Interactions between 2,3,7,8-TCDD and PCBs as tumor promoters: limitations of TEFs

The assessment of the carcinogenic risk of polychlorinated dioxins (PCDDs), furans (PCDFs), and biphenyls (PCBs) by TEFs is hampered by species- and tissue-specific responses that cannot readily be explained by differences in the Ah receptor levels but may be due to events subsequent to ligand binding to the Ah receptor. Moreover, PCDDs and related compounds accumulate in the environment, in animal and human tissues as highly complex mixtures. Thus, comprehensive risk assessment should include all Ah receptor ligands and agents that modulate the Ah receptor-mediated responses. Tumor promoter studies with mixtures of PCDDs and halogenated biphenyls have shown additive, synergistic, and antagonistic effects. To analyse the interactions of TCDD and PCBs as tumor promoters in more detail, we established an in vitro assay, i.e., the enhancement (promotion) of malignant transformation of carcinogen-initiated C3H/M2 mouse fibroblasts after treatment with tumor promoters. The coplanar PCB 126, a potent Ah receptor agonist, and the diortho-substituted PCB153, to which no TEF value has been ascribed, are promoters of malignant transformation. A defined mixture of PCB126 and TCDD had an additive promoting effect, while PCB 153 antagonized the TCDD-mediated promotion. Thus, the TEF-approach may be insufficient to estimate the tumor-promoting activities of PCDDs, PCDFs, and PCBs in mammalian tissues in which diortho-substituted PCBs are greatly accumulated.     

Toxic equivalency factors (TEFs) for PCBs, PCDDs, PCDFs for humans and wildlife

An expert meeting was organized by the World Health Organization (WHO) and held in Stockholm on 15-18 June 1997. The objective of this meeting was to derive consensus toxic equivalency factors (TEFs) for polychlorinated dibenzo-p-dioxins (PCDDs) and dibenzofurans (PCDFs) and dioxinlike polychlorinated biphenyls (PCBs) for both human, fish, and wildlife risk assessment. Based on existing literature data, TEFs were (re)evaluated and either revised (mammals) or established (fish and birds). A few mammalian WHO-TEFs were revised, including 1,2,3,7,8-pentachlorinated DD, octachlorinated DD, octachlorinated DF, and PCB 77. These mammalian TEFs are also considered applicable for humans and wild mammalian species. Furthermore, it was concluded that there was insufficient in vivo evidence to continue the use of TEFs for some di-ortho PCBs, as suggested earlier by Ahlborg et al. [Chemosphere 28:1049-1067 (1994)]. In addition, TEFs for fish and birds were determined. The WHO working group attempted to harmonize TEFs across different taxa to the extent possible. However, total synchronization of TEFs was not feasible, as there were orders of a magnitude difference in TEFs between taxa for some compounds. In this respect, the absent or very low response of fish to mono-ortho PCBs is most noticeable compared to mammals and birds. Uncertainties that could compromise the TEF concept were also reviewed, including nonadditive interactions, differences in shape of the dose-response curve, and species responsiveness. In spite of these uncertainties, it was concluded that the TEF concept is still the most plausible and feasible approach for risk assessment of halogenated aromatic hydrocarbons with dioxinlike properties.     

Ethoxyresorufin-O-deethylase (EROD) inducing potencies of planar chlorinated aromatic hydrocarbons in primary cultures of hepatocytes from different developmental stages of the chicken

In vitro induction of ethoxyresorufin O-deethylase (EROD) activity in cell cultures is an extensively validated tool for measuring overall potencies of mixtures of halogenated aromatic hydrocarbons (HAHs) in samples from the abiotic or biotic environment. For risk assessment with special attention to effects in wild birds, an assay was developed that makes use of chicken embryo hepatocytes. However, it was questioned whether compound-specific responses are consistent at the various developmental stages. The results of our present study show that there are considerable differences between early and late embryonal and post-hatching stages. The induction of EROD was measured in primary chicken hepatocyte cultures. The cells were isolated at day 14 and day 19 of embryonal development and at day 1 post hatching. Hepatocytes were exposed in vitro to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), 2,3,7,8-tetrachlorodibenzofuran (TCDF), 3,3',4,4',5-pentachlorobiphenyl (PCB 126, IUPAC nomenclature) and 2,3',4,4',5-pentachlorobiphenyl (PCB 118). The respective compounds were chosen as representatives for dioxins, furans, non-ortho PCBs, and mono-ortho PCBs. These groups of chemicals have been identified as environmental contaminants with major dioxin-like effects that are mediated by a common receptor, the arylhydrocarbon (Ah) receptor. At all developmental stages, TCDF was more potent than TCDD. Relative potencies (RP = EC50TCDD/EC50HAH) decreased in the order TCDF < TCDD < PCB 126 < PCB 118. Depending on the developmental stage, TCDF was 1.2 to 3.4 times more potent than TCDD. PCB 126 was equipotent or less potent by a factor of 3 than TCDD. PCB 118 was 100 to 300 times less potent than TCDD. Both the mean effective concentration (EC50) and the maximum EROD activity (Ymax) of all compounds were lower in hepatocyte cultures from 14-day-old embryos than those from 19-day-old embryos or 1-day-old hatchlings. RPs were comparable in 19-day-old embryos and in hatchlings, but significantly different in 14-day-old embryos.     

Potency of mixtures of polychlorinated biphenyls as inducers of dioxin receptor-regulated CYP1A activity in rat hepatocytes and H4IIE cells

Among the polychlorinated biphenyls (PCBs), a family of widespread environmental pollutants, the most toxic non-ortho-substituted coplanar (non-ortho coplanar) congeners are thought to act as strong dioxin (aryl hydrocarbon) receptor agonists leading to adverse effects, such as body weight loss, immunosuppression, thymic atrophy, hepatotoxicity, tumor promotion, and disturbances of steroid hormone action. Since PCBs are present in environmental and tissue samples as complex mixtures, we investigated the possible interaction of non-ortho coplanar congeners with other major PCBs, which are less active or inactive as dioxin receptor agonists. As a parameter for dioxin receptor activation, induction of CYP1A-catalyzed 7-ethoxyresorufin O-deethylase (EROD) was determined in rat hepatocytes in primary culture and in the rat hepatoma cell line H4IIE. In rat hepatocytes, individual EC50-values and 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) equivalency factors (TEFs) for the non-ortho and mono-ortho coplanar PCBs 126, 169, 105, 118 and 156, were in good agreement with published data from in vivo experiments, while in H4IIE cells coincidence was lower. However, in both cell systems TEFs for PCB 77 were significantly higher than reported from experiments in rats. In an approximately equipotent mixture the six potent PCB congeners showed perfect additive behaviour in both cell systems. In contrast, addition of a tenfold surplus of abundant mono- and di-ortho PCBs (28, 52, 101, 138, 153 and 180) led to an almost threefold higher TEF than predicted. This finding suggests a moderate synergistic enhancement of the inducing potency of potent PCBs by less potent congeners, present in abundance in environmental and tissue samples.     

PCBs and dioxin-like compounds in plasma of adult Inuit living in Nunavik (Arctic Quebec)

Inuit people residing in the Arctic are unusually exposed to organochlorines through their traditional diet which includes large quantities of sea mammal fat. Recently, 499 Inuit adults from Nunavik (Arctic Quebec) participated in a large health survey and donated a blood sample for organochlorine and heavy metal analysis. Twenty pooled plasma samples were formed, each made of individual samples from the same age group, sex, and region of residence, to allow for dioxin-like compound determination. The mean total concentration of PCBs and dioxin-like compounds (the latter expressed in 2,3,7,8-TCDD toxic equivalents) were respectively 4.1 mg/kg lipids and 184.2 ng/kg lipids, compared to 0.13 mg/kg lipids and 26.1 ng/kg lipids for three control pooled plasma samples from Southern Quebec. Total PCBs and dioxin-like compound concentrations were strongly correlated (r = 0.98; p < 0.0001), increased with age and were greater in men than in women. Although the body burdens of PCBs and dioxin-like compounds are close to those which induced adverse health effects in laboratory animals, dietary benefits from the sea-food based diet still outweigh the hypothetical health risks.     

Dioxin-like PCBs in the environment-human exposure and the significance of sources

Dioxin-like PCBs represent an important component of the Sigma-TEQ in many environmental media. Specifically, in animal produce and in fish PCBs dominate the Sigma-TEQ ingested by humans. This in turn leads to high background body burdens in humans with PCB-TEQ greater than that associated with PCDD/Fs. High fish consumers are apparently subject to elevated TEQ exposure from dioxin-like PCBs. This has important implications for exposure assessment studies which have previously only been concerned with PCDDs and PCDFs. Unlike PCDD/Fs, dioxin-like PCBs are not controlled within the food chain. Sources and pathways of exposure are poorly defined. Aroclor formulations and their subsequent usage are considered to be the most important sources in terms of human exposure to some TEF-rated congeners, notably PCB-118, PCB-156 and part of PCB-126. Emissions from combustion sources contribute additional PCB-126. More research is needed to place these compounds in an integrated risk evaluation framework.     

Species and organ dependence of PCB contamination in fish, foxes, roe deer, and humans

According to previous experimental results, PCBs are deposited in muscle fat in animals and in humans, although they also reach the brain, the liver, and the lungs. The aim of the present study was to determine the concentrations of the so-called "indicator PCBs" (PCB nos. 28, 52, 101, 138, 153, 180), as described by the German ordinance for maximum concentrations of contaminants in foodstuffs, in muscle tissue, liver, and brain of four different species: fish, fox, roe deer, and humans, all exposed to PCBs directly in their environment. Potential target organs for the accumulation of these congeners were also to be identified. Furthermore, the organs or tissues were to be identified in which PCBs are accumulated, and unusual patterns of accumulation or breakdown of particular PCBs, for example the "dioxin-like PCBs" (coplanar PCBs) determined. For humans, the lungs were also included in these studies. Statistical comparison of PCB concentrations in samples from wild animals and humans showed that in spite of its relatively high fat concentration, brain tissue in all of the species examined (with the exception of fish) appeared to be better protected against accumulation of PCB than liver or muscle tissue. This protection may be the result of the blood-brain barrier, as witnessed by the relatively uniform concentration of PCBs throughout the various organs of fish, since the blood-brain barrier of fish is considerably less efficient than that of mammals. No peculiarities were found in regard to distribution of the coplanar PCBs over the other congeners in this study. This applies to the brain and other organs or tissues of the four species that were examined. Accumulations of PCBs and coplanar PCBs in the liver were only found in fox and roe deer. In contrast, humans were found to have accumulations of the high-chlorinated biphenyls studied here as well as PCB no. 118 in muscle tissue fat and not in the liver. Unexpectedly, low-chlorinated biphenyls were found to accumulate in the human lung. The results of this study show that the lung represents a target organ for the accumulation of potentially metabolically activated low-chlorinated biphenyls, indicating that the possible biological effects of PCBs on the lungs will need to receive more attention in the future.     

3,4,3',4'-Tetrachlorobiphenyl acts as an estrogen in vitro and in vivo

Polychlorinated biphenyls (PCBs) are one of the most widespread, persistent man-made products in the ecosystem giving rise to serious environmental contamination and potential hazard to health. The PCBs, in common with other compounds such as the dioxins, have been shown to exert some biological actions mediated through the aryl hydrocarbon receptor. Evidence for interaction of PCBs with other nuclear receptors has been sparse. Here we present evidence that 3,4,3',4'-tetrachlorobiphenyl (TCB) (PCB77), a PCB with high toxicity and significant bioaccumulation, can act as an estrogen with actions mediated through the estrogen receptor. Evidence is presented from multiple assay systems including 1) ligand binding to estrogen receptor in a competitive binding assay, 2) ligand ability to induce estrogen receptor binding to DNA, 3) ligand regulation of gene expression from a transfected exogenous (ERE-tk-CAT) or an endogenous (pS2) estrogen-regulated gene, 4) ligand regulation of cell growth in estrogen-dependent human breast cancer cell lines MCF7 and ZR-75-1, and 5) ligand activity in the immature mouse uterine weight bioassay in vivo. These results demonstrate that TCB (PCB77) can be included in the increasing list of environmental pollutants that possess the ability to mimic estrogen action and be termed an environmental estrogen. Since the concentrations of TCB used here (10(-9) M; 292 ng/liter) are not incompatible with levels of PCB/TCB found in human tissues, these results may have physiological relevance. Use of multiple approaches to study estrogenic action demonstrates that one congener can act as both an agonist and antagonist of estrogen action and that the magnitude of these effects can alter according to the molecular environment.     

Damage occurs early in systemic vasculitis and is an index of outcome

The use of products containing PCB in buildings resulted in indoor air contaminations. The search for appropriate measures is hampered by several different uncertainties in the regulatory toxicological process. These refer to problems in exposure assessment including measurement approaches, the toxicological evaluation of health risks including the derivation of a tolerable intake and the use of TCDD toxicity equivalency factors and finally the legal consequences of health risk evaluation. Since no consensus on these aspects has been achieved, the regulatory consequences vary considerably from one German state government to the other. FAO/WHO have not been able to arrive at a satisfactory supranational recommendation of a tolerable intake for PCB.     

Serum concentration of calcium, 1,25 vitamin D and parathyroid hormone are not correlated with coronary calcifications. An electron beam computed tomography study

As a consequence of contamination by effluents from local electronics manufacturing facilities, the New Bedford Harbor and estuary in southeastern Massachusetts is among the sites in the United States that are considered the most highly contaminated by polychlorinated biphenyls (PCBs). Since 1993, measures of intrauterine PCB exposure have been obtained for a sample of New Bedford area infants. Among 122 mother-infant pairs, we identified four milk samples with total PCB levels that were significantly higher than the rest, with estimated total PCBs ranging from 1,100 to 2,400 ng/g milk fat compared with an overall mean of 320 ng/g milk fat for the 122 women. The congener profile and history of one case was consistent with past occupational PCB exposures. Otherwise, the source of PCB exposures in these cases was difficult to specify. Environmental exposures including those from fish consumption were likely, whereas residence adjacent to a PCB-contaminated site was considered an unlikely exposure source. In all four cases, the infants were full-term, healthy newborns. Because the developing nervous system is believed to be particularly susceptible to PCBs (for example, prenatal PCB exposures have been associated with prematurity, decrements in birth weight and gestation time, and behavioral and developmental deficits in later infancy and childhood, including decrements in IQ), it is critical to ascertain if breast-feeding is a health risk for the women's infants. Despite the potential for large postnatal PCB exposures via breast milk, there is limited evidence of significant developmental toxicity associated with the transmission of moderate PCB concentrations through breast milk. Breast-feeding is associated with substantial health benefits including better cognitive skills among breast-fed compared with formula-fed infants. We conclude, based on evidence from other studies, that the benefits of breast-feeding probably outweigh any risk from PCB exposures via breast milk among the four New Bedford infants. In this case report, PCB analysis of breast milk and infant cord serum was a research tool. PCB analysis of milk is rarely done clinically, in part because it is difficult to use the results of such analyses to predict health risks. Substantial effort is needed to achieve a better understanding of the clinical and public health significance of PCB exposures, particularly among potentially susceptible groups such as infants and children. Such efforts are critical to improving the clinical and public health management of widespread and ongoing population exposures to PCBs.     

A mutation in the neurofibromatosis type 2 tumor-suppressor gene, giving rise to widely different clinical phenotypes in two unrelated individuals

Polychlorinated biphenyls (PCBs) are industrial chemicals that are long-lasting global environmental contaminants. PCBs have been reported to adversely affect reproduction in laboratory and wild animals by reducing the incidence of breeding and the survival rate of young. The present study was undertaken to determine the toxic potential of PCBs on in vitro fertilization (IVF) in the mouse. Aroclor 1221, 1254, and 1268, and 3, 3', 4, 4'-tetrachlorobiphenyl (TCB), a PCB congener, were added to IVF medium at various concentrations (0.01, 0.1, 1, and 10 micrograms/mL). Cumulus masses containing oocytes were obtained from superovulated B6D2F1 mice and cultured in medium containing PCB to which capacitated sperm were added. Oocytes were assessed for fertilization 20 to 24 h after insemination. A-1221, A-1268, and TCB reduced the fertilization rate at the 1 microgram/mL and 10 micrograms/mL doses, while inhibition of fertilization by A-1254 reached significance at 0.1 microgram/ml. Furthermore, all of these chemicals caused an increased incidence of degenerative ova and abnormal 2-cell embryos at the higher dose levels (1 microgram/mL and 10 micrograms/mL). The results suggest that higher dosages of PCB and TCB adversely affect fertilization and cause an increased incidence of degeneration of oocytes and abnormality in the early mouse embryos.     

Polychlorinated biphenyl (PCB) and dichlorodiphenyl dichloroethylene (DDE) exposure among Native American men from contaminated Great Lakes fish and wildlife

The New York State Department of Health is performing an investigation of Mohawk men, women, and infants who live at the Akwesasne Reserve along the St. Lawrence River in New York, Ontario, and Quebec Three large industrial facilities bordering the Akwesasne Reserve have seriously contaminated the soil and the sediments and fish of the adjacent St. Lawrence River with polychlorinated biphenyls (PCBs). The main study goals are to investigate the associations among the consumption of locally caught fish, residential exposure, body burdens of PCBs, and liver enzyme induction. Contamination with PCBs, polychlorinated dibenzofurans, polychlorinated dibenzodioxins, polyaromatic hydrocarbons, dichlorodiphenyl dichloroethylene (DDE) and other chemicals has been documented in locally caught fish, ducks, and other wildlife. The contamination of fish and wildlife is a major concern of the Mohawk people, since their tradition and culture emphasize the interdependence of man and his environment and because many residents formerly depended heavily on local fish and waterfowl for food. The focus of this research from 1986-1992 was on nursing women and infants. The major purpose of the current project is to determine if there are associations between dietary, residential, and occupational exposures to PCBs and DDE and individual body burdens in Mohawk men, specifically the husbands, partners, fathers, brothers, or other male relatives of the women in our other studies. In other fish-eating populations, adult men have tended to demonstrate higher PCB and DDE body burdens than women and children. Exposure estimates based on the reported consumption of locally caught fish and wildlife and residential histories will be correlated with the specific pattern of PCB congeners found in serum, thereby establishing a direct relationship between two potential sources of exposure and body burdens. Liver function will be examined through the caffeine breath test (CBT), a sensitive, noninvasive method of assessment of enzyme induction, one of the earliest detectable biological responses to PCBs in laboratory animals. This test appears promising as a method to detect subtle subclinical effects before the onset of overt clinical symptoms. The project is among the first to explore differences in dietary and other exposures, body burdens, and potential adverse health effects due to specific PCB congeners in men and women from the same source population.     

Effect of Oil on Polychlorinated Biphenyl Phase Partitioning during Land Biotreatment of Impacted Sediment

This study evaluated the partitioning of polychlorinated biphenyls (PCBs) during long-term, passive, land biotreatment of PCB-impacted industrial lagoon sediments. Over six years under field conditions, two land treatment units (LTUs) experienced 40% total PCB reductions from initial concentrations of 8–10?mg/kg. A third LTU with 113?mg/kg initial total PCBs showed little reduction over five years. In each unit throughout the study, oil concentrations declined at a rate greater than that for PCBs. Measured aqueous equilibrium concentrations for the PCB-impacted sediments were typically an order of magnitude or more smaller than values estimated using correlations based on total organic matter partitioning. Measured aqueous PCB concentrations agreed with predictions based on equilibration with a PCB-containing oil phase, best modeled by Raoult’s law. It was postulated that, as a consequence of PCB oil-phase partitioning, biotreatment would lead to higher PCB concentrations in the oily matter and thus increased PCB partitioning to the aqueous phase if the degradation of oily matter proceeded faster compared to PCBs. Such was the case in this study, wherein low-level aqueous phase PCB concentrations of tetrachloro PCBs increased several fold over the years as oily matter was degraded. The contribution of oil to PCB partitioning needs to be incorporated in the assessment of risk and treatability goals for land biotreatment of contaminated sediments from industrial sites.     

The ecotoxicity of chlorate to aquatic organisms: a critical review

In order to assess the risk posed by chlorate in aquatic ecosystems, data on the effects of chlorate on aquatic organisms (microorganisms, algae, invertebrates, and fish) and mesocosm studies have been collated and critically reviewed. The geometric mean E(L)C50 values for both freshwater and marine species were (as ClO3-): microorganisms, 38,583 mg.liter-1; microalgae, 563 mg.liter-1; invertebrates, 2442 mg.liter-1; fish, 3815 mg.liter-1. Marine macro red algae were insensitive to chlorate, whereas marine macro brown algae (e.g., Fucus sp.) appeared to be exceptionally sensitive to chlorate, adverse long-term effects having been reported at concentrations as low as 0.015 mg ClO3-.liter-1. Evidence for the mechanism by which chlorate is thought to be particularly toxic to these species is also reviewed. It is concluded that, based on the species reported, chlorate is nontoxic (acute toxicity > 100 mg.liter-1) to most of the freshwater and marine species examined. However, chlorate is highly toxic (acute toxicity < 0.1 mg.liter-1) to certain macro brown algal species. For macro brown algae, the NOEC after 6 months was reported to be approximately 0.005 mg ClO3-.liter-1. It is also concluded that an improved understanding of the actual mode of action of chlorate in sensitive species is desirable. Together with further information on the environmental fate of chlorate, this will improve the risk assessment for chlorate in the aquatic environment.     

Effects of Perinatal Exposure to PCBs on Neuropsychological Functions in the Rotterdam Cohort at 9 Years of Age.

PCBs are known for their neurotoxic properties, especially on the developing brain. To increase insight into the neurotoxic effects of PCB exposure, the authors studied the effects of perinatal exposure to environmental levels of these compounds on different neuropsychological domains. In 9-year-old children of the Rotterdam PCB--dioxin cohort, higher prenatal PCB levels were associated with longer response times (RTs), more variation in RTs, and lower scores on the Tower of London (TOL; Shallice, 1982). A longer breast-feeding duration was associated with lower TOL scores and with better spatial organizational skills. There was some evidence of negative effects of lactational exposure to PCBs on scores on the TOL. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Evaluation of Potential Risks from Ash Disposal Site Leachate

A risk-based approach is used to evaluate potential human health risks associated with a discharge from an ash disposal site into a small stream. The RIVRISK model was used to estimate downstream concentrations and corresponding risks. The modeling and risk analyses focus on boron, the constituent of greatest potential concern to public health at the site investigated, in Riddle Run, Pennsylvania. Prior to performing the risk assessment, the model is validated by comparing observed and predicted results. The comparison is good and an uncertainty analysis is provided to explain the comparison. The hazard quotient (HQ) for boron is predicted to be greater than 1 at presently regulated compliance points over a range of flow rates. The reference dose (RfD) currently recommended by the United States Environmental Protection Agency (U.S. EPA) was used for the analyses. However, the toxicity of boron as expressed by the RfD is now under review by both the U.S. EPA and the World Health Organization. Alternative reference doses being examined would produce predicted boron hazard quotients of less than 1 at nearly all flow conditions.     

废弃矿山固废环境风险评价方法与分级监管建议

中国是矿业大国,矿种丰富,造成历史遗留矿山众多。因矿种类型复杂、不同地区气候差异大、水文地质条件不同以及周边环境敏感度迥异,致使其环境风险不明,环境污染底数不清,目前仍缺乏针对历史遗留矿山环境风险的评价方法体系。本研究尝试建立了一种基于层次分析法的历史遗留矿山环境风险评估方法,选择具有主导作用、代表性的12项指标构建了基于评价目标层、评价准则层与评价因子层的历史遗留矿山固废环境风险评价三级指标体系,包括矿种类别、固废属性、自然条件、管理措施、保护目标与环境质量等,构建了判断矩阵并通过一致性检验,明确了各影响要素的权重。根据实际赋分情况,将历史遗留矿山环境风险等级分为一般、较大和严重三个等级。在此基础上提出了针对不同风险等级应采取的管理措施：自然衰减、风险管控与修复治理。最后将建立的评价方法应用于某地区的10个历史遗留矿山的环境风险评价,结果显示该地区一般、较大和严重风险的矿山数量分别为7、2和1,评价结果可为历史遗留矿山的差异性环境监管工作提供参考。     

Dioxins, dibenzofurans, dioxin-like PCBs, and DDE in U.S. fast food, 1995

Food, especially dairy products, meat, and fish, is the primary source of environmental exposure to dioxins in the general population. Little data exists on dioxin levels in the popular and widely consumed "fast foods". Data presented in a previously published pilot study was limited to measuring only the levels of dioxins and dibenzofurans in three types of U.S. fast food. This study adds to the previous paper by presenting data, in addition to dioxins and dibenzofurans, on the closely related dioxin-like polychlorinated biphenyls (PCBs), and the persistent metabolite of DDT, 1,1-dichloro-2,2-bis (p-chlorophenyl) ethylene (DDE), in four types of popular U.S. fast food. These include McDonald's Big Mac Hamburger, Pizza Hut's Personal Pan Pizza Supreme, Kentucky Fried Chicken (KFC) three piece original recipe mixed dark and white meat luncheon package, and H?agen-Daz chocolate-chocolate chip ice cream. Dioxin plus dibenzofuran dioxin toxic equivalents (TEQ) ranged from 0.03 to 0.28 TEQ pg/g wet or whole weight for the Big Mac, from 0.03 to 0.29 for the Pizza, from 0.01 to 0.31 for the KFC, and from 0.03 to 0.49 TEQ pg/g for the ice cream. Daily TEQ consumption per kilogram body weight (kg/BW), assuming an average 65 kg adult and a 20 kg child, from one serving of each of these fast food ranged between 0.046 and 1.556 pg/kg in adults whereas in children the values were between 0.15 and 5.05 pg/kg. Total measured PCDD/Fs in the Big Mac, Personal Pan Pizza, KFC, and the H?agen-Daz ice cream varied from 0.58 to 9.31 pg/g. Measured DDE levels in the fast foods ranged from 180 to 3170 pg/g. Total mono-ortho PCB levels ranged up to 500 pg/g or 1.28 TEQ pg/g for the KFC and for di-ortho PCBs up to 740 pg/g or 0.014 TEQ pg/g for the pizza sample. Total PCB values in the four samples ranged up to 1170 pg/g or 1.29 TEQ pg/g for the chicken sample.     

Fate and risk evaluation of persistent organic contaminants and related compounds in Victoria Harbour, Hong Kong

The Environment Protection Department of Hong Kong has a monitoring program for persistent organic contaminants in sediments of Victoria Harbour, the main harbour of Hong Kong. A fugacity model has been used, based on this sedimentary data, to estimate inputs to the system (probably from sewage, stormwater and industrial discharges) as well as the fate of the contaminants, particularly in terms of the aqueous and biotic concentrations. The risk of deleterious effects on the natural marine system, as well as on the consumers of seafood from the system, was carried out using the estimated aqueous and biotic concentrations together with accepted environmental quality guidelines. The result of our analysis indicated that the chlorohydrocarbons, PCBs (as Aroclor 1254) total DDT and total HCH pose a significant risk, and probably have caused damage to the marine ecosystem as well as posing a hazard to seafood consumers. Much higher concentrations of the less toxic total alkanes, nonaromatic hydrocarbons, linear alkyl benzenes and the compounds giving a unresolved complex mixture (UCM) cannot be evaluated due to a lack of environmental guidelines and the complexity of these substances. However, it is probable that these substances add adverse effects to those due to the other contaminants.