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At least 19 recordsLinked to original sources
PubMed2006

Occurrence of polybrominated biphenyls, polybrominated dibenzo-p-dioxins, and polybrominated dibenzofurans as impurities in commercial polybrominated diphenyl ether mixtures.

The objective of this study was to determine the concentrations and compositions of polybrominated biphenyls (PBBs), polybrominated dibenzo-p-dioxins (PBDDs), and polybrominated dibenzofurans (PBDFs) as contaminants in the commercial polybrominated diphenyl ether (PBDE) mixtures DE-71, DE-79, and DE-83 and to ascertain the lot-to-lot variations in the proportions of these contaminants. Commercial PBDE mixtures tested in the present study contained both PBBs and PBDFs, as impurities, at concentrations in the range of several tens to several thousands of nanograms per gram. Concentrations of total PBDFs were greater than those of total PBBs in DE-79 and DE-83 mixtures. PBDDs were not detected at levels above the limit of detection. Profiles of PBB and PBDF congeners varied with the degree of bromination of the commercial PBDE mixtures (i.e., more highly brominated mixtures of PBDEs contained heavily brominated homologues of PBBs and PBDFs). On the basis of the production/ usage of commercial PBDE mixtures in 2001, potential global annual emissions of PBBs and PBDFs were calculated to be 40 and 2300 kg, respectively. Results of our study suggestthat PBDFs can also be formed during the production of commercial PBDE mixtures, in addition to their formation during pyrolysis of brominated flame retardants.

Benzofurans↗
PubMed1999

Polychlorinated biphenyls, polybrominated biphenyls, and dioxin reduction during processing/cooking food.

This chapter presents information on the levels of environmental contaminants found in recent market basket surveys as well as the effect of processing and cooking on the reduction of these contaminants. Although consumers have expressed concern over the level of environmental contaminants in the food supply, market basket surveys involving over 8,000 analyses of foods ready-to-eat, found measurable amounts (ppb levels) of PCBs in only 24 foods. Processing/cooking has been shown to reduce PCBs by 20-100%. Although PBBs got into the food chain as the result of one incredible accident and thus are not expected to be found in foods today, cooking/processing was also effective in reducing PBBs. Dioxins are the result of combustion processes and chemical manufacturing processes. TCDD levels found in Great Lakes fish were in the low part per trillion level. Again, cooking and processing resulted in substantially less TCDD in fish as eaten.

Animals↗
PubMed1979

Action of exogenously administered steroid hormones following perinatal exposure to polybrominated biphenyls.

Polybrominated biphenyls (PBBs) have produced a variety of effects including alterations in the endocrine system and in the activity of microsomal mixed-function oxidases (MFOs). Because steroid hormones are substrates for MFOs, effects of PBBs on the endocrine system may be a consequence of enhanced steroid hormone catabolism. Therefore, as a first step in evaluating the effect of PBBs on steroid hormone catabolism. Therefore, as a first step in evaluating the effect of PBBs on steroid hormone metabolism, it was of interest to determine effects of perinatal exposure to PBBs on the response to exogenously adminstered steroid hormones. Rats were exposed to 0, 10, or 100 ppm PBBs from d 8 of gestation until d 28 postpartum, when experiments were conducted. Responses to labeled steroid hormones were generally modified in a manner directly related to PBB dose and were correlated with changes in serum and target tissue retroactivity. Stimulated metabolism of steroid hormones may account, at least in part, for endocrine-related alterations produced by PBBs. Although the potential for decreased reproductive capacity following PBBs cannot yet be accurately predicted, these experiments suggest that fertility may be reduced following PBBs as a consequence of accelerated steroid hormone metabolism and/or excretion.

Animals↗
PubMedDate not supplied

Comparative toxicity of polychlorinated biphenyl and polybrominated biphenyl in the rat liver: light and electron microscopic alterations after subacute dietary exposure.

The comparative toxicity of polychlorinated biphenyl (PCB) and polybrominated biphenyl (PBB) in livers was studied in male Holtzman rats. Four-week-old animals were fed at dietary levels of 0, 5, 50, or 500 ppm for 5 weeks and then sacrificed. The mean liver-body weight ratios of the 50 and 500 ppm groups were increased. Histopathologic examination of the livers revealed fatty degenerative change associated with both compounds. This change was more marked at 500 than at 50 ppm. Various sized lamellar cytoplasmic inclusions were detected in livers of animals fed 500 ppm of either compound. However, the inclusions were more numerous in the PBB-treated rats. Several animals fed 50 ppm PBB had a few inclusions. In rats that received 500 ppm PBB, hypertrophic degenerative hepatocytes were present around the central veins. On the periphery of this change there were occasionally multinucleated hepatocytes. Electron microscopic examination at a dose level of 5 ppm in both the PCB and PBB groups showed a slight proliferation of smooth endoplasmic reticulum (SER), a moderate increase of lipid droplets and some liposomes, and a marked proliferation of Golgi condensing vesicles containing lipoprotein particles. A decreased number of mitochondria and lysosomes was also observed. At 50 ppm, similar but more marked ultrastructural alterations were seen. In addition, an increased number of branched and cup-shaped profiles of mitochondria and a decreased number of Golgi condensing vesicles containing lipoprotein particles were observed. Concentric membranous cytoplasmic whorls were encountered only in the 50 ppm PBB-treated rats. At 500 ppm the number of mitochondria decreased in both groups. There was also a marked increase in the number of SER and liposomes concomitant with a decreased number of Golgi condensing vesicles containing lipoprotein granules. Membranous whorls were also present in the 500 ppm groups.

Animals↗
PubMed1983

The comparative biologic and toxic potencies of polychlorinated biphenyls and polybrominated biphenyls.

Aroclor 1254 and fireMaster BP-6, two commercial polychlorinated biphenyl (PCB) and polybrominated biphenyl (PBB) preparations, exhibit comparable biologic and toxic effects. In the present study the commercial PBB was more active than Aroclor 1254 in causing thymic atrophy in male Wistar rats. However, a direct comparison of the relative effects of bromine vs chlorine substituents is not possible with the commercial PBB and PCB mixtures due to their complex congeneric composition. This study reports the synthesis and biologic and toxic effects of a series of laterally substituted 3,3',4,4'-tetrahalobiphenyls which contain the following variable molecular Cl/Br ratios; Br4, Br3Cl, Br2Cl2 (two isomers), BrCl3, and Cl4. 3,3',4,4'-Tetrabromobiphenyl and 3,4,4'-tribromo-3'-chlorobiphenyl (150 mumol/kg)-pretreated animals significantly inhibited the growth rate of and caused thymic atrophy in immature male Wistar rats whereas those isostereomers with reduced Br (and increased Cl) content were either less active or inactive. Pretreatment of male Wistar rats with 10 mumol/kg of the 3,3',4,4'-tetrahalobiphenyls and determination of their effects as inducers of the hepatic microsomal drug-metabolizing enzymes also illustrated the effects of the relative Cl/Br ratios on induction potencies. Both 3,3',4,4'-tetrabromo- and 3,4,4'-tribromo-3'-chlorobiphenyl maximally induced the cytochrome P-448-dependent monooxygenases, benzo[a]pyrene and 4-chlorobiphenyl hydroxylase; the order of potency of the other isostereomers was 4,4'-dibromo-3,3'-dichloro- congruent to 3,4-dibromo-3',4'-dichlorobiphenyl greater than 4-bromo-3,3',4'-trichloro- greater than 3,3',4,4'-tetrachlorobiphenyl. With few exceptions this order of potency was observed for the induction of benzo[a]pyrene hydroxylase and ethoxyresorufin O-deethylase in rat hepatoma cells in culture and for their relative binding affinities to the rat cytosolic receptor protein. The data clearly demonstrate that the biologic activities of this group of isosteric halogenated biphenyls are enhanced with increasing bromine substitution and also support the hypothesis that the activities of this class of chemicals are mediated through the receptor.

Animals↗
PubMed1987

Hypothyroidism and abnormalities in the kinetics of thyroid hormone metabolism in rats treated chronically with polychlorinated biphenyl and polybrominated biphenyl.

Studies were directed at the question of whether polychlorinated biphenyl (PCB; Aroclor 1254) and polybrominated biphenyl (PBB; Fire Master BP-6), when administered in the diets of female Sprague-Dawley rats over long periods of time (5-7 months) and at low dosages (0, 1, 5, 10, and 50 ppm), would depress the thyroid. By examining serum T3 and T4, kinetics of T4 metabolism, and in vivo thyroid response to exogenous TSH injections, an estimate of the degree of hypothyroidism was made, and abnormalities in T4 disappearance from serum were encountered. Serum T3 and T4 levels were greatly suppressed in a dose-related manner by PCB or PBB treatment. There was a diminished response of serum T3 and T4 to TSH injection in rats pretreated with PCB or PBB (5 and 10 ppm), the exception being T3 in the 5 ppm PCB treatment group. Had the PCB and PBB treatment-induced suppression of T4 and T3 been on the hypothalamo-pituitary axis, the response of the treated rats to exogenous TSH might have exceeded that of controls; however, the opposite occurred. Disappearance of injected doses of L-[125I]T4 diminished as treatment concentrations of PCB or PBB increased. Disappearance slopes (r = 0.98) and fractional turnover rate constants (k) were decreased (t1/2 was lengthened) at each treatment level compared to the control values. The T4 distribution space (per 100 g BW) was expanded with increasing dosage by as much as 8-fold in the 50 pmm PCB treatment group. T4 MCRs were not increased by PCB or PBB treatment; thus, decreases in serum T3 and T4 were not caused by increased catabolism. T4 production rates were decreased at all treatment levels, but maximally 6-fold by 50 ppm PCB treatment. Together these data indicate that PCB-PBB-induced decreases in serum T3 and T4 result primarily from direct damage to the thyroid rather than any enhanced hepatic or other peripheral catabolism per se. Expanded T4 distribution space demonstrated that nonthyroid damage was also an important factor in reducing serum T4. Cell membrane damage associated with PCB-PBB intoxication may have expanded pools for T4 dilution. The findings are consistent with reported histological and ultrastructural damage caused by PCB and PBB. It also appears that TSH plays little role in PCB-PBB-induced hypothyroidism.

Animals↗
PubMed1989

Determinants of polychlorinated biphenyls (PCBs), polybrominated biphenyls (PBBs), and dichlorodiphenyl trichloroethane (DDT) levels in the sera of young children.

Serum samples from 285 4-year-old Michigan children were evaluated for levels of 11 environmental contaminants. Polychlorinated biphenyls (PCBs) were found in half the samples tested; polybrominated biphenyls (PBBs) in 13-21 percent; dichlorodiphenyl trichloroethane (DDT), in more than 70 percent. Nursing (Mothers' milk) was the principal source of these exposures. Congener-specific analysis documented the presence of at least one highly toxic PCB congener, 2,3',4,4',5-pentachlorobiphenyl. The data demonstrate the multigenerational impact of female exposure to persistent organic environmental contaminants.

Body Burden↗
PubMed1984

The transfer of polychlorinated biphenyls (PCBs) and polybrominated biphenyls (PBBs) across the human placenta and into maternal milk.

Cord serum and maternal milk levels of polychlorinated biphenyls (PCBs) and polybrominated biphenyls (PBBs) were examined in relation to maternal serum levels. Maternal serum levels were significantly higher than cord serum levels for both types of compounds. Placental passage was indicated by significant maternal to cord serum correlations for both PCBs (r = .42) and PBBs (r = .81). Correlations between maternal serum and milk levels were similar. Higher PBB correlations were probably due to greater reliability in the measurement of PBB levels in serum and milk.

Environmental Pollutants↗
PubMed1984

Polychlorinated biphenyls (PCBs) and polybrominated biphenyls (PBBs): biochemistry, toxicology, and mechanism of action.

Polychlorinated and polybrominated biphenyls are industrial chemical mixtures which have been implicated in numerous human poisonings in Taiwan and Japan (PCBs) and Michigan (PBBs). Moreover, these polyhalogenated biphenyls have been widely detected in the environment including the air, water, fish, wildlife, human adipose tissue, and blood and breast milk. A major problem associated with the analysis and toxicology of this group of chemicals is their chemical complexity (e.g., there are 209 possible PCB isomers and congeners) and the remarkable effects of structure on activity. This article will discuss the effects of structure on the biologic and toxic effects of individual PCB and PBB congeners as well as reconstituted mixtures. The results clearly show that like "dioxin" (or 2,3,7,8-TCDD), the PCBs and PBBs elicit their effects through a cytosolic receptor protein which preferentially binds with the toxins which are approximate isostereomers of 2,3,7,8-TCDD. The evidence for this mechanism of action will be discussed in detail.

Acne Vulgaris↗
PubMed1982

Inhibition of purified rabbit muscle phosphorylase a and phosphorylase b by polychlorinated biphenyls, polychlorinated biphenylols and polybrominated biphenyls.

Polychlorinated biphenyls, polychlorinated biphenylols and polybrominated biphenyls inhibited both rabbit muscle phosphorylase a and phosphorylase b (1,4-alpha-D-glucan:orthophosphate alpha-d-glucosyltransferase, EC 2.4.1.1). The degree of inhibition was dependent upon the relative hydrophobicity of the compounds and steric hinderance. 2,4,5,2',4',5'-Hexabromobiphenyl and Firemaster BP-6 were the most effective inhibitors (Ki, 15 . 10(-6) M). Phosphorylase b was inhibited by compounds of all three groups. 2,4,5,2',4',5'-Hexachlorobiphenyl and 2,4,5,2',4',5'-hexabromobiphenyl did not significantly inhibit phosphorylase a. All of the compounds inhibited phosphorylase a less than phosphorylase b, except 2',3',4',5,5'-pentachloro-2-biphenylol, which was equally effective on each enzyme. Kinetic analysis showed the inhibition was non-competitive and mixed. The results indicate that the compounds bind to hydrophobic site(s) on phosphorylase, access to which is limited by phosphorylation of serine 24.

Animals↗
PubMed1975

Effects of polychlorinated biphenyls and terphenyls and polybrominated biphenyls on pentobarbital sleeping times of Japanese quail.

Polychlorinated biphenyls (Aroclor 1221, 1232, 1242, 1248, 1254, 1260, 1262, and 1268), polychlorinated terphenyls (Aroclor 5460), a mixture of polychlorinated biphenyls and terphenyls (Aroclor 4465) and polybrominated biphenyls (BP-6) were administered in a single dose, 100 mg/kg body weight injected orally, to mature male and female Japanese quail. Two hr after Aroclor treatment, pentobarbital sleeping times were prolonged (2 to 3 times control) in both male and female quail. Twenty-four hr after treatment, sleeping times were similar to those of controls. However, 48 hr after treatment with Aroclor 1248 through Arolcor 5460 and with BP-6, sleeping times of males were only 1/2 those of controls, whereas after treatment with Aroclor 1221, 1232 and 1242, sleeping times were similar to those of controls. The reduction in sleeping times of male quail 48 hr after administration of PCBs was correlated with the percentage of chlorine in the PCB with greater reductions in male than female quail. The response after three days ad libitum feeding of 300 ppm of each substance was the same as the response 48 hr after a single oral injection. Although very few birds died from the toxicity of the Aroclors and BP-6, mortality was greatly increased during anesthesia when the pentobarbital was administered two hr after single oral dosing.

Animals↗
PubMed1977

The biological effects of polybrominated biphenyls in avian species.

Polybrominated biphenyl (PBB), structurally similar to polychlorinated biphenyl (PCB), affects feed intake, egg production, and hatchability of fertile eggs in chickens and quail. Subcutaneous edema of the neck and shoulder are common abnormalities of hatched chicks from PBB-fed dams. No characteristic teratogenicity is evident. Offspring hatched are less viable during their first 3 weeks of life. PBB does not produce thinner egg shells or lower egg weights. The ratio of PBB egg content to dietary level is 1.3-1.5:1.0. The biological half-life of PBB in eggs is calculated to be 17 days. Tissue residues are higher in males than females because egg production is a major excretory route for PBB. Polybrominated biphenyl feeding causes tissue changes in size, structure and/or function in the liver, thyroid, testes, comb, heart, spleen, bursa of Fabricus, and blood. Liver enlargement, porphyria and microsomal enzyme induction results from PBB administration. The spleen, bursa and comb are reduced in size, whereas the thyroid increases after PBB feeding. A characteristic of PBB and PCB toxicity is hydropericardium and general edema.

Animals↗
PubMed1982

Performance and health of offspring of cows experimentally exposed to polybrominated biphenyls.

Offspring of cows experimentally given polybrominated biphenyls(fire-Master BP-6) were studied from May 1976 through January 1981. Daily doses were 0,.25, and 250 mg for 60 days for Groups I, II, and III, and 250 mg for 180 or 202 days for Group V. Concentrations of polybrominated biphenyls in fat of dosed animals in Groups I, II, and III, and V were .05, .20, 25, and 30 micrograms/g at the end of dosing. Residue concentrations in body fat declined with a half life of about 1 yr. Seventy-five calves were born to these cows and their offspring, representing first through fifth parturition. Fifteen calves died, 10 of which were in Groups III and V. All deaths in Groups III and V were attributable to dystocia. Incidence od dystocia and calf mortality were related to birth weight of the calf which in turn was correlated with concentrations of polybrominated biphenyls in blood and tissues of the dam. Other variables that influenced birth weight were sex of calf, length of gestation, and parturition number of dam. There were no significant differences in growth and performance of calves from the four dosed groups. Clinical signs of polybrominated biphenyl toxicosis were not evident, and general health of offspring was not influenced. Number of inseminations for conception was greater among offspring from Groups III and V. Mechanisms for this dysfunction have not been determined.

Animals↗