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Pentachlorophenol (PCP) and Dichlorodiphenyltrichloroethane (DDT) are environmental contaminants found in human blood. Previous studies have shown that PCP and DDT inhibit the lytic function of highly purified human natural killer (NK) lymphocytes and decrease the expression of several surface proteins on NK cells. Interleukin-1 βeta (IL-1β) is a cytokine produced by lymphocytes and monocytes, and anything that elevates its levels inappropriately can lead to chronic inflammation, which among other consequences can increase tumor development and invasiveness. Here, PCP and DDT were examined for their ability to alter secretion of IL-1β from immune cell preparations of various complexity: NK cells; monocyte-depleted (MD) peripheral blood mononuclear cells (PBMCS); and PBMCs. Cells were exposed to concentrations of PCP ranging from 5 to 0.05 µM and DDT concentrations of 2.5-0.025 μM for 24, 48 h, and 6 days. Results showed that both PCP and DDT increased IL-1β secretion from all of the immune cell preparations. The specific concentrations of PCP and DDT that increased IL-1β secretion varied by donor. Immune cells from all donors showed compound-induced increases in IL-1β secretion at one or more concentration at one or more length of exposure. The mechanism of PCP stimulation of IL1-β secretion was also addressed, and it appears that the MAPKs, ERK1/2 and p38, may be utilized by PCP to stimulate secretion of IL-1β.

We performed toxicity tests with two species of pulmonate snails (Lymnaea stagnalis and Physa gyrina) and four taxa of nonpulmonate snails in the family Hydrobiidae (Pyrgulopsis robusta, Taylorconcha serpenticola, Fluminicola sp., and Fontigens aldrichi). Snails were maintained in static-renewal or recirculating culture systems with adults removed periodically to isolate cohorts of offspring for toxicity testing. This method successfully produced offspring for both species of pulmonate snails and for two hydrobiid species, P. robusta and Fluminicola sp. Toxicity tests were performed for 28 days with copper, ammonia, and pentachlorophenol in hard reconstituted water with endpoints of survival and growth. Tests were started with 1-week-old L. stagnalis, 2-week-old P. gyrina, 5- to 13-week-old P. robusta and Fluminicola sp., and older juveniles and adults of several hydrobiid species. For all three chemicals, chronic toxicity values for pulmonate snails were consistently greater than those for hydrobiid snails, and hydrobiids were among the most sensitive taxa in species sensitivity distributions for all three chemicals. These results suggest that the toxicant sensitivity of nonpulmonate snails in the family Hydrobiidae would not be adequately represented by results of toxicity testing with pulmonate snails.

As part of the ecological risk assessment for Portland Harbor Superfund site, a study was conducted to address the question of whether the use of surrogate species in the risk assessment would be protective of lamprey ammocoetes. The study evaluated the acute toxicity of six chemicals: pentachlorophenol, copper, diazinon, aniline, naphthalene, and lindane; these chemicals represent the toxic modes of action of oxidative phosphorylation uncoupler, gill dysfunction, acetylcholinesterase inhibitor, polar narcosis, narcosis, and central nervous system interference, respectively. Field-collected lamprey ammocoetes were exposed to each of the six chemicals in a definitive 96-h flow-through acute water-only toxicity test. LC(50)s were calculated for pentachlorophenol at 31 μg/l, copper at 46 μg/l, diazinon at 8.9 mg/l, and aniline at 430 mg/l. Species sensitivity distributions based on LC(50)s for aquatic organisms indicated that lamprey ammocoetes were relatively sensitive to pentachlorophenol (15th percentile). The sensitivity of lamprey ammocoetes to copper approximated the average of aquatic species tested (46th percentile). Lamprey ammocoetes were relatively insensitive to diazinon and aniline (72nd and 90th percentile, respectively). The 96-h LC(50) for naphthalene was estimated at 10 mg/l, based on 50% mortality in the highest concentration. Based on a comparison with LC(50)s for four other fish species, ranging from 2.0 to 6.6 mg/l, lamprey ammocoetes were relatively insensitive to naphthalene. A 96-h LC(50) could not be derived for lindane, with 12.5% mortality in the highest test concentration of 2.68 mg/l. LC(50)s for numerous other fish species ranged from 0.001 to 0.24 mg/l, indicating that lamprey ammocoetes were relatively insensitive to lindane. The study concluded that the use of surrogate species in the ecological risk assessment for Portland Harbor would be protective of lamprey ammocoetes.

In this study, the effect of environmental toxins such as pentachlorophenol (PCP), tetrachlorocatechol (TeCC) and tetrachloroguaiacol (TeCG) on human peripheral blood lymphocytes was investigated. All the compounds studied increased the size and granularity of the lymphocytes in the concentrations range from 5 to 600 ppm. The PCP caused the strongest increase in the size of the cells, whereas lymphocytes granularity was more strongly increased by TeCC and PCP than by TeCG. The PCP and its derivatives in the concentrations range from 1 to 125 ppm significantly depleted ATP level. It was also observed that PCP most strongly decreased ATP content at its highest concentration of 125 ppm. Moreover, PCP caused the highest loss of lymphocytes viability in the concentrations range from 125 to 600 ppm. The TeCC in the concentrations of 1 and 5 ppm significantly increased the level of strand breaks in DNA, whereas lower damage was noted for PCP, and particularly for TeCG. The increase in carbonyl groups content was more strongly induced by TeCG and TeCC than by PCP in the concentrations range from 0.04 to 1 ppm; however, in a concentration of 5 ppm, all the compounds studied increased this parameter to a similar degree. DNA and protein damage was the most probably induced by free radical formation, as it was observed that all the compounds examined, and TeCC, in particular, were able of oxidize a fluorescent probe 6-carboxy-2',7'-dichlorodihydrofluorescein in the concentrations range from 0.01 to 1 ppm.

Early life-stage toxicity tests with copper and pentachlorophenol (PCP) were conducted with two species listed under the United States Endangered Species Act (the endangered fountain darter, Etheostoma fonticola, and the threatened spotfin chub, Cyprinella monacha) and two commonly tested species (fathead minnow, Pimephales promelas, and rainbow trout, Oncorhynchus mykiss). Results were compared using lowest-observed effect concentrations (LOECs) based on statistical hypothesis tests and by point estimates derived by linear interpolation and logistic regression. Sublethal end points, growth (mean individual dry weight) and biomass (total dry weight per replicate) were usually more sensitive than survival. The biomass end point was equally sensitive as growth and had less among-test variation. Effect concentrations based on linear interpolation were less variable than LOECs, which corresponded to effects ranging from 9% to 76% relative to controls and were consistent with thresholds based on logistic regression. Fountain darter was the most sensitive species for both chemicals tested, with effect concentrations for biomass at < or = 11 microg/L (LOEC and 25% inhibition concentration [IC25]) for copper and at 21 microg/L (IC25) for PCP, but spotfin chub was no more sensitive than the commonly tested species. Effect concentrations for fountain darter were lower than current chronic water quality criteria for both copper and PCP. Protectiveness of chronic water-quality criteria for threatened and endangered species could be improved by the use of safety factors or by conducting additional chronic toxicity tests with species and chemicals of concern.

Uptake, biotransformation, and elimination rates were determined for pentachlorophenol (PCP), methyl parathion (MP), fluoranthene (FU), and 2,2',4,4',5,5'-hexachlorobiphenyl (HCBP) using juvenile Hyalella azteca under water-only exposures. A two-compartment model that included biotransformation described the kinetics for each chemical. The uptake clearance coefficients (k(u)) were 25.7 +/- 2.9, 11.5 +/- 1.1, 184.4 +/- 9.3, and 251.7 +/- 9.0 (ml g(-1) h(-1)) for PCP, MP, FU, and HCBP, respectively. The elimination rate constant of the parent compound (k(ep)) for MP was almost an order of magnitude faster (0.403 +/- 0.070 h(-1)) than for PCP and FU (0.061 +/- 0.034 and 0.040 +/- 0.008 h(-1)). The elimination rate constants for FU and PCP metabolites (k(em)) were similar to the parent compound elimination 0.040 +/- 0.005 h(-1) and 0.076 +/- 0.012 h(-1), respectively. For MP, the metabolites were excreted much more slowly than the parent compound (0.021 +/- 0.001 h(-1)). For PCP, FU, and MP whose metabolites were measured, the biological half-life (t(1/2p)) of the parent compound was shorter than the half-life for metabolites (t(1/2m)) because the rate is driven both by elimination and biotransformation processes. Thus, H. azteca is capable of metabolizing compounds with varying chemical structures and modes of toxic action, which may complicate interpretation of toxicity and bioaccumulation results. This finding improves our understanding of H. azteca as a test organism, because most biomonitoring activities do not account for biotransformation and some metabolites can contribute significantly to the noted toxicity.

Pentachlorophenol (PCP) induces liver cancer in mice, possibly due to covalent binding of PCP metabolites to critical macromolecules. In this work, covalent binding was related to PCP biotransformation and specific (cysteinyl) adducts of chlorinated quinones in liver and blood of Sprague-Dawley rats and B6C3F1 mice dosed with [(14)C]PCP. Using a sequential scheme of scintillation counting along with selective cleavage of cysteinyl adducts by Raney nickel, we quantified total radiobinding, total covalent binding, non-cysteinyl protein binding, and specific protein adducts in liver nuclei (Np), liver cytosol (Cp), hemoglobin (Hb), and serum albumin (Alb). Almost all of the radiobinding to Np (>98%) was attributed to covalent binding in both rats and mice. Regarding Cp, more covalent binding was observed in mice than in rats (100% versus 67%, P=0.015). Very little binding was attributed to serum Alb (rats 1.3%, mice 2.6%, P=0.046) or Hb (not detected in either species). These results indicate that the liver was the main organ for PCP metabolism and that relatively little of the dose of reactive metabolites became systemically available. Cysteinyl binding accounted for 76-91% of total covalent binding to Np and 68-76% of total covalent binding to Cp. In addition, five times more PCP was bioactivated in the livers of mice than in those of rats (2.14% of the dose bound to Cp in mice and 0.416% in rats). These results reinforce previous studies, suggesting that the liver was a target organ of PCP carcinogenicity and that mice were more susceptible to liver damage than rats. However, the sum of all quantified adducts accounted for only 7-8% of total cysteinyl binding to Np and 2% to Cp, suggesting that other uncharacterized binding species may be important to the toxicity of PCP.

An in vivo study of the effects of pentachlorophenol was carried out with a pre-acclimatized fish species, Heteropneustes fossilis, using four sub-lethal concentrations, 0.1, 0.2, 0.3 and 0.4 ppm, and three sampling times, 48, 72 and 96 h. Cytogenetic preparations were stained by the haematoxylin-eosin technique. The incidence of micronuclei was scored by a manual and an automated method. Small-sized micronuclei appeared in the cytoplasm in addition to the main nucleus. The frequency of micronucleated erythrocytes peaked at 4 days (96 h) exposure. The percentage of single micronuclei increased with longer exposures. The Mann-Whitney U test showed all micronuclei frequencies were significantly different from control (P<0.05). No statistical difference was observed between scores obtained by the manual and automated methods. A linear relationship between the percentage of micronucleated erythrocytes and dose was confirmed at all levels. Computer image analysis of morphological variations of erythrocytes indicated a 1:5 ratio of micronuclei and main nucleus accompanied by a reduction in cell volume by 600 dot units. Pentachlorophenol-mediated genotoxicity was confirmed in this fish for the first time. Possible consequences of genotoxicity and cytotoxicity are discussed.

The Dreissena-Monitor is a biological early warning system for the continuous monitoring of river water quality, based on the valve movements of two groups of 42 zebra mussels (Dreissena polymorpha). Laboratory experiments with Cd, PCP, and 2-chloro-4-nitro-aniline were conducted in combination with suspended particles (a mixture of stinging nettle powder, bentonite, and quartz powder). An increase of suspended particles up to a nominal concentration of 540 mg/L within 5 min did not evoke any reactions by the mussels significantly different from normal. The distribution between water and solids was analyzed for Cd and 2-chloro-4-nitroaniline, with the result that the former quickly adsorbed to the particles, whereas the latter did not bind to the particles at all. The behavior of the zebra mussels revealed that the detection of 2-chloro-4-nitro-aniline was not affected by the presence of suspended matter. In the cases of Cd and PCP, D. polymorpha was able to detect these substances when they were particle-associated at least as well or better as when they were dissolved in the water. The results are discussed with respect to the physiology of the organisms and the bioavailability of toxicants, as well as to the consequences these results may have under field conditions.

Objective: This study evaluates whether wood dust and/or wood preservatives develop a carcinogenic potential against the tissues of the airways of rats., Methods: The formation of tumors of the respiratory tract after exposure to wood dust was studied in six groups of approximately 60 female Fischer 344 rats exposed by long-term inhalation to mean concentrations of (1) 18 mg/m3 of untreated oak wood dust, (2) wood preservatives containing ca. 1 microgram/m3 lindane and 0.2 microgram/m3 of pentachlorophenol (PCP) in the exposure air, or lindane and 18 micrograms/m3 of PCP (group lindane/PCP vapors, and group oak wood treated with lindane/PCP), (3) 21 or 39 micrograms/m3 of sodium dichromate (calculated as CrO3, group chromate aerosol and group oak wood with chromate), and 72 micrograms/m3 of N-nitrosodimethylamine vapors as positive control. The negative control group consisted of 115 animals (sham-exposed)., Results: Tumors of the nasal cavity developed in two rats exposed to chromate aerosol or in combination with wood dust (2/102, 2%). Malignant tumors of the lower respiratory tract were induced only in exposed groups of rats (three adenocarcinomas of the lung and four bronchiolar lung carcinomas, 7/254, 2.8%). More respiratory tract tumors were observed in rats exposed to chromate or wood with chromate (5/102, 5%), also in groups exposed to oak wood dust (oak untreated, oak + chromate, oak + lindane/PCP; together 5/155, 3.2%). Analysis of 'unpreserved' oak wood dust revealed up to 5 micrograms/m3 of chromate. When this exposure was taken into account, eight of nine animals with respiratory tract tumors (including nasal cavity) had exposure to chromate, while only one tumor occurred in the group lindane/PCP. Otherwise the incidence of systemic tumors was increased in animals exposed to lindane/PCP, due in particular to a significantly increased incidence of liver tumors (OR = 3.7; 1.24-11.3; P = 0.019). Fatal (mucoepidermoid) tumors were induced by N-nitrosodimethylamine (NDMA) in the positive control (14/46, 30%). No such tumors of the respiratory tract were observed in the negative control., Conclusions: Tumors in the respiratory tract were found only in exposed animals, predominantly in the groups which inhaled oak wood dust and chromate stain. Chromate may play a decisive role for the etiology of tumors of the nasal cavity in wood workers. This assumption should be supported by further dose-response studies.

Mature specimens of the isopod Oniscus asellus were maintained on soil and leaf litter to which was added different concentrations of either benzo[a]pyren (B[a]P), 2,2',5,5'-tetrachlorobiphenyl (PCB52), gamma-hexachlorocyclohexane (gamma-HCH), or pentachlorophenol (PCP) for a maximum of 14 days. Time-dependent investigation of the body level of the 70 kD stress protein group (hsp70) in the isopods revealed a significant but transient induction of the hsp70 response after about 24 h of exposure to PCB52 or B[a]P. Despite continuous exposure, the hsp70 level decreased subsequently and ended up close to or below the control level independent of the concentration of PCB52 or B[a]P in the substrate. All applied PCP or gamma-HCH concentrations also resulted in an initial peak of hsp70 response after 24 h of exposure and a second peak after several days of exposure, as well as an elevated hsp70 level throughout the period of exposure. Although acute stress conditions posed by all four organic chemicals were monitored by stress protein induction, hsp70 can act as a biomarker of chronic exposure and effect for PCP and gamma-HCH only.

Numerous wood preserving waste (WPW) sites in the United States pose genotoxic hazards. WPWs consist of complex mixtures containing toxic, including genotoxic, compounds which are derived from the preservatives coal tar creosote and pentachlorophenol (PCP) and other polychlorinated aromatics. The genotoxicity of WPW extracts, which has not been tested in mammals, cannot be evaluated on the basis of data for individual components because of possible compound interactions. Therefore, whole extracts need to be assayed. 32P-postlabeling represents a powerful tool to determine DNA adduct formation by complex genotoxic mixtures, such as cigarette smoke, diesel exhaust, and coke oven and foundry emissions in experimental animals and humans. In the present study, a mouse bioassay was used in combination with 32P-postlabeling to determine DNA adduct formation induced by hexane/acetone extracts of two samples from a WPW site. Female ICR mice were treated dermally with extract corresponding to 3 mg residue or vehicle control once per day for 2 days and killed 24 h later. Skin, lung, liver, kidney, and heart DNA preparations were assayed by nuclease P1-enhanced postlabeling. Adduct profiles were tissue-specific and displayed a multitude of non-polar DNA adducts with levels amounting to one adduct in 1.6 x 10(6) DNA nucleotides in skin (both extracts) and one adduct in 3.2 x 10(7) or 1.2 x 10(7) DNA nucleotides in liver (extract 1 or extract 2). Based on their chromatographic properties, these adducts appeared largely derived from polycyclic aromatic hydrocarbons (PAHs) present in the extracts. One of the major adducts was identified as the 32P-labeled derivative of the reaction product of 7 beta, 8 alpha-dihydroxy-9 alpha, 10 alpha-epoxy-7, 8,9,10-tetrahydrobenzo[a]pyrene (BPDE I) with N2 of deoxyguanosine. Total non-polar DNA adduct levels were highest in skin and lung, amounting to 17.4 and 24.0% of the skin values for extracts 1 and 2, respectively, in lung while the corresponding levels in liver were 5.0 and 12.6%. These results were in accord with the carcinogenic potencies of PAHs in these organs. Extract 2 induced higher adduct levels in internal organs, although its PAH concentrations were lower than those of extract 1, i.e. lung, liver, kidney, and heart had 1.4, 2.5, 1.9, and 1.7 times higher total adduct levels and 1.6, 3.3, 1.6, and 1.9 times higher benzo[a]pyrene adduct levels. With the exception of total adducts in lung, the differences between the two extracts were all significant, suggestive of compound interactions. The benzo[a]pyrene adduct levels in the five tissues correlated linearly with total adduct levels and thus represented a surrogate for the latter. Overall, the results suggest that DNA adducts in mouse tissues, as analyzed by 32P-postlabeling, are suitable biomarkers and dosimeters of the genotoxicity of WPW extracts.

We recently reported that co-administration to female mice of tamoxifen or 4-hydroxytamoxifen (4-OH-tamoxifen) with pentachlorophenol (PCP), but not with 2,6-dichloro-4-nitrophenol (DNCP) results in strong intensification of a specific subgroup, termed group I, of tamoxifen-DNA adducts in female mouse liver. As both PCP and DCNP are sulfotransferase inhibitors, we concluded that the intensification of tamoxifen group I adducts is probably not due to inhibition of sulfation by these phenols of a tamoxifen metabolite. Since epoxide derivatives of 4-OH-tamoxifen are potential candidates involved in tamoxifen-induced DNA damage, the hypothesis was developed and tested that PCP inhibits epoxide detoxication. As 4-OH-tamoxifen metabolites were unavailable to us, we employed indirect approaches to test this hypothesis. In the first set of experiments we determined whether PCP would augment DNA adduct formation from the benzo[a]pyrene metabolite, 9-hydroxybenzo[a]pyrene (9-OH-BP), as 9-OH-BP-4,5-epoxide is known to be involved in the metabolic activation of this compound. Female mice were given a single i.p. dose of 9-OH-BP (50 mumol/kg) either alone or in combination with PCP (75 mumol/kg), and hepatic DNA adducts were measured 24 h later by nuclease P1-enhanced bisphosphate 32P-postlabeling. Co-administration of PCP with 9-OH-BP resulted in a statistically significant 1.5- to 1.7-fold increase in 9-OH-BP adduct levels versus 9-OH-BP controls. In order to determine whether PCP inhibits the enzymatic detoxication of epoxides in vitro, in a second set of experiments, the effects of PCP on liver microsomal epoxide hydrolase (mEH) and purified equine liver glutathione S-transferase (GST) activities were studied using, respectively, styrene-7,8-oxide and 1-chloro-2,4-dinitrobenzene (CDNB) as substrates. Incubation of mouse liver microsomes with PCP (10-100 microM) strongly inhibited (by 21-97%) mEH activity in a dose-dependent manner, the IC50 being 35 microM. DCNP was ineffective as a mEH inactivator. PCP also inhibited purified equine liver GST activity, with an IC50 of 23.5 microM. Taken together, the results of this study strongly support the hypothesis that PCP inhibited enzymatic detoxication of epoxides in vivo and in vitro. By this mechanism PCP would lead to enhancement of DNA damage caused by 9-OH-BP, and possibly other drugs and their metabolites, which undergo epoxidation prior to DNA binding.

The variation of acute toxicity data among nematode species belonging to different taxonomic and ecological groups was investigated. Twelve different nematode species were extracted from the soil and directly exposed to cadmium and pentachlorophenol. LC50-values were estimated after 24, 48, 72, and 96 h of exposure in aqueous solutions. The species exhibited large differences in sensitivity. LC50-values (72 h) for pentachlorophenol ranged from 0.5 to more than 34.5 mumol/L and for cadmium from 29 to more than 800 mumol/L. These toxicity data could be described by a log-logistic distribution function. LC50-values for cadmium were not correlated with those for pentachlorophenol. Species of the subphylum Secernentia were less sensitive to pentachlorophenol than species of the subphylum Penetrantia, while no differences were observed for cadmium. In addition, no relationship was found between toxicity data and life-history strategies. Slow colonizers (K-strategists, sensu lato) were not more sensitive to cadmium and pentachlorophenol than opportunistic species (r-strategists, sensu lato). Nematodes appeared to be as sensitive to pentachlorophenol as other soil invertebrates. Nematodes were generally tolerant to cadmium.

Pentachlorophenol (PCP) is a widespread contaminate of soils and ground water throughout North America. Earlier studies have indicated that microbial biodegradation leads to the formation of intermediate metabolites which are more toxic than the parent compound. Microbial degradation is by three general pathways: dechlorination, methylation, and oxidation. The relative toxicity of PCP and 25 of its identified intermediates of microbial transformation was evaluated in the static Tetrahymena pyriformis population growth assay. Dechlorination of chlorophenols resulted in a decrease in toxicity because of a decrease in both hydrophobicity and reactivity. Moreover, dechlorination of chloroanisoles resulted in a decrease in toxicity due to a decrease in hydrophobicity. Since there was a decrease in reactivity, methylation of chlorophenols resulted in a decrease in toxicity. Oxidation of chlorophenols resulted in enhanced toxicity owing to increased reactivity and concomitant decreased hydrophobicity.

Sub-adult African clawed frogs (Xenopus laevis) were fed pentachlorophenol (PCP)-injected mealworms containing 64.8 to 2604 ug of PCP per gram of worm for 27 days. There was no mortality and no significant bioaccumulation of PCP in the frogs. After three weeks, frogs fed 2,604 micrograms/g of PCP ceased eating. The no observed adverse effects level (NOAEL) based on significantly reduced food consumption (PCP-injected mealworms) was 638 micrograms/g. This corresponded to a NOAEL based on PCP intake of about 8 micrograms PCP/g frog/day. A toxicity threshold model estimated that about 800 micrograms/L of waterborne PCP may be a threshold for adverse effects in Xenopus or similar amphibians. Further study is needed to verify threshold estimates.

A Gram-negative bacterium, Pseudomonas sp. strain SR3, was isolated from soil at a former wood treatment plant in north central Florida. The ability of this bacterium to degrade pentachlorophenol (PCP) was confirmed by growing cells in a basal salts medium in which PCP was the only source of carbon and energy. Degradation from a measured concentration of 39-40 micrograms PCP/ml to 0.0006 micrograms PCP/ml was observed within 120 h of incubation in the presence of PCP-induced cells of Pseudomonas sp. strain SR3. The initial cell density in these cultures was 6 x 10(6) cfu/ml. Microtox 5 min EC50 toxicity tests revealed that aqueous solutions of PCP, measured concentrations 39-40 micrograms/ml were toxic but that final biodegraded samples, 0.0006 micrograms PCP/ml were nontoxic. However, bioassays with embryonic inland silversides, Menidia beryllina, showed that the biodegraded samples were embryotoxic or teratogenic. Water containing added PCP at concentrations up to 30 times higher than measured in the final biodegraded samples was less toxic/teratogenic. These results indicate that while biodegradation of PCP was nearly complete, intermediate metabolites of the degradation process or undegraded impurities in PCP were toxic or teratogenic. Thus, the M. beryllina bioassay allows extremely sensitive assessment of toxicity associated with biodegraded environmental pollutants and may be a useful criterion for determining whether bioremediated water or soil is safe for discharge back into the environment.

Chronic toxicity 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 +/- 12 h old were exposed for their entire lifespan (i.e., 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.(ABSTRACT TRUNCATED AT 250 WORDS)

Chemical analyses revealed that polycyclic aromatic hydrocarbons (PAHs) 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 PAHs and other organics. A study was conducted to determine the efficacy of ultrafiltration for removal of organics from groundwater at this U.S. Environmental Protection Agency, 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. A concentration of 100% streamwater caused significant (alpha less than or equal to 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% concentrations greater than 90% of hatched larvae appeared normal. The Microtox EC50 was 30% permeate water.

The acute toxicity of a technical formulation of pentachlorophenol (PCP) and pure pentachlorophenol to three age classes of Daphnia magna, and adult D. pulex and D. galeata mendotae was determined by static toxicity tests. The influence of a number of factors on toxicity of PCP was also examined. The 48-hr LC50 estimates for adult daphnids of the three species exposed to pure PCP 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 PCP; however, toxicity of both forms of PCP 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 PCP was equally toxic to all age classes of D. magna but susceptibility to technical PCP decreased with maturation. D. g. mendotae was ten times more sensitive than D. pulex to PCP. Pure PCP was significantly more toxic to D. magna at pH 5.5 than 7.0 with mean 48-hr LC50 values of 0.082 and 1.78 mg PCP/L, respectively. At 12 degrees C, the toxicity of both forms of PCP to D. g. mendotae and D. pulex did not differ significantly from that at 20 degrees C; however, technical PCP was significantly more toxic to D. magna at 12 degrees C for an exposure duration of 48 hr.(ABSTRACT TRUNCATED AT 250 WORDS)

The morbidity and mortality of workers occupationally exposed to wood treating chemicals used in Hawaii for the years 1960 to 1981 were evaluated. The specific chemical exposures investigated were CCA (chromated copper-arsenate), TBTO (tributyl tin oxide) and PCP (pentachlorophenol). Results of detailed medical histories, laboratory and physiological tests, and physical examinations of 88 wood treaters were compared with those of 58 matched controls. The occupationally exposed cases had a significantly higher mean level of urinary PCP as compared to the controls (mean of 174 ppb vs. 35 ppb, micrograms/kg). There were no significant differences between the groups for the other urinary pesticide residues. The medical histories and physical examinations revealed no significant variations between the wood treaters and the comparison group. Review of all organ systems and laboratory data showed no clinically significant differences between exposed and nonexposed cohorts, although elevated hepatic enzymes in both groups merit further study. The results indicated no adverse health effects or increased incidence of mortality resulting from exposure to wood preservative chemicals in wood treaters who had worked in the industry for 0.33 to 26.3 years with a median of 6.5 years. Only 6 deaths were reported, 5 of cardiovascular disease, one of cause undetermined and none of cancer. Total number of deaths were less than the 8 anticipated for this age group.

Age-dependent effects of technical pentachlorophenol (PCP) on male rat livers were investigated after a 15 day treatment with PCP, 30 mg/kg/d body weight. The liver tissues were investigated morphometrically at light and electron microscopical levels. Statistically significant alterations of nuclei and organelles of the hepatocytes were described.

Survival, growth, and reproduction of Hyalella azteca were determined under various test conditions. Reproduction by a cohort begins when the amphipods are 5 to 6 weeks old, peaks at 8 to 12 weeks, and then declines due to continuing adult mortality. Full life-cycle tests can be completed in 12 to 14 weeks at 25 degrees C. Reproduction is poor when only artificial plastic substrate is provided. A substrate of cotton gauze results in dramatic improvements in both reproduction and growth. Better reproduction can be obtained by culturing the amphipods in some sediments, but this makes weekly enumeration difficult. Increased mortality during chronic exposure to cadmium was observed at 1 microgram/L for H. azteca and 3.2 micrograms/L for Gammarus fasciatus. Reproduction during longer exposure was not reduced at concentrations lower than those causing increased mortality within six weeks. Chronic toxicity of pentachlorophenol was observed at 100 micrograms/L for both species. Chronic toxicity to Daphnia magna was similar to that of the amphipods for cadmium, but lower for pentachlorophenol. Amphipods are at least as sensitive as Daphnia to a variety of toxicants during chronic exposure.

A bioassay using Pseudomonas fluorescens was affected by the sequence of exposure to pentachlorophenol (PCP) and 2,3,4,5-tetrachlorophenol (TCP). Surviving cells from standardized cell suspensions initially treated with PCP at concentrations ranging from 10 to 75 micrograms/ml, followed by removal of the toxicant, were not affected by a second dose of PCP at the same concentration. However, if the second dose was TCP, the test organism was sensitive to the second exposure. The most toxic sequence was an initial exposure to TCP followed by a second exposure to PCP. The response of the test organism to PCP and TCP was clearly dependent upon both the toxicant concentrations used and the sequence of toxicant addition.

Seven commercially available wood-related compounds have been tested for mutagenicity by the use of the Ames and fluctuation test-systems. All compounds were found to be non-mutagenic. Among these compounds, 2,6-dimethoxy-p-benzoquinone showed a very weak and questionable mutagenic activity against Salmonella typhimurium TA 100. In this connection, probable causes of nasal adenocarcinoma of woodworkers are briefly discussed.

The toxicity of phenol (P), pentachlorophenol (PCP), and dinitrophenol (DNP) was determined separately and in different combinations with a test fish, Notopterus notopterus, using the procedure of Schubert et al. (1978) that provided a simple, sensitive, and quantitative index of synergism, antagonism and additivity. The combination (P + DNP)/PCP was found to be the most synergistic, while (PCP + DNP)/P was antagonistic in nature. The (DNP + P)/PCP combination was additive in its effect. The other combinations were also synergistic, but to a lesser extent than the (P + DNP)/PCP combination.

Embryos of fathead minnows were more resistant to phenol, 2,4-dimethylphenol (2,4-DMP), 2,4-dichlorophenol (2,4-DCP), and pentachlorophenol (PCP) than were larval or juvenile life stages. Growth of 28-day-old fish was the most sensitive indicator of stress during exposures to phenol, 2,4-DMP, and PCP, whereas survival was the most sensitive indicator of toxic effects from 2,4-DCP exposure. Based on these effects, the estimated maximum acceptable toxicant concentration for fathead minnows in Lake Superior water lies between 1,830 and 3,570 micrograms/L for phenol; 1,970 and 3,110 micrograms/L for 2,4-DMP; 290 and 460 micrograms/L for 2,4-DCP; and 44.9 and 73.0 micrograms/L for PCP.