Mobilization of Environmental Toxicants Following Bariatric Surgery.

OBJECTIVE: Persistent organic pollutants (POPs) are lipophilic environmental toxicants that accumulate in adipose tissue. Weight loss leads to mobilization and increased redistribution of these toxicants. Many are obesogens and endocrine disruptors. Increased exposure could pose long-term health risks. The study objective was to measure the changes in serum concentrations of lipophilic POPs during significant weight loss. METHODS: This study enrolled 27 patients at a university hospital in a longitudinal, 6-month, observational study examining changes in POP blood levels after bariatric surgery. The primary outcome was the changes in the concentrations of 24 polychlorinated biphenyls (PCBs), 9 organochlorine pesticides (OCPs), 11 polybrominated diphenyl ethers, 2,2',4,4',5,5'-hexabromobiphenyl, and 4 perfluorochemicals (PFCs). RESULTS: Older adults (those born before 1976) had baseline levels of PCBs, OCPs, and PFCs that were two- to fivefold higher than younger adults (those born after 1976). Older adults had greater increases in PCBs, OCPs, and polybrominated diphenyl ethers associated with weight loss. Conversely, younger adults had greater increases in PFCs associated with weight loss. On average, blood POP levels increased as weight loss occurred. CONCLUSIONS: Although weight loss is considered beneficial, the release and redistribution of POPs to other lipid-rich organs such as the brain, kidneys, and liver warrant further investigation. Interventions should be considered to limit organ exposure to POPs when weight loss interventions are planned.

Concentration dependence of human and mouse aryl hydrocarbon receptor responsiveness to polychlorinated biphenyl exposures: Implications for aroclor mixtures.

1. Aryl hydrocarbon receptor (AhR) ligands, including 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) and polychlorinated biphenyls (PCBs), are endocrine disrupting chemicals associated with nonalcoholic fatty liver disease. This study documents the species-specific differences between mouse (high affinity mAhR) and human AhR (hAhR) activation by PCB congeners and Aroclor mixtures. 2. AhR activation by TCDD or PCBs 77, 81, 114, 114, 126, and 169 was measured using luciferase reporter constructs transfected into either Hepa1c1c7 mouse or HepG2 human liver cell lines. The EC50 values were lower in Hepa1c1c7 cells than HepG2 cells for all compounds tested except PCB 81. The results for TCDD and PCB 126 were validated in primary human and mouse hepatocytes by measuring CYP1A1 gene transcript levels. 3. Because humans are exposed to PCB mixtures, several mixtures (Aroclors 1254; 1260; and 1260 + 0.1% PCB126 each at 10 µg/ml) were then tested. Neither Aroclor 1254 nor Aroclor 1260 increased luciferase activity by the transfected AhR reporter construct. The Aroclor 1260 + 0.1% PCB 126 mixture induced mAhR-mediated transactivation, but not hAhR activation in cell lines. 4. In summary, significant concentration-dependent differences exist between human and mouse AhR activation by PCBs. Relative effect potencies differed, in some cases, from published toxic equivalency factors.

Bioaccumulation and cycling of organochlorine pesticides (OCPs) and polychlorinated biphenyls (PCBs) in three mangrove reserves of south China.

Total 22 organochlorine pesticides (OCPs) compounds and 31 polychlorinated biphenyls (PCBs) congeners in mangrove sediments and tissues (leaf, branch, root and fruit) of nine species from three Mangrove Reserves of China were studied. The mean concentrations of total DDTs, HCHs, OCPs and PCBs in sediments were 2.84, 0.06, 3.84 and 0.17 ng g-1 dw, while those in tissues were 1.85, 0.22, 9.43 and 1.61 ng g-1 dw, respectively. The elevated OCPs and PCBs levels in mangrove leaves may be caused by atmospheric sedimentation. The biota sediment accumulation factor (BSAF) values of both OCPs (mean: 3.4) and PCBs (mean: 9.9) are generally larger than one, implying mangroves' bioaccumulation and their ability to intercept pollutants. The BSAFs of PCBs in mangrove tissues were negatively correlated with the PCB congener's octanol-water partition coefficients (KOW, R = 0.58, n = 31, p < 0.001), suggesting that lower chlorinated CB congeners are more bioaccumulative in mangroves. In order to better understanding the fate of these organochlorine compounds, the cycling (including the standing accumulation, the annual absorption, the annual net retention, the annual return, and the turnover period) of OCPs and PCBs in the Mangrove Reserves were estimated, and the results indicated that mangroves are playing important roles in retaining OCPs and PCBs.

Estimating the Bioconcentration Factors of Hydrophobic Organic Compounds from Biotransformation Rates Using Rainbow Trout Hepatocytes.

Determining the biotransformation potential of commercial chemicals is critical for estimating their persistence in the aquatic environment. In vitro systems are becoming increasingly important as screening methods for assessing the potential for chemical metabolism. Depletion rate constants (kd) for several organic chemicals with high octanol-water partition coefficient (Kow) values (9-methylanthracene, benzo(a)pyrene, chrysene, and PCB-153) in rainbow trout hepatocytes were determined to estimate biotransformation rate constants (kMET) that were used in fish bioconcentration factor (BCF) models. Benzo[a]pyrene was rapidly biotransformed when incubated singly; however, its depletion rate constant (kd) declined 79% in a mixture of all four chemicals. Chrysene also exhibited significant biotransformation and its depletion rate constant declined by 50% in the mixture incubation. These data indicate that biotransformation rates determined using single chemicals may overestimate metabolism in environments containing chemical mixtures. Incubations with varying cell concentrations were used to determine whether cell concentration affected kd estimates. No statistically significant change in depletion rate constants were seen, possibly due to an increase in nonspecific binding of hydrophobic chemicals as cell density increased, decreasing overall biotransformation. A new model was used to estimate BCFs from kMET values calculated from empirically derived kd values. The inclusion of kMET in models resulted in significantly lower BCF values (compared kMET = 0). Modelled BCF values were consistent with empirically derived BCF values from the literature.

Biotransformation, antioxidant and histopathological biomarker responses to contaminants in European and American yellow eels from the Gironde and St. Lawrence estuaries.

Since the early 1980s, populations of American (Anguilla rostrata) and European eels (Anguilla anguilla) have suffered a sharp decline. The causes of their decline are likely multifactorial and include chemical pollution. A field study was conducted in eight sites varying in organic and metal contamination along the St. Lawrence (Eastern Canada) and Gironde (France) systems to investigate the relationships among contaminants, biological characteristics and biotransformation, antioxidant and histopathological biomarkers in eels from both species. For A. rostrata, no major influences of persistent organic contaminants on biomarkers were identified. For A. anguilla, eels from the most contaminated site expressed higher surface of MelanoMacrophage Centers (MMCs) and eels from another contaminated site expressed higher amount of spleen lipofuscin pigment. These two histopathological biomarkers were also associated with aging. Compared to eels from the cleanest French site, higher hepatic catalase activity and density of MMC in eels from contaminated sites was related to higher concentration of organic (DDT and metabolites, sum of PCBs, sum of PBDEs) and inorganic (Hg and Cd) contaminants. In both species, a higher deposition of spleen hemosiderin pigment was measured in eels from the most brackish sites compared to eels living in freshwater environments. Our results suggest an association between higher hemosiderin pigment and metal contamination (As for A. anguilla and Pb for A. rostrata). Parasitism by A. crassus was observed in European eels from freshwater sites but not in eels from brackish habitats. Overall, contamination may pose a greater risk for the health of European compared to American eels.

PCB 28 metabolites elimination kinetics in human plasma on a real case scenario: Study of hydroxylated polychlorinated biphenyl (OH-PCB) metabolites of PCB 28 in a highly exposed German Cohort.

Polychlorinated biphenyls (PCBs) are suspected of carcinogenic, neurotoxic and immunotoxic effects in animals and humans. Although background levels of PCBs have been slowly decreased after their ban, they are still among the most persistent and ubiquitous pollutants in the environment, remaining the subject of great concern. PCB 28 is a trichlorinated PCB found in high concentrations not only in human plasma but also in indoor air in Europe, yet little is known about its metabolic pathway and potential metabolites in humans. The present study aims to elucidate the kinetics of metabolite formation and elimination by analyzing four hydroxylated PCBs (OH-PCBs) in human plasma as potential metabolites of the PCB 28 congener. For this purpose, the study was conducted in plasma samples of highly PCB-exposed individuals (N=268), collected from 2010 to 2014 as a representation of a real case scenario with longitudinal data. OH-PCBs have been predicted, synthesized in the course of this study and further identified and quantitated in human plasma. This is the first time that previously unknown PCB 28 metabolites have been measured in human plasma and half-lives have been estimated for PCB metabolites, which could then provide further understanding in the toxicological consequences of exposure to PCBs in humans.

Potent mutagenicity of some non-planar tri- and tetrachlorinated biphenyls in mammalian cells, human CYP2E1 being a major activating enzyme.

Polychlorinated biphenyls (PCBs) have been classified as human carcinogens. Mutagenicity of lower chlorinated biphenyls as well as activation of transcription factors by some other congeners may contribute to the carcinogenicity of PCBs. Recently, we reported that human CYP2E1 activates mono- and dichlorobiphenyls to mutagens. However, mutagenicity of other PCBs and the involvement of other CYPs remained unknown. In this study, Chinese hamster V79-derived cell lines genetically engineered for expression of individual human CYP enzymes and a human hepatocyte (L-02) line endogenously expressing various CYPs were used to determine the activities of several tri- and tetrachlorobiphenyls to induce micronuclei and gene mutations. 2,3,4'-Trichlorobiphenyl, 2,3,3'-trichlorobiphenyl, 2,4,4',5-tetrachlorobiphenyl and 2,2',5,5'-tetrachlorobiphenyl efficiently induced micronuclei and/or gene mutations in V79-derived cells at low micromolar concentrations, depending on human CYP2E1, while they were inactive in parental V79-Mz cells and weakly positive or inactive in V79-derived cells expressing human CYP1A1, 1A2, 1B1 or 3A4. The induction of gene mutations in human CYP2E1-expressing V79 cells by 2,3,4'-trichlorobiphenyl and 2,4,4',5-tetrachlorobiphenyl was more potent than that of N-nitrosodimethylamine, a strong carcinogen activated by CYP2E1. As representative PCB compounds, 2,3,3'-trichlorobiphenyl and 2,3,4'-trichlorobiphenyl induced micronuclei in L-02 cells, and this effect was blocked by specific CYP2E1 inhibition, wherein the effects of benzo[a]pyrene and aflatoxin B1 (activated by some CYPs other than CYP2E1) were unaffected. This study demonstrates that some non-planar tri- and tetrachlorobiphenyls are potent mutagens in mammalian cells-more potent than previously tested mono- and dichlorobiphenyls-and that among several human CYP enzymes, CYP2E1 is most efficient in activating these environmental contaminants.

A Preliminary Link between Hydroxylated Metabolites of Polychlorinated Biphenyls and Free Thyroxin in Humans.

BACKGROUND: Polychlorinated biphenyls (PCBs) and their hydroxylated metabolites (HO-PCBs) interfere with thyroid hormone action both in vitro and in vivo. However, epidemiologic studies on the link between PCB exposure and thyroid function have yielded discordant results, while very few data are available for HO-PCBs. OBJECTIVES: Our study aimed at investigating the relationship between clinically available markers of thyroid metabolism and serum levels of both PCBs and HO-PCBs. SUBJECTS AND METHODS: In a group of 180 subjects, thyroid-stimulating hormone (TSH) and free thyroxin (fT4), 29 PCBs (expressed both in lipid weight and in wet weight) and 18 HO-PCBs were measured in serum. RESULTS: In regression models, adjusted for gender, age, current smoking behavior, BMI and total lipid levels, serum levels of 3HO-PCB118 and 3HO-PCB180, and PCB95(lw), PCB99(lw) and PCB149(lw) were independent, significant predictors of fT4. A stepwise, multiple regression with gender, age, current smoking behavior, BMI and total lipid levels and all five previously identified significant compounds retained age, BMI, PCB95(lw), PCB99(lw) and 3HO-PCB180 as significant predictors of fT4. TSH levels were not predicted by serum levels of any of the PCBs or HO-PCBs. CONCLUSIONS: Our study indicates that in vivo, circulating fT4 levels can be linked to serum levels of several PCBs and hydroxylated PCB metabolites.

Bioanalytical and instrumental screening of the uptake of sediment-borne, dioxin-like compounds in roach (Rutilus rutilus).

To examine the uptake of dioxin-like compounds (DLCs), common roaches (Rutilus rutilus) were exposed for 28 days to differently contaminated sediments from two major European rivers in a purpose-built facility. Dietary transfer of DLCs was investigated by exposing fish to sediments inoculated or non-inoculated with black worms (Lumbriculus variegatus). Dioxin-like polychlorinated biphenyls (DL-PCBs), polychlorinated dibenzo-p-dioxins and dibenzofurans (PCDD/Fs), measured via high-resolution gas chromatography/high-resolution mass spectrometry (HRGC/HRMS) in sediments and whole fish, were used to calculate toxicity equivalent quotients (TEQs). TEQs were compared with biological toxicity equivalent quotients (BEQs) determined via the 7-ethoxyresorufin-O-deethylase (EROD) assay, performed with mammalian (H4IIE) and fish (RTL-W1) liver cell lines. TEQs and BEQs indicated an uptake of sediment-borne DLCs by roach, which was independent of sediment contamination levels, but rather reflected sediment-specific characteristics. For most sediment treatments, DLC uptake did not increase with time. Highest congener-specific uptake (DL-PCB 123) was 10-fold compared to control. Exposure to worm-inoculated sediment of highest overall DLC contamination caused a 2-fold (TEQ and H4IIE BEQ) greater uptake of DLCs by fish compared to the respective non-inoculated treatment. H4IIE cells showed the greatest sensitivity (0.37 ± 0.25 pM TCDD) and the strongest correlation with TEQs (r (2) = 0.79), hence, they seem to be best suited for DLC screening of sediments and biota, amended by compound-specific instrumental analysis if required.

Intervention to reduce PCBs: learnings from a controlled study of Anniston residents.

Nonabsorbable dietary lipid reduces the absorption of dietary PCBs and increases the excretion of previously absorbed stored PCBs. Absorption of all PCB congeners will presumably be interrupted by nonabsorbable lipid; however excretion will be enhanced only for PCBs that have not been metabolized and also for their lipophilic metabolites. Our study with the nonabsorbable lipid, olestra, in a controlled trial in Anniston residents with elevated PCB levels demonstrated that it is possible to enhance removal of PCBs from the body in the clinically meaningful time frame of 1 year. The rate of disappearance of PCBs in participants who ate 15 g/day of olestra was significantly faster than the rate determined during the 5 years prior to intervention. The rate of disappearance was not changed from the pretrial rate in participants who ingested vegetable oil. Consideration of the role of body weight and fat is an important factor in the design of intervention trials of this kind, and the results of this trial suggest that the level of body fat in individuals will influence the rate of removal from the body. Previously reported data from animals and from a case report indicate that weight loss combined with nonabsorbable dietary lipid will maximize removal of PCBs and presumably other stored organochlorine compounds. The design of future intervention trials should include a focus on body fat levels and changes. Future trials should also include the testing of dietary compounds other than olestra that have affinity for PCBs, such as plant-derived polyphenols.

Hydroxyl metabolite of PCB 180 induces DNA damage signaling and enhances the DNA damaging effect of benzo[a]pyrene.

Non-dioxin-like (NDL) polychlorinated biphenyls (PCBs) and their hydroxyl metabolites (OH-PCBs) are ubiquitous environmental contaminants in human tissues and blood. The toxicological impact of these metabolites is poorly understood. In this study rats were exposed to ultrapure PCB180 (10-1000mg/kgbw) for 28days and induction of genotoxic stress in liver was investigated. DNA damage signaling proteins (pChk1Ser317 and γH2AXSer319) were increased dose dependently in female rats. This increase was paralleled by increasing levels of the metabolite 3'-OH-PCB180. pChk1 was the most sensitive marker. In in vitro studies HepG2 cells were exposed to 1µM of PCB180 and 3'-OH-PCB180 or the positive control benzo[a]pyrene (BaP, 5µM). 3'-OH-PCB180, but not PCB180, induced CYP1A1 mRNA and γH2AX. CYP1A1 mRNA induction was seen at 1h, and γH2AX at 3h. The anti-oxidant N-Acetyl-l-Cysteine (NAC) completely prevented, and 17ß-estradiol amplified the γH2AX induction by 3'-OH-PCB180. As 3'-OH-PCB180 induced CYP1A1, a major BaP-metabolizing and activating enzyme, interactions between 3'-OH-PCB180 and BaP was also studied. The metabolite amplified the DNA damage signaling response to BaP. In conclusion, metabolism of PCB180 to its hydroxyl metabolite and the subsequent induction of CYP1A1 seem important for DNA damage induced by PCB180 in vivo. Amplification of the response with estradiol may explain why DNA damage was only seen in female rats.

Impact of soil characteristics on relative bioavailability of NDL-PCBs in piglets.

Children may be orally exposed to organic pollutants through involuntary soil ingestion. This study was aimed at determining the impact of the characteristics (organic carbon (OC), black carbon (BC), clay contents and pH) of ten contaminated soils on the bioavailability of non-dioxin-like polychlorobiphenyls (NDL-PCBs). Five juvenile male piglets were exposed to increasing amounts of each of the soils. These soil-fed groups were compared by a relative bioavailability approach (RBA) to a reference group fed with corn oil spiked with increasing doses of Aroclor 1254. After 10days of oral exposure, the animals were sacrificed and NDL-PCB concentrations were determined by GC-MS in the adipose tissue. The relative bioavailability (RBA) factors were calculated for PCB 101, 138, 153 and 180. Despite high variations in the amount of black carbon (0.50gkg(-1)-6.0gkg(-1)d.w.) and organic matter (12gkg(-1)-180gkg(-1)d.w.), only 3 soils exhibited a significantly lower RBA for all NDL-PCBs, compared to the oil-group. High levels of OC (>100gkg(-1)) and BC content (3.0gkg(-1)) were related to a significant reduction in RBA. Overall, RBA was higher than 45% independently of the soil and the PCB congener.

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.

Role of AHR, AHRR and ARNT in response to dioxin-like PCBs in Spaurus aurata.

The aryl hydrocarbon receptor (AHR) mediates a variety of biological responses to ubiquitous dioxin and PCB dioxin-like. AHR together with ARNT, AHRR, represent a novel basic helix-loop-helix/PAS family of transcriptional regulators. Their interplay may affect the xenobiotic response. The aim of this study was to investigate, by histological, immunohistochemical investigations and western-blot analysis, the expression of AHR, ARNT and AHRR in liver of seabrem (Spaurus aurata) after exposure at different time to dioxin-like PCB126 in order to deep the knowledge about their specific role. The findings showed a significant increase of AHR and ARNT expression in juvenile fishes after 12 h than control group. The induction of AHR and ARNT is also significant at 24 and 72 hours compared to the control group. Furthemore, induction of AHRR expression has proved to increase both 12 h but this induction does not seem significant to 24 and 72 hours. The most important data of this work is that the induction of AHRR, when the action of the toxic persistence substances, as dioxin and PCB-126, it is not enough to reduce AHR signaling and thus its hyperactivation leads to toxic effects in seabrem (Spaurus aurata). All this confirms the importance of AHR ligands as new class of drugs that can be directed against severe disease such as cancer.

Adipose tissue PCB levels and CYP1B1 and COMT genotypes in relation to breast cancer risk in postmenopausal Danish women.

Exposure to PCBs may be an etiologic factor for breast cancer. The cytochrome P450 1B1 (CYP1B1) and catechol-O-methyltransferase (COMT) enzymes are involved in estrogen metabolism and PCB metabolism, both of which may relate to breast cancer susceptibility. Polymorphisms in genes regulating these enzymes control efficiency. Our objective was to assess whether CYP1B1 and COMT gene polymorphisms modulate the effect of PCBs in breast cancer risk, among postmenopausal Danish women. Neither CYP1B1 Leu432Val polymorphisms nor adipose tissue PCBs were independently associated with breast cancer risk. When assessing the independent effect of the COMT Val158Met polymorphism, we observed reduced risk for breast cancer amongst hormone replacement therapy using women who were homozygous carriers of the variant allele compared with those carrying the wild-type variant (RR = 0.41; 95% CI: 0.29-0.89). We found no statistically significant interactions between any of the PCB groups and CYP1B1 or COMT polymorphisms on the risk of breast cancer.

Estimation of health risk by using toxicokinetic modelling: a case study of polychlorinated biphenyl PCB153.

To assess potential PCB153-associated human health effects and risks, it is necessary to model past exposure. PCB153 blood concentrations, obtained from the AMAP biomonitoring programme, in Inuit women covering the years 1994-2006 at Disko Bay, 1999-2005 at Nuuk, and 1992-2007 at Nunavik were used to extrapolate body burden and exposure to the whole lifespan of the population by the one-compartment toxicokinetic model. By using risk characterisation modelling, calculated Hazard Quotients were higher than 1 between the years 1955 and 1987 for the 90th population percentile and during 1956-1984 for the 50th population percentile. Cancer risk for overall exposure of PCB153 ranged from 4.6×10(-5) to 1.8×10(-6) for the 90th percentile and 3.6×10(-5) to 1.4×10(-10) for the 50th percentile between 1930 and 2049, when central estimates or upper-bound slope factors were applied. Cancer risk was below 1×10(-6) for the same time period when a lower slope factor was applied. Significant future research requirements to improve health risk characterisation include, among others, larger sample sizes, better analytical accuracy, fewer assumptions in exposure assessment, and consequently, a better choice of the toxicity benchmark used to develop the hazard quotient.

Biological and tumor-promoting effects of dioxin-like and non-dioxin-like polychlorinated biphenyls in mouse liver after single or combined treatment.

To assess the impact of a mixture containing dioxin-like and non-dioxin-like polychlorinated biphenyls (PCBs), male mice were initiated with N-nitroso-diethylamine and subsequently treated with PCB126, an Ah-Receptor agonist, and PCB153, acting via activation of the constitutive androstane receptor. The two congeners were given at two dose levels: the low dose was adjusted to induce ~150-fold increases in cytochrome P450 (Cyp)1a1 (PCB126) and Cyp2b10 mRNAs (PCB153), and the high dose was chosen as twice the low dose. To keep the liver PCB levels constant, mice were given initial loading doses followed by weekly maintenance doses calculated on the basis of the PCBs' half-lives. Mice were treated with the individual congeners (low and high dose) or with a mixture consisting of the low doses of the 2 PCBs. The following results were obtained: (1) the 2 PCBs produced dose-dependent increases in Cyp1a1 and Cyp2b10 mRNA, protein, and activity when given individually; (2) combined treatment caused more than additive effects on Cyp1a1 mRNA expression, protein level, and ethoxyresurofin activity; (3) changes in the levels of several proteins were detected by proteome analysis in livers of PCB-treated mice; (4) besides these biological responses, the individual PCBs caused no significant increase in the number of glucose-6-phospatase (G6Pase)-deficient neoplastic lesions in liver, whereas a moderate significant effect occurred in the combination group. These results suggest weak but significant response-additive effects of the 2 PCBs when given in combination. They also suggest that the Cyp biomarkers tend to overestimate the carcinogenic response produced by the PCBs in mouse liver.

Uptake of organochlorine pesticides (OCPs) and polychlorinated biphenyls (PCBs) by river water fish: the case of River Chenab.

Organochlorine pesticides (OCPs) and polychlorinated biphenyls (PCBs) were investigated in eleven edible fish species (5 herbivorous and 6 carnivorous) collected from the River Chenab, Pakistan, during 2007-2009. Total OCP and PCB concentrations (ng g(-1) wet weight, ww) ranged between 13-107 (mean: 38) and 3.1-93.7 (mean: 20) for five herbivorous fish species and 21.6-365 (mean: 148) and 2.5-108 (mean: 30) for six carnivorous species, respectively. The trends of detected organochlorine pesticides (OCPs) in fish samples were: DDTs>PCBs>chlordanes>HCHs. The mean concentration(s) (ng g(-1) ww) of OCPs were relatively higher in all fish species collected near industrial areas followed by urban and agricultural areas. Risk assessment of OCPs and PCBs indicated that fish intake may pose health risk to humans with a consumption rate of >8 g/person/day. The hazardous ratios for the 50th and 95th percentile data of OCPs and PCBs in fish exceeded the value of 1, suggesting that the daily exposure to OCPs and PCBs yield a lifetime cancer risk greater than 1 in 10,000.

Biomarker responses and accumulation of hazardous substances in mussels (Mytilus trossulus) transplanted along a pollution gradient close to an oil terminal in the Gulf of Finland (Baltic Sea).

Baltic Sea blue mussels (Mytilus trossulus) were used as sentinel organisms to detect the biological effects of chemical contamination in the low salinity environment. Mussels naturally adapted to a salinity of ca. 6.0 PSU were caged for 30 days at four sites along an assumed pollution gradient (salinity ca. 4.5 PSU) in the vicinity of Finland's largest oil refinery and harbor Kilpilahti in the Gulf of Finland. Tissue concentrations and accumulation rates of especially organic contaminants (PAHs, PCBs and organotins) were clearly elevated at the innermost coastal stations near the harbor area. Biological effects of contaminant exposure on caged mussels were evaluated by measuring a suite of biomarkers including catalase, glutathione S-transferase, superoxide dismutase, glutathione reductase, lipid peroxidation, acetylcholinesterase activity and lysosomal membrane stability. Mussels transplanted near the harbor area were able to elevate their antioxidant defense in response to environmental contamination. Reduced morphometric condition index and soft tissue growth rate together with increased lipid peroxidation and low lysosomal membrane stability were also observed at the most contaminated site. The results suggest that caging of M. trossulus for four weeks at lower salinity is a feasible method for the detection of environmental pollution also in low salinity areas of the Baltic Sea.

[Human biomonitoring and variation of haematic parameters in a population exposed to PCB and dioxin near a steel plant in the lower Susa Valley]. / Biomonitoraggio umano e variazione dei parametri ematici in una popolazione esposta a PCB e diossine presso un'acciaieria in bassa Val di Susa.

OBJECTIVE: to evaluate the degree of exposure to PCB in a population resident in the lower Susa Valley and its effects on general and endocrine homeostasis. DESIGN, SETTING, PARTICIPANTS AND MAIN OUTCOME MEASURES: in the lower Susa Valley (Piedmont, Italy), there is a steel secondary casting plant (i.e. by fusion of scrap iron), active since the '50s. The emissions of PCB and dioxin coming from the furnace were found in samples of herb, pulse and ground in a preliminary environmental characterisation study. During 2005-2006 we run an epidemiologic study of biomonitoring (measuring as outcome common haematochemical parameters, hormonal parameters, haematic PCB) on a sample of subjects resident in the municipalities with higher levels of PCB and dioxin contamination (exposed subjects), that was compared with another sample (unexposed) of subjects residing in other areas of the Susa Valley. RESULTS: the final sample consisted of 244 subjects (119 unexposed and 125 exposed), balanced by gender, age, education and representative of the Susa Valley population. The greater part of hormonal and toxic parameters showed worse values among exposed than among unexposed, including PCB median value (2.30 µg/l among exposed vs. 1.90 µg/l among unexposed). The difference however was not statistically significant and the values were lower than the population reference values (7.2 µg/l). Haematic PCB values were significantly and positively correlated with age and alcohol consumption and not significantly with male gender. The distribution of the principal haematochemical parameters (hemochrome, total, LDL and HDL cholesterol, triglycerides, glucose, creatinine, bilirubin, transaminases, gamma-glutamiltranspeptidase, proteine electrophoresis) showed also, on the whole, worse values among exposed compared to unexposed, even if the difference was not statistically significant for single values. CONCLUSIONS: the exposed population showed higher values of PCB haematic values and alterations of the hormonal and common heamatochemical parameters compared to unexposed population, even if within reference limits.