Bioconcentration and intracellular storage of hexachlorobenzene in charophytes and their potential role in monitoring and remediation actions.

It has been hypothesized that highly hydrophobic substances (LogK(OW) > 5) including many persistent organic pollutants cannot overtake protective tissues and diffuse inside the body of plants due to steric hindrance or very slow diffusion. We investigated the bioaccumulation of hexachlorobenzene (HCB, LogK(OW) = 5.5) in a benthic charophycean macro-alga: Chara rudis. Chara species are a group of common freshwater algae with a complex body structure encompassing a protective layer of cortex cells surrounding large internode cells. The charophyte cell wall has many features in common with that of higher plants; therefore, they are useful models to investigate bioaccumulation mechanisms in general. We found that HCB diffused through the cortex and reached the cytoplam of internode cells. More than 90% of the HCB mass found in the organism was in the cortex and 10% in the internode cell cytoplasm. The cortex reached a pseudoequilibrium partitioning with water, and the bioconcentration factor was in the same range as that of lower aquatic organisms such as phytoplankton. Charophytes are therefore very efficient accumulators of hydrophobic compounds. Based on the structural and ecological features of charophytes, we speculated on their possible use as biomonitors and bioremediation tools.

Biomonitoring equivalents for hexachlorobenzene.

Recent efforts worldwide have resulted in a growing database of measured concentrations of chemicals in blood and urine samples taken from the general population. However, few tools exist to assist in the interpretation of the measured values in a health risk context. Biomonitoring equivalents (BEs) are defined as the concentration or range of concentrations of a chemical or its metabolite in a biological medium (blood, urine, or other medium) that is consistent with an existing health-based exposure guideline. This study reviews available health-based exposure guidance values for hexachlorobenzene (HCB) from Health Canada, the United States Environmental Protection Agency (US EPA), the US Agency for Toxic Substances and Disease Registry (ATSDR) and World Health Organization (WHO). HCB liver tissue concentrations in chronic rodent bioassays and information on human elimination rates and tissue distribution of HCB were extrapolated to estimate serum lipid-adjusted HCB concentrations that are consistent with the exposure guidance values for HCB. Estimated serum lipid-adjusted HCB concentrations ranging from 16 to 250 ng/g lipid were consistent with non-cancer-based exposure guidance values from various agencies. Concentrations associated with cancer risk-specific doses at target risk levels of interest were also estimated. These BE values may be used as screening tools for evaluation of population biomonitoring data for HCB in a risk assessment context and can assist in prioritization of the potential need for additional risk assessment efforts for HCB relative to other chemicals.

Bioaccumulation of organochlorine compounds in large, threatened elasmobranchs off northern New South Wales, Australia.

Persistent organic pollutants (POPs) include polychlorinated biphenyls (PCBs) dichlorodiphenyltrichloroethane (DDT) and hexachlorobenzene (HCB), which are resistant to biodegradation and therefore accumulate in the marine environment. In Australia, POPs occur in high concentrations primarily in costal water near farming regions and urban centres. From contaminated sediments and biota, POPs are transferred and biomagnified in larger marine organisms. We quantified POPs concentrations in 57 individuals from ten species of sharks and rays caught in bather-protection gillnets deployed off northern New South Wales, Australia. Polychlorinated biphenyls, DDTs and HCB were detected in all species. For some individuals, concentrations were at levels known to have deleterious sub-lethal effects. Overall, the POP concentrations analysed in this study were comparable to those in similar species from more polluted regions, and may have negative impacts on longer-term health. Future research is warranted to investigate spatio-temporal patterns of species-specific contaminant loads and their implications.

Effects of aging and sediment composition on hexachlorobenzene desorption resistance compared to oral bioavailability in rats.

Studies were conducted to assess the effects of black carbon, clay type and aging (1-1.5yr) on desorption and bioavailability of hexachlorobenzene (HCB) in spiked artificial sediments. Tenax (a super sorbent)-mediated desorption was used to examine the effects of these parameters on the physicochemical availability of HCB. The Tenax-mediated desorption of HCB from the four aged artificial sediments exhibited biphasic kinetics. The fast desorbing fractions ranged from 64.8% to 22.3%, showing reductions of 4.0-18.9% compared with freshly-spiked sediments. Statistical analysis on the fast desorbing fractions showed that all three treatment effects (i.e., montmorillonite clay, black carbon content, and aging) were significant. Two sediments with higher black carbon content exhibited much greater aging effects (i.e., greater reduction in fast desorbing fraction) than the other two sediments without the addition of black carbon. For both freshly-spiked and aged sediments, the desorption resistant sediment-bound HCB (i.e., slow desorbing fraction) correlated reasonably well to previously reported rat fecal elimination of HCB, which is a measure of the non-bioavailable fraction of sediment-bound HCB. A similar correlation was also observed between fast desorbing fraction and previously reported accumulation of HCB in the rat body (carcass+skin). These observations suggest that physicochemical availability, as defined by the desorption of HCB from sediments, provides a reasonable prediction of the oral bioavailability of sediment-bound HCB to rats. These results showed that montmorillonite clay, black carbon and aging reduced physicochemical availability and ultimately bioavailability of sediment-bound HCB.

Determination of the dietary absorption efficiency of hexachlorobenzene with the channel catfish (Ictalurus punctatus).

This study was designed to experimentally measure the assimilation efficiency of hexachlorobenzene (HCB) in a warm-water, benthic-feeding fish species, the channel catfish (Ictalurus punctatus). Catfish were exposed to (14)C-radiolabeled HCB in catfish food over a 28-day exposure period, followed by a 14-day clearance period. Over the experimental period, the total (14)C residues were measured in fish tissue and a simple two-box kinetic model was applied to the data to simulate uptake and clearance dynamics. No detectable metabolism of HCB by catfish was found. A two-box kinetic model effectively modeled the uptake and clearance of (14)C-HCB in catfish, with a calculated assimilation efficiency of the chemical into the whole catfish of 67% (growth corrected). The growth-corrected pseudo first-order elimination half-life of (14)C-HCB from whole catfish was determined to be 29 days (k(2)=0.024 day(-1)).

Selective bioaccumulation of chlorinated pesticides and metabolites in Arctic seabirds.

Chlorinated pesticides and metabolites (CPs) were quantified in the seabird species: little auk (Alle alle), Brünnich's guillemot (Uria lomvia), black guillemot (Cepphus grylle) and black-legged kittiwake (Rissa tridactyla). The purpose was to evaluate avian accumulation of selected CPs based on their concentrations and relative patterns, their relation to dietary descriptors (stable isotopes of carbon and nitrogen), to enzymes involved in biotransformation, as well as CPs' accumulation potential relative to the recalcitrant polychlorinated biphenyl PCB-153. In all species, the CP pattern was dominated by p,p'-dichlorodiphenyltrichloroethane (DDE) and hexachlorbenzene (HCB). Except for HCB, concentrations were not related to trophic position. Most CPs were quantified in black guillemot, indicating a slower elimination compared to other seabird species. Brünnich's guillemot showed efficient elimination of chlordanes, whereas the opposite was found for little auk. Kittiwake showed higher accumulation of persistent CP and metabolites than auks, whereas accumulation of less recalcitrant CPs was low.

Effect of organic carbon content, clay type, and aging on the oral bioavailability of hexachlorobenzene in rats.

Bioavailability of lipophilic chemicals is influenced by the physicochemical properties of soils/sediment such as particle size, pH, clay, and organic carbon content. The present study investigated the effects of sediment composition and aging on the oral bioavailability of hexachlorobenzene (HCB) in rats. Formulated sediments were prepared using various ratios of kaolinite and montmorillonite clay, sand, peat moss, and black carbon, spiked with (14)C-HCB, and orally administered to rats prior to and after one year of aging in dark at 10 degrees C. In the nonaged sediments there was a 21 to 45% reduction in the oral bioavailability of HCB when compared to the corn oil standard without any clear pattern of the impact of the sediment clay and/or organic carbon content. One year of aging resulted in statistically significant (p = 0.049) reduction in the oral bioavailability of HCB from the sediments compared to the corn oil standard and nonaged sediment indicating stronger interactions between HCB and sediment contents with aging. The mean reduction in oral bioavailability after one year of aging ranged from approximately 5 to 14% greater than that observed for nonaged sediments. The fecal elimination of the HCB-derived radioactivity from the one-year-aged sediments was much higher than the nonaged sediments, consistent with the lower absorption from the gastrointestinal tract due to lower desorption of HCB from the aged sediments. Increase in the fecal elimination and decrease in oral bioavailability of (14)C-HCB was related to the increase in clay and black carbon.

An updated physiologically based pharmacokinetic model for hexachlorobenzene: incorporation of pathophysiological states following partial hepatectomy and hexachlorobenzene treatment.

Physiologically based pharmacokinetic (PBPK) modeling is generally used for describing xenobiotic disposition in animals and humans with normal physiological conditions. We describe here an updated PBPK model for hexachlorobenzene (HCB) in male F344 rats with the incorporation of pathophysiological conditions. Two more features contribute to the distinctness of this model from the earlier published versions. This model took erythrocyte binding into account, and a particular elimination process of HCB, the plasma-to-gastrointestinal (GI) lumen passive diffusion (i.e., exsorption), was incorporated. Our PBPK model was developed using data mined from multiple pharmacokinetic studies in the literature, and then modified to simulate HCB disposition under the conditions of our integrated pharmacokinetics/liver foci bioassay. This model included plasma, erythrocytes, liver, fat, rapidly and slowly perfused compartments, and GI lumen. To account for the distinct characteristics of HCB absorption, the GI lumen was split into an upper and a lower part. HCB was eliminated through liver metabolism and the exsorption process. The pathophysiological changes after partial hepatectomy, such as alterations in the liver and body weights and fat volume, were incorporated in our model. With adjustment of the transluminal diffusion-related parameters, the model adequately described the data from the literature and our bioassay. Our PBPK model simulation suggests that HCB absorption and exsorption processes depend on exposure conditions; different exposure conditions dictate different absorption and exsorption rates. This model forms a foundation for our further exploration of the quantitative relationship between HCB exposure and development of preneoplastic liver foci.

Toxicity of hexachlorobenzene and its transference from microalgae (Chlorella kessleri) to crabs (Chasmagnathus granulatus).

The aim of this work was to study the transference of hexachlorobenzene from a green alga (Chlorella kessleri) to an estuary crab (Chasmagnathus granulatus), and to analyze the toxic effects that the xenobiotic has on the latter. The effect of hexachlorobenzene uptake was evaluated measuring oxidative stress, Uroporphyrinogen decarboxylase activity and morphometric parameter alteration, and also performing a histological analysis of crab hepatopancreas. Results demonstrated that hexachlorobenzene enters the alga, is accumulated in it, and then transferred into the crab, causing a decrease in Uroporphyrinogen decarboxylase activity in both organisms. The high malondialdehyde levels detected in crab hepatopancreas after the toxic treatment suggested the existence of hexachlorobenzene-induced lipid peroxidation. Antioxidant defenses such as superoxide dismutase activity and reduced glutathione content fell below normal values on the fourth week of treatment. At the same time, the hepatosomatic index, used as a morphometric parameter, reduced 20% with respect to the control. The histological analysis revealed epithelium disorganization in hepatopancreas tubules, confirming the existence of structural damage caused by hexachlorobenzene.

Age dependence of the accumulation of organochlorine pollutants in brown trout (Salmo trutta) from a remote high mountain lake (Redó, Pyrenees).

Polychlorobiphenyls (PCBs), hexachlorocyclohexanes (HCHs), hexachlorobenzene (HCB) and DDT were examined in the muscle of brown trout (Salmo trutta) from a high mountain lake located in the Pyrenees (Catalonia, Spain) that was used as a model of these lacustrine environments. Results indicate that fish age is the main factor of variability among specimens in this population that is subjected to atmospheric inputs of the organochlorine compounds (OC). Increases of 2- and 20-fold between fish aged 1 year and 15 years old are found. The observed pattern cannot be explained in terms of fish size, condition factor, or muscle lipid content. Higher molecular weight compounds (higher lipophilicity) are better correlated with fish age than low molecular weight compounds. A transformation from 4,4'-DDT to 4,4'-DDE occurs in fish after ingestion; this results in amplified age-dependent signals, especially in male specimens. In contrast, PCB congener #180 has lower age dependence than the general OC group, which could be due to its high hydrophobicity (log K(ow) > 7). In any case, selective accumulation of hydrophobic compounds is already observed among younger fish (age, 1 year). Due to this effect, the relative OC composition does not reflect the main OC pollutants in the lake waters.

Historical intake and elimination of polychlorinated biphenyls and organochlorine pesticides by the Australian population reconstructed from biomonitoring data.

Quantifying the competing rates of intake and elimination of persistent organic pollutants (POPs) in the human body is necessary to understand the levels and trends of POPs at a population level. In this paper we reconstruct the historical intake and elimination of ten polychlorinated biphenyls (PCBs) and five organochlorine pesticides (OCPs) from Australian biomonitoring data by fitting a population-level pharmacokinetic (PK) model. Our analysis exploits two sets of cross-sectional biomonitoring data for PCBs and OCPs in pooled blood serum samples from the Australian population that were collected in 2003 and 2009. The modeled adult reference intakes in 1975 for PCB congeners ranged from 0.89 to 24.5ng/kgbw/day, lower than the daily intakes of OCPs ranging from 73 to 970ng/kgbw/day. Modeled intake rates are declining with half-times from 1.1 to 1.3years for PCB congeners and 0.83 to 0.97years for OCPs. The shortest modeled intrinsic human elimination half-life among the compounds studied here is 6.4years for hexachlorobenzene, and the longest is 30years for PCB-74. Our results indicate that it is feasible to reconstruct intakes and to estimate intrinsic human elimination half-lives using the population-level PK model and biomonitoring data only. Our modeled intrinsic human elimination half-lives are in good agreement with values from a similar study carried out for the population of the United Kingdom, and are generally longer than reported values from other industrialized countries in the Northern Hemisphere.

A novel model to characterize postnatal exposure to lipophilic environmental toxicants and application in the study of hexachlorobenzene and infant growth.

BACKGROUND: Infants are exposed to persistent environmental contaminants through breast milk, yet studies assessing the health effects of postnatal exposure are lacking. Existing postnatal exposure assessment is either too simple (lactation exposure model, LEM) or requires complex physiologically-based pharmacokinetic (PBPK) models. OBJECTIVES: We present equations for postnatal exposure calculations. We applied these equations to study the effect of hexachlorobenzene (HCB) on infant growth in the two first years of life. METHODS: HCB was measured in breast milk samples in 449 mother-child pairs participating in the Norwegian birth cohort study HUMIS. We used these concentrations, mother's weight, height and age, together with child's weight at 8 age points, and proportion of milk consumed each month, to calculate HCB concentrations in the infant over age. We then estimated the association between HCB and infant growth using a linear mixed model. RESULTS: Children exposed to HCB via mother's milk reached concentrations 1-5 times higher than the mother. HCB was associated with lower weight gain in the first 2years (-33g per unit HCB and month, 95% CI: -38, -27 at 6months). Associations were stronger during the first 3months (-57g per unit HCB and month, 95% CI: -67, -49 at 1month), indicating a critical window of effect. Our equations gave more precise estimates than the LEM. CONCLUSION: Our equations for postnatal exposure of lipophilic environmental toxicants give better results than the LEM and are easier to implement than the complex PBPK models. HCB exposure, especially during the first three months of life, has a negative effect on infant growth up to 2years.

Influence of iron on the induction of hepatic tumors and porphyria by octachlorostyrene in C57BL/10ScSn mice.

Octachlorostyrene (OCS) is an environmental contaminant, present in fish of Northern European waters and the Great Lakes of America. It has many distribution and toxic similarities to hexachlorobenzene (HCB). Administration of OCS at 0.01% of the diet to C57BL/10ScSn mice within iron overload for 18 months gave only a low incidence of hepatic nodular hyperplasia (2/10 survivors) and no hepatocellular adenomas or carcinomas. In contrast, with a similar regime, HCB causes severe liver cancer or nodules in all exposed mice. Whole body autoradiography of mice given [14C]OCS or [14C]HCB showed no gross variations in distribution or covalent binding of the radiolabelled compound to account for the difference between the chemicals in the development of tumours. In 12-week studies, the CYP1A subfamily was induced to a greater degree by HCB than OCS and iron-enhanced uroporphyria was significantly greater with HCB. The findings are consistent with the proposal that uroporphyria and liver cancer induced in mice by HCB are associated through related mechanisms, but occur to a significantly lesser extent with OCS.

Dose-response relationships in hexachlorobenzene-induced porphyria.

The rate of development of hexachlorobenzene (HCB)-induced porphyria in female Wistar rats was determined using HCB dosage and porphyrin analysis protocols designed to determine factors which contribute to the delay commonly observed between initial exposure to HCB and the detection of porphyria. Measurements were made of HCB and porphyrin concentrations in the livers, kidneys, and spleens of female Wistar rats exposed continuously (up to 56 days) or for 1 day to HCB (at dietary concentrations of 1000 ppm and 100 ppm). The experiments showed that when a corn oil solution of HCB was added to the diet at a concentration of 1000 ppm, HCB accumulated rapidly in all organs, and the delay in appearance of elevated liver highly carboxylated porphyrins (HCPs) was at most 4 days (approximately 8-fold elevation of HCPs on day 4). One day of exposure to this diet was sufficient to cause elevated liver HCPs, thus showing that continuous exposure to HCB was not required to cause porphyria in this species. Solid HCB added directly to the diet (1000 ppm) resulted in less rapid HCB accumulation and less rapid development of porphyria. The experiments demonstrated that the appearance of a delay in HCB-induced porphyria in the Wistar rat is caused by the rate at which HCB is absorbed, and by using total hepatic porphyrins (rather than HCPs) as the indicator of the disorder. The experiments also showed that HCB-induced liver enlargement and neurotoxicity are not necessarily associated with the severity of porphyria.

Excretion of hexachlorobenzene and metabolites in feces in a highly exposed human population.

A set of 53 individuals from a population highly exposed to airborne hexachlorobenzene (HCB) were selected to study the elimination kinetics of this chemical in humans. The volunteers provided blood, 24-hr urine, and feces samples for analysis of HCB and metabolites. The serum HCB concentrations ranged from 2.4 to 1,485 ng/mL (mean +/- SD, 124 +/- 278), confirming that this human population has the highest HCB blood levels ever reported. All analyzed feces samples contained unchanged HCB (range, 11-3,025 ng/g dry weight; mean +/- SD, 395 +/- 629). The HCB concentration in feces strongly correlated with HCB in serum (r = 0.85; p < 0.001), suggesting an equilibrium in feces/serum that is compatible with a main pulmonary entrance of the chemical and low intestinal excretion of nonabsorbed foodborne HCB. The equilibrium is also compatible with a nonbiliary passive transfer of the chemical to the intestinal lumen. Two HCB main metabolites, pentachlorophenol (PCP) and pentachlorobenzenethiol (PCBT), were detected in 51% and 54% of feces samples, respectively. All urine samples contained PCP and PCBT, confirming the conclusions of a previous study [Environ Health Perspect 105:78-83 (1997)]. The comparison between feces and urine showed that whereas daily urinary elimination of metabolites may account for 3% of total HCB in blood, intestinal excretion of unchanged HCB may account for about 6%, thus showing the importance of metabolism in the overall elimination of HCB. The elimination of HCB and metabolites by both routes, however, appears to be very small (< 0.05%/day) as compared to the estimated HCB adipose depots. Features of HCB kinetics that we present in this study, i.e., nonsaturated intestinal elimination of HCB and excretion in feces and urine of inert glutathione derivatives, may explain, in part, the absence of porphyria cutanea in this human population heavily exposed to HCB.

Comparison of the urinary metabolite profiles of hexachlorobenzene and pentachlorobenzene in the rat.

The urinary metabolite profile of hexachlorobenzene (HCB) and pentachlorobenzene (PCBz) in the rat is compared after dietary exposure for 13 weeks. Both HCB and PCBz are oxidized to pentachlorophenol (PCP) and tetrachlorohydroquinone (TCHQ), which were the only two mutual metabolites formed. Additional urinary metabolites of HCB are N-acetyl-S(pentachlorophenyl)cysteine (PCTP-NAC), which appeared to be quantitatively the most important product, and mercaptotetrachlorothioanisole (MTCTA), which was excreted as a glucuronide. PCBz is more extensively metabolized to the major metabolites 2,3,4,5-tetrachlorophenol (TCP), mercaptotetrachlorophenol (MTCP) and the glucuronide of pentachlorothiophenol (PCTP), and the minor metabolites methylthiotetrachlorophenol (MeTTCP), hydroxytetrachlorophenyl sulphoxide (HTCPS), and bis(methylthio)-trichlorophenol (bis-MeTTriCP). The biotransformation of HCB and PCBz was modulated by selective inhibition of cytochrome P450IIIA in rats which received combined treatment of HCB or PCBz with triacetyloleandomycin (TAO). Rats receiving this diet had a strongly diminished excretion of both PCP and TCHQ, as compared to rats fed HCB or PCBz alone, indicating the involvement of P450IIIA in the oxidation of both compounds. However, the excretion of 2,3,4,5-TCP was not diminished by co-treatment of rats with PCBz and TAO, indicating that: (i) the oxidation of PCBz to PCP and 2,3,4,5-TCP does not proceed via a common intermediate; and (ii) oxidation of PCBz to 2,3,4,5-TCP is not mediated by P450IIIA. Co-treatment of rats with PCBz and TAO had a differential effect on the excretion of sulphur-containing metabolites, resulting in a decrease in the excretion of PCTP glucuronide, whereas no change was observed in the excretion of MTCP, as compared to rats receiving PCBz alone. The observed differences in HCB and PCBz metabolites clearly deserve further in vitro studies to elucidate their origin.

Hexachlorobenzene toxicity in the monkey primordial germ cell without induced porphyria.

Hexachlorobenzene is a persistent chlorinated organic chemical that has been detected in many tissues from a variety of species including human ovary and human ovarian follicular fluid. When administered in high dosage to nonhuman primates, hexachlorobenzene causes destruction of ovarian primordial germ cells in association with systemic toxicity. The purpose of these experiments was to assess relative ovarian germ cell sensitivity at much lower dosages of hexachlorobenzene that do not produce systemic effects and additionally to evaluate oocyte function by means of the response to superovulation, fertilization, and embryo cleavage during a cycle of in vitro fertilization in the cynomolgus monkey. Hexachlorobenzene in dosages of 0.1, 1.0, and 10.0 mg/kg/day was administered orally by gelatin capsule for 90 days. There was a dose-dependent accumulation of HCB in serum and other tissues without any change in the serum estradiol response to human menopausal gonadotropin, oocyte recovery, oocyte maturation, oocyte fertilization in vitro, and early embryo cleavage rate. There was a dose-related toxic effect observed in primordial germ cells at the lowest dose despite no evidence of systemic or hepatic effects. As there were no changes in the urinary porphyrin excretion, the mechanism of hexachlorobenzene ovotoxicity may be distinct from hexachlorobenzene-induced cytochrome P-450-dependent inhibition of uroporphobilinogen decarboxylase in the liver, although such intraovarian metabolism cannot be excluded.

The association between local fish consumption and DDE, mirex, and HCB concentrations in the breast milk of Mohawk women at Akwesasne.

A study was conducted to assess the extent to which the consumption of local fish contaminated with p,p'-dichlorodiphenyl dichloroethylene (p,p'-DDE), mirex, and hexachlorobenzene (HCB) has impacted the concentrations of these compounds in the milk of nursing Mohawk women residing along the St. Lawrence River. From 1986 to 1992, 97 Mohawk women were interviewed, and each donated a one-time sample of at least 50 ml of breast milk. The comparison population consisted of 154 Caucasians from other rural areas in New York State. After adjustment for potential confounders, Mohawk mothers who gave birth from 1986 to 1990 had significantly higher geometric mean p,p'-DDE milk concentrations than did the control group, but no significant differences were observed from 1991 to 1992. In contrast, mirex was significantly elevated among the Mohawks throughout the study period, while HCB showed no difference at any point. Mohawk women with the greatest estimated cumulative lifetime exposure to p,p'-DDE from local fish consumption had a significantly higher geometric mean milk level of that compound relative to control women, but no differences in mirex or HCB concentrations in breast milk by local fish consumption were found. The reduction in breast milk p,p'-DDE concentrations among the Mohawk women from 1986 to 1990 parallels a corresponding decrease in local fish consumption, and may be the result of the advisories that have been issued over the past decade recommending against the consumption of local fish by pregnant and nursing Mohawk women. Elevations in the concentrations of mirex in the breast milk of the Mohawks are consistent with the fact that it is a common contaminant in the region and throughout the Lake Ontario-St. Lawrence River Basin.

High-fat diet enhances the accumulation of hexachlorobenzene (HCB) by pregnant rats during continuous exposure to HCB.

To investigate the influence of a high-fat diet on HCB distribution and accumulation, pregnant rats in study 1 were fed a high-fat or control diet containing HCB, and, in study 2, pregnant rats were given a single HCB dose by intragastric gavage and HCB-free high-fat or control diet. In study 1, the high-fat diet group had higher HCB concentrations in fat tissues and liver than did the controls. In study 2, although the total amounts of HCB in the fat tissue and liver were greater in the high-fat diet group than in the controls, no significant differences in HCB concentration were observed between the two groups. The high-fat diet group also showed more fecal excretion of HCB. Therefore, HCB accumulation in rats fed a high-fat diet was enhanced more by continuous exposure to HCB than by administration of a single dose.

Bioconcentration of lipophilic organochlorines in ovine dentine.

The bioconcentration of lipophilic organochlorines in ovine dentine in comparison to adipose tissue was examined. Sheep were given a single dose (0.2-1.4 mg/kg body wt) of individual polychlorobiphenyl (PCB) congeners (tetrachlorobiphenyls IUPAC Nos. 54 and 80, and hexachlorobiphenyls IUPAC Nos. 155 and 169) and organochlorine pesticides 1,1-bis(4-chlorophenyl)-2,2-dichloroethene) (4,4'-DDE) and hexachlorobenzene (HCB). They were killed 2 months after the dose and teeth and adipose tissue were collected. For the extraction of organochlorines, dentine was treated ultrasonically with sulfuric acid and hexane. The concentration of organochlorines in dentine and adipose tissue was determined by high-resolution gas chromatography with electron-capture detection. The bioconcentration of 'planar' compounds (PCB-169, HCB) in dentine, compared to adipose tissue, was lower than that of 'non-planar' (PCB-155, 4,4'-DDE). Ratios of the non-planar to planar compounds PCB-155/-169 and 4,4'-DDE/HCB in dentine were 1.4 and 7.2, and in adipose tissue 0.5 and 2.4, respectively. The dentine:adipose tissue bioconcentration ratios (on a lipid basis) of PCB-54, -80, -155, -169, 4,4'-DDE and HCB were 47, 16, 0.3, 0.1, 3.2 and 1.0, respectively. The results indicate that the bioconcentration of organochlorines in different tissues cannot be based on lipid content only. It is suggested that the physicochemical properties of individual organochlorines, i.e. lipophilicity (K(ow)), diffusivity, metabolism and tissue-specific interactions, play a part in the different bioconcentrations of individual organochlorine pollutants in dentine compared to adipose tissue.