuation: ... Fire: If tank, rail car or
tank truck is involved in a fire, ISOLATE for 800 meters (1/2 mile) in all
directions; also, consider initial evacuation for 800 meters (1/2 mile) in all
directions.
Fire: Small fires: Dry chemical, CO2 or water
spray. Large fires: Dry chemical, CO2, alcohol-resistant foam or water spray.
Move containers from fire area if you can do it without risk. Dike fire control
water for later disposal; do not scatter the material. Fire involving tanks or
car/trailer loads: Fight fire from maximum distance or use unmanned hose holders
or monitor nozzles. Do not get water inside containers. Cool containers with
flooding quantities of water until well after fire is out. Withdraw immediately
in case of rising sound from venting safety devices or discoloration of tank.
ALWAYS stay away from tanks engulfed in fire.
Spill or leak: ELIMINATE all ignition sources
(no smoking, flares, sparks or flames in immediate area). Do not touch damaged
containers or spilled material unless wearing appropriate protective clothing.
Stop leak if you can do it without risk. Prevent entry into waterways, sewers,
basements or confined areas. Absorb or cover with dry earth, sand or other
non-combustible material and transfer to containers. DO NOT GET WATER INSIDE
CONTAINERS.
First aid: Move victim to fresh air. Call 911
or emergency medical service. Apply artificial respiration if victim is not
breathing. Do not use mouth-to-mouth method if victim ingested or inhaled the
substance; induce artificial respiration with the aid of a pocket mask equipped
with a one-way valve or other proper respiratory medical device. Administer
oxygen if breathing is difficult. Remove and isolate contaminated clothing and
shoes. In case of contact with substance, immediately flush skin or eyes with
running water for at least 20 minutes. For minor skin contact, avoid spreading
material on unaffected skin. Keep victim warm and quiet. Effects of exposure
(inhalation, ingestion or skin contact) to substance may be delayed. Ensure that
medical personnel are aware of the material(s) involved, and take precautions to
protect themselves.
Health: Toxic; may be fatal if inhaled,
ingested or absorbed through skin. Inhalation or contact with some of these
materials will irritate or burn skin and eyes. Fire will produce irritating,
corrosive and/or toxic gases. Vapors may cause dizziness or suffocation. Runoff
from fire control or dilution water may cause pollution. /Organochlorine
pesticide, liquid, flammable, poisonous; Organochlorine pesticide, liquid,
flammable, toxic; Organochlorine pesticide, liquid, poisonous, flammable;
Organochlorine pesticide, liquid, toxic, flammable/
Fire or explosion: Highly flammable: Will be
easily ignited by heat, sparks or flames. Vapors may form explosive mixtures
with air. Vapors may travel to source of ignition and flash back. Most vapors
are heavier than air. They will spread along ground and collect in low or
confined areas (sewers, basements, tanks). Vapor explosion and poison hazard
indoors, outdoors or in sewers. Those substances designated with a "P"
may polymerize explosively when heated or involved in a fire. Runoff to sewer
may create fire or explosion hazard. Containers may explode when heated. Many
liquids are lighter than water. /Organochlorine pesticide, liquid, flammable,
poisonous; Organochlorine pesticide, liquid, flammable, toxic; Organochlorine
pesticide, liquid, poisonous, flammable; Organochlorine pesticide, liquid,
toxic, flammable/
Public safety: Call Emergency Response
Telephone Number. ... Isolate spill or leak area immediately for at least 100 to
200 meters (330 to 660 feet) in all directions. Keep unauthorized personnel
away. Stay upwind. Keep out of low areas. Ventilate closed spaces before
entering. /Organochlorine pesticide, liquid, flammable, poisonous;
Organochlorine pesticide, liquid, flammable, toxic; Organochlorine pesticide,
liquid, poisonous, flammable; Organochlorine pesticide, liquid, toxic,
flammable/
Protective clothing: Wear positive pressure
self-contained breathing apparatus (SCBA). Wear chemical protective clothing
which is specifically recommended by the manufacturer. It may provide little or
no thermal protection. Structural firefighters' protective clothing provides
limited protection in fire situations ONLY; it is not effective in spill
situations. /Organochlorine pesticide, liquid, flammable, poisonous;
Organochlorine pesticide, liquid, flammable, toxic; Organochlorine pesticide,
liquid, poisonous, flammable; Organochlorine pesticide, liquid, toxic,
flammable/
Evacuation: ... Fire: If tank, rail car or
tank truck is involved in a fire, isolate for 800 meters (1/2 mile) in all
directions; also, consider initial evacuation for 800 meters (1/2 mile) in all
directions. /Organochlorine pesticide, liquid, flammable, poisonous;
Organochlorine pesticide, liquid, flammable, toxic; Organochlorine pesticide,
liquid, poisonous, flammable; Organochlorine pesticide, liquid, toxic,
flammable/
Fire: CAUTION: All these products have a very
low flash point. Use of water spray when fighting fire may be inefficient. Small
fires: Dry chemical, CO2, water spray or alcohol-resistant foam. Large fires:
Water spray, fog or alcohol-resistant foam. Move containers from fire area if
you can do it without risk. Dike fire control water for later disposal; do not
scatter the material. Use water spray or fog; do not use straight streams. Fire
involving tanks or car/trailer loads: Fight fire from maximum distance or use
unmanned hose holders or monitor nozzles. Cool containers with flooding
quantities of water until well after fire is out. Withdraw immediately in case
of rising sound from venting safety devices or discoloration of tank. ALWAYS
stay away from tanks engulfed in fire. For massive fire use unmanned hose
holders or monitor nozzles; if this is impossible, withdraw from area and let
fire burn. /Organochlorine pesticide, liquid, flammable, poisonous;
Organochlorine pesticide, liquid, flammable, toxic; Organochlorine pesticide,
liquid, poisonous, flammable; Organochlorine pesticide, liquid, toxic,
flammable/
Spill or leak: Fully encapsulating, vapor
protective clothing should be worn for spills and leaks with no fire. ELIMINATE
all ignition sources (no smoking, flares, sparks or flames in immediate area).
All equipment used when handling the product must be grounded. Do not touch or
walk through spilled material. Stop leak if you can do it without risk. Prevent
entry into waterways, sewers, basements or confined areas. A vapor suppressing
foam may be used to reduce vapors. Small spills: Absorb with earth, sand or
other non-combustible material and transfer to containers for later disposal.
Use clean non-sparking tools to collect absorbed material. Large spills: Dike
far ahead of liquid spill for later disposal. Water spray may reduce vapor; but
may not prevent ignition in closed spaces. /Organochlorine pesticide, liquid,
flammable, poisonous; Organochlorine pesticide, liquid, flammable, toxic;
Organochlorine pesticide, liquid, poisonous, flammable; Organochlorine
pesticide, liquid, toxic, flammable/
First aid: Move victim to fresh air. Call 911
or emergency medical service. Apply artificial respiration if victim is not
breathing. Do not use mouth-to-mouth method if victim ingested or inhaled the
substance; induce artificial respiration with the aid of a pocket mask equipped
with a one-way valve or other proper respiratory medical device. Administer
oxygen if breathing is difficult. Remove and isolate contaminated clothing and
shoes. In case of contact with substance, immediately flush skin or eyes with
running water for at least 20 minutes. Wash skin with soap and water. Keep
victim warm and quiet. Effects of exposure (inhalation, ingestion or skin
contact) to substance may be delayed. Ensure that medical personnel are aware of
the material(s) involved, and take precautions to protect themselves. /Organochlorine
pesticide, liquid, flammable, poisonous; Organochlorine pesticide, liquid,
flammable, toxic; Organochlorine pesticide, liquid, poisonous, flammable;
Organochlorine pesticide, liquid, toxic, flammable/
Health: Highly toxic, may be fatal if inhaled,
swallowed or absorbed through skin. Avoid any skin contact. Effects of contact
or inhalation may be delayed. Fire may produce irritating, corrosive and/or
toxic gases. Runoff from fire control or dilution water may be corrosive and/or
toxic and cause pollution. /Organochlorine pesticide, liquid, poisonous;
Organochlorine pesticide, liquid, toxic; Organochlorine pesticide, solid,
poisonous; Organochlorine pesticide, solid, toxic/
Fire or explosion: Non-combustible, substance
itself does not burn but may decompose upon heating to produce corrosive and/or
toxic fumes. Containers may explode when heated. Runoff may pollute waterways. /Organochlorine
pesticide, liquid, poisonous; Organochlorine pesticide, liquid, toxic;
Organochlorine pesticide, solid, poisonous; Organochlorine pesticide, solid,
toxic/
Public safety: CALL Emergency Response
Telephone Number. ... Isolate spill or leak area immediately for at least 25 to
50 meters (80 to 160 feet) in all directions. Keep unauthorized personnel away.
Stay upwind. Keep out of low areas. /Organochlorine pesticide, liquid,
poisonous; Organochlorine pesticide, liquid, toxic; Organochlorine pesticide,
solid, poisonous; Organochlorine pesticide, solid, toxic/
Protective clothing: Wear positive pressure
self-contained breathing apparatus (SCBA). Wear chemical protective clothing
which is specifically recommended by the manufacturer. It may provide little or
no thermal protection. Structural firefighters' protective clothing provides
limited protection in fire situations ONLY; it is not effective in spill
situations. /Organochlorine pesticide, liquid, poisonous; Organochlorine
pesticide, liquid, toxic; Organochlorine pesticide, solid, poisonous;
Organochlorine pesticide, solid, toxic/
Evacuation: ... Fire: If tank, rail car or
tank truck is involved in a fire, ISOLATE for 800 meters (1/2 mile) in all
directions; also, consider initial evacuation for 800 meters (1/2 mile) in all
directions. /Organochlorine pesticide, liquid, poisonous; Organochlorine
pesticide, liquid, toxic; Organochlorine pesticide, solid, poisonous;
Organochlorine pesticide, solid, toxic/
Fire: Small fires: Dry chemical, CO2 or water
spray. Large fires: Water spray, fog or regular foam. Move containers from fire
area if you can do it without risk. Dike fire control water for later disposal;
do not scatter the material. Use water spray or fog; do not use straight
streams. Fire involving tanks or car/trailer loads: Fight fire from maximum
distance or use unmanned hose holders or monitor nozzles. Do not get water
inside containers. Cool containers with flooding quantities of water until well
after fire is out. Withdraw immediately in case of rising sound from venting
safety devices or discoloration of tank. ALWAYS stay away from tanks engulfed in
fire. For massive fire, use unmanned hose holders or monitor nozzles; if this is
impossible withdraw from area and let fire burn. /Organochlorine pesticide,
liquid, poisonous; Organochlorine pesticide, liquid, toxic; Organochlorine
pesticide, solid, poisonous; Organochlorine pesticide, solid, toxic/
Spill or leak: Do not touch damaged containers
or spilled material unless wearing appropriate protective clothing. Stop leak if
you can do it without risk. Prevent entry into waterways, sewers, basements or
confined areas. Cover with plastic sheet to prevent spreading. Absorb or cover
with dry earth, sand or other non-combustible material and transfer to
containers. DO NOT GET WATER INSIDE CONTAINERS. /Organochlorine pesticide,
liquid, poisonous; Organochlorine pesticide, liquid, toxic; Organochlorine
pesticide, solid, poisonous; Organochlorine pesticide, solid, toxic/
First aid: Move victim to fresh air. Call 911
or emergency medical service. Apply artificial respiration if victim is not
breathing. Do not use mouth-to-mouth method if victim ingested or inhaled the
substance; induce artificial respiration with the aid of a pocket mask equipped
with a one-way valve or other proper respiratory medical device. Administer
oxygen if breathing is difficult. Remove and isolate contaminated clothing and
shoes. In case of contact with substance, immediately flush skin or eyes with
running water for at least 20 minutes. For minor skin contact, avoid spreading
material on unaffected skin. Keep victim warm and quiet. Effects of exposure
(inhalation, ingestion or skin contact) to substance may be delayed. Ensure that
medical personnel are aware of the material(s) involved, and take precautions to
protect themselves. /Organochlorine pesticide, liquid, poisonous; Organochlorine
pesticide, liquid, toxic; Organochlorine pesticide, solid, poisonous;
Organochlorine pesticide, solid, toxic/
Odor Threshold:
Odor thresholds for PCP soln at 30 deg and 60
deg C were 857 and 12,000 ug/l, respectively.
Detection: 1.6 mg/l.
Skin, Eye and Respiratory Irritations:
Dust or vapor irritates skin. ...
Eye and skin irritant.
All chlorophenol ... dusts are ... irritating
to the respiratory tract. /Chlorophenols/
Dust and vapor of pentachlorophenol
are irritating to the eyes, causing lacrimation.
NFPA Hazard Classification:
Health: 3. 3= Materials that, on short
exposure, could cause serious temporary or residual injury, including those
requiring protection from all bodily contact. Fire fighters may enter the area
only if they are protected from all contact with the material. Full protective
clothing, including self-contained breathing apparatus, coat, pants, gloves,
boots, and bands around legs, arms, and waist, should be provided. No skin
surface should be exposed.
Flammability: 0. 0= This degree includes any
material that will not burn.
Reactivity: 0. 0= This degree includes
materials that are normally stable, even under fire exposure conditions, and
that do not react with water. Normal fire fighting procedures may be used.
Fire Fighting Procedures:
If material on fire or involved in fire:
Extinguish fire using agent suitable for type of surrounding fire. Material
itself does not burn or burns with difficulty.
Extinguish fire using agent suitable for
surrounding fire. Use dry chemical, foam, carbon dioxide, or water spray. Water
may be ineffective. Approach fire from upwind to avoid hazardous vapors and
toxic decomposition products. Use water spray to keep fire-exposed containers
cool.
Toxic Combustion Products:
Hydrogen chloride, chlorinated phenols, and
carbon monoxide may be released upon decomposition.
Hazardous Reactivities & Incompatibilities:
Contact with strong oxidizers may cause fires
or explosions.
Reacts with acids, alkalies, oxidizing
materials, and other organic materials.
Strong oxidizers, acids, alkalis.
Hazardous Decomposition:
Hydrogen chloride, chlorinated phenols, and
carbon monoxide may be released upon decomposition.
Decomposes to produce hydrogen chloride and
other irritants and toxic gases.
Immediately Dangerous to Life or Health:
2.5 mg/cu m
Protective Equipment & Clothing:
Wear rubber gloves ... & overalls.
Five commercial glove materials were tested
for permeation using two pentachlorophenol
(PCP) formulations. When challenged with a 4.3% PCP in diesel oil soln, both
Dayton Flexible Products Triflex (PVC) & the Best 64 NFW (natural rubber)
gloves exhibited breakthrough times 30 sec after exposure. The Playtex #835
(latex/neoprene) glove exhibited breakthrough after 60 min, but showed a 5-fold
greater rate of permeation than the Dayton & the Best glove. Neither the
Edmont Sol-Vet (nitrile rubber) not the Granet Glo-Gluv (PVC) gloves had been
permeated after testing for 8 & 16 hr, respectively. ... The results show
that different gloves offer differing resistance to permeation by PCP based upon
the composition of the gloves & the PCP formulation tested.
Recommendations for respirator selection. Max
concn for use: 2.5 mg/cu m: Respirator Classes: Any chemical cartridge
respirator with organic vapor cartridge(s) in combination with a dust, mist, and
fume filter. May require eye protection. Any powered, air-purifying respirator
with organic vapor cartridge(s) in combination with a dust, mist, and fume
filter. May require eye protection. Any supplied-air respirator. May require eye
protection. Any self-contained breathing apparatus with a full facepiece.
Recommendations for respirator selection.
Emergency or planned entry into unknown concn or IDLH conditions: Respirator
Classes: Any self-contained breathing apparatus that has a full facepiece and is
operated in a pressure-demand or other positive pressure mode. Any supplied-air
respirator that has a full facepiece and is operated in pressure-demand or other
positive pressure mode in combination with an auxiliary self-contained breathing
apparatus operated in pressure-demand or other positive pressure mode.
Recommendations for respirator selection.
Escape from suddenly occuring respiratory hazards: Respirator Classes: Any
air-purifying, full-facepiece respirator (gas mask) with a chin-style, front- or
back-mounted organic vapor canister having a high-efficiency particulate filter.
Any appropriate escape-type, self-contained breathing apparatus.
Wear appropriate personal protective clothing
to prevent skin contact.
SRP: Contaminated protective clothing should
be segregated in such a manner so that there is no direct personal contact by
personnel who handle, dispose, or clean the clothing. Quality assurance to
ascertain the completeness of the cleaning procedures should be implemented
before the decontaminated protective clothing is returned for reuse by the
workers. Contaminated clothing should not be taken home at end of shift, but
should remain at employee's place of work for cleaning.
Wear appropriate eye protection to prevent eye
contact.
Eyewash fountains should be provided in areas
where there is any possbility that workers could be exposed to the substance;
this is irrespective of the recommendation involving the wearing of eye
protection.
Facilities for quickly drenching the body
should be provided within the immediate work area for emergency use where there
is a possibility of exposure. [Note: It is intended that these facilities
provide a sufficient quantity or flow of water to quickly remove the substance
from any body areas likely to be exposed. The actual determination of what
constitutes an adequate quick drench facility depends on the specific
circumstances. In certain instances, a deluge shower should be readily
available, whereas in others, the availability of water from a sink or hose
could be considered adequate.]
Decontamination: Wear positive-pressure SCBA
and protective equipment specified by references such as the DOT Emergency
Response Guidebook or the CANUTEC Initial Emergency Response Guide. If special
chemical protective clothing is required, consult the chemical manufacturer or
specific protective clothing compatibility charts. Delay entry until trained
personnel and proper protective equipment are available. Remove patient from
contaminated area. Quickly remove and isolate patient's clothing, jewelry, and
shoes. Gently brush away dry particles and blot excess liquids with absorbent
material. Rinse patient with warm water, 30 deg C/86 deg F, if possible. Wash
patient with Tincture of Green soap or a mild liquid soap and large quantities
of water. Refer to decontamination protocol in Section Three.
PRECAUTIONS FOR "CARCINOGENS": ...
Dispensers of liq detergent /should be available./ ... Safety pipettes should be
used for all pipetting. ... In animal laboratory, personnel should ... wear
protective suits (preferably disposable, one-piece & close-fitting at ankles
& wrists), gloves, hair covering & overshoes. ... In chemical
laboratory, gloves & gowns should always be worn ... however, gloves should
not be assumed to provide full protection. Carefully fitted masks or respirators
may be necessary when working with particulates or gases, & disposable
plastic aprons might provide addnl protection. ... Gowns ... /should be/ of
distinctive color, this is a reminder that they are not to be worn outside the
laboratory. /Chemical Carcinogens/
Preventive Measures:
ALL CLOTHING WORN DURING ONE SPRAYING
OPERATION SHOULD BE LEFT AT WORKPLACE & LAUNDERED BEFORE REUSE. WASHING WITH
SOAP & WATER IS MUST BEFORE EATING, DRINKING OR SMOKING. AT END OF EACH DAY,
WORKMEN SHOULD SHOWER & CHANGE INTO CLEAN CLOTHING.
Penta Concentrate: Vapor will cause injury if
adequate ventilation is not insured. Do not use this product indoors or any
other confined areas where vapors may concentrate ...
Contact lenses should not be worn when working
with this chemical.
If material not on fire and not involved in
fire: Keep material out of water sources and sewers. Build dikes to contain flow
as necessary.
Avoid breathing vapors. Keep upwind. Wear
boots, protective gloves, and goggles. Wash away any material which may have
contacted the body with copious amounts of water or soap and water.
Environmental considerations: Land spill: Dig
a pit, pond, lagoon, or holding area to contain liquid or solid material. /SRP:
If time permits, pits, ponds, lagoons, soak holes, or holding areas should be
contained with a flexible impermeable membrane liner./ Cover solids with a
plastic sheet to prevent dissolving in rain or fire fighting water.
Environmental considerations: Water spill: Use
natural deep water pockets, excavated lagoons, or sand bag barriers to trap
material at bottom. If dissolved, in region of 10 ppm or greater concentration,
apply activated carbon at ten times the spilled amount. Remove trapped material
with suction hoses. Use mechanical dredges or lifts to remove immobilized masses
of pollutants and precipitates or greater concentration.
SRP: Contaminated protective clothing should
be segregated in such a manner so that there is no direct personal contact by
personnel who handle, dispose, or clean the clothing. Quality assurance to
ascertain the completeness of the cleaning procedures should be implemented
before the decontaminated protective clothing is returned for reuse by the
workers. Contaminated clothing should not be taken home at end of shift, but
should remain at employee's place of work for cleaning.
The worker should immediately wash the skin
when it becomes contaminated.
Work clothing that becomes wet or
significantly contaminated should be removed and replaced.
Workers whose clothing may have become
contaminated should change into uncontaminated clothing before leaving the work
premises.
SRP: The scientific literature for the use of
contact lenses in industry is conflicting. The benefit or detrimental effects of
wearing contact lenses depend not only upon the substance, but also on factors
including the form of the substance, characteristics and duration of the
exposure, the uses of other eye protection equipment, and the hygiene of the
lenses. However, there may be individual substances whose irritating or
corrosive properties are such that the wearing of contact lenses would be
harmful to the eye. In those specific cases, contact lenses should not be worn.
In any event, the usual eye protection equipment should be worn even when
contact lenses are in place.
PRECAUTIONS FOR "CARCINOGENS":
Smoking, drinking, eating, storage of food or of food & beverage containers
or utensils, & the application of cosmetics should be prohibited in any
laboratory. All personnel should remove gloves, if worn, after completion of
procedures in which carcinogens have been used. They should ... wash ... hands,
preferably using dispensers of liq detergent, & rinse ... thoroughly.
Consideration should be given to appropriate methods for cleaning the skin,
depending on nature of the contaminant. No standard procedure can be
recommended, but the use of organic solvents should be avoided. Safety pipettes
should be used for all pipetting. /Chemical Carcinogens/
PRECAUTIONS FOR "CARCINOGENS": In
animal laboratory, personnel should remove their outdoor clothes & wear
protective suits (preferably disposable, one-piece & close-fitting at ankles
& wrists), gloves, hair covering & overshoes. ... Clothing should be
changed daily but ... discarded immediately if obvious contamination occurs ...
/also,/ workers should shower immediately. In chemical laboratory, gloves &
gowns should always be worn ... however, gloves should not be assumed to provide
full protection. Carefully fitted masks or respirators may be necessary when
working with particulates or gases, & disposable plastic aprons might
provide addnl protection. If gowns are of distinctive color, this is a reminder
that they should not be worn outside of lab. /Chemical Carcinogens/
PRECAUTIONS FOR "CARCINOGENS": ...
Operations connected with synth & purification ... should be carried out
under well-ventilated hood. Analytical procedures ... should be carried out with
care & vapors evolved during ... procedures should be removed. ... Expert
advice should be obtained before existing fume cupboards are used ... & when
new fume cupboards are installed. It is desirable that there be means for
decreasing the rate of air extraction, so that carcinogenic powders can be
handled without ... powder being blown around the hood. Glove boxes should be
kept under negative air pressure. Air changes should be adequate, so that concn
of vapors of volatile carcinogens will not occur. /Chemical Carcinogens/
PRECAUTIONS FOR "CARCINOGENS":
Vertical laminar-flow biological safety cabinets may be used for containment of
in vitro procedures ... provided that the exhaust air flow is sufficient to
provide an inward air flow at the face opening of the cabinet, &
contaminated air plenums that are under positive pressure are leak-tight.
Horizontal laminar-flow hoods or safety cabinets, where filtered air is blown
across the working area towards the operator, should never be used ... Each
cabinet or fume cupboard to be used ... should be tested before work is begun (eg,
with fume bomb) & label fixed to it, giving date of test & avg air-flow
measured. This test should be repeated periodically & after any structural
changes. /Chemical Carcinogens/
PRECAUTIONS FOR "CARCINOGENS":
Principles that apply to chem or biochem lab also apply to microbiological &
cell-culture labs ... Special consideration should be given to route of admin.
... Safest method of administering volatile carcinogen is by injection of a soln.
Admin by topical application, gavage, or intratracheal instillation should be
performed under hood. If chem will be exhaled, animals should be kept under hood
during this period. Inhalation exposure requires special equipment. ... Unless
specifically required, routes of admin other than in the diet should be used.
Mixing of carcinogen in diet should be carried out in sealed mixers under fume
hood, from which the exhaust is fitted with an efficient particulate filter.
Techniques for cleaning mixer & hood should be devised before expt begun.
When mixing diets, special protective clothing &, possibly, respirators may
be required. /Chemical Carcinogens/
PRECAUTIONS FOR "CARCINOGENS": When
... admin in diet or applied to skin, animals should be kept in cages with solid
bottoms & sides & fitted with a filter top. When volatile carcinogens
are given, filter tops should not be used. Cages which have been used to house
animals that received carcinogens should be decontaminated. Cage-cleaning
facilities should be installed in area in which carcinogens are being used, to
avoid moving of ... contaminated /cages/. It is difficult to ensure that cages
are decontaminated, & monitoring methods are necessary. Situations may exist
in which the use of disposable cages should be recommended, depending on type
& amt of carcinogen & efficiency with which it can be removed. /Chemical
Carcinogens/
PRECAUTIONS FOR "CARCINOGENS": To
eliminate risk that ... contamination in lab could build up during conduct of
expt, periodic checks should be carried out on lab atmospheres, surfaces, such
as walls, floors & benches, & ... interior of fume hoods & airducts.
As well as regular monitoring, check must be carried out after cleaning-up of
spillage. Sensitive methods are required when testing lab atmospheres. ...
Methods ... should ... where possible, be simple & sensitive. /Chemical
Carcinogens/
PRECAUTIONS FOR "CARCINOGENS": Rooms
in which obvious contamination has occurred, such as spillage, should be
decontaminated by lab personnel engaged in expt. Design of expt should ... avoid
contamination of permanent equipment. ... Procedures should ensure that
maintenance workers are not exposed to carcinogens. ... Particular care should
be taken to avoid contamination of drains or ventilation ducts. In cleaning
labs, procedures should be used which do not produce aerosols or dispersal of
dust, ie, wet mop or vacuum cleaner equipped with high-efficiency particulate
filter on exhaust, which are avail commercially, should be used. Sweeping,
brushing & use of dry dusters or mops should be prohibited. Grossly
contaminated cleaning materials should not be re-used ... If gowns or towels are
contaminated, they should not be sent to laundry, but ... decontaminated or
burnt, to avoid any hazard to laundry personnel. /Chemical Carcinogens/
PRECAUTIONS FOR "CARCINOGENS": Doors
leading into areas where carcinogens are used ... should be marked distinctively
with appropriate labels. Access ... limited to persons involved in expt. ... A
prominently displayed notice should give the name of the Scientific Investigator
or other person who can advise in an emergency & who can inform others (such
as firemen) on the handling of carcinogenic substances. /Chemical Carcinogens/
Stability/Shelf Life:
STABLE; PROLONGED HEATING ABOVE 200 DEG C
PRODUCES TRACES OF OCTACHLORODIBENZO-PARA-DIOXIN.
Shipment Methods and Regulations:
No person may /transport,/ offer or accept a
hazardous material for transportation in commerce unless that person is
registered in conformance ... and the hazardous material is properly classed,
described, packaged, marked, labeled, and in condition for shipment as required
or authorized by ... /the hazardous materials regulations (49 CFR 171-177)./
The International Air Transport Association (IATA)
Dangerous Goods Regulations are published by the IATA Dangerous Goods Board
pursuant to IATA Resolutions 618 and 619 and constitute a manual of industry
carrier regulations to be followed by all IATA Member airlines when transporting
hazardous materials.
The International Maritime Dangerous Goods
Code lays down basic principles for transporting hazardous chemicals. Detailed
recommendations for individual substances and a number of recommendations for
good practice are included in the classes dealing with such substances. A
general index of technical names has also been compiled. This index should
always be consulted when attempting to locate the appropriate procedures to be
used when shipping any substance or article.
PRECAUTIONS FOR "CARCINOGENS":
Procurement ... of unduly large amt ... should be avoided. To avoid spilling,
carcinogens should be transported in securely sealed glass bottles or ampoules,
which should themselves be placed inside strong screw-cap or snap-top container
that will not open when dropped & will resist attack from the carcinogen.
Both bottle & the outside container should be appropriately labelled. ...
National post offices, railway companies, road haulage companies & airlines
have regulations governing transport of hazardous materials. These authorities
should be consulted before ... material is shipped. /Chemical Carcinogens/
PRECAUTIONS FOR "CARCINOGENS": When
no regulations exist, the following procedure must be adopted. The carcinogen
should be enclosed in a securely sealed, watertight container (primary
container), which should be enclosed in a second, unbreakable, leakproof
container that will withstand chem attack from the carcinogen (secondary
container). The space between primary & secondary container should be filled
with absorbent material, which would withstand chem attack from the carcinogen
& is sufficient to absorb the entire contents of the primary container in
the event of breakage or leakage. Each secondary container should then be
enclosed in a strong outer box. The space between the secondary container &
the outer box should be filled with an appropriate quantity of shock-absorbent
material. Sender should use fastest & most secure form of transport &
notify recipient of its departure. If parcel is not received when expected,
carrier should be informed so that immediate effort can be made to find it.
Traffic schedules should be consulted to avoid ... arrival on weekend or holiday
... /Chemical Carcinogens/
Storage Conditions:
Temperature: ambient.
Venting: open.
Store in cool, dry, well ventilated location.
Separate from acids, alkalies, oxidizing materials, and other organic materials.
Penta Ready, Penta
WR: Keep container closed. Do not leave in sunshine. Do not use,
pour, spill, or store near heat or open flame. Destroy or return this container
when empty. Do not reuse empty container.
Penta Concentrate: Not for use or storage
around the house.
PRECAUTIONS FOR "CARCINOGENS":
Storage site should be as close as practical to lab in which carcinogens are to
be used, so that only small quantities required for ... expt need to be carried.
Carcinogens should be kept in only one section of cupboard, an explosion-proof
refrigerator or freezer (depending on chemicophysical properties ...) that bears
appropriate label. An inventory ... should be kept, showing quantity of
carcinogen & date it was acquired ... Facilities for dispensing ... should
be contiguous to storage area. /Chemical Carcinogens/
Cleanup Methods:
1) VENTILATE AREA OF SPILL. 2) COLLECT SPILLED
MATERIAL IN MOST CONVENIENT & SAFE MANNER & DEPOSIT IN SEALED CONTAINERS
FOR RECLAMATION OR ... DISPOSAL ... LIQ CONTAINING PENTACHLOROPHENOL
SHOULD BE ABSORBED IN VERMICULITE, DRY SAND, EARTH OR SIMILAR MATERIAL.
Biological treatment is principal secondary
treatment method but other ... methods employed at some wood preservative plants
are carbon absorption, membrane filtration ... and oxidation by chlorine,
hydrogen peroxide, and ozone. The reduction in concn of pentachlorophenol
... /in biological treatment/ is thought to occur by adsorption upon biomass
rather than by degradation.
Avoid contact with solid and dust. Keep people
away. Stop discharge if possible. Isolate and remove discharged material. Notify
local health and pollution control agencies.
Survey report six case histories employing
EPA's hazardous materials spills treatment trailer are reviewed. The trailer's
... treatment system has three mixed-media filters and three activated carbon
columns to remove suspended, precipitated, and organic soluble materials. Spills
of PCB, pentachlorophenol, kepone,
tremide (chlordane, heptachlor, aldrin, and dieldrin), toxaphene, and
dinitrobutylphenol were treated by the EPA trailer, which was generally
successful in mitigating environmental effects by filtering and
carbon-adsorption. 90% removal was achieved for 21 of 23 compounds.
Adsorption studies for the removal of the
pesticide pentachlorophenol found in a
number of water supplies were carried out using various materials including
kaolinite, bentone SD-3 and powdered activated carbon. It was found that
adsorption on kaolinite was negligible, whereas bentone SD-3 presented an
adsorption efficiency from 10 to 100 fold less than equivalent quantities of
powdered activated carbon. The effect of the pH on the removal of pentachlorophenol
by activated carbon was studied. The removal efficiency of pentachlorophenol
by activated carbon is better in acidic media. A clear dependence of adsorption
on the pH appeared to be the result of a marked variation on the pesticide
solubility as a function of the pH. Adsorption of pentachlorophenol/phenate
(5 mg/l) diminishes markedly at pH values above the pKa of this weak acid (equal
to 5.9 : 0.1) when the pentachlorophenol
exists almost entirely in ionic form in aqueous solution, and is enhanced at low
pH when the percentage of molecular species (whose concentration can be
determined from pKa value) becomes significant. These remarks and the adsorptive
capacities (163 mg.g-1 = 0.6 mmol/g at pH = 5.2 and 79 mg/g = 0,3 mmol/g at pH =
12.7), suggest a negative interaction between pentachlorophenol
and activated carbon which seems to be confirmed by the results with bentone
SD-43 (tables 1 to 4), and the values of the electrokinetic potential of these
materials. This study emphasizes the effect of organic coadsorbates (eg,
dissolved humic substances and the pesticide lindane) on the adsorption capacity
of activated carbon for pentachlorophenol.
Two different natural organic matters were studied as coadsorbates: purified
humic acids from a commercial source (at 10 mg/l) and fulvic acids extracted
from a top soil horizon (at 20 mg/l). Pentachlorophenol
absorption was not affected by humic acids, whereas an increase of adsorption
seemed to be observed in the presence of fulvic acids. Pentachlorophenol
does not affect the adsorption of the humic acids, but improves slightly the
removal of fulvic acids. This suggests an association between the two kinds of
organic compounds, the resulting complex, fulvic acids/pentachlorophenol,
being more adsorbed than the compounds themselves. The coadsorbate lindane (0.65
mg/l) which is easily adsorbed by activated carbon seemed also to improve
slightly the removal efficiency of pentachlorophenol
by activated carbon.
Chemical analyses revealed that polycyclic
aromatic hydrocarbons and other organic compounds were present in a perennial
freshwater stream that flowed through the abandoned American Creosote works and
into Pensacola Bay, Florida. Moreover, groundwater pumped from a well depth of
21 m at a location adjacent to the site was heavily contaminated with polycyclic
aromatic hydrocarbons and other organics. A study was conducted to determine the
efficacy of ultrafiltration for removal of organics from groundwater at this
USEPA, Super Fund site. Ultrafiltration reduced the concentration of total
identified organics from 210.0 mg/l in groundwater to 1.5 mg/l in the post
filtration permeate. Tests for toxicity/teratogenicity in embryonic inland
silversides, Menidia beryllina; and Microtox 15 min EC50's were conducted with:
(1) streamwater, (2) untreated groundwater, (3) feedwater used in the
ultrafiltration system and (4) permeate water that passed through the
ultrafiltration system. Concentration of 100% streamwater caused significant
(alpha : 0.05) teratogenic responses in fish embryos and larvae; the Microtox
EC50 was 3.7% streamwater. Groundwater and feedwater caused significant embryo
toxic or teratogenic responses at concentrations of 100, 10, and 1%; the
Microtox EC50's were 0.85 and 0.48%, respectively. In contrast, only 100%
permeate water caused significant increases in terata, compared to the control
response; at 10 and 1% concentration > 90% of hatched larvae appeared normal.
The Microtox EC50 was 30% permeate water.
PRECAUTIONS FOR "CARCINOGENS": A
high-efficiency particulate arrestor (HEPA) or charcoal filters can be used to
minimize amt of carcinogen in exhausted air ventilated safety cabinets, lab
hoods, glove boxes or animal rooms ... Filter housing that is designed so that
used filters can be transferred into plastic bag without contaminating
maintenance staff is avail commercially. Filters should be placed in plastic
bags immediately after removal ... The plastic bag should be sealed immediately
... The sealed bag should be labelled properly ... Waste liquids ... should be
placed or collected in proper containers for disposal. The lid should be secured
& the bottles properly labelled. Once filled, bottles should be placed in
plastic bag, so that outer surface ... is not contaminated ... The plastic bag
should also be sealed & labelled. ... Broken glassware ... should be
decontaminated by solvent extraction, by chemical destruction, or in specially
designed incinerators. /Chemical Carcinogens/
Disposal Methods:
Generators of waste (equal to or greater than
100 kg/mo) containing this contaminant, EPA hazardous waste numbers D037; F027
must conform with USEPA regulations in storage, transportation, treatment and
disposal of waste.
Pentachlorophenol
is a waste chemical stream constituent which may be subjected to ultimate
disposal by controlled incineration. Incineration (600 deg to 900 deg) coupled
with adequate scrubbing and ash disposal facilities.
A potential candidate for rotary kiln
incineration at a temperature range of 820 to 1,600 deg C and residence times of
seconds for liquids and gases, and hours for solids.
The following wastewater treatment
technologies have been investigated for pentachlorophenol:
Concentration process: Biological Treatment.
The following wastewater treatment
technologies have been investigated for pentachlorophenol:
Concentration process: Solvent Extraction.
Before draining, aqueous soln of low concn
must be purified of the poisonous pentachlorophenol
by filtering methods such as adsorption of the harmful material by activated
charcoal. After this step, the charcoal is regenerated by controlled oxidation
in a rotary kiln incinerator installation (600-900 deg C). The escaping hydrogen
chloride gas is removed by scrubbers. Concentrated wastes are destroyed in
special waste incinerators which have suitable installations to scrub the
liberated hydrogen chloride gas. Recommendable method: Incineration. Not
recommendable methods: Discharge to sewer, open burning & use as fuel.
Peer-review: Dissolve in excess solvent before burning. (Peer-review conclusions
of an IRPTC expert consultation (May 1985))
PRECAUTIONS FOR "CARCINOGENS": There
is no universal method of disposal that has been proved satisfactory for all
carcinogenic compounds & specific methods of chem destruction ... published
have not been tested on all kinds of carcinogen-containing waste. ... summary of
avail methods & recommendations ... /given/ must be treated as guide only.
/Chemical Carcinogens/
PRECAUTIONS FOR "CARCINOGENS": ...
Incineration may be only feasible method for disposal of contaminated laboratory
waste from biological expt. However, not all incinerators are suitable for this
purpose. The most efficient type ... is probably the gas-fired type, in which a
first-stage combustion with a less than stoichiometric air:fuel ratio is
followed by a second stage with excess air. Some ... are designed to accept ...
aqueous & organic-solvent solutions, otherwise it is necessary ... to absorb
soln onto suitable combustible material, such as sawdust. Alternatively, chem
destruction may be used, esp when small quantities ... are to be destroyed in
laboratory. /Chemical Carcinogens/
PRECAUTIONS FOR "CARCINOGENS": HEPA
(high-efficiency particulate arrestor) filters ... can be disposed of by
incineration. For spent charcoal filters, the adsorbed material can be stripped
off at high temp & carcinogenic wastes generated by this treatment conducted
to & burned in an incinerator. ... LIQUID WASTE: ... Disposal should be
carried out by incineration at temp that ... ensure complete combustion. SOLID
WASTE: Carcasses of lab animals, cage litter & misc solid wastes ... should
be disposed of by incineration at temp high enough to ensure destruction of chem
carcinogens or their metabolites. /Chemical Carcinogens/
PRECAUTIONS FOR "CARCINOGENS": ...
Small quantities of ... some carcinogens can be destroyed using chem reactions
... but no general rules can be given. ... As a general technique ... treatment
with sodium dichromate in strong sulfuric acid can be used. The time necessary
for destruction ... is seldom known ... but 1-2 days is generally considered
sufficient when freshly prepd reagent is used. ... Carcinogens that are easily
oxidizable can be destroyed with milder oxidative agents, such as saturated soln
of potassium permanganate in acetone, which appears to be a suitable agent for
destruction of hydrazines or of compounds containing isolated carbon-carbon
double bonds. Concn or 50% aqueous sodium hypochlorite can also be used as an
oxidizing agent. /Chemical Carcinogens/
PRECAUTIONS FOR "CARCINOGENS":
Carcinogens that are alkylating, arylating or acylating agents per se can be
destroyed by reaction with appropriate nucleophiles, such as water, hydroxyl
ions, ammonia, thiols & thiosulfate. The reactivity of various alkylating
agents varies greatly ... & is also influenced by sol of agent in the
reaction medium. To facilitate the complete reaction, it is suggested that the
agents be dissolved in ethanol or similar solvents. ... No method should be
applied ... until it has been thoroughly tested for its effectiveness &
safety on material to be inactivated. For example, in case of destruction of
alkylating agents, it is possible to detect residual compounds by reaction with
4(4-nitrobenzyl)-pyridine. /Chemical Carcinogens/
Occupational Exposure Standards:
OSHA Standards:
Permissible Exposure Limit: Table Z-1 8-hr
Time-Weighted Avg: 0.5 mg/cu m. Skin Designation.
Threshold Limit Values:
8 hr Time Weighted Avg (TWA): 0.5 mg/cu m,
skin
Excursion Limit Recommendation: Excursions in
worker exposure levels may exceed three times the TLV-TWA for no more than a
total of 30 min during a work day, and under no circumstances should they exceed
five times the TLV-TWA, provided that the TLV-TWA is not exceeded.
Biological Exposure Index (BEI): Determinant:
total pentachlorophenol in urine;
Sampling Time: prior to last shift of workweek; BEI: 2 mg/g creatinine. The
determinant may be present in biological specimens collected from subjects who
have not been occupationally exposed, at a concentration which could affect
interpretation of the result. Such background concentrations are incorporated in
the BEI value.
A3: Confirmed animal carcinogen with unknown
relevance to humans.
Biological Exposure Index (BEI): Determinant:
free pentachlorophenol in plasma;
Sampling Time: end of shift; BEI: 5 mg/l. The determinant may be present in
biological specimens collected from subjects who have not been occupationally
exposed, at a concentration which could affect interpretation of the result.
Such background concentrations are incorporated in the BEI value.
NIOSH Recommendations:
Recommended Exposure Limit: 10 Hr
Time-Weighted Avg: 0.5 mg/cu m, skin.
Immediately Dangerous to Life or Health:
2.5 mg/cu m
Manufacturing/Use Information:
Major Uses:
AS A MOLLUSCICIDE
TO INHIBIT FERMENTATION IN VARIOUS MATERIALS
Used as a preharvest defoliant on selected
crops /Former/
In various products, pentachlorophenol
has been used as a herbicide, algacide, defoliant, wood preservative, germicide,
fungicide, and molluscicide. As a wood preservative, it is commonly applied as a
0.1% solution in mineral spirits, NO 2 fuel oil, or kerosene. It is used in
pressure treatment of lumber at 5% concentration. Weed killers contain higher
concentrations. PCP is no longer available for over-the-counter sale in the USA.
Insecticide for termite control; pre-harvest
defoliant; general herbicide. Has been recommended for use in the preservation
of wood, wood products, starches, dextrins, glues.
The main commercial use of pentachlorophenol
is as a wood preservative...it is used as a fungicide to protect wood from
fungal decay and wood-boring insects...it is used as a pre-harvest defoliant in
cotton and as a general pre-emergence, non-selective contact herbicide...it has
been used as a bactericide in drilling fluids, as a fungicide in adhesives and
textiles and for slime control in pulp and paper manufacture...pentachlorophenol
has also been used to control the snails that are the hosts of schistosomiasis.
Pentachlorophenol
is used to control termites and, frequently, as an ester (such as
pentachlorophenyl laurate) to protect wood from fungal rots and wood-boring
insects, and as a general herbicide. The sodium salt is used as a general
disinfectant, e.g. for trays in mushroom houses.
Manufacturers:
Vulcan Materials Co, Hq, PO Box 530390,
Birmingham, AL 35253, (205) 877-3000; Vulcan Chemicals Group, PO Box 530390,
Birmingham, AL 35253; Production site: Wichita, KS 67277
Methods of Manufacturing:
Prepared by the chlorination of
2,4,5-trichlorophenol.
Pentachlorophenol
is produced commercially in the USA by direct chlorination of phenol with
chlorine gas in the presence of a catalyst at gradually rising temperatures up
to 200 deg C. Other contaminants formed in pentachlorophenol
production are isomers of hexa, hepta, and octachlorodibenzo-para-dioxin and
isomers of tetra, penta, hexa, hepta, and octachlorodibenzofuran.
Pentachlorophenol
is prepared either by catalytic chlorination of phenol or by alkaline hydrolysis
of hexachlorobenzene.
General Manufacturing Information:
Once used in tremendous volumes as an
insecticide and fungicide in preserving wood products, /pentachlorophenol/
is being phased out of use because of the discovery that many commercial
products were contaminated by polychlorinated dibenzodioxins and dibenzofurans,
predominantly by hexa-, hepta-, and octachlorinated congeners.
Formulations/Preparations:
The cmpd may be used alone or in combination
with other agents such as ... 2,4-dinitrophenol, sodium fluoride, the dichromate
salts, sodium arsenate, or arsenious oxide.
Grades or Purity: 86-100%.
Dowicide EC-7: Pentachlorophenol
88%; Other chemicals 12%.
Penta Concentrate contains 9.7 lbs/gal PCP
/Los Angeles Chemical Co/
Penta Ready contains
5.3% PCP /Los Angeles Chemical Co/
Penta WR contains
5.0% PCP /Los Angeles Chemical Co/
The formulated product is available as
granules, wettable powder and oil-miscible liquid...pentachlorophenol
is also formulated as blocks, pellets, prills, and concentrates.
For the treatment of wood in the USA, pentachlorophenol
is usually administered as a 5% solution in a mineral spirit solvent, such as
No. 2 fuel oil or kerosene, or in dichloromethane, isopropyl alcohol, or
methanol. Formulations may also contain co-solvents and anti-blooming agents.
Impurities:
Technical PCP has been reported to contain
chlorodiphenylethers, chlorodibenzo-p-dioxins, chlorodibenzofurans, and
hydroxychlorodiphenylethers; the octachlorodibenzo-p-dioxin content is typically
500-1500 ppm.
Fourteen technical pentachlorophenol
and three sodium pentachlorophenate samples were obtained from several
manufacturers and analyzed for various chlorinated phenolic impurities.
Reversed-phase liquid chromatography with an electrochemical (coulometric mode)
detector was used for qualitative and quantitative determinations.
2,4-Dichlorophenol, 3,5-dichlorophenol, 2,3,4-trichlorophenol,
2,4,6-trichlorophenol, 3,4,5-trichlorophenol, 2,3,5,6-tetrachlorophenol,
2,3,4,6-tetrachlorophenol, and 2,3,4,5-tetrachlorophenol were detected as
contaminants in the various samples.
Commercial pentachlorophenol
(PCP) contains significant quantities of tetrachlorophenol (TCP). The ratio of
PCP to TCP in Dowicide G-ST, a commercial PCP formulation, was 2.5 + or - 0.1.
COMMERCIAL GRADE PCP CONTAINS 88.4% PCP, 4.4%
TETRACHLOROPHENOL, 6.2% HIGHER-CHLORINATED PHENOXYPHENOLS, LESS THAN 0.1%
TRICHLOROPHENOL & VARIOUS DIBENZO-P-DIOXINS & DIBENZOFURANS. /SRP:
2,3,7,8-TETRACHLORODIBENZO-P-DIOXIN HAS NOT BEEN FOUND./
The identification of
2-bromo-3,4,5,6-tetrachlorophenol, a halogenated phenol, in commercial pentachlorophenol
samples is described. The concentration of the phenol impurity in the samples
was on the order of 0.1%.
... Pentachlorophenol
available after about 1973 contained only 1 ppm of the hexachloro- and 26 ppm of
the octachlordibenzo-p-dioxin.
Impurities in commercial pentachlorophenol
preparations are as follows: tetrachlorophenol, 4.4-10.2%; trichlorophenol, less
than or equal to 1%; chlorinated phenoxyphenols, 5-6.2%; octachlorodibenzodioxin,
5.5-3600 mg/kg; heptachlorodibenzodioxin, 0.6-520 mg/kg; hexachlorodibenzodioxin,
<0.03-100 mg/kg; octachlorodibenzofuran, <0.1-260 mg/kg;
heptachlorodibenzofuran, <0.1-400 mg/kg; hexachlorodibenzofuran, <0.03-90
mg/kg; pentachlorodibenzofuran, <0.03-40 mg/kg; and tetrachlorodibenzofuran
<0.02-0.45 mg/kg. In addition, chlorinated cyclohexenones and
cyclohexadienones, hexachlorobenzene and polychlorinated biphenyls are found.
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 hexachlorodibenzo-p-dioxin have been detected in
technical-grade pentachlorophenol. The
1,2,3,6,7,8- and 1,2,3,7,8,9-hexachlorodibenzo-p-dioxins predominated in
commercial samples of technical-grade pentachlorophenol
(Dowicide 7) and sodium pentachlorophenate. Octachlorodibenzo-p-dioxin is
present in relatively high amounts in unpurified technical-grade
2,3,7,8-Tetrachlorodibenzo-p-dioxin has been
confirmed only once in commercial pentachlorophenol
samples.
Consumption Patterns:
Wood Preservative, 90%; Sodium
Pentachlorophenate, 10% (1983)
In the USA, it was estimated that 97% of the pentachlorophenol
usage was as a wood preservative, 1% as a general herbicide and the remainder
for miscellaneous smaller applications.
U. S. Production:
(1975) 1.79X10+10 G
(1980) 2.12X10+10 G
2.04X10+10 g
Four manufacturers in the USA produced a total
of 18,000-23,000 tonnes of pentachlorophenol
annually from 1945 to 1978. Less than 14,000 tonnes were produced in 1980 by two
manufacturers. In 1987, about 12,000 tonnes were produced by the sole US
producer.
U. S. Imports:
(1980) 1.49X10+8 G
(1982) 5.47X10+7 G
(1983) 274,730 lb
U. S. Exports:
(1978) 1.11X10+9 G
(1983) 8.89X10+8 G
1.83X10+9 G
Laboratory Methods:
Clinical Laboratory Methods:
A method incorporating hydrolysis is essential
to relate pentachlorophenol urinary
excretion to absorbed dose. HPLC with a fixed wavelength detector at 313 nm was
used.
Chlorinated phenols in urine are ... detected
by electron-capture gas chromatography using a double support-bonded diethylene
glycol succinate column ... Avg recoveries of >80% were obtained.
/Chlorinated phenols/
DETECTED IN /NON-HUMAN/ MILK (5 UG/KG);
BIOLOGICAL TISSUE (0.1 UG/KG); HUMAN ADIPOSE TISSUE (5 UG/KG), PLASMA (20 UG/L),
BLOOD & URINE (10 UG/L) BY GAS CHROMATOGRAPHY FITTED WITH ELECTRON CAPTURE
DETECTION.
Negative chemical ionization mass spectrometry
has been used to examine a commercial pentachlorophenol
formulation in a series of environmental and human samples.
Pentachlorophenol
has been found to be present in human adipose tissue as an ester of palmitic
acid. Levels of pentachlorophenol in
human fat tissue range from 4-250 ppb. Current extraction procedures do not
hydrolyze the ester bond, eliminating pentachlorophenol
present in ester form. New procedures for extraction and simultaneous monitoring
of pentachlorophenol and
palmitoylpentachlorophenol or a procedure designed that would hydrolyze
palmitoylpentachlorophenol before extraction of pentachlorophenol
would accurately assess pentachlorophenol
exposure.
A GC method for determining pentachlorophenol
in biological fluids was developed. Samples analyzed were urine, water, serum,
or fish, tissue. Urine and water samples were digested at 100 deg C for 1 hr in
a sealed vial and later were extracted with toluene. Serum samples were
acidified and then digested and extracted as above. Fish tissue washomogenized,
acidified to pH 2, and rehomogenized; the emulsion was extracted with methylene
chloride, extracted with alkali, and finally with toluene and digested as above.
All samples were treated with an internal standard, diluted as appropriate, and
subjected to gas chromatography at 300 deg C using fused silica capillary
columns. Samples were injected at 1 microliter volume and detection of compounds
was facilitated by electron capture at 350 deg C. A calibration standard of pure
pentachlorophenol was run; the time of
chromatographic run was 1 hr. Good resolution was achieved. Concentrations as
low as 0.5 ppb wre detected by this method. The precision of the method was 1.2%
for pentachlorophenol. The upper limit
of detection was 200 ppb. Samples of water, urine, serum, and fish tissue
contained a detectable concentration. Corrections were made to compensate for
instrument drift. This method offers high sensitivity and precision for
examining pentachlorophenol.
A gas chromatographic procedure for
determining pentachlorophenol in blood
and urine was described. Two ml samples of urine and 10 ml samples of blood were
used. Theblood and urine samples were analyzed on a GC column fitted with a
(63)Ni electron capture detector.
NIOSH Method 230. Analyte: Pentachlorophenol.
Specimen: Urine. Procedure: Gas chromatography. For pentachlorophenol
this method has a working range from 20 to 180 ug for a 2 -ml urine sample. The
precision/RSD is 0.15 (est). Applicability: In urine. Interference: Chlorinated
or other electrophilic organic compounds having the same chromatographic
retention time as pentachlorophenol.
NIOSH Method 8303. Analyte: Pentachlorophenol.
Specimen: Urine end of shift, mid to late in work week. Procedure: Gas
chromatography, electron capture detector. For pentachlorophenol
this method has an estimated detection limit of 1 ug/l/sample. The presision/RSD
is 0.03 and the recovery is 0.947. The working range is 1 to 1000 ug/l for a
100-ml sample. Applicability: This method measures free and conjugated pentachlorophenol
after hydrolysis and is useful when monitoring chronic pentachlorophenol
exposure via skin contact, ingestion or inhalation. Urine contains about 82%
free pentachlorophenol and 13% pentachlorophenol
glucuronide. Interferences: Numerous potential interferences from urine include
chloronaphthylenes, polychlorinated biphenyls and diuron.
NIOSH Method 8001. Analyte: Pentachlorophenol.
Specimen: Whole blood in 5 ml tubes. Procedure: Gas chromatography, electron
capture detector. For pentrachlorophenol this method has an estimated detection
limit of 0.001 ug pentachlorophenol/ml
blood. The presision/RSD is 0.02 and the recovery is 90%. The working range is
0.01 to 1 ug pentachlorophenol/ml
blood for a 5-ml sample. Interferences: Chloronaphthalenes, polychlororinated
biphenyl and diuron are also hexane-extractable but are separated from pentachlorophenol
by column.
Analytic Laboratory Methods:
DETECTED IN RIVER & WASTE WATERS BY UV
& IR SPECTROPHOTOMETRY. DETECTED IN SEDIMENT, SEWAGE & SOIL BY GAS
CHROMATOGRAPHY WITH ELECTRON CAPTURE DETECTION.
Negative chemical ionization mass spectrometry
has been used to examine a commercial pentachlorophenol
formulation in a series of environmental and human samples.
PENTACHLOROPHENOL
WAS DETECTED IN WOOD SHAVINGS (10 UG/KG) BY GAS CHROMATOGRAPHY/ELECTRON CAPTURE
DETECTION. EXTRACTION/CLEANUP PROCEDURE: DIGEST (POTASSIUM HYDROXIDE), ACIDIFY,
STEAM DISTILL, EXTRACT (TOLUENE), ETHYLATE.
Product analysis is by titration with alkali.
Residues may be determined by colorimetry of derivatives.
EPA Method 3540. Soxhlet Extraction. A solid
sample is mixed with anhydrous sodium sulfate and extracted using an appropriate
solvent in a Soxhlet extractor. The sample is then dried and concentrated using
a Kuderna-Danish apparatus. This is a procedure for extracting nonvolatile and
semivolatile organic compounds from solids such as soils, sludges, and waste.
EPA Method 3550. Sonication Extraction. A 2-
to 3-g solid sample is mixed with anhydrous sodium sulfate to form a
free-flowing powder, then solvent extracted using a horn-type sonicator,
followed by vacuum filtration or centrifugation for organic components of equal
or less than 20 mg/kg. This method is applicable to the extraction of
nonvolatile and semivolatile organic compounds from solids such as soils,
sludges, and waste. Interferences include chlorofluorocarbons and methylene
chloride.
EPA Method 8040. Method for the determination
of phenols in solid waste by gas chromatography with flame ionization detection
(FID) or derivatization to pentafluorobenzyl- bromide (PFB) derivatives followed
by gas chromatography with electron capture detection (ECD). ECD is used to
reduce detection limits of some phenols and/or interferences. Under the
prescribed conditions for pentachlorophenol,
the method detection limit is 0.59 ug/l using FID and 7.4 ug/l using ECD.
Precision and method accuracy were found to be directly related to analyte
concentration and essentially independent of the sample matrix.
EPA Method 8250. Packed Column Gas
Chromatography/Mass Spectrometry Technique for the determination of semivolatile
organic compounds in extracts prepared from all types of solid waste matrices,
soil, and groundwater. This method is applicable to quantify most neutral,
acidic, and basic organic compounds that are soluble in methylene chloride and
capable of being eluted with derivatization as sharp peaks from a gas
chromatographic packed column. Under the prescribed conditions, pentachlorophenol
has a detection limit of 3.6 ug/l. Precision and method accuracy were found to
be directly related to the concentration of the analyte and essentially
independent of the sample matrix.
EPA Method 515. Capillary Column Gas
Chromatography with electron capture detection for the determination of
chlorinated herbicides in drinking water. For pentachlorophenol
the estimated detection limit is 0.0005 ug/l, and the method detection limit is
not given. Using the packed column, mean recovery is 63% with a standard
deviation of 11% with a spike level of 1.01 ug/l in reagent water. Using a
capillary column, mean recovery, standard deviation, and spike level are not
given.
Method 6420 B. Liquid - Liquid Extraction GC
with flame ionization detection or derivatization and ECD. The method is
applicable to the determination of a wide variety of phenols including pentachlorophenol.
The method detection limit is 7.4 ug/l using flame ionization detection and 0.59
ug/l using ECD.
Method 6420 C. Liquid - Liquid Extraction
GC/MS for the determination of phenols including pentachlorophenol
in water and wastewater. For pentachlorophenol
the method detection limit is 3.6 ug/l. Precision and method bias were found to
be related directly to the compound concentration and essentially independent of
the sample matrix.
EPA Method 604. GC Method with flame
ionization detection. This method is applicable for analysis of phenols
including pentachlorophenol in
municipal and industrial discharges. Under the prescribed conditions for pentachlorophenol,
the method has a detection limit of 7.4 ug/l. Precision and method accuracy were
found to be directly related to the concentration of the parameter and
essentially independent of the sample matrix.
EPA Method 625. GC/MS for the analysis of
acid/base/neutral extractables including pentachlorophenol
in municipal and industrial discharges. Under the prescribed conditions for pentachlorophenol,
the method has a detection limit of 3.6 ug/l. Precision and method accuracy were
found to be directly related to the concentration of the parameter and
essentially independent of the sample matrix. Interferences: PCBs.
EPA Method 1625. Isotope Dilution Capillary
Column GC/MS for the determination of semivolatile organic compounds in
municipal and industrial discharges. By adding a known amount of an isotopically
labeled compound to every sample prior to purging, a correction of recovery of
the pollutant can be made. If isotopically labeled compounds are not available,
an internal standard method is used. Under the prescribed conditions for both
the isotopically labeled and unlabeled pentachlorophenol,
the method has a minimum detection level of 50 ug/l.
EPA 8270. Capillary Column GC/MS. This method
is used for the determination of semivolatile organic compounds in extracts
prepared from all types of solid waste matrices, soils, and groundwater. This
method is applicable to quantify most acidic, basic, and neutral organic
compounds that are soluble in methylene chloride and are capable of being eluted
without derivatization as sharp peaks from a capillary column (DB-5 or
equivalent). The Practical Quantitation Limit for pentachlorophenol
is 50 ug/l in ground water and 3300 ug/kg in low soil/sediment. The precision
and a method accuracy were found to be directly related to the concentration of
the analyte and essentially independent of the sample matrix.
NIOSH Method 3297. Analyte: Pentachlorophenol.
Matrix: Air. Procedure: HPLC Method Evaluation: Method was validated over the
range of 0.2654 to 1.131 mg/cu m using a 190 l sample. Method detection limit:
Not given. Precision (CVT): 0.072. Interferences: No specific interferences.
Most of the analytical methods used today
involve acidification of the sample to convert pentachlorophenol
to its nonionized form, extraction into an organic solvent, possible cleaning by
back-extraction into a basic solution, and determination by gas chromatography
with ECD or other chromatographic methods as ester or ether derivatives.
Depending on sampling procedures and matrices, detection limits as low as 0.05
ug/cu m in air and 0.01 ug/L in water can be achieved.
AREAL Method IP-8. Determination of
Organochlorine Pesticides in Indoor Air. Range= 0.01 ug/cu m indoor air.
AREAL Method TO-10. Determination of
Organochlorine Pesticides In Ambient Air Using Low Volume Polyurethane Foam (PUF)
Sampling With Gas Chromatography/ Electron Capture Detector (GC/ECD).
CLP Method LC_SV. The Analysis of Water for
Low Concentration Semivolatile Organic Compounds by Gas Chromatography/Mass
Spectrometry. Contract required quantitation limit=20 ug/l.
CLP Method MC_SVOA. Analysis of Semivolatile
Organics in Multi- Concentration Water Samples by Gas Chromatography with a Mass
Spectrometer. Contract required quantitation limit= 20 ug/l.
EAD Method 1653. Chlorinated Phenolics in
Wastewater by In-situ Acetylation and GCMS. Method detection limit= 0.280 ug/l.
EMSLC Method 515.1. Determination of
Chlorinated Acids in Water by Gas Chromatography with an Electron Capture
Detector. Revision 4.0. Estimated detection limit= 0.076 ug/l.
EMSLC Method 525.1. Determination of Organic
Compounds in Drinking Water by Liquid-Solid Extraction and Capillary Column Gas
Chromatography and Mass Spectrometry. Revision 2.2. Method detection limit=0.30
ug/l.
EMSLC Method 555. Determination of Chlorinated
Acids in Water by High Performance Liquid Chromatography with a Photodiode Array
Ultraviolet Detector. Revision 1.0. Method detection limit= 1.6 ug/l.
NCASI Method CP-85.01. Determination of
Chlorinated Phenolics in Water by In-Situ Acetylation using Gas Chromatography
with Electron Capture Detection. Lower detection limit= 0.6 ug/l.
OSW Method 8151. Determination of Chlorinated
Herbicides by GC Using Methylation Or Pentafluorobenzylation Derivatization:
Capillary Column Technique. Estimated detection limit= 0.076 ug/l; 0.160 ug/kg
in soil/waste.
EAD Method 1625. Semivolatile Organic
Compounds by Isotope Dilution GCMS. Method detection limit= 210 ug/kg.
CLP Method MC_SVOA. Analysis of Semivolatile
Organics in Low Concentration Soil Samples by Gas Chromatography with a Mass
Spectrometer. Contract required quantitation limit= 830 ug/kg; 25000 ug/kg (for
medium concentrations).
EPA-B Method PMD-PCP. Determination of Pentachlorophenol
by High Performance Liquid Chromatography.
EPA-B Method PMD-PCP. Determination of Pentachlorophenol
by Gas Chromatography (FID-IS) Using On-Column Derivatization with MSFTA.
FDA Method 221.1. Method for Chlorophenoxy
Acids and Pentachlorophenol by Gas
Chromatography.
FDA Method 221.1. Method for Chlorophenoxy
Acids and Pentachlorophenol by Gas
Chromatography.
NIOSH Method 8001. Determination of Pentachlorophenol
in Blood by Gas Chromatography with Electron Capture Detection. Range= 0.01 ug/ml.
NIOSH Method 8303. Determination of Pentachlorophenol
in Urine by Gas Chromatography with Electron Capture Detection.
NIOSH Method 5512. Determination of Pentachlorophenol
by High Performance Liquid Chromatography with UV Detection. Detection limit=
0.010 ug/cu m.
AOAC Method 985.24. Pentachlorophenol
in Gelatin. Gas Chromatographic Method.
Sampling Procedures:
Commercially available air sampling tubes were
evaluated for personnel sampling of several pesticides. Commercial Chromosorb
102 sorbent air sample tubes designed into 66 and 33 mg portions separated by
either glass wool or polyurethane plugs were used.
This paper presents the analytical results of
personal breathing zone, area air, and surface wipe samples collected at a
typical pentachlorophenol
manufacturing plant. The personal breathing zone samples showed that workers
were exposed to hexachlorobenzene concentrations ranging from less than 0.0001
to 0.12 mg/cu m. Area air samples taken throughout the manufacturing plant
showed that hexachlorobenzene concentrations ranged from less than 0.0001 to
0.63 mg/cu m. Surface wipe samples showed contamination ranging from less than
0.1 to 3.7 micrograms/wipe.
EPA Method 8040. For the detection of phenolic
compounds, a representative sample (solid or liquid) is collected in a glass
container equipped with a Teflon-lined cap. Care is taken to avoid sample
contact with any plastic. Maximum sample holding time until extraction is 7
days, after extraction is 40 days.
NIOSH Method 5512. Analyte: Pentachlorophenol.
Matrix: Air. Sampler: Filter and bubbler (mixed cellulose ester membrane with
stainless steel backup screen/ethylene glycol). Flow Rate: 0.5 to 1.0 l/min:
Sample Size: 180 liters. Shipment: Place filter in bubbler containing 15 ml
ethylene glycol after sampling. Sample Stability: At least 8 days at 25 deg C.
NIOSH Method 230. Analyte: Pentachlorophenol.
Matrix: Urine. Procedure: Benzene extraction. Flow Rate: Not given. Sample Size:
2 ml.
NIOSH Method 5297. Analyte: Pentachlorophenol.
Matrix: Air. Procedure: Filter and bubbler collection, ethylene glycol,
extraction. Flow Rate: 1 to 5 l/min. Sample Size: 180 liters.
NIOSH Method 8303. Analyte: Pentachlorophenol.
Specimen: Urine end of shift mid to late in work week. Volume: 100 ml in
polyethylene bottle. Preservative: 2 to 3 drops concentrated hydrochloric acid
acid after collection. Shipment: Ship frozen in dry ice. Sample Stability: 40
days if kept frozen.
NIOSH Method 8001. Analyte: Pentachlorophenol.
Specimen: Whole blood in 5 ml tubes. Volume: 5 ml. Preservative: None. Shipment:
Polyethylene shippers with sample container kept at 10 deg C. Sample Stability:
Unknown.
Special References:
Special Reports:
ARSENAULT RD; PROC AM WOOD-PRESERV ASSOC 72:
122-48 (1976). REVIEW WITH 118 REFERENCES ON ENVIRONMENTAL FATE, INDUSTRIAL
SAFETY & RESP BREAKDOWN PRODUCTS OF PENTACHLOROPHENOL.
U.S. Dept of Int, Fish and Wildlife Serv;
Metabolism of Pesticides-Update III U.S. Dept Int Special Sci Report- Wildlife
No 232 (1980)
NRC ASSOC COMM SCI CRITERIA ENVIRON QUAL CAN;
CHLORINATED PHENOLS: CRITERIA FOR ENVIRONMENTAL QUALITY; NATL RES COUNC CAN
ASSOC COMM SCI CRITERIA ENVIRON QUAL PUBL, ISSUE (18578): 17-191 (1982)
USEPA; Pentachlorophenol
(Non-Wood Uses): Special Review Document No. 2/3 (1987) EPA/540/9-87/124
USEPA; Ambient Water Quality Criteria
Document: Pentachlorophenol (1986) EPA
440/5-86/009
O'Donoghue JL; Neurotox Ind Commer Chem 2:
139-53 (1985). A review with 157 references on the neurotoxicity of phenol, pentachlorophenol,
hexachlorophene, and 2,4-dichlorophenoxyacetic acid.
USEPA; Drinking Water Criteria Doc: Pentachlorophenol
(Final Draft) (1984) EPA/600/X-84/177-1
Exon JH; Vet Hum Toxicol 26 (6): 508-20
(1984). A review of chlorinated phenols.
NCI/DCE; Monograph on Human Exposure to
Chemicals in the Workplace: Pentachlorophenol.
SRC-TR-84-535 (1984) Contract N01-CP-26002-03. The report presents a summary and
evaluation of information relevant to an occupational hazard assessment of pentachlorophenol.
Grimm HG; VDI-Ber 609: 69-88 (1987). Review of
pentachlorophenol pollution along with
human exposure data.
Rosner G; Staub-Reinhalt Luft 47 (7-8):
198-203 (1987). A review of pentachlorophenol-dioxin
health hazards.
Choudhury H et al; Toxicol Indust Health 2
(4): 483-571 (1986). The Environmental Protection Agency (EPA) health and
environmental effects profile of pentachlorophenol
is presented. Physical and chemical properties of pentachlorophenol
are summarized. Production and uses of pentachlorophenol
are discussed. ...
Govt Reports Announcements & Index 15:
1-74 (1987) NTIS/PB87-859914. This bibliography contains citations concerning
laboratory and field studies regarding the toxicity of the pesticide pentachlorophenol.
Topics include dosage effects, uptake, bioaccumulation, and metabolism by
various organisms, detection methods, and synergistic effects with other harmful
compounds. Cases of human poisoning and occupational hazards associated with pentachlorophenol
are also treated.
Alberta Community & Occupat Health,
Medical Servics; Medical Monitoring of Workers Exposed to Pentachlorophenol
p.8 (12/86). This guideline is for the prevention of adverse effects and
includes /the following/: background on pentachlorophenol;
entry, metabolism and excretion; health effects; protective measures; health and
biological monitoring; treatment of pentachlorophenol
intoxication.
Govt Reports Announcements & Index 19:
1-64 (1987) NTIS/PB-87-863767. This bibliography contains citations concerning
toxicological studies of pentachlorophenol
and its effects on humans, aquatic and laboratory animals, and livestock. Topics
include pentachlorophenol
determination and analysis methods, pentachlorophenol
accumulation in animals, assessment and control of PCP contamination in waters
and soils, health risk assessment of pesticides and insecticides, and pentachlorophenol
degradation and decomposition techniques. Biochemical studies of occupational
exposure and clinical reports are included.
Govt Reports Announcements & Index 18:
1-38 (1987) NTIS/PB87-863528. This bibliography contains citations concerning
toxicology studies of pentachlorophenol
and its effects on humans, and aquatic and laboratory animals. Topics include pentachlorophenol
determination and analysis methods, water quality criteria, health risk
assessment of pentachlorophenol
pesticides and insecticides, human exposure in the workplace and hazard
assessment, and techniques of pentachlorophenol
degradation and destruction. Reports on pentachlorophenol
wood preservatives are also included.
Smejtek P; J Membr Sci 33 (2): 249-68 (1978).
A discussion and review ... on the membrane toxicity of pentachlorophenol,
a herbicide and wood preservative. Experimental data on membrane-pentachlorophenol
interactions from multiple studies were compared. These data include membrane
electroconductivity, toxicity, microelectrophoresis, and spectrophotometry.
DHHS/ATSDR; Toxicological Profille for Pentachlorophenol
(Update) (1994) ATSDR/TP-93/13
DHHS/NTP; Toxicology & Carcinogenesis
Studies of Two Pentachlorophenol
Technical Grade Mixtures in B6C3F1 (Feed Studies) Mice Technical Report Series
No. 349 (1989) NIH Publication No. 89-2804
Synonyms and Identifiers:
Related HSDB Records:
761
[PENTACHLOROPHENOL, SODIUM SALT]
(Analog)
2863
[PENTACHLOROBENZENE] (Analog)
Synonyms:
AI3-00134
**PEER REVIEWED**
Caswell No. 641
**PEER REVIEWED**
Chlon
**PEER REVIEWED**
DOWICIDE 7
**PEER REVIEWED**
Dowicide 7 Antimicrobial
**PEER REVIEWED**
Dowicide EC-7
**PEER REVIEWED**
Dura Treet II
**PEER REVIEWED**
EP 30
**PEER REVIEWED**
EPA Pesticide Chemical Code 063001
**PEER REVIEWED**
Forpen-50 Wood Preservative
**PEER REVIEWED**
FUNGIFEN
**PEER REVIEWED**
GRUNDIER ARBEZOL
**PEER REVIEWED**
LAUXTOL
**PEER REVIEWED**
LIROPREM
**PEER REVIEWED**
NCI-C55378
**PEER REVIEWED**
NCI-C56655
**PEER REVIEWED**
Ontrack WE Herbicide
**PEER REVIEWED**
Osmose Wood Preserving Compound
**PEER REVIEWED**
PCP
**PEER REVIEWED**
PENCHLOROL
**PEER REVIEWED**
Pentachlorphenol
(German)
**PEER REVIEWED**
Penta Concentrate
**PEER REVIEWED**
Penta Ready
**PEER REVIEWED**
Penta WR
**PEER REVIEWED**
PERMASAN
**PEER REVIEWED**
Santophen 20
**PEER REVIEWED**
Ortho Triox Liquid Vegetation Killer
**PEER REVIEWED**
Watershed Wood Preservative
**PEER REVIEWED**
Weed and Brush Killer
**PEER REVIEWED**
Woodtreat
**PEER REVIEWED**
Formulations/Preparations:
The cmpd may be used alone or in combination
with other agents such as ... 2,4-dinitrophenol, sodium fluoride, the dichromate
salts, sodium arsenate, or arsenious oxide.
Grades or Purity: 86-100%.
Dowicide EC-7: Pentachlorophenol
88%; Other chemicals 12%.
Penta Concentrate contains 9.7 lbs/gal PCP
/Los Angeles Chemical Co/
Penta Ready contains
5.3% PCP /Los Angeles Chemical Co/
Penta WR contains
5.0% PCP /Los Angeles Chemical Co/
The formulated product is available as
granules, wettable powder and oil-miscible liquid...pentachlorophenol
is also formulated as blocks, pellets, prills, and concentrates.
For the treatment of wood in the USA, pentachlorophenol
is usually administered as a 5% solution in a mineral spirit solvent, such as
No. 2 fuel oil or kerosene, or in dichloromethane, isopropyl alcohol, or
methanol. Formulations may also contain co-solvents and anti-blooming agents.
Shipping Name/ Number DOT/UN/NA/IMO:
UN 3155; Pentachlorophenol
IMO 6.0; PENTACHLOROPHENOL
UN 2761; Organochlorine pesticides, solid,
toxic, not otherwise specified (compounds & preparations)
UN 2762; Organochlorine pesticides, liquid,
flammable, toxic, not otherwise specified, flashpoint less than 23 deg C
(compounds & preparation)
UN 2995; Organochlorine pesticides, liquid,
toxic, flammable, not otherwise specified, flashpoint 23 deg C or more.
UN 2996; Organochlorine pesticides, liquid,
toxic, not otherwise specified.
IMO 3.0; Organochlorine pesticides, liquid,
flammable, toxic not otherwise specified, flashpoint less than 23 deg C.
IMO 6.1; Organochlorine pesticides, solid or
liquid, toxic, flammable, not otherwise specified, flashpoint 23 deg C or more.
Standard Transportation Number:
49 613 80; Pentachlorophenol
EPA Hazardous Waste Number:
D037; A waste containing pentachlorophenol
may or may not be characterized as a hazardous waste following testing by the
Toxicity Characteristic Leaching Procedure as prescribed by the Resource
Conservation and Recovery Act (RCRA) regulations.
F027; A hazardous waste from nonspecific
sources when a component of a discarded unused formulation.
Administrative Information:
Hazardous Substances Databank Number:
894
Last Revision Date: 20021108
Last Review Date: Reviewed by SRP on 5/7/1998
Update History:
Complete Update on 11/08/2002, 1 field
added/edited/deleted.
Complete Update on 10/16/2002, 13 fields added/edited/deleted.
Field Update on 01/14/2002, 1 field added/edited/deleted.
Complete Update on 08/09/2001, 1 field added/edited/deleted.
Complete Update on 05/16/2001, 1 field added/edited/deleted.
Complete Update on 01/31/2001, 2 fields added/edited/deleted.
Complete Update on 09/12/2000, 1 field added/edited/deleted.
Complete Update on 03/22/2000, 1 field added/edited/deleted.
Complete Update on 03/09/2000, 1 field added/edited/deleted.
Complete Update on 02/02/2000, 1 field added/edited/deleted.
Complete Update on 09/21/1999, 1 field added/edited/deleted.
Complete Update on 08/26/1999, 1 field added/edited/deleted.
Complete Update on 07/27/1999, 9 fields added/edited/deleted.
Complete Update on 03/29/1999, 1 field added/edited/deleted.
Complete Update on 01/27/1999, 1 field added/edited/deleted.
Complete Update on 11/12/1998, 2 fields added/edited/deleted.
Complete Update on 09/29/1998, 74 fields added/edited/deleted.
Field Update on 06/02/1998, 1 field added/edited/deleted.
Field Update on 02/25/1998, 1 field added/edited/deleted.
Complete Update on 10/20/1997, 1 field added/edited/deleted.
Complete Update on 09/17/1997, 1 field added/edited/deleted.
Complete Update on 09/16/1997, 4 fields added/edited/deleted.
Complete Update on 08/13/1997, 1 field added/edited/deleted.
Complete Update on 04/07/1997, 2 fields added/edited/deleted.
Complete Update on 02/28/1997, 1 field added/edited/deleted.
Complete Update on 02/25/1997, 1 field added/edited/deleted.
Complete Update on 06/06/1996, 2 fields added/edited/deleted.
Complete Update on 04/18/1996, 1 field added/edited/deleted.
Complete Update on 04/09/1996, 9 fields added/edited/deleted.
Field Update on 03/21/1996, 1 field added/edited/deleted.
Field Update on 01/19/1996, 1 field added/edited/deleted.
Complete Update on 12/08/1995, 1 field added/edited/deleted.
Complete Update on 10/19/1995, 1 field added/edited/deleted.
Complete Update on 01/23/1995, 1 field added/edited/deleted.
Complete Update on 12/22/1994, 1 field added/edited/deleted.
Complete Update on 11/18/1994, 1 field added/edited/deleted.
Complete Update on 11/04/1994, 1 field added/edited/deleted.
Complete Update on 09/08/1994, 2 fields added/edited/deleted.
Complete Update on 08/19/1994, 1 field added/edited/deleted.
Complete Update on 08/02/1994, 1 field added/edited/deleted.
Complete Update on 05/05/1994, 1 field added/edited/deleted.
Complete Update on 04/05/1994, 16 fields added/edited/deleted.
Field Update on 03/21/1994, 1 field added/edited/deleted.
Complete Update on 01/27/1994, 22 fields added/edited/deleted.
Complete Update on 09/15/1993, 84 fields added/edited/deleted.
Field Update on 08/20/1993, 1 field added/edited/deleted.
Field Update on 08/03/1993, 1 field added/edited/deleted.
Field update on 12/16/1992, 1 field added/edited/deleted.
Field Update on 11/27/1992, 1 field added/edited/deleted.
Field Update on 09/04/1992, 1 field added/edited/deleted.
Field Update on 09/04/1992, 1 field added/edited/deleted.
Field Update on 04/16/1992, 1 field added/edited/deleted.
Complete Update on 01/23/1992, 1 field added/edited/deleted.
Complete Update on 09/26/1991, 1 field added/edited/deleted.
Complete Update on 07/08/1991, 1 field added/edited/deleted.
Field update on 11/09/1990, 1 field added/edited/deleted.
Complete Update on 10/22/1990, 7 fields added/edited/deleted.
Field Update on 05/14/1990, 1 field added/edited/deleted.
Field Update on 03/06/1990, 1 field added/edited/deleted.
Field Update on 01/15/1990, 1 field added/edited/deleted.
Complete Update on 01/11/1990, 4 fields added/edited/deleted.
Complete Update on 04/03/1989, 101 fields added/edited/deleted.
Complete Update on 03/12/1987
GLCC
RELATED TOXIC SUBSTANCES FOUND IN THE CAMP POND AND CAMP WATER WELL 2003 AND
2004
GREAT LAKES CHEMICAL CORPORATION AND THE PATHFINDERS CAMP