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At least 19 recordsLinked to original sources
PubMed1979

Comparison of the compositions of Aroclor 1242 and Aroclor 1016.

The complete polychlorinated biphenyl compositions of two American products, Aroclor 1242 and its more modern replacement, Aroclor 1016, have been determined by gas-liquid chromatography (GLC) on twelve liquid phases of differing selectivities. Attempts were made to determine the degree of contamination of these Aroclors with chlorinated naphthalenes, using GLC with multiple ion-monitoring mass spectrometry. Chlorinated dibenzofurans, indetectable in Aroclor 1016, were tentatively identified by negative chemical-ionization mass spectrometry and their retention times relative to dieldrin on two GLC liquid phases. Quantitation of the dibenzofurans was initially accomplished using an electron-capture detector, and confirmed by negative chemical-ionization mass spectrometry. Aroclor 1242 contained less than 0.05 mol.% chloronaphthalenes, while Aroclor 1016 contained less than 0.06 mol.% of these compounds. Aroclor 1242 had approximately 150 ppb of chlorinated dibenzofurans, of which 43% was the toxic 2,3,7,8-tetrachloro isomer.

Aroclors↗
PubMed1977

Inhibitory effect of a polychlorinated biphenyl (Aroclor 1254) on aflatoxin B1 carcinogenesis in rainbow trout (Salmo gairdneri).

Duplicate lots of 120 rainbow trout (Salmo gairdneri) fingerlings were fed for 1 year semipurified diets containing 6 ppb aflatoxin B1 (AFB1), 100 ppm Aroclor 1254 (a polychlorinated biphenyl), and 6 ppb AFB1 plus 100 ppm Aroclor 1254. Appropriate controls were also maintained. Samples were taken at 1, 2, 4, 6, 9, and 12 months to monitor tumor incidence, Aroclor 1254 accumulation, and histopathology of liver, spleen, and kidney tissues. At the end of the year, 26 of 37 (70.3%) trout fed 6 ppb AFB1 had hepatocellular carcinomas, compared to 14 of 46 (30.4%) trout fed 6 ppb AFB1 plus 100 ppm Aroclor 1254, a highly significant reduction in tumor incidence in the trout on the Aroclor 1254-containing diet. None of the control or Aroclor 1254-fed fish had liver tumors. Levels of Aroclor 1254 increased rapidly during the first 6 months, then plateaued at approximately 80 ppm on a whole-fish basis. AFB1 inhibited growth but Aroclor 1254 did not. Glycogen depletion of hepatocytes and hyperemia, and white pulp depletion of the spleen were the only changes induced by Aroclor 1254.

Aflatoxins↗
PubMed1977

Tissue distribution of PCB components in swine and sheep fed three different rations containing Aroclors 1242 and 1254.

Growing swine and sheep were fed three dietary variations containing 20 ppm of Aroclors 1242 or 1254 for 13 to 15 weeks. Generally, Aroclor 1254 residues were higher; higher 1242 residues in swine blood, spleen, and ovary are attributed to persistent major components of this Aroclors. Some minor differences in total PCB were observed with varying diets, but peak composition did not vary. Some lower chlorinated components maintained higher levels in the blood relative to other components; other components were selectively accumulated in tissues such as fat and muscle. Blood and fat residues in sheep declined during the last weeks of feeding. Microsomal oxidase levels were elevated in response to PCB and diet in both species, but the response was greater in sheep. Sheep liver microsomes were capable of metabolizing pure analogs and components of Aroclor 1242. Major differences in Aroclor profiles can be demonstrated between swine and sheep residues and total residues can be estimated by measuring selected peaks in blood and backfat. The peaks which provide the most reliable estimate of total PCB residue vary with species and Aroclor.

Animal Feed↗
PubMed1979

Studies on the mutagenicity of p-phenylenediamine in Salmonella typhimurium. Presence of PCB's in rat-liver microsomal fraction induced by Aroclor.

The mutagenicity of fresh solutions of p-phenylenediamine (PPD) and Aroclor 1254 was investigated. The histidine-requiring strains of Salmonella typhimurium were used in the absence and presence of uninduced and/or Aroclor-induced rat-liver homogenate. The presence of polychlorinated biphenyls (PCBs) was also examined by chromatographic methods in Aroclor-induced rat-liver homogenate. In the absence of metabolic activation, as well as in the presence of uninduced rat-liver homogenate, PPD was not mutagenic in the strains used. In the presence of Aroclor-induced S9 a twofold increase (or less) was observed in the number of revertant colonies over those of the controls in TA1538 and TA98. There was no increase in the number of revertant colonies over those of the controls when PPD was dissolved in NH4OH solution and the solution mixed with H2O2 before the addition of S9 mix. Aroclor 1254 was not mutagenic in TA1538 or TA98. However, the presence of PCBs in Aroclor-induced rat-liver homogenate (induced S9) was identified by gas-liquid chromatography (GLC), high-performance liquid chromatography (HPLC) and gas--liquid chromatography/mass spectrometry (GC/MS).

Animals↗
PubMedDate not supplied

Use and health effects of Aroclor 1242, a polychlorinated biphenyl, in an electrical industry.

Aroclor 1242, a chlorinated biphenyl, is widely used as a dielectric medium in transformers and capacitors. In this survey, thirty-four occupationally exposed workers were examined. Complaints consisted of a burning sensation of the face and hands, nausea, and a persistent body odor. One had chloracne, and five suffered from an eczematous rash on the legs and hands. Although hepatic function tests were normal, the mean blood Aroclor level in the exposed group (approximately 400 ppb) was significantly higher than in the control group. A tentative value of 200 ppb is suggested for Aroclor 1242 as an acceptable level for occupationally exposed workers. The use of an efficient exhaust ventilation to maintain air concentrations below the threshold limit value, and the regular measurements of hepatic function and of blood Aroclor concentrations in exposed workers are recommended.

Absorption↗
PubMed1979

Biochemical basis of aroclor 1254 and pesticide toxicity in vitro. 1. Effects on intracellular ATP concentration.

Aroclor 1254 and op'-DDT inhibit lymphocyte mitogenic response to PHA. We use petri dish purified lymphocytes for studying the biochemical basis of chemical toxicity. Aroclor 1254 and DDT decrease lymphocyte intracellular ATP concentration. The inhibitory effect on ATP production is due to the suppression of mitochondrial respiration as judged by decreased oxygen consumption. Lymphocyte glycolysis measured by lactate production is not inhibited by Aroclor 1254 to any significant extent. ATP is required for various biosynthetic reactions following mitogenic stimulation. The inhibition of mitochondrial respiration which leads to decreased ATP concentration may be responsible for Aroclor inhibition of lymphocyte mitogenic response to PHA.

Adenosine Triphosphate↗
PubMed1979

Effects of the hepatic S9 fraction from aroclor-1254-treated rats on the mutagenicity of benzo[alpha]pyrene and 2-aminoanthracene in the Salmonella/microsome assay.

The mutagenicity of benzo[alpha]pyrene and 2-aminoanthracene for Salmonella typhimurium TA98 in the plate-incorporation test was studied using liver S9 from untreated and aroclor-1254-treated rats. The induction of liver S9 protein, arylhydrocarbon hydroxylase (AHH), and cytochrome P448/450 was followed with time. There was no change in protein concentrations with induction; AHH and cytochrome levels were increased at 1, 3, 5 and 7 days post Aroclor treatment. Benzo[alpha]pyrene mutagenicity was enhanced with Aroclor treatment while 2-aminoanthracene mutagenicity was depressed. The benzo[alpha]pyrene mutagenicity showed a positive correlation with the levels of AHH and cytochrome on the plate; 2-aminoanthracene showed a negative correlation with activity in induced samples.

Animals↗
PubMed1979

The induction of hepatic and extrahepatic xenobiotic metabolism in the rat and ferret by a polychlorinated biphenyl mixture (Aroclor 1254).

1. The effect of a single i.p. dose (500 mg/kg) of a polychlorinated biphenyl mixture (Aroclor 1254) on hepatic and extrahepatic xenobiotic metabolism in male rat, and male and female ferret, was studied. 2. Aroclor 1254 treatment induced hepatic microsomal N-demethylase activities, and cytochrome P-450 and protein content in both rat and ferret. Liver size and aniline 4-hydroxylase were also increased in rat, but not ferret. The polychlorinated biphenyl mixture appeared to be a mixed-type inducer of hepatic xenobiotic metabolism in both species. 3. Aroclor 1254 treatment produced large increases in activities of benzo(a)pyrene hydroxylase and 7-ethoxycoumarin O-deethylase in whole homogenates of the liver, small intestinal mucosa, kidneys and lungs of both species. Maximal stimulation of xenobiotic metabolism occurred in the kidney of both the rat and ferret. In contrast, UDP-glucuronyltransferase activity was only stimulated in liver, intestine and kidney of the rat and in liver and intestine of the ferret. 4. These results suggest a general species similarity in the response to the polychlorinated biphenyl mixture between the rat and ferret.

Animals↗
PubMed1975

Effect of polychlorinated biphenyls (Aroclor 1254) on inducible and repressible microsomal N-demethylases in the mouse and rat.

A comparative study of the effects of the polychlorinated biphenyl mixture Aroclor 1254, 3-methylcholanthrene, and starvation on hepatic dimethylnitrosamine (DMN) demethylase (a repressible enzyme) and azo dye N-demethylase (an inducible enzyme) has been carried out. As previously observed with polycyclic hydrocarbons and phenobarbital, Aroclor in rats is a potent inducer of liver tissue proliferation and of azo dye N-demethylase. However, in mice, although the inducing effect on liver tissue proliferation and azo dye N-demethylase activity is maintained, there is no change in DMN demethylase activity as a result of Aroclor administration. As in rats, 3-methylcholanthrene induces the azo dye N-demethylase in mice. This hydrocarbon, which is known to substantially repress the DMN demethylase in rats, has, however, no effect on this enzyme in mice. While starvation is known to have a substantial inducing effect on DMN demethylase in rats, in mice starvation brings about a moderate induction of DMN demethylase.

Animals↗
PubMed1976

Apparent pharmacokinetics of PCB components in growing pigs and lambs when fed a ration containing Aroclor 1254.

Young growing lambs and pigs were fed a ration containing 200 ppm of Aroclor 1254 for 35 days and then switched to "clean" feed. Blood and fat samples were collected periodically throughout the experiment and analyzed for components of Aroclor 1254 and total PCB. Several components are apparently accumulated and eliminated at different rates within each species, as seen by comparing gas chromatograph tracings, accumulation ratios and apparent rate constants of elimination. Differences in accumulation and elimination of Aroclor components, some of which were apparently caused by differences in growth rates, were also seen between pigs and lambs. Variable growth rates of different species of food producing animals are an important factor to consider when dealing with tissue distribution and residues of polychlorinated biphenyls for determination of carcass disposition, as well as accumulation of toxic concentrations in the animal body.

Adipose Tissue↗
PubMed1978

The effect of polychlorobiphenyls (Aroclor 1242) on bicarbonate-C14 uptake by Euglena gracilis.

Aroclor 1242 is inhibitory to long-term batch growth of Euglena gracilis at 10 ppm. Exposure to PCB's, subsequent to an initial drop of 50% in the first 30 minutes, does not appear to inhibit photosynthesis on a per cell basis over the time span of four hours. Consequently our experimental findings suggest that inhibition of population growth does not lie directly in the photosynthetic pathway despite the initial inhibition by Aroclor 1242 on Euglena gracilis in "light". "Dark" absorption of bicarbonate appears to decrease with increased PCB exposure. This decrease may be causally related to the population growth inhibition observed.

Animals↗
PubMed1975

Further studies on the use of enzyme profiles to monitor residue accumulation in wildlife: plasma enzymes in starlings fed graded concentrations of Morsodren, DDE, Aroclor 1254 and malathion.

Wild-trapped starlings (Sturnus vulgaris) were fed concentrations of Morsodren (2, 4, and 8 ppm), DDE or Aroclor 1254 (5, 25, and 100 ppm), or malathion (8, 35, and 160 ppm) that were found to be sublethal in pen-reared Coturnix quail fed these amounts for 12 weeks. Plasma enzymes had to be measured earlier than planned in starlings fed Morsodren (at three weeks) or the organochlorine compounds (at seven weeks) because of unexpected, subsequent mortality. Variations in enzyme response were greater in wild than in pen-reared birds, but not enough to mask the toxicant-induced changes in enzyme activity. Cholinesterase activities decreased in birds fed Morsodren or malathion, and increased in those fed the organochlorine compounds. Lactate dehydrogenase activities increased two-fold in starlings fed Morsodren and two- to four-fold in those fed the organochlorine compounds, but only 50% in those fed malathion. Further examination of enzyme profiles showed that creatine kinase and aspartate aminotransferase activities increased two- to four-fold in birds fed Morsodren or the organochlorine compounds but not at all in those fed malathion. Thus the classes of environmental contaminants fed to starlings could be easily distinguished by these enzymatic parameters. Evaluation of enzymatic profiles appears to be a potentially valuable technique to monitor the presence of toxicants in wild populations, especially if used to complement standard chemical residue analyses. Here the residue analyses showed, after three weeks feeding, that mercury in the carcasses reflected the concentrations fed daily, whereas accumulation in the livers was two- to four-fold greater. After seven weeks feeding, liver residues of either organochlorine compound were about three-fold higher than the concentrations fed daily. However, four times as much DDE as Aroclor 1254 had accumulated in the carcasses.

Animals↗
PubMed1977

A study of the effects of methyl mercury, cadmium, arsenic, selenium, and a PCB, (Aroclor 1254) on adrenal and testicular steroidogeneses in vitro, by the gray seal Halichoerus grypus.

An in vitro study on the effects of the contaminants polychlorinated biphenyl (Aroclor 1254) (PCB), methyl mercury (MeHg), arsenic (As), cadmium (Cd), and selenium (Se) on the biosynthesis of steroid hormones in the gray seal (Halichoerus grypus) indicated altered steroid biosynthesis. Biotransformed delta4-androstene-3, 17-dione (delta 4A), dehydroepiandrosterone, 11-ketotestosterone (11-KT), and testosterone (T) were detected in all seal testicular incubates. Yields of 11-KT were greatly increased in the presence of Aroclor 1254. All contaminants except As and Se stimulated the in vitro biosyntheses of T, with the greatest increase in production of T being in the Cd-treated tissue. Cortisol (F), corticosterone (B), aldosterone (ALDO) but no cortisone (E), were biosynthesized by the seal adrenal tissue. Corticosterone (B) was the principal transformation product in all incubations with less B produced by the treated adrenals than by the control. The lowest yeild of B was achieved by the Se-treated adrenal. The yeild of ALDO was also lower in all contaminant treated incubations, with Se and Cd giving the greatest inhibition. More F was biosynthesized by all the treated adrenals than by the control. The greatest increase of production of F(6-fold) from progesterone was by the As-treated adrenal.

Acetylation↗
PubMed1979

Non-mutagenicity for Salmonella of the chlorinated hydrocarbons aroclor 1254, 1,2,4-trichlorobenzene, mirex and kepone.

A polychlorinated biphenyl mixture, Aroclor 1254, two commercial grade insecticides, mirex and kepone, and a pesticide breakdown product, 1,2,4-trichlorobenzene were evaluated for mutagenicity and hepatic enzyme induction potential in the Salmonella/microsomal assay. None was found to revert strains TA1535, TA1537, TA98 or TA100 when tested with or without metabolic activation. Liver microsomal extracts (S9) from rats induced with 1,2,4-trichlorobenzene were shown to differ from S9 of either control or Aroclor 1254-induced rats in the capacity to activate 2-aminoanthracene mutagenesis.

Aroclors↗
PubMed1975

Induction of liver tumor in Sherman strain female rats by polychlorinated biphenyl aroclor 1260.

Sherman strain female rats (200) were fed 100 ppm of polychlorinated biphenyl (Aroclor 1260) for apporximately 21 months, and 200 female rats were kept as controls. The rats were killed when 23 months old. Twenty-six of 184 experimental animals and 1 of 173 controls had hepatocellular carcinomas. None of the controls but 146 of 184 experimental rats had neoplastic nodules in their livers, and areas of hepatocellular alteration were noted in 28 of 173 controls and 182 of 184 experimental animals. Thus the polychlorinated biphenyl Aroclor 1260, when fed in the diet, had a hepatocarcinogenic effect in these rats. The incidence of tumors in other organs did not differ appreciably between the experimental and control groups.

Animals↗