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PubMedDate not supplied

Hycrest crested wheatgrass accelerates the degradation of pentachlorophenol in soil.

We investigated the effects of vegetation on the fate of pentachlorophenol (PCP) in soil using a novel high-flow sealed test system. Pentachlorophenol has been widely used as a wood preservative, and this highly toxic biocide contaminates soil and ground water at many sites. Although plants are known to accelerate the rates of degradation of certain soil contaminants, this approach has not been thoroughly investigated for PCP. The fate of [14C]PCP, added to soil at a concentration of 100 mg/kg, was compared in three unplanted and three planted systems. The plant used was Hycrest, a perennial, drought-tolerant cultivar of crested wheatgrass [Agropyron desertorum (Fischer ex Link) Schultes]. The flow-through test system allowed us to maintain a budget for 14C-label as well as monitor mineralization (breakdown to 14CO2) and volatilization of the test compound in a 155-d trial. In the unplanted systems, an average of 88% of the total radiolabel remained in the soil and leachate and only 6% was mineralized. In the planted system, 33% of the radiolabel remained in the soil plus leachate, 22% was mineralized, and 36% was associated with plant tissue (21% with the root fraction and 15% with shoots). Mineralization rates were 23.1 mg PCP mineralized kg-1 soil in 20 wk in the planted system, and for the unplanted system 6.6 mg PCP kg-1 soil for the same time period. Similar amounts of volatile organic material were generated in the two systems (1.5%). Results indicated that establishing crested wheatgrass on PCP-contaminated surface soils may accelerate the removal of the contaminant.

Biodegradation, Environmental↗
PubMed1985

Assessment of pentachlorophenol toxicity in newborn calves: clinicopathology and tissue residues.

Newborn Holstein bull calves were fed either analytical pentachlorophenol (aPCP) or technical pentachlorophenol (tPCP) for 6 wk to establish and compare the clinical and pathologic manifestations of toxicity. Four groups of three calves/group were each fed either 1 or 10 mg X (kg body weight)-1 X d-1 of either aPCP or tPCP. A fifth group served as control. Dosages of both PCP preparations were normalized to contain equal concentrations of PCP. Toxic effects were observed only at the 10 mg/kg dose in the tPCP-treated calves. These effects included decreased body weight gain, anorexia, decreased serum protein concentration, elevated serum gamma glutamyl transferase, and decreased triiodothyronine (T3) and thyroxine (T4) concentrations. Histologic lesions included cortical atrophy in the thymus and squamous metaplasia and hyperkeratous changes in the Meibomian gland of the eyelid. Thyroid function, which was assessed in vivo by measuring the rate of T3 and T4 production over 4 h after thyrotropin-releasing hormone (TRH)-challenge, was not impaired suggesting an extrathyroidal site of toxic action. Although serum chemistry indicators were suggestive of hepatic injury there were no discernable lesions. Organ weight analyses were inconclusive but there was a tendency toward enlargement of liver, kidneys and thyroid and decreased weight of lungs, spleen and thymus. A toxic effect clearly related to PCP and not its contaminants was depressed active transport of p-aminohippurate measured in kidney slices in vitro. Steady state concentrations of PCP in serum were about 40 and 90 ppm for the 1 and 10 mg/kg groups, respectively. Concentrations of PCP among the major organs were comparable.

Animals↗
PubMed1978

A pharmacokinetic study of pentachlorophenol poisoning and the effect of forced diuresis.

A pharmacokinetic study of an intentional pentachlorophenol ingestion by an elderly human has been undertaken. Information on the presence or absence of forced diuresis either continuously or for a short restricted period indicates that such treatment would materially reduce the body burden of pentachlorophenol. It is suggested that forced diuresis is the treatment of preference for such intoxication at this time.

Chlorophenols↗
PubMed1978

Effect of technical grade pentachlorophenol on rumen microorganisms.

The toxicity of technical grade pentachlorophenol to rumen microorganisms was tested by an in vitro fermentation procedure. Rumen fluid was collected from a fistulated mature steer fed a diet of all alfalfa hay. The compound was dissolved in absolute ethanol and added in vitro at concentrations ranging from 0 to 100 ppm. Digestion of cellulose and production of volatile fatty acids over 24 and 48 h of incubation was used to assess toxicity. Both cellulose digestion and propionic acid production were decreased at the 10 ppm concentration. The results suggest that technical grade pentachlorophenol has the potential to interfere with utilization of cellulose in ruminants.

Animals↗
PubMed2000

[Pentachlorophenol poisoning. Report of 4 cases and review of the literature].

Pentachlorophenol (PCP) was, and still is, one of the most frequently used fungicides and pesticides. The use of PCP has been more restricted during the last few years. PCP's most important industrial application is as a wood preservative. The pentachlorophenol can be absorbed into the body by all the routes of occupational exposure. Some epidemiological observations suggest that exposure to PCP solutions may result in an increased risk for certain diseases in humans, e.g., immunodeficiency, blood disorders, malignancies, congenital anomalies. Chronic poisoning is difficult to detect since symptoms are often vague. Acute poisoning is due to interference with oxidative phosphorylation and can present itself as an unexpected case of sudden death. Four cases of PCP poisoning, including one fatalitie, occurred in two small wood preservative plants. All cases presented with increased serum creatinine phosphokinasa. The clinical finding are reported, and treatment modalities commented. At present there is no antidote for PCP. The basis for treatment is intensive supportive care to maintain vital bodily function. In one patient plasmapheresis was used and rapid recover was obtained. It is suggested that such therapy may be lifesaving in such intoxications.

Adult↗
PubMed1998

Health effects of occupational pentachlorophenol exposure in timber sawmill employees: a preliminary study.

AIMS: To study the health effects of pentachlorophenol (PCP) exposure in the timber sawmill industry. METHOD: A questionnaire-based, non-random survey was undertaken amongst a group of current and ex-workers who had identified their health concerns as being related to PCP exposure. RESULTS: Low, medium and high exposure groups were identified. A significant dose-response was found between past exposure to Pentachlorophenol and reported symptoms of fever/sweating (47% in the high exposure group), weight loss (33% in the high exposure group), persisting fatigue (74% in the high exposure group), nausea (40% in the medium and high exposure groups) and responses to a screening test for neuropsychological dysfunction (Questionnaire 16) (81% in the high exposure group). No associations were observed with other chronic diseases, apart from emphysema and chronic bronchitis. CONCLUSIONS: This study is based on a self selected sample of PCP-exposed workers whose precise exposure levels are unclear. Thus the findings presented should be regarded as preliminary. Nevertheless, they support clinical experiences and point to the need for further investigation.

Adult↗
PubMed2001

Direct electrochemistry of pentachlorophenol hydroxylase.

The direct electrochemistry of the flavin-containing monooxygenase, pentachlorophenol hydroxylase (PCPH), at an edge plane graphite electrode was observed and a catalytic response, linear with concentration, was found with the substrate pentachlorophenol (PCP).

Bioreactors↗
PubMed1965

INDUSTRIAL PENTACHLOROPHENOL POISONING IN WINNIPEG.

Enquiry into the occupational history of a patient presenting with stupor, hyperpyrexia and profuse sweating, and dying at a Winnipeg hospital a few hours later in coma, finally led to the identification of pentachlorophenol-a substance widely used as a wood preservative-as the cause of death of this worker and the cause of non-fatal intoxication in four other workers engaged by wood-processing plants. In these latter four cases the prominent clinical symptoms were sweating, weight loss and gastrointestinal complaints. A review of the literature revealed that pentachlorophenol exerts its toxicity following cutaneous absorption or inhalation by interference with oxidative phosphorylation, resulting in excessive release of heat. This substance has been the cause of several deaths in other countries. Observance of simple precautionary measures that ensure adequate ventilation and skin protection should suffice in making this industrially useful product safe.

Canada↗
PubMed1992

Dioxin intoxication from chronic exposure of horses to pentachlorophenol-contaminated wood shavings.

Investigations into the cause of health problems on a horse-breeding farm led to the discovery of high concentrations (630 to 9,810 mg/kg of bedding) of pentachlorophenol in wood shavings used as bedding for horses over a period of 2 to 4 years. Toxicologic signs in the horses were characteristic of toxic effects associated with exposure of polychlorinated dibenzo-p-dioxins and dibenzofurans. Tissue residue analysis confirmed presence of toxic polychlorinated dibenzo-p-dioxin and dibenzofuran isomers known to be in pentachlorophenol, substantiating the bioavailability of polychlorinated dibenzo-p-dioxins and dibenzofurans in the wood shavings. The findings provide evidence that residue concentrations in the range of 2 ng/g of toxic polychlorinated dibenzo-p-dioxin isomers in liver or fat correlate with toxicologic effects in horses.

Animals↗
PubMed2005

[Toxicity effects of pentachlorophenol on Brachydanio rerio].

With embryo development technique, this paper determined the toxicity of pentachlorophenol (PCP) to Brachydanio rerio embryos. The results showed that the special effect duration of PCP on embryos was within 6 hours after embryos incubation. PCP could markedly inhibit the development of Brachydanio rerio embryos, and cause its malformation and even death. There were different toxicity endpoints which could be observed in embryos exposed to PCP with different time. The lethal effect sensitivity of embryos incubated after 48 hours was getting lower when the exposure time was getting shorter, the LC50 being the minimum (70.8 microg x L(-1)) for 0 hpf embryos, and the maximum (831.8 microg x L(-1)) for 24 hpf embryos. The acute toxicological endpoint of Brachydanio rerio embryos was in order of edema, no blood-circulation and heartbeat > incubation rate > stopping growth, and the most sensitive endpoints of Brachydanio rerio embryos to pentachlorophenol were no blood-circulation and half lethal concentration at 48 hrs.

Animals↗
PubMed1986

Porphyrins and pentachlorophenol in rat-liver mitochondria in hexachlorobenzene-induced porphyria.

This study investigated the extent of impairment in functional parameters of liver mitochondria from rats treated for 60 days with hexachlorobenzene (HCB). 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.

Animals↗
PubMed1999

Theoretical and Experimental (400-10 000 cm-1) Study of the Vibrational Spectrum of Pentachlorophenol.

Geometric and vibrational spectroscopic data (bond distances and angles, vibrational frequencies, infrared intensities) of pentachlorophenol-OH (PCP-OH) and pentachlorophenol-OD (PCP-OD) are calculated by density functional theory (B3LYP) using the 6-311G(d, p) basis set. Except for the vibrations involving the OH bond, the agreement between the experimental and calculated fundamental frequencies between 3600 and 400 cm-1 is very good. The theoretical method failed, however, to reproduce quantitatively the experimental intensities. The infrared spectra between 3600 and 10 000 cm-1 are studied, and the overtones or combination bands are assigned by comparing the spectra of PCP-OH and PCP-OD. The difference between the experimental and theoretical frequencies of the nu(OH) and nu(OD) frequencies can be mainly accounted for by the neglect of the anharmonicities of these vibrations in calculations. The binary or ternary combinations characterized by the highest coupling constants and the highest intensities are those involving the nu(OH), delta(OH), gamma(OH), and nu(C-O) vibrations. Copyright 1999 Academic Press.

Journal Article↗
PubMed2004

Evaluation of a polyclonal antiserum to pentachlorothiophenol-acetic acid-KLH immunogen: binding properties and use with heterologous PCP derivatives in ELISA for pentachlorophenol.

A polyclonal antiserum to pentachlorothiophenol-acetic acid-KLH was generated in sheep and assessed by solid phase ELISA. The assessment procedure included use of double checkerboard analysis in the absence and in the presence of analyte loads, estimation of cross reactivities of chlorophenol pesticides, assessment of the effect of pH, Tween 20, and Thames water matrix. The antiserum was highly specific for pentachlorophenol and enabled minimum detection limits of less than 0.2 ng mL(-1) in river water matrix. Particularly important was the significant improvement of assay performance in the absence of Tween 20 and at pH 4 and the very low cross reactivity (less than 0.01%) for other commonly used chlorophenols-2,4,5-trichlorophenol and 2,4,6-trichlorophenol, 2-methyl-4-chlorophenoxyacetic acid, and 2,4-dichlorophenoxy acetic acid. The study re-affirms the importance of the judicious choice of hapten derivatives in the synthesis of immunogens and assay reagents for pentachlorophenol analysis by competitive immunoassays.

Acetic Acid↗
PubMed1991

Induction of mutation in V79 Chinese hamster cells by tetrachlorohydroquinone, a metabolite of pentachlorophenol.

Tetrachlorohydroquinone (TCHQ) and tetrachlorocatechol (TCC), two metabolites of the environmental mutagen and carcinogen pentachlorophenol, were tested without exogenous activation in V79 Chinese hamster cells for the induction of mutation at the hypoxanthine phosphoribosyl transferase (HPRT) locus to 6-thioguanine resistance (TGr) and at the Na/K-ATPase locus to ouabain resistance (OuaR). Treatment was for 24 h at 37 degrees C. TCHQ produced statistically significant increases in the frequency of TGr mutants. The lowest observed effective dose (LOED) was 20 microM, where the relative cloning efficiency was 63%. The relationship between the dose of TCHQ and the frequency of TGr mutants was approximately linear over the range of 0-60 microM with an estimated slope (+/- 95% confidence limits) of 1.1 +/- 0.3 mutants per 10(6) clonable cells per microM. At the highest tested dose of TCHQ, 60 microM, the relative cloning efficiency was reduced to 7%. In contrast to TCHQ, TCC was unable to induce TGr mutants at doses up to 120 microM. The relative cloning efficiency at this dose was 5%. Both TCHQ and TCC were unable to induce OuaR mutants. The results suggest that TCHQ is at least partly responsible for the genotoxic activity of pentachlorophenol. TCHQ can produce reactive oxygen species, which may cause large genetic damage such as deletions, resulting in mutation to TGr but not to OuaR.

Animals↗
PubMed1990

Toxicity of municipal wastewater effluents contaminated by pentachlorophenol in Southwest Missouri.

Toxicity of effluents from two sewage treatment plants in Joplin, Missouri, was tested using Ceriodaphnia dubia and Pimephales promelas. No test organisms survived in effluents from either plant, in effluents diluted with water from Turkey Creek (the receiving stream), or in water from Turkey Creek. Mortality was complete in all but the most dilute treatments of effluents, in which reconstituted water was used as the diluent. High concentrations of pentachlorophenol (130-970 microg liter(-1)) in effluents and the receiving stream likely caused mortality during the 7-day tests. Detectable concentrations of other phenolic compounds indicated the presence in Turkey Creek of other toxic by-products of pentachlorophenol manufacture. This study demonstrated the utility of biological tests of whole effluents to determine toxicity of wastewater effluents.

Journal Article↗
PubMed2005

Removal of pentachlorophenol from aqueous solutions by dolomitic sorbents.

The partial decomposition of dolomite carried out within the temperature range 600-1000 degrees C provides new sorbents, called dolomitic sorbents. Their surface properties and identification by X-ray diffraction are discussed. The lowest specific surface area value was found for the raw dolomite, while the highest value was achieved by the D-1000 sample. The adsorption equilibrium of pentachlorophenol from aqueous solutions on the examined sorbents was investigated at 30, 40, and 50 degrees C via a bath process. Langmuir, Freundlich, Langmuir-Freundlich, and Redlich-Petersen models were fitted to experimental equilibrium data, and their goodnesses of fit are compared. The adjustable parameters of Langmuir-Freundlich and Redlich-Petersen isotherms were estimated by nonlinear least-squares analysis. Langmuir and Freundlich models were found insufficient to explain the adsorption equilibrium, while Langmuir-Freundlich and Redlich-Petersen isotherms provide the best correlation of the pentachlorophenol adsorption onto dolomitic sorbents.

Journal Article↗
PubMed2002

Subcellular localization of pentachlorophenol 4-monooxygenase in Sphingobium chlorophenolicum ATCC 39723.

We have studied the subcellular localization of pentachlorophenol 4-monooxygenase (PCP4MO) in Sphingobium chlorophenolicum ATCC 39723 during induction by pentachlorophenol (PCP). Using a monoclonal antibody CL6 specific to the native and recombinant PCP4MO, the enzyme was primarily found soluble as determined by immunoblot and ELISA analyses of cellular fractions. However, the enzyme was observed both in the soluble and membrane-bound forms during induction for 2-4 h, suggesting its translocation out from the cytoplasm. Electron microscopy confirmed that PCP4MO was predominantly present in the cytoplasm at 1 h, whereas at 4 h significant amount was detected also in the membrane and periplasm. After 6 h, the majority of PCP4MO was in the periplasm and only small amount was bound to the inner membrane or present in the cytoplasm. The results indicate that after biosynthesis PCP4MO in S. chlorophenolicum is exported via the inner membrane to the final location in the periplasm.

Alphaproteobacteria↗
PubMed1993

Cloning, sequence analysis, and expression of the Flavobacterium pentachlorophenol-4-monooxygenase gene in Escherichia coli.

The pcpB gene of Flavobacterium sp. strain ATCC 39723 was cloned by using a degenerate primer designed from the N-terminal sequence of the purified enzyme. The nucleotide sequence of pcpB was determined and found to encode an open reading frame of 1,614 nucleotides, yielding a predicted translation product of 538 amino acids, in agreement with the estimated size of the purified protein analyzed by sodium dodecyl sulfate-polyacrylamide gel electrophoresis. The transcriptional start of pcpB was found to be 80 bp upstream of the translational start, and the transcript was found to be induced in Flavobacterium sp. strain ATCC 39723 by the presence of pentachlorophenol but to be constitutive in the Escherichia coli pcpB clone. DNA hybridizations with genomic DNAs from Arthrobacter sp. strain ATCC 33790 and Pseudomonas sp. strain SR3 revealed a similar-size 3.0-kb EcoRI fragment, whereas there was no positive hybridization with genomic DNA from Rhodococcus chlorophenolicus. Cell extracts from an E. coli pcpB overexpression strain, as well as the whole cells, were proficient in the dechlorination of pentachlorophenol to tetrachlorohydroquinone. Protein data base comparisons of the predicted translation products revealed regions of homology with other microbial monooxygenases, including phenol-2-monooxygenase and tryptophan-2-monooxygenase.

Amino Acid Sequence↗