Technical Grade Pentachlorophenol Research Articles

The immunotoxic effects of dual exposure to PCP and TCDD

Pentachlorophenol (PCP) was a commonly used fungicide, herbicide, insecticide, and bactericide in industrial, agricultural, and domestic settings; however, it was also contaminated with polychlorinated dibenzo-p-dioxins (PCDDs) and polychlorinated dibenzofurans (PCDFs). It has been reported that technical grade PCP had immunosuppressive effects and that the immune system was the major target of PCDD/PCDFs toxicity. Although the immune response after exposure to PCP or 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) has been studied, the toxic effects of exposure to both PCP and TCDD have not yet been reported. The aim of this study was to evaluate the effects on immune cells from mice intraperitoneally immunized with OVA and subsequently treated with PCP or TCDD alone or in combination by gavage. The animals were terminated on day 7 and 14, and the spleen and plasma samples were collected for immunotoxicity evaluation. The numbers and populations of splenocytes, T cell-derived cytokines produced by splenocytes, splenocyte-generated cytotoxicity and OVA-specific antibodies in plasma were investigated. Our results indicate that the spleen/body weight ratio and splenocyte number was reduced by TCDD alone; in addition, this reduction was enhanced when TCDD was combined with PCP. Exposure to TCDD alone or in conjunction with PCP suppressed many ovalbumin (OVA)-stimulated cytokines, including IL-2, IFN-γ, IL-4, IL-5, and IL-10. Furthermore, the immunoglobulins IgG and IgM were suppressed in mice administered by PCP alone, but the suppressive effects were greater in mice treated with TCDD alone or in combination with PCP. Co-exposure to PCP and TCDD resulted in an antagonistic effect on TCDD-induced suppression of IFN-γ and IL-10. Our results demonstrate that PCP alone is immunotoxic, regardless of the presence of TCDD. PCP led to mild changes in cytokine secretion, and it compromised splenocyte-generated cytotoxicity and IgM and IgG antibody production on day 7. The finding that PCP antagonizes TCDD-induced IFN-γ suppression could be due to the competitive binding of PCP to AhR (aryl hydrocarbon receptor).

Seasonal Variation in Plankton Community Responses of Mesocosms Dosed with Pentachlorophenol

Seasonal variations in plankton community response to pentachlorophenol (PCP) were studied in four mesocosm experiments using enclosures in a small lake. The mesocosms (860 l) were dosed with single applications of technical grade PCP (0, 4, 10, 24, 36, 54, 81 and 121 microg/l PCP) and monitored for 20 days. Multivariate statistical analyses showed that plankton community taxonomic composition varied with season. In winter and spring, communities were most stable in time; species diversity and abundance were lowest in winter. Seasonally, the communities varied little with respect to the dominant species, which were the copepod Calamoecia lucasi, the alga Peridinium sp. and the rotifer Ascomorpha ovalis. The direct effects of the PCP additions varied little between seasons, but indirect effects were evident at lower treatment levels in autumn. Indirect effects were not evident in winter. Minor variations in plankton community responses to PCP with season were apparent in the following order of decreasing sensitivity; autumn > or = winter/spring > or = summer. At the species level, C. lucasi showed the largest response. The responses observed were greatest in autumn, with decreased abundance at PCP concentrations > or = 24 microg/l. In the other seasons, effects were observed at levels of 54 or 81 microg/l and higher. Ascomorpha ovalis was the most responding rotifer in winter and spring, whereas Anuraeopsis fissa responded more strongly in autumn and summer. The dinoflagellate alga Peridinium sp. had the largest negative response in all but winter, when Dinobryon cylindricum did. Cryptomonas sp. responded positively to PCP in all seasons, increasing in abundance in the highest treatments, possibly due to reduced grazing pressure, reduced competition, or increased decomposition. The plankton community no-observed effect-concentration (NOEC) was 24-36 microg/l PCP. Results reported here suggest that the Australian and New Zealand water quality guideline values for PCP are sufficient to protect plankton communities against adverse effects.

Investigation of the potential release of polychlorinated dioxins and furans from PCP-treated utility poles

The United States (US) Environmental Protection Agency (EPA) estimated that the use of technical grade pentachlorophenol (PCP) between 1970 and 1995 to treat wood was approximately 400 000 metric tons in the US, and that between 4800 and 36 000 g of 2,3,7,8-tetrachlorodibenzo- p-dioxin toxic equivalents (TEQs) were incorporated annually in treated wood. The EPA has been unable, however, to estimate the rate of release of polychlorinated dibenzo -p-dioxins and dibenzofurans (CDD/Fs) from treated utility poles into the environment. There is some evidence that CDD/Fs leach from treated poles into the surrounding soils, but these studies do not allow for the calculation of a rate of release from this mechanism. Another possible release mechanism is the volatilization of dioxins into the atmosphere, but there are no data to demonstrate, much less quantify, this release. While not directly measuring the release of dioxins from treated utility poles into the environment, this study was designed to examine the potential for such release. The general approach taken was to collect PCP-treated poles of varying ages, to remove and analyze multiple samples from each pole cross-section, and to compare the spatial distribution of CDD/F congeners among poles of different ages. Evidence of concentration–depth profile changes over time may provide insight into the potential for dioxins to migrate through and then out of PCP-treated utility poles. It was found that the CDD/F concentrations were consistently higher in the outer portions of the poles than the center. This trend tends to be most marked in older poles and for the lower chlorinated congeners. The trend for dioxins to concentrate in the outer portions of the pole over time suggest migration within the poles, and this migration may result in some environmental release. Other possible explanations were also offered.

Effects of temperature and chemical formulation on the acute toxicity of pentachlorophenol toSimocephalus vetulus(Schoedler, 1858) (Crustacea: Cladocera)

Abstract The influence of temperature on the acute toxicity of a technical formulation (86%) and pure formulation (99%) of pentachlorophenol (PCP) to less than 24‐h‐old Simocephalus vetulus neonates was determined with 48‐h static toxicity tests. The technical grade PCP was significantly more toxic to S. vetulus than the pure PCP (P < 0.05). Sensitivity of S. vetulus to technical PCP also significantly increased with temperature (P < 0.05), but a significant temperature effect was not found with the pure PCP. The mean 48‐h LC50 values for neonates exposed to technical PCP were 140 and 199 μg l−1 at 22°C and 16°C, respectively, and for those exposed to pure PCP were 262 and 304 μg l−1, respectively.

Effects of pentachlorophenol (PCP) on the pituitary and thyroidal hormone regulation in the rat

Investigations on rats after repeated application of pentachlorophenol (PCP) should clarify whether thyroid side effects caused by this xenobiotic can be seen in a dose range which does not cause major toxic effects. Female rats of the Wistar strain were treated with 3 and 30 mg PCP/kg body wt. daily by gavage for 28 days. To assess the potential impact of impurities the study was performed both with pure and technical grade PCP at the dosage of 3 mg · kg −1 · day −1, and at a level of 30 mg · kg −1· day −1 with pure PCP only. The effects in animals on normal iodine diet were compared to those in animals on a low iodine diet. No decrease of body wt. was noticed, only the liver weights were increased slightly in animals treated with 30 mg · kg −1· day −1 PCP. However distinct effects on thyroid hormones as well as on thyrotropin (TSH) were observed: a pronounced fall of circulating thyroxine (T 4) and triiodothyronine (T 3) levels was accompanied by lower levels of both free thyroid hormones and TSH, and the T 4:T 3 ratio was decreased in serum. Furthermore the intrathyroidal hormone stores were reduced. An interference of PCP at pituitary or hypothalamic level is assumed as a major mode of action. Additional effects of the test substance on peripheral conversion can be suspected.

Inhibition by pentachlorophenol of production of reactive-oxygen intermediates by medaka phagocytic blood cells

Phagocytes isolated from the pronephros of the Japanese medaka ( Oryzias latipes) produce reactive-oxygen intermediates (ROI) that mediate various protective functions by virtue of their antimicrobial and antineoplastic properties. Pentachlorophenol (PCP) is a common marine and estuarine contaminant that is bioconcentrated in the tissues of exposed fish. This study shows that PCP exposure, at sublethal concentrations, produces a dose-dependent suppression of ROI generation by medaka phagocytes. Inhibition of phagocytosis-associated ROI detected by nitroblue-tetrazolium (NBT) reduction was seen after 20 h of PCP exposure, or after only 1 h of exposure by using luminol-augmented chemiluminescence (CL). The inhibition produced by pure PCP was slightly enhanced with dioxin-contaminated technical grade PCP. Inhibition of CL was reversible after the cells were placed in PCP-free medium. The data suggest that PCP exerts direct immunotoxicological effects on medaka blood cells.

Biodegradation of pentachlorophenol in soil: the response to physical, chemical, and biological treatments

The effects of physical, chemical, and biological treatments on biodegradation of pentachlorophenol (PCP) were studied in a silt-loam soil contaminated with 175 mg PCP/kg and uniformly 14C-labelled PCP. Biodegradation of 14C-labelled PCP and technical-grade PCP were monitored over 210 days incubation. Mineralization of labelled PCP was significantly (p=0.05) influenced by soil treatments. Negligible biodegradation occurred in either the sterile control soil or the uninoculated control soil, with less than 1% of added 14C recovered as 14 CO2. Inoculation of unamended soil with a strain of Flavobacterium (ATCC 39723) known to degrade PCP increased biodegradation of PCP; approximately 60% of the [14C]PCP was recovered as 14CO2. Increased soil water content (60% versus 30% w/w) enhanced biodegradation (67% recovery of 14C as CO2), while increased chloride ion concentration and anoxic conditions were inhibitory (20 and 1% recoveries, respectively). Residual soil PCP concentrations were also influenced by various treatments. In the sterile control soil and noninoculated control, after 210 days incubation, concentrations of PCP were 143 and 1223 mg/kg, respectively, while the PCP concentration in the inoculated soil was 21 mg/kg. When soil organic matter was increased by adding finely ground red clover leaf and stem material, the residual PCP concentration was reduced to 6 mg/kg after 210 days. Increased soil water content resulted in a residual PCP concentration of 5 mg/kg. High-pressure liquid chromatography of soil extracts revealed no accumulation of partial PCP degradation products. The results indicated that biodegradation of PCP in soil was significantly influenced by various soil amendments.

Activity of the anion exchange protein (band 3) of human erythrocytes as affected by hydroxychloro aromatic chemicals

The membranous segment of the anion transport protein (band 3) of the human erythrocyte membrane has been shown [T. L. Miller and R. J. Smith, Archs Biochem. Biophys. 250, 128 (1986)] to be destabilized by relatively low concentrations of many hydroxychloroaromatic compounds (HO-Cl x -Ar), including hydroxychlorodiphenyl ethers (HO-Cl x ,-DPE), major contaminants of technical grade pentachlorophenol (PCP). In the present study, HO-Cl x -DPE also caused a concentration-dependent inhibition of the rate of sulfate exchange mediated by band 3 in human erythrocytes. The most active compound studied, 2-HO-Cl 9-DPE, was about nine times more potent in inhibiting sulfate exchange than 2-HO-′,4,4′-Cl 3-DPE, the least active compound studied. The potency of HO-Cl x ,-DPE as inhibitors of anion exchange generally increased with the degree of chlorination. The concentration-dependent decreases in the sulfate exchange rate elicited by 2-HO-Cl 9-DPE and 2-HO-2′,4,4′-Cl 3-DPE paralleled the effects of these compounds on the stability of band 3.

The acute oral LD50 of technical pentachlorophenol in developing rats

The acute oral LD50s for technical-grade pentachlorophenol (T-PCP) were calculated by the Litchfield-Wilcoxon method during the ontogenetic growth of 10- to 134-d-old rats. Signs of toxicity included accelerated respiration, hyperpyrexia, collapse, asphyxial convulsions and death followed by rapid rigor mortis. Young rats (not yet weaned, 10 and 20 d old) and adults (70 and 134 d old) were more susceptible to the toxic and lethal effects of T-PCP than were juveniles (25 to 50 d old). The LD50 (mg/kg) ranged from 50 to 180 for preweaned rats, from 220 to 230 for juveniles and from 80 to 120 for adults.

Complete reductive dechlorination and mineralization of pentachlorophenol by anaerobic microorganisms.

Anaerobically digested municipal sewage sludge which had been acclimated to monochlorophenol degradation for more than 2 years was shown to degrade pentachlorophenol (PCP). Di-, tri-, and tetrachlorophenols accumulated when PCP was added to the individual acclimated sludges. When the 2-chlorophenol- (2-CP), 3-CP-, and 4-CP-acclimated sludges were mixed in equal volumes, PCP was completely dechlorinated. The same results were obtained in sludge acclimated to the three monochlorophenol isomers simultaneously. With repeated PCP additions, 3,4,5,-trichlorophenol, 3,5-dichlorophenol, and 3-CP accumulated in less than stoichiometric amounts. All chlorinated compounds disappeared after PCP additions were stopped. All chlorinated compounds disappeared after PCP additions were stopped. Incubations with [14C]PCP resulted in 66% of the added 14C being mineralized to 14CO2 and 14CH4. Technical-grade PCP was found to be degraded initially at a rate very similar to that of reagent-grade PCP, but after repeated additions, the technical PCP was degraded more slowly. Pentabromophenol was also rapidly degraded by the mixture of acclimated sludges. These results clearly show the complete reductive dechlorination of PCP by the combined activities of three chlorophenol-degrading populations.

Effects of pure and technical grade pentachlorophenol on cultured rat hepatocytes

Technical grade pentachlorophenol (tPCP) markedly induced monooxygenase activity in primary cultured rat hepatocytes, whereas pure PCP had no inducing effect. Phase II metabolism of the monooxygenase product, however, was equally inhibited after pretreating the cells with either of the PCP preparations.

Chlorinated dibenzo-p-dioxin and dibenzofuran levels in human adipose tissue and milk samples from the north and south of Vietnam

Although 2,3,7,8-TCDD has been found to be extremely toxic to a variety of laboratory aminals, human epidemiology studies, where exposure to 2,3,7,8-TCDD has been less well characterized than in animal toxicologic studies, have been less conclusive in characterizing the extent of toxicity. In order to determine whether the newly refined techniques of human adipose tissue biopsy including isomer specific and sensitive measurement of PCDDs and PCDFs might be able to assist in finding populations within the same country with high and low levels of dioxins, adipose tissue samples were taken and levels analyzed from the north and south of Vietnam. It seemed reasonable, based on previous work, that high levels of 2,3,7,8-TCDD might still be found in adipose tissue in selected patients living in areas sprayed with Agent Orange and other 2,3,7,8-TCDD containing herbicides, and that lower levels should be found in patients not exposed to 2,3,7,8-TCDD from herbicides or other sources, such as persons who had always resided in the north of Vietnam. Of 9 specimens from patients hospitalized in Hanoi who had never been south, none had detectable adipose tissue levels of 2,3,7,8-TCDD at a detection limit of 2 or 3 ppt on a wet weight basis. Of 15 specimens from Ho Chi Minh City hospitalized patients the mean of positive specimens (12 of 15) was 28 on a lipid basis. The mean of the positive values from the south is about 2 to 3 times higher than found in the North American Continent control patients where the mean is about 6–10 ppt and much higher than in the north of Vietnam. In the northern specimens, the levels were non-detectable with a sensitivity of between 2 and 3 ppt. Other PCDD and PCDF isomers not found in Agent Orange, the penta- through octachlorinated dibenzo-dioxins and dibenzofurans, were similar in isomer type and quantity in the south of Vietnam to what we previously reported in North America. Adipose tissue from the north of Vietnam contained the lowest levels of four through eight chlorinated dioxins and furans thus far reported. The initial data suggests that populations exist in the south of Vietnam with elevated levels of 2,3,7,8-TCDD at the present time, fourteen years after the last known 2,3,7,8-TCDD (Agent Orange) application, superimposed on a preexisting body burden of dioxins and dibenzofurans from sources other than Agent Orange such as technical grade pentachlorophenol or products of incineration contaminated with higher chlorinated PCDDs or PCDFs. In light of the recent finding that unexpected levels of PCDDs and PCDFs exist in the general adult population of industrialized countries, ca. 1,000 to 1,200 ppt, wet weight of total dioxin and furan isomers in adipose tissues, it seems reasonable that the extent of human toxicity of dioxins may be more readily characterized in Vietnam than in industrialized countries. Because 2,3,7,8-TCDD was applied in 1962–1970, although not yet cleaned up, the levels of 2,3,7,8-TCDD in the environment, the food chain, and in humans, would be expected to decrease with time. Therefore, if studies are not initiated in a timely fashion, the opportunity to better characterize the extent of the toxicity of TCDD to humans as well as the persistence of TCDD in the environment in Vietnam may be lost.

Humoral immunotoxicity of polychlorinated diphenyl ethers, phenoxyphenols, dioxins and furans present as contaminants of technical grade pentachlorophenol

Previous studies have demonstrated that the humoral immune response in mice as measured by the splenic IgM response to sheep erythrocytes (SRBC) is highly sensitive to suppression by technical grade (86%) pentachlorophenol (T-PCP) whereas analytical grade (> 99%) PCP is not immunosuppressive. In the present studies, we have examined several contaminant fractions and purified isomers from T-PCP for their humoral immunosuppressive effect. C57BL/6 mice were treated with a single oral dose of the various contaminants 2 days prior to SRBC challenge and the peak splenic IgM antibody response was measured 5 days later. Under these exposure conditions, T-PCP produced a dose-related suppression of the antibody response whereas analytical grade PCP was without effect. The dose of T-PCP producing 50% immunosuppression relative to the vehicle-treated control (ID 50) was 83 mg/kg. Results from studies using contaminant fractions extracted from T-PCP indicated that a chlorinated dioxin/furan fraction was significantly immunosuppressive, whereas a chlorinated phenoxyphenol fraction and a chlorinated diphenyl ether fraction were without effect when administered at dose levels expected to occur in the ID 50 dose of T-PCP. Several purified phenoxyphenol isomers representing the major pre- and isopredioxins in T-PCP were also not immunosuppressive, nor was octachlorodibenzo- p-dioxin. The 1,2,3,6,7,8-hexachlorodioxin (HxCDD), 1,2,3,4,6,7,8-heptachlorodioxin (HpCDD), and 1,2,3,4,6,7,8-heptachlorofuran (HpCDF) isomers were all significantly immunosuppressive. The single, oral ID 50s were 7.1, 85 and 208 μg/kg for HxCDD, HpCDD and HpCDF, respectively. Coadministration of HxCDD and HpCDD produced an additive immunosuppresive effect suggesting that the toxic dioxin and furan isomers present in T-PCP function in concert to produce the degree of immune suppression observed following T-PCP exposure. When analytical grade PCP was coadministered with HpCDD, the degree of immune suppression was equivalent to that produced by HpCDD alone, indicating no significant influence of PCP on dioxin-induced immunosuppression. The enhanced susceptibility of Ah-responsive C57BL/6 mice to T-PCP induced immune suppression as compared to Ah-nonresponsive DBA/2 mice and the correlation of immune suppression with P 1-450 associated monoxygenase induction provided further evidence for the role of the toxic Ah-interactive dioxin and furan contaminants in T-PCP as the mediators of T-PCP immunotoxicity.

Suppression of mouse complement activity by contaminants of technical grade pentachlorophenol.

Pentachlorophenol (PCP) is an antimicrobial agent used chiefly for the preservation of wood. Subchronic oral exposure (14 days) to Technical Grade PCP significantly inhibited the functional activity of female B6C3F1 mouse complement when measured in a microtiter hemolytic assay. When evaluated one day following the final exposure the highest administered dose (100 mg/kg) significantly suppressed the Classical complement pathway, the Spontaneous C1 autoactivation pathway, the Alternate pathway and the level of complement component, C3. Reconstitution studies using C5-deficient serum also demonstrated deleterious effects on this complement component. The Classical pathway was the most sensitive to Technical Grade PCP effects. Animals treated with 100 mg/kg Technical Grade PCP had CH 50 levels 30% of vehicle controls. Animals treated for 14 days and allowed a 15 day recovery period had CH 50 values 36% of control and animals which recovered for 30 days had only 52% of the complement activity of control animals. C3 recovery studies also demonstrated continued suppression on days 15 and 30 post-final exposure. Doses of 10 and 30 mg/kg did not produce the marked effects observed with the highest dose; however, a dose-dependent trend was observed for all responses. Animals treated with 100 mg/kg of EC-7, a PCP preparation with reduced amounts of contaminating dioxins and dibenzofurans, did not demonstrate detrimental effects on the complement system.

Pentachlorophenol toxicity to amphipods and fathead minnows at different test pH values

AbstractJuvenile amphipods (Gammarus pseudolimnaeus and Crangonyx pseudogracilis) and fathead minnows (Pimephales promelas) were exposed to pentachlorophenol (PCP) at pH values of 6.5, 7.5, 8.0 and 8.5 for 96 h, and early life stages of fathead minnows were exposed for 32 d at the same pH values to determine the relationship between test pH and the acute and chronic toxicity of PCP. Residue analyses were performed on fathead minnows after 32 d to determine the relationship between test pH and PCP bioaccumulation. Technical‐grade PCP (88% active ingredient; Dowicide EC7) was used as the toxicant source.Acute exposures with all three species showed that PCP toxicity was decreased with increased test pH. The slopes of this relationship were similar for the amphipods, but were different from that observed for fathead minnows. Early life stage exposures of fathead minnows showed that chronic PCP toxicity and bioaccumulation were similarly decreased when pH values were increased. The decrease in chronic PCP toxicity appeared to be due to the reduction in PCP accumulation as a direct result of the increased ionization of PCP at higher pH values, indicating that the ionized form was less toxic per unit concentration than was the un‐ionized form. However, these studies suggest that chronic as well as acute toxicity may be caused by both forms of PCP when significant concentrations are present in solution.

Effects of dietary technical pentachlorophenol exposure on T cell, macrophage and natural killer cell activity in C57Bl/6 mice.

The effects of technical grade pentachlorophenol (T-PCP) exposure on several immunological parameters were examined in adult C57Bl/6 mice following eight weeks of dietary exposure. Immune function tests included mitogen-induced lymphocyte blastogenesis, mixed lymphocyte reactivity (proliferation and cytotoxicity), spontaneous and boosted levels of natural killer (NK) cytotoxicity, and phagocytic activity of resident, thioglycollate-induced, and P815-tumor activated peritoneal macrophages. Thymic and splenic weights, spleen cellularity, percentages of splenic T and B cells, and bone marrow cellularity were also determined. The only statistically significant functional alteration observed in T-PCP exposed mice in these studies was a reduction in the lymphoproliferative response in mixed lymphocyte culture which occurred in the absence of any apparent effect on the generation of cytotoxic cells. Mitogen responses, NK cytotoxicity and macrophage phagocytosis were unaltered by exposure to T-PCP. No changes were observed in spleen or thymus weights or in spleen or bone marrow cellularity. A dose-responsive trend toward reduced T cell and increased B cell percentages in the spleen of T-PCP exposed mice was noted. The apparent functional resistance of T cells, macrophages, and NK cells to T-PCP is in contrast to the marked sensitivity of the humoral immune response to T-PCP induced suppression. The results are discussed in relation to the dioxin contaminants present in T-PCP.

Effect of pentachlorophenol on the growth and mortality of embryonic and juvenile steelhead trout

The toxicity of sodium pentachlorophenate to early life stages of steelhead trout (Salmo gairdneri) was investigated, using a flowthrough exposure system. A 96-hr LC50 of 66 μg/ L was derived for previously unexposed ten-week-old fry. A 72-day test, beginning 24 hr after fertilization, yielded a chronic toxicity threshold of 14 μg/L. These results, and the acute/chronic ratio of 4.7, compare reasonably well with values in the literature. Yolk sac edema and cranial malformations, which are commonly observed in chronic tests with technical grade pentachlorophenol, were rare in this test with purified (99%) material.

Identification of Chlorinated Phenyl and Phenoxy Substituted Dibenzodioxin, Dibenzofuran, and Diphenyl Ether Homologs in Commercial Grade Pentachlorophenol

Abstract As part of a bioassay study by the National Toxicology Program, technical grade pentachlorophenol (PCP) was analyzed for chlorinated impurities using capillary gas chromatography/mass spectrometry (GC/MS). Several high molecular weight impurities eluting after octachlorodibenzodioxin were detected during the analysis of this material. These impurities were tentatively identified according to structural classes as chlorinated triphenyl ethers, dibenzodioxin phenyl ethers, phenyldibenzodioxins, and dibenzofuran phenyl ethers.

Subchronic Administration of Technical Pentachlorophenol to Lactating Dairy Cattle: Performance, General Health, and Pathologic Changes1,2

Technical grade pentachlorophenol (penta) was fed subchronically to lactating dairy cattle to establish whether exposure approximating farm environments containing substantial penta-treated wood represents a hazard to animal health. Four Holstein cattie in early lactation were fed .2mg penta/kg body weight per day for 75 to 84 days followed by 2mg penta/kg body weight per day for 56 to 60 days. Each treated cow was paired with a control cow of equivalent stage of lactation. Milk production, feed intake, and body weight were not affected by either dose except that treated cattle were more efficient converters of feed to milk during the early stage of the 2mg/kg period. Neither milk fat production nor somatic cell count in milk were affected by exposure to penta. Postmortem examination revealed enlargement of liver, lungs, kidneys, and adrenals and thickening of the urinary bladder wall. Chronic interstitial nephritis and subacute urocystitis were the major pathologic changes in penta-treated cattle. In vitro testing of kidney slices confirmed significant loss of renal function. The relationship of lesions to administration of penta is not clear.

Dioxin levels in raw and cooked liver, loin steaks, round, and patties from beef fed technical grade pentachlorophenol

Dioxin levels in raw and cooked liver, loin steaks, round, and patties from beef fed technical grade pentachlorophenol