Pentachlorophenol

Hazardous Air Pollutants (HAPs)

Other Classes -> Chlorophenols

Carcinogens

Chlorinated/Brominated phenol

Semi-Volatile Organic Compound (SVOC) and(or) Waste-water effluent contaminant

Pesticide -> EPA IRIS

Herbicides

Active substance -> EU Pesticides database: Not approved

Pesticide (Pentachlorophenol) -> USDA PDB

log Kow = 5.12

5.12

5.01

4.79

Phenolic odor

Very pungent odor, only when hot

Benzene-like odor

1.98 at 59 °F (USCG, 1999) - Denser than water; will sink

1.978 g/mL

DENSITY OF SATURATED AIR: 1.0000011 (AIR= 1); PERCENT IN SATURATED AIR: 0.0000145% BY VOLUME AT 20 °C; 1 MG/L IS EQUIVALENT TO 91.9 PPM & 1 PPM IS EQUIVALENT TO 0.01088 MG/L AT 25 °C

1.98 g/cm³

Relative density of the vapour/air-mixture at 20 °C (air = 1): 1.00

1.98

White monoclinic, crystalline solid

Needle-like crystals

Colorless to white crystalline solid

less than 1 mg/mL at 68 °F (NTP, 1992)

Slightly soluble in ligroin; very soluble in diethyl ether

Soluble in most organic solvents, for example acetone 215 g/L at 20 °C. Slightly soluble in ... parafins.

Sol in dilute alkali, carbitol, cellosolve

Solubilities (g/100 g of solution at 20 °C): 2 g in carbon tetrachloride; 8.5 in o-dichlorobenzene; 3.1 g in diesel oil; 32 in pine oil; 1.5 in Stoddard solvent

For more Solubility (Complete) data for Pentachlorophenol (7 total), please visit the HSDB record page.

Danger

H301: Toxic if swallowed [Danger Acute toxicity, oral]

P203, P260, P261, P262, P264, P264+P265, P270, P271, P273, P280, P284, P301+P316, P302+P352, P304+P340, P305+P351+P338, P316, P318, P319, P320, P321, P330, P332+P317, P337+P317, P361+P364, P362+P364, P391, P403+P233, P405, and P501 (click each P-code to see the statement)

Danger

H300 (33.3%): Fatal if swallowed [Danger Acute toxicity, oral]

P203, P260, P261, P262, P264, P264+P265, P270, P271, P273, P280, P284, P301+P316, P302+P352, P304+P340, P305+P351+P338, P316, P318, P319, P320, P321, P330, P332+P317, P337+P317, P361+P364, P362+P364, P391, P403+P233, P405, and P501 (click each P-code to see the statement)

Hazard Traits - Bioaccumulation; Carcinogenicity; Dermatotoxicity; Endocrine Toxicity; Environmental Persistence; Hematotoxicity; Hepatotoxicity and Digestive System Toxicity; Immunotoxicity; Nephrotoxicity and Other Toxicity to the Urinary System; Neurotoxicity; Respiratory Toxicity

2002/2076

Substance: Pentachlorophenol

The New Jersey Worker and Community Right to Know Act requires public and private employers to provide information about hazardous substances at their workplaces. (N.J.S.A. 34:5A-1 et. seq.)

Special Hazards of Combustion Products: Generates toxic and irritating vapors. (USCG, 1999)

· Non-combustible, substance itself does not burn but may decompose upon heating to produce corrosive and/or toxic fumes.

Not combustible. Liquid formulations containing organic solvents may be flammable.

Not combustible but if involved in a fire decomposes to produce hydrogen chloride and other irritants and toxic gases. May be in hydrocarbon solution.

Formulated products may be flammable.

Dust or vapor irritates skin and mucous membranes, causing coughing and sneezing. Ingestion causes loss of appetite, respiratory difficulties, anesthesia, sweating, coma. Overexposure can cause death. (USCG, 1999)

· TOXIC and/or CORROSIVE; inhalation, ingestion or skin contact with material may cause severe injury or death.

Pentachlorophenol is a manufactured chemical that does not occur naturally. Pure pentachlorophenol exists as colorless crystals. Impure pentachlorophenol (the form usually found at hazardous waste sites) is dark gray to brown and exists as dust, beads, or flakes. Humans are usually exposed to impure pentachlorophenol (also called technical grade pentachlorophenol). Pentachlorophenol was widely used as a pesticide and wood preservative. Since 1984, the purchase and use of pentachlorophenol has been restricted to certified applicators. It is no longer available to the general public. It is still used industrially as a wood preservative for utility poles, railroad ties, and wharf pilings.

Pentachlorophenol was once one of the most widely used biocides in the United States, but it is now a restricted use pesticide and is no longer available to the general public. It was primarily used as a wood preservative. Pentachlorophenol is extremely toxic to humans from acute (short-term) ingestion and inhalation exposure. Acute inhalation exposures in humans have resulted in neurological, blood, and liver effects, and eye irritation. Chronic (long-term) exposure to pentachlorophenol by inhalation in humans has resulted in effects on the respiratory tract, blood, kidney, liver, immune system, eyes, nose, and skin. Human studies are inconclusive regarding pentachlorophenol exposure and reproductive effects. Human studies suggest an association between exposure to pentachlorophenol and cancer. Oral animal studies have reported increases in liver tumors and two uncommon tumor types. EPA has classified pentachlorophenol as a Group B2, probable human carcinogen.

PCP causes the uncoupling of oxidative phosphorylation resulting in the release of cellular energy as heat. Technical grade PCP is contaminated with furans, dioxins, and other chlorinated congeners. Liver injury and mild and transient renal dysfunction associated with pentachlorophenol poisoning have been reported. [ATSDR Case Studies #23] In acute poisoning, PCP causes hyperpyrexia, vascular collapse, and acute renal failure. [LaDou, p. 417] PCP has caused chloracne in exposed workers. TLV Basis: Irritation (upper respiratory and eye); Impairment (CNS and cardiovascular); [ACGIH] Cases of aplastic anemia and leukemia were temporally associated with exposure to pentachlorophenol, but causality was not established. [EPA Pesticides] PCP was manufactured in the US from 1937 to 1980. Twenty percent of production workers developed chloracne as a result of high dioxin (TCDD) exposure. [PMID 19786897] See TCDD. PCP was classified by the Working Group as carcinogenic to humans (Group 1), based on sufficient evidence that PCP causes non-Hodgkin lymphoma in humans. In all of the available epidemiological studies, exposure to PCP was positively associated with non-Hodgkin lymphoma. [IARC, News Release, 24 October 2016]

3155 154

3155 154

Excerpt from ERG Guide 154 [Substances - Toxic and/or Corrosive (Non-Combustible)]:

In case of fire in the surroundings, use appropriate extinguishing media.

Fresh air, rest. Half-upright position. Artificial respiration may be needed. Refer for medical attention.

Remove contaminated clothes. Rinse and then wash skin with water and soap. Refer for medical attention . Wear protective gloves when administering first aid.

First rinse with plenty of water for several minutes (remove contact lenses if easily possible), then refer for medical attention.

Rinse mouth. Give a slurry of activated charcoal in water to drink. Give one or two glasses of water to drink. Refer for medical attention .

· CALL 911. Then call emergency response telephone number on shipping paper. If shipping paper not available or no answer, refer to appropriate telephone number listed on the inside back cover.

· ELIMINATE all ignition sources (no smoking, flares, sparks or flames) from immediate area.

EYES: First check the victim for contact lenses and remove if present. Flush victim's eyes with water or normal saline solution for 20 to 30 minutes while simultaneously calling a hospital or poison control center. Do not put any ointments, oils, or medication in the victim's eyes without specific instructions from a physician. IMMEDIATELY transport the victim after flushing eyes to a hospital even if no symptoms (such as redness or irritation) develop.

General First Aid:

(General first aid procedures)

· Wear positive pressure self-contained breathing apparatus (SCBA).

Biological Exposure Indices (BEI) [ACGIH] - PCP in urine (with hydrolysis) prior to last shift of workweek: Nq (Biological monitoring should be considered for this compound based on the review; however, a specific BEI could not be determined due to insufficient data.) [TLVs and BEIs]

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 surrounding fire using suitable agent. Approach fire from upwind to avoid hazardous vapors and toxic decomposition products. Use water spray to keep fire-exposed containers cool.

Where possible, automatically transfer material from drums or other storage containers to process containers. Sources of ignition such as smoking and open flames are prohibited where this chemical is handled, used, or stored. Metal containers involving the transfer of this chemical should be grounded and bonded. A regulated, marked area should be established where this chemical is handled, used or stored ...

Temperature: ambient.

Venting: open.

Store in cool, dry, well ventilated location. Separate from acids, alkalies, oxidizing materials, and other organic materials.

For more Storage Conditions (Complete) data for Pentachlorophenol (7 total), please visit the HSDB record page.

Shovel into suitable dry container.

1) Ventilate area of spill. 2) Collect spilled material in most convenient and safe manner and 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.

For more Cleanup Methods (Complete) data for Pentachlorophenol (8 total), please visit the HSDB record page.

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 °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.

For more Disposal Methods (Complete) data for Pentachlorophenol (11 total), please visit the HSDB record page.

Personal protection: chemical protection suit and filter respirator for organic gases and particulates adapted to the airborne concentration of the substance. Do NOT let this chemical enter the environment. Sweep spilled substance into covered sealable containers. If appropriate, moisten first to prevent dusting. Carefully collect remainder. Then store and dispose of according to local regulations.

Level of 15 ppb(1), 10-120 ppb in blood from users of pentachlorophenol-contaminated water were reported(2). Serum of 123 residents of pentachlorophenol-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 pentachlorophenol 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).

Urine of 118 residents of pentachlorophenol-treated log homes ranged from 1-340 ppb, 69 ppb mean, while 143 controls ranged from 1-7 ppb, mean 3.4 ppb(1). All urine samples from 197 Arkansas children contained pentachlorophenol(2). The median and max pentachlorophenol concn was 14 and 240 ppb. All 87 urine samples collected randomly in Saskatchewan, Canada, contained pentachlorophenol at concentrations 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)(3). A second study of 38 urine samples from "normal, healthy" humans living in Saskatchewan, Canada, reported pentachlorophenol concentrations from 0.1 to 3.6 ng/mL with an average concentration of 0.9 ng/mL and a median concentration of 0.5 ng/mL(3). Levels in samples of seminal fluid obtained from volunteer Florida State University students have been reported as 100-200 ppb(4) and in adipose tissue obtained from autopsy samples from the University of Florida at 250-500 ppb(4) and 23 ppb in autopsy samples taken in 10 women from Dade County, FL(5). 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(6).

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 approximately 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 concentrations in persons living in log homes and workers occupationally exposed to pentachlorophenol was conducted. The study group consisted of 35 persons exposed to pentachlorophenol in six workplaces and 123 persons living in 45 homes constructed of pentachlorophenol treated logs. The comparisons consisted of 143 persons living in conventional homes and not occupationally exposed to pentachlorophenol. Urine and blood samples were collected and analyzed for pentachlorophenol. Among the comparisons, urine pentachlorophenol 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 pentachlorophenol treated log homes, serum pentachlorophenol concentrations ranged from 69 to 1340 ppb, mean 420 ppb. The serum pentachlorophenol concns decreased with increasing age. Subjects in the 2 to 7 year old group had significantly higher serum pentachlorophenol concns than those over 15 years old. The serum pentachlorophenol 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 pentachlorophenol concentrations. Urine pentachlorophenol concns ranged from 1 to 340 ppb, mean 69 ppb. When the urine pentachlorophenol concns were corrected for creatinine concns, they correlated well with the serum pentachlorophenol concns. Serum pentachlorophenol concentrations in the pentachlorophenol workers ranged from 26 to 84900 ppb. The lowest concentrations occurred in workers constructing homes from pentachlorophenol treated logs and the highest in workers exposed to pentachlorophenol in chemical factories. Urine pentachlorophenol concentrations in four workers ranged from 2400 to 13800 ppb, mean 10000 ppb(1).

A mean concn of 12 ng/g pentachlorophenol was detected in Swedish human milk samples between 1984 and 1985(1). Milk from 10 to 20 Swedish women, from 1972 to 1989, contained pentachlorophenol at 0.0125 to 0.036 ug/g fat(2). Pentachlorophenol was detected at a median concn of 2 pg/g, ranging from 10-570 pg/g, in 15 Swedish mothers between 2000 and 2001(3). Bavaria, Germany - 0.03-2.83 ppb - 21 donors(4). Pentachlorophenol concentration in 90 maternal serum samples from The Netherlands ranged from 300 to 8500 pg/g serum, fresh weight basis, with a median concentration of 970 pg/g. The concentration in chord serum was 420 to 1900 pg/g serum, fresh weight basis, with a median concentration of 1500 pg/g serum(5).

If the compound has been ingested, rapid gastric lavage should be performed using 5% sodium bicarbonate. For skin contact, the skin should be washed with soap and water. If the compound has entered the eyes, they should be washed with large quantities of isotonic saline or water. In serious cases, atropine and/or pralidoxime should be administered. Anti-cholinergic drugs work to counteract the effects of excess acetylcholine and reactivate AChE. Atropine can be used as an antidote in conjunction with pralidoxime or other pyridinium oximes (such as trimedoxime or obidoxime), though the use of '-oximes' has been found to be of no benefit, or possibly harmful, in at least two meta-analyses. Atropine is a muscarinic antagonist, and thus blocks the action of acetylcholine peripherally.

Investigation of the toxicological effects of pentachlorophenol (PCP) and bisphenol A (BPA) alone and in combination was carried out following the method of the early life stage (ELS) test on zebrafish embryos. Both chemicals revealed lethal and sub-lethal effects, such as no blood flow, cardiac edema, delayed hatching, and tail malformations. According to their median effective concentrations (EC(50) values) in the single exposure, the toxic level of PCP was about two orders of magnitude higher than that of BPA. Result of the joint action modes varied depending on different endpoints. Synergistic action was observed based on the endpoint of 24 hr mortality and antagonistic effect displayed based on the endpoint of 72 hr cardiac edema. It was also found that the toxicity of PCP would be enhanced with the addition of BPA even below its no observed effect concentration (NOEC) level at the endpoint of 32 hr with no blood flow, and the level of the increase was influenced by the toxic unit (TU) ratio.

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.

For more Interactions (Complete) data for Pentachlorophenol (6 total), please visit the HSDB record page.

Cancer, Developmental (effects during periods when organs are developing) , Hepatic (Liver)

Hepatic

Eyes, skin, respiratory system, cardiovascular system, liver, kidneys, central nervous system

Acute exposure to cholinesterase inhibitors can cause a cholinergic crisis characterized by severe nausea/vomiting, salivation, sweating, bradycardia, hypotension, collapse, and convulsions. Increasing muscle weakness is a possibility and may result in death if respiratory muscles are involved. Accumulation of ACh at motor nerves causes overstimulation of nicotinic expression at the neuromuscular junction. When this occurs symptoms such as muscle weakness, fatigue, muscle cramps, fasciculation, and paralysis can be seen. When there is an accumulation of ACh at autonomic ganglia this causes overstimulation of nicotinic expression in the sympathetic system. Symptoms associated with this are hypertension, and hypoglycemia. Overstimulation of nicotinic acetylcholine receptors in the central nervous system, due to accumulation of ACh, results in anxiety, headache, convulsions, ataxia, depression of respiration and circulation, tremor, general weakness, and potentially coma. When there is expression of muscarinic overstimulation due to excess acetylcholine at muscarinic acetylcholine receptors symptoms of visual disturbances, tightness in chest, wheezing due to bronchoconstriction, increased bronchial secretions, increased salivation, lacrimation, sweating, peristalsis, and urination can occur. Certain reproductive effects in fertility, growth, and development for males and females have been linked specifically to organophosphate pesticide exposure. Most of the research on reproductive effects has been conducted on farmers working with pesticides and insecticdes in rural areas. In females menstrual cycle disturbances, longer pregnancies, spontaneous abortions, stillbirths, and some developmental effects in offspring have been linked to organophosphate pesticide exposure. Prenatal exposure has been linked to impaired fetal growth and development. Neurotoxic effects have also been linked to poisoning with OP pesticides causing four neurotoxic effects in humans: cholinergic syndrome, intermediate syndrome, organophosphate-induced delayed polyneuropathy (OPIDP), and chronic organophosphate-induced neuropsychiatric disorder (COPIND). These syndromes result after acute and chronic exposure to OP pesticides.

LC50; Species: Anas platyrhychos (Mallard duck, 10 day old) oral (5-day diet) approx 4500 ppm

LC50; Species: Anas platyrynchus (Mallard duck) diet 3763 ppm for 5 days /88.9% ai/

LD50; Species: Anas platyrhynchos (Mallard, 3 month old female) oral 380 mg/kg (mean)

LD50; Species: Colinus virginianus (Bobwhite quail) oral 627 mg/kg /88.0% ai/

For more Ecotoxicity Values (Complete) data for Pentachlorophenol (181 total), please visit the HSDB record page.

TERRESTRIAL FATE: Based on a classification scheme(1), Koc values ranging from 1250 for the dissociated form to 25,000 for the undissociated form(2), indicate that pentachlorophenol is expected to have low to no mobility in soil(SRC). The pKa of pentachlorophenol is 4.70(3), indicating that this compound will almost entirely exist in the anion form in the environment and anions generally do not adsorb more strongly to soils containing organic carbon and clay than their neutral counterparts(4). Volatilization from moist soil is not expected because the acid exists as an anion and anions do not volatilize. Pentachlorophenol is not expected to volatilize from dry soil surfaces(SRC) based upon a vapor pressure of 1.1X10-4 mm Hg at 25 °C(5). As much as 55% of added pentachlorophenol was photodegraded in a sandy clay loam soil in 14 days(6), suggesting the photolysis of the dissociated form may be an important terrestrial fate process(SRC). Screening biodegradability tests give conflicting results(7-13); pentachlorophenol does biodegrade but may require several weeks for acclimation(SRC).

AQUATIC FATE: Based on a classification scheme(1), Koc values ranging from 1250 for the dissociated form to 25,000 for the undissociated form(2), indicate that pentachlorophenol is expected to adsorb to suspended solids and sediment in water(SRC). A pKa of 4.70(3) indicates pentachlorophenol will exist almost entirely in the anion form at pH values of 5 to 9 and therefore volatilization from water surfaces is not expected to be an important fate process(4). According to a classification scheme(5), measured BCF values of 5(6) to 5370(7), suggest that bioconcentration in aquatic organisms is low to very high(SRC), with the value being greatly influenced by environmental pH(8). Pentachlorophenol has a pH-dependent absorption max of 303 nm(9) and will rapidly photodegrade in surface water when exposed to direct sun light(10); a measured half-life for the photolysis in solution has been reported to be 0.86 hrs(11). Screening biodegradability tests give conflicting results(12-18); pentachlorophenol does biodegrade but may require several weeks for acclimation(SRC).

AQUATIC FATE: 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 concns 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 concn 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 concn of pentachlorophenol) increased with increasing pentachlorophenol input, which was explicable by an increase in the pentachlorophenol degrader population with increasing pentachlorophenol concn. 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.

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 20 °C(2), should exist almost entirely in vapor phase 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(SRC), calculated from its rate constant of 0.55X10-12 cu cm/molecule-sec at 25 °C(SRC) that was derived using a structure estimation method(3). Pentachlorophenol has a pH-dependent absorption max of 303 nm(4) and therefore may be susceptible to direct photolysis by sunlight.

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(1).

The substance can be absorbed into the body by inhalation, through the skin and by ingestion.

inhalation, skin absorption, ingestion, skin and/or eye contact

Oral (L127) ; inhalation (L127) ; dermal (L127)

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. (This listing does not include formulations containing Hexachlorophene sythesized from prepurified 2,4,5-trichlorophenol as the sole component.)

EPA has previously identified and required the submission of the generic (i.e., active ingredient-specific) data required to support reregistration of wood preservative products containing pentachlorophenol as an active ingredient. The Agency has reviewed these generic data, and has determined that the data are sufficient to support a reregistration eligibility decision for the wood preservative uses of pentachlorophenol (see Appendix B). EPA considered the available information and, after a thorough evaluation of the risks and benefits associated with each use, has determined that the wood preservative uses of pentachlorophenol presented in Appendix A will not pose unreasonable risks to humans or the environment provided that (1) all risk mitigation measures are implemented, (2) label amendments are made as described in Section V, and (3) confirmatory data requirements are satisfied. Accordingly, should a registrant fail to implement any of the conditions and requirements for reregistration identified in this document, the Agency may take regulatory action to address the potential risk concerns from the use of pentachlorophenol.

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.

Criteria of concern: oncogenicity, mutagenicity, and teratogenicity. Action: In order to avoid cancellation, 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.

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 continued use. Under this pesticide reregistration program, EPA examines newer health and safety data for pesticide active ingredients initially registered before November 1, 1984, and determines whether the use of the pesticide does not pose unreasonable risk in accordance to newer saftey standards, such as those described in the Food Quality Protection Act of 1996. Pesticides for which EPA had not issued Registration Standards prior to the effective date of FIFRA '88 were divided into three lists based upon their potential for human exposure and other factors, with List B containing pesticides of greater concern than those on List C, and with List C containing pesticides of greater concern than those on List D. 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 RED /Reregistration Eligibility Decision/ 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 have made commitments to conduct the studies and pay the fees required for reregistration, and are meeting those commitments in a timely manner.

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.

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. The rule for determining when notification is required is stated in 40 CFR 302.4 (section IV.D.3.b).

Toxic pollutant designated pursuant to section 307(a)(1) of the Federal Water Pollution Control Act and is subject to effluent limitations.

Pentachlorophenol is 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. This designation includes any isomers and hydrates, as well as any solutions and mixtures containing this substance.

(AZ) ARIZONA 220 ug/L

(ME) MAINE 3 ug/L

(MN) MINNESOTA 1 ug/L

Maximum contaminant levels (MCL) for synthetic organic contaminants apply to community water systems and non-transient, non-community water systems: Pentachlorophenol, MCL 0.001 mg/L.

EPA 1 ug/L

As with other chlorophenols, the biochemical action of pentachlorophenol is active uncoupling of oxidative phosphorylation. The molecular basis for this is not clear. PCP binds to mitochondrial protein and inhibits mitochondrial ATP-ase activity. Thus, both the formation of ATP and the release of energy to the cell from the breakdown of ATP to ADP are prevented. Electron transport is not inhibited by PCP, although reactions dependent on available high-energy bonds, such as oxidative and glycolytic phosphorylation, are affected. Binding to enzymic protein has been reported and may lead to the inhibition of other cellular enzymes. There is an increase in cellular oxygen demand during the uncoupling of oxidative phosphorylation. This causes the initial rise in respiration rate reported in individuals poisoned by PCP. PCP is toxic to the liver, kidneys, and central nervous system. The toxicity of PCP is increased by impurities in some formulations. In some instances, it is very difficult to know whether the impurities have affected the poisoning. Dermatitis and chloracne are caused by contaminants such as PCDDs and PCDFs.

... Acute exposure of rat cerebellar granule neurons (CGNs) to uM concn of pentachlorophenol (PCP) induced the transcriptional activity of genes related to the classical apoptosis pathway (caspase 3, caspase 8, Bad), oxidative stress and glutathione metabolism (glutathione peroxidase-1, catalase, glutathione-S-transferase-3 and superoxide dismutase-1), and mitogenic response (cyclin D1, cdk2, cdk4, cdkn2b). Results from Western blot also shown /significant/ increases in the expression of cyclins D1, E and A and cdk4. The mitogenic response was also related to a /significant/ increase in the phosphorylation of retinoblastoma protein (Rb). PCP would cause apoptosis up-regulating the transcriptional activity of p53 gene and also increasing their activation by phosphorylation, concomitant with a decrease in the sirtuin 1 content. In conclusion, acute exposure of CGNs to PCP induces the classical p53 apoptotic pathway, promotes the up-regulation of several genes related to oxidative stress and the over-expression of molecules involved in the cell cycle control.

Chlorophenols and their derivatives are a major component of environmental pollutants that are potential immunotoxicants. Deaminase assay performed on peripheral blood mononuclear cells (PBMCs) exposed to chlorophenolic compounds and its derivatives demonstrated a decreased proliferation rate and cell death. Chlorophenolic exposure also led to impaired production of IL-21 and IL-9 along with many other cytokines and chemokines that potentiate the inflammatory response. Using the PBMC activation model and gene expression profiling provide insights into mechanisms by which the chlorophenolic compounds and their derivatives, especially pentachlorophenol (PCP) dysregulate the inflammatory response. PCP represses IL21 and IL9 expression thus affecting various downstream signaling pathways. /It was proposed/ that PCP ... imparts its cytotoxicity by evading the immune response by simultaneously affecting multiple signaling pathways in lymphocytes.

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 at the mitochondrial /membrane/, cells continue to respire but soon are depleted of ATP necessary for growth. /Chlorophenols/

For more Mechanism of Action (Complete) data for Pentachlorophenol (9 total), please visit the HSDB record page.

Median half-life is about 15 days; Urine concentrations reach a steady state after several months in the workplace. [TLVs and BEIs]

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).

For more Biological Half-Life (Complete) data for Pentachlorophenol (8 total), please visit the HSDB record page.

... 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 and in vitro in rat to tetra- and tri-chlorohydroquinone ... Dechlorination is mediated by liver-microsomal enzymes, and 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 and 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 and Cephaloascus fragrans.

For more Metabolism/Metabolites (Complete) data for Pentachlorophenol (13 total), please visit the HSDB record page.

Pentachlorophenol is a known human metabolite of pentachlorobenzene and HEXACHLOROBENZENE.

Substances or energies, for example heat or light, which when introduced into the air, water, or land threaten life or health of individuals or ECOSYSTEMS.

Compounds or agents that combine with an enzyme in such a manner as to prevent the normal substrate-enzyme combination and the catalytic reaction.

Pesticides used to destroy unwanted vegetation, especially various types of weeds, grasses (POACEAE), and woody plants. Some plants develop HERBICIDE RESISTANCE.

Pesticides designed to control insects that are harmful to man. The insects may be directly harmful, as those acting as disease vectors, or indirectly harmful, as destroyers of crops, food products, or textile fabrics.

Chemicals used to destroy pests of any sort. The concept includes fungicides (FUNGICIDES, INDUSTRIAL); INSECTICIDES; RODENTICIDES; etc.

Substances which, when ingested, inhaled, or absorbed, or when applied to, injected into, or developed within the body in relatively small amounts may, by their chemical action, cause damage to structure or disturbance of function. (From Dorland, 27th ed)

The aim of the present study was to understand the placental transfer of polychlorinated biphenyls (PCBs), specific hydroxylated PCB metabolites (OH-PCBs), and pentachlorophenol (PCP) in blood serum, in a birth cohort from eastern Slovakia. During the period 2002-2004, cord blood specimens were collected in parallel with maternal specimens from women delivering in the two eastern Slovak districts of Michalovce and Svidnik/Stropkov. A total of 92 pairs of mother-cord specimens at delivery were selected for this study. 4-OH-CB107, 3-OH-CB153, 4-OH-CB146, 3'-OH-CB138, 4-OH-CB187, and 4'-OH-CB172 were quantified. The median concentrations of Sigma(17)PCBs, Sigma(6)OH-PCBs, and PCP in cord serum were 0.92, 0.33, and 0.69 ng/g wet wt, respectively, and highly correlated with the corresponding maternal serum levels (correlations were R(2) = 0.61, 0.78, and 0.82, respectively). The median cord to mother ratios of the Sigma(17)PCBs, Sigma(6)OH-PCBs, and PCP were 0.18, 0.75, and 1.10, respectively. The median ratio of the Sigma(6)OH-PCBs to the Sigma(17) PCBs in the cord serum was 0.38 from wet wt based concn, which was about four times higher than the ratio of these compounds in maternal serum (0.09). PCP was more abundant than any PCB or OH-PCB congener measured in cord serum. The higher cord to maternal ratios of OH-PCB metabolites as compared with the parent cmpd suggests either a higher placental transfer rate or greater metabolism in the fetus as compared with the maternal compartment. These findings are consistent with their preferential binding to TTR that can cross the placenta. The cord to maternal ratio varies by congener (e.g., 4-OH-CB107 = 0.58, 4-OH-CB146 = 0.74, 3'-OH-CB138 = 1.01).

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 month period, serum and urine levels ... were 348.4 to 3963 ug/L and 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; and only trace (0.05%), in expired air. High activity observed in gallbladder and its contents, wall of stomach fundus, contents of GI tract, and liver.

For more Absorption, Distribution and Excretion (Complete) data for Pentachlorophenol (22 total), please visit the HSDB record page.

Pentachlorophenol was once one of the most widely used biocides in the United States, but it is now a restricted use pesticide and is no longer available to the general public.

Used as an industrial wood preservative for power-line poles, cross arms, fence posts, railroad ties, and wharf pilings; no longer used to treat wood products for log homes, outdoor furniture, or playground equipment; registered by EPA as a restricted-use pesticide since 1984; no longer registered for use as a pesticide (termiticide), fungicide, herbicide, molluscicide, disinfectant, or paint anti-fouling agent; it's use as a slimicide in cooling towers is being phased out; non-wood uses account for less than 2% of US consumption; PCP is manufactured at only one facility in the US (Wichita, Kansas). [ATSDR ToxProfiles] Production in the US ended in 1992; [ACGIH]

In 1987, EPA restricted the use of PCP to certified applicators.

Pulp and Paper Processing [Category: Industry]

Woodworking [Category: Hobbies]

For pentachlorophenol (USEPA/OPP Pesticide Code: 063001) ACTIVE products with label matches. /SRP: Registered for use in the U.S. but approved pesticide uses may change periodically and so federal, state and local authorities must be consulted for currently approved uses./

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.

Pentachlorophenol ... contains chlorinated dibenzodioxins and chlorinated dibenzofurans (CDDs and CDFs) and hexachlorobenzene (HCB) as contaminants formed during the manufacture process. However, pentachlorophenol is only one of many sources of CDDs, CDFs, and HCB in the environment making it difficult to quantify the portion of the aggregate environmental risk from CDDs, CDFs, and HCB that is attributable to pentachlorophenol ... CDDs and CDFs have been identified as micro-contaminants in technical grade pentachlorophenol. CDDs and CDFs have been found throughout the world at low concentrations in air, soil, water, sediment, fish and shellfish, and other food products such as meat and dairy products. CDDs and CDFs are members of a family of polychlorinated isomers of "dioxin-like" compounds. Physical and chemical properties and toxicity vary with the degree of chlorination. The most toxic congener of the family is 2,3,7,8-tetrachlorodibenzo-p-dioxin (2,3,7,8-TCDD). The dioxin/furan contaminants of pentachlorophenol present a unique case for purposes of risk characterization. Up to 17 CDD/CDF congeners are produced as contaminants in the manufacture of technical grade pentachlorophenol. All of these contaminants have chlorine substitution in at least the 2,3,7, and 8 positions, thus imparting these contaminants with "dioxin like" activity. Thus, all must be considered in the risk assessment for the contaminants of pentachlorophenol. HCB has also been identified as a micro-contaminant in technical grade pentachlorophenol, and is not a naturally occurring compound. It is present in the environment through emissions into the atmosphere due to the manufacture of PCP and numerous emission processes, industrial discharge of HCB containing wastes into waterways as well as due to the manufacturing processes of some pesticides. Since HCB is a micro-contaminant in technical grade pentachlorophenol, it must also be considered in the risk assessment for the contaminants of pentachlorophenol.

For more Impurities (Complete) data for Pentachlorophenol (9 total), please visit the HSDB record page.

(1978) 1.11X10+9 G

(1983) 8.89X10+8 G

1.83X10+9 G

(1980) 1.49X10+8 G

(1982) 5.47X10+7 G

(1983) 274,730 lb

(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 tons of pentachlorophenol annually from 1945 to 1978. Less than 14,000 tons were produced in 1980 by two manufacturers. In 1987, about 12,000 tons were produced by the sole US producer.

World production of PCP is estimated to be of the order of 30 000 tons per year (1989).

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.

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 °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.

PCP can be obtained either from phenol by direct chlorination or from hexachlorobenzene by hydrolysis. Direct chlorination requires two steps: Chlorine gas is bubbled through liquid phenol, chlorophenol, or polychlorophenol at 30 - 40 °C to produce 2,4,6-trichlorophenol, which is then converted to PCP by further chlorination at a higher temperature in the presence of a catalyst, e.g., aluminum).The other method involves alkaline hydrolysis of hexachlorobenzene in methanol and dihydric alcohols, water, and solvents at 130 - 170 °C. A number of (very) toxic byproducts are produced in small quantities during the synthesis (e.g., polychlorinated dibenzofurans, chlorinated dibenzo-p-dioxins). This has led to severe restriction in the use of this compound in Western countries.

Chlorination of phenol.

Penta 5 Sure-Treat Wood Preserver: Active Ingredient 4.3% Pentachlorophenol

Pentacon-7: Active Ingredient 6.27% Pentachlorophenol

KMG-B Penta OL Technical Pentachlorophenol, Vulcan Glazd Penta: Active Ingredient 86.0% Pentachlorophenol

Pentacon-10: Active Ingredient 8.96% Pentachlorophenol

For more Formulations/Preparations (Complete) data for Pentachlorophenol (67 total), please visit the HSDB record page.

Chemical Classes -> Nitrosamines/ethers/alcohols, Pesticides (chemicals used for killing pests, such as rodents, insects, or plants), Phenols/phenoxy acids

Pharmaceuticals

HERBICIDES

ANTIMICROBIAL AGENTS

Phenol, 2,3,4,5,6-pentachloro-: ACTIVE

The WHO Recommended Classification of Pesticides by Hazard identifies Pentachlorophenol (technical grade) as Class IB: highly hazardous; Main Use: insecticide; fungicide, other than for seed treatment; herbicide. According to the PIC /Prior Informed Consent/ Convention, export of /pentachlorophenol/ can only take place with the prior informed consent of the importing Party ... (further information can be found at : http://www.pic.int/)..

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.

Currently, there are six products containing pentachlorophenol as an active ingredient. ... Indoor applications are prohibited. ... restricted use pesticide for sale and use by certified applicators only.

Previously, PCP was widely used as a herbicide, defoliant, and preharvest desiccant. However, as PCP is not a very specific herbicide in terms of inhibiting special target species ..., non-target crop and wildlife species can also be adversely affected, though no data are available in this respect.

For more General Manufacturing Information (Complete) data for Pentachlorophenol (7 total), please visit the HSDB record page.