PCB Levels In Blood Research Articles

Prenatal PCB-153 Exposure and Decreased Birth Weight: The Role of Gestational Weight Gain

Prenatal PCB-153 Exposure and Decreased Birth Weight: The Role of Gestational Weight Gain

Protective effects of selenium against DNA adduct formation in Inuit environmentally exposed to PCBs

Dietary habits that expose populations to potential toxicants as well as protective agents simultaneously are a realistic scenario where a meaningful assessment of the interactions and net benefit or damage can be made. A group of Inuit from Salluit, Northern Canada are exposed to high levels of PCBs and selenium, both present in the Inuit traditional foods such as blubber from sea mammals and fatty fish. Blood samples were collected from 83 Inuit, 22–70 years old. Blood selenium and PCB levels were determined previously and ranged from 227 to 2069 µg/L and 1.7 to 143 µg/L, respectively. DNA isolated from white blood cells were analyzed by modified 32P-postlabeling adductomics technology that detects a multitude of highly polar to lipophilic adducts. The levels of 8-oxodG adducts ranged from 470 to 7400 adducts/10 9 nucleotides. Other as yet unidentified polar adducts showed a 30 to 800-fold inter-individual variability. Adduct levels were negatively associated with PCB and selenium levels. The subjects were classified into high and low ratio groups, with respect to selenium/PCB. In the high ratio group, the coefficient of selenium is significantly negatively correlated with 8-oxodG ( r = − 0.38, p = 0.014) and total adducts ( r = − 0.41, p = 0.009) while there was no correlation within the low selenium/PCB group. This study suggests that increasing selenium has mitigating effect in reducing DNA adducts and therefore, possible negative effects of PCB were not seen. A protective effect of selenium is highlighted.

Dioxin, dibenzofuran, and coplanar PCB levels in Laotian blood and milk from agent orange-sprayed and nonsprayed areas, 2001.

Agent Orange, a phenoxyherbicide contaminated with 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), was used by American military forces during the United States-Vietnam war between 1962 and 1971 primarily as a defoliant to destroy forests where enemy troops might find cover. Agent Orange was used mainly in Vietnam, but also to a lesser extent in Laos and Cambodia. In Laos, there have been no prior studies of TCDD contamination from Agent Orange, despite known defoliation and documented records of Agent Orange spraying. This article presents findings of TCDD in human blood and milk from two geographic areas in Laos: Vientiane, a nonsprayed area, and Sepone, an Agent Orange-sprayed area. German and Canadian laboratories used high-resolution gas chromatography-mass spectrometry to measure 7 dioxin, 10 dibenzofuran, and 4 non-ortho or coplanar polychlorinated biphenyls in Laotian blood and milk samples. Most subjects tested in this Laos Ministry of Health Study showed low dioxin and dibenzofuran levels, consistent with what would be expected in a primarily rural nonindustrial country. These findings are consistent with relatively low dioxin and dibenzofuran levels recently found in food from these same areas. The chemically and toxicologically related non-ortho PCBs were measured but were found at low levels compared to specimens from other countries, presumably because of less industrialization and industrial pollution in Laos.

Revised and new reference values for some persistent organic pollutants (POPs) in blood for human biomonitoring in environmental medicine

Reference values for environmental pollutants related to the German population are established continuously by the Human Biomonitoring Commission of the German Federal Environmental Agency. The revised and new reference values for organochlorine compounds in whole blood are derived from the German Environmental Survey 1998 (adults aged 18 – 69 years) and from a survey performed with children (age 9 – 11 years) in south-west Germany 1998/99. The levels of organochlorine compounds in blood of adults increased with increasing age. Therefore the reference values are revised for different age groups (age groups: 18 – 19, 20 – 29, 30 – 39, 40 – 49, 50 – 59, 60 – 69). The reference values for PCB 138 in whole blood range from 0.4 to 2.2 μg/l, for PCB 153 from 0.6 to 3.3 μg/l, for PCB 180 from 0.3 to 2.4 μg/l, for β-HCH from 0.3 to 0.9 μg/l and for HCB from 0.4 to 5.8 μg/l. The reference values for DDE among adults in East Germany are higher compared to those in West Germany. The reference values of DDE in blood for adults in West Germany increase from 1.5 μg/l to 11 μg/l for the different age groups. The corresponding results for East Germany are 3 and 31 μg/l. The following reference values in blood of children (age 9 – 11 years) are recommended: 0.3 μg/l for PCB 138, 0.4 μg/l for PCB 153, 0.3 μg/l for PCB 180, 0.9 μg/l for sum of PCB (138+153+180), 0.3 μg/l for β-HCH, 0.3 μg/l for HCB and 0.7 μg/l for DDE. In comparison with the former evaluation the revised reference values for PCB, β-HCH and HCB levels in blood were reduced especially for younger adults

Organochlorine levels in maternal and umbilical cord blood plasma in Arctic Canada

A baseline for exposure to organochlorine and metal contaminants has been established for mothers and newborns in the Northwest Territories and Nunavut areas of Arctic Canada. Maternal and umbilical cord blood plasma organochlorine levels are described for Inuit, Dene, Métis, Caucasian and Other non-Aboriginal participants. Overall, 523 women volunteered to participate by giving their written informed consent between May 1994 and June 1999, resulting in the collection of 386 maternal blood samples, 407 cord blood samples and 351 maternal/cord pairs. Nearly half of all the participants regularly smoked cigarettes, including 77% of the Inuit participants. Maternal and cord results are presented for PCBs (as Aroclor 1260 and 14 congeners) and organochlorine pesticides, including p, p′-DDT, p, p′-DDE, beta-hexachlorocyclohexane (β-HCH), hexachlorobenzene (HCB), cis and trans nonachlor, heptachlor epoxide, oxychlordane, mirex, dieldrin and toxaphene. Maternal PCB levels (as Aroclor 1260) averaged 4.42 (±9.03) μg/l in Inuit, which was 3.3 times higher than those found in Dene/Métis, and 3.4 times higher than levels in Caucasians. Mean DDE levels were 2.8 times higher in the Other non-Aboriginal group (Chinese, Filipino, East Indian and multiple ethnicity) than in the Inuit group, at 3.99 μg/l and 1.42 μg/l, respectively. Cord blood PCB levels (as Aroclor 1260) averaged 1.16 (±2.42) μg/l for Inuit participants, which was 3.3–4 fold higher than the other ethnic groups. PCBs, p, p′-DDE and hexachlorobenzene were detected in all maternal samples, and p, p′-DDE was detected in all cord samples. Regression coefficients for maternal/cord pairs are presented for selected organochlorines. Other results from this study, including maternal and cord metals data, will be presented elsewhere.

PCB Concentrations and Metabolism Patterns in Common Terns ( Sterna hirundo) from Different Breeding Colonies in The Netherlands

PCB levels in blood of common terns ( Sterna hirundo) from Terneuzen, a breeding colony in The Netherlands with relatively low breeding success, were significantly higher than in birds from two Dutch reference colonies, one nearby (Oesterdam) and one further away (the Isle of Griend). However, a detailed analysis of the patterns of PCB congeners in birds from the different colonies indicated that birds from Terneuzen and to a lesser extent birds from the Oesterdam showed Ah-receptor mediated activity of P 450 iso-enzymes. It is concluded that the induction of this enzyme activity in Terneuzen may be related to PCBs as well as other non-identified compounds. In contrast to this, it is likely that at the Oesterdam non-identified compounds are mainly responsible for the enzyme activity, resulting in a shift of PCB congener patterns.

Effects of postnatal exposure of monkeys to a PCB mixture on concurrent random interval-random interval and progressive ratio performance.

Behavioral impairment as a consequence of PCB exposure beginning in utero has been reported in both humans and animals. The present study assessed the behavioral consequences of postnatal exposure to PCBs. Male monkeys (Macaca fascicularis) were dosed from birth to 20 weeks of age with 7.5 microg/kg/day of a PCB mixture representative of the PCBs typically found in human breast milk (eight monkeys) or vehicle (four monkeys). Blood PCB levels at 20 weeks of age were 0.30-0.37 ppb for control and 1.84-2.84 ppb for treated monkeys, and fat levels were 50-198 and 1694-3560 ppb for the two groups, respectively. Beginning at about 5.0 years of age, monkeys performed under concurrent schedules of reinforcement in which separate random intervals were in effect on two buttons independently. After steady-state performance was reached, the relative reinforcement ratio on the buttons was changed a total of four times, and performance both during transition and steady state was examined. There was no evidence for treatment-related differences in performance across the series of changes in schedule contingencies. The negative results failed to support the hypothesis that performance on an intermittent schedule, combined with the requirement for shifting response strategy, would prove particularly sensitive to postnatal PCB exposure. Following the concurrent schedules, monkeys were tested under a progressive ratio (PR) schedule preceded by a training procedure consisting of a within-session series of increasing fixed ratios. PCB-treated monkeys emitted more responses than controls over the first few sessions of the PR, which may be indicative of retarded acquisition of their steady-state PR performance. These results extend previous studies in these monkeys on the characterization of PCB-induced behavioral deficits.

Effects of postnatal exposure of monkeys to a PCB mixture on spatial discrimination reversal and DRL performance.

Behavioral impairment as a consequence of PCB exposure beginning in utero has been reported in both humans and animals. The present study assessed the behavioral consequences of postnatal exposure to PCBs. Male monkeys (Macaca fascicularis) were dosed from birth to 20 weeks of age with 7.5 microg/kg/ day of a PCB mixture representative of the PCBs typically found in human breast milk (eight monkeys) or vehicle (four monkeys). Blood PCB levels at 20 weeks of age were 0.30-0.37 ppb for control and 1.84-2.84 ppb for treated monkeys, and fat levels were 50-198 and 1694-3560 ppb for the two groups, respectively. At about 4.5-5.0 years of age, monkeys performed on a series of three spatial discrimination reversal tasks, followed by a differential reinforcement of low rate (DRL) 30-s schedule of reinforcement. There were no differences between groups for the number of errors across reversals for any of the discrimination reversal tasks, whereas the PCB-treated group tended to have shorter median response latencies than the control group. On the DRL schedule, there were robust differences in performance between the treated and control groups. Treated monkeys displayed shorter mean and median interresponse times (IRTs), obtained fewer reinforcements, and emitted more nonreinforced responses. The treated groups also had more short IRTs (< or =10 s) than control monkeys. Performance of the treated group did not improve to control levels over the 51 sessions of the DRL 30-s schedule; their performance remained much less efficient than that of controls. The results of this study extend previous research in this cohort of monkeys, and provide further evidence that PCB exposure limited to the early postnatal period and resulting in environmentally relevant body burdens produces long-term behavioral effects.

Determinants of polychlorinated biphenyl levels in plasma from 42-month-old children.

We report on the PCB levels in plasma from 42-month-old children and the factors that determine these levels. We measured the levels of the PCB congeners 118 (2,4,5-3'4' pentachlorobiphenyl (CB)), 138 (2, 3,4-2'4'5'hexaCB), 153 (2,4,5-2'4'5'hexaCB), and 180 (2,3,4, 5-2'4'5'heptaCB) in cord plasma, breast milk, and plasma from 42-month-old children (n = 126) living in the Groningen area, The Netherlands. The sum of the levels of these four congeners was calculated for cord plasma (SigmaPCBcord), breast milk (SigmaPCBmilk), and 42-month plasma (SigmaPCB42mo). SigmaPCBcord was used as a measure of prenatal exposure. Postnatal exposure was assessed in terms of the SigmaPCBmilk and the duration of lactation. In addition, maternal factors including age, body weight and height, parity, and formal education were recorded. In 42-month-old children who have been fully breast-fed for at least six weeks as babies, the median SigmaPCB42mo was 4.5 times as high as that in formula-fed children (0.81 microg/L vs. 0.18 microg/L). The PCB levels in cord blood and human milk and the duration of breast-feeding predict the plasma PCB level at 42 months. Each additional week of full breast-feeding is estimated to result in an increase of 0.3% of the milk PCB level. We concluded that lactation is a major source for the child's PCB body burden at 42 months.

PCB levels in bird blood and relationship to MFO responses

A non destructive methods of risk evaluation using blood is proposed for birds. Japanese quail ( Coturnix coturnixjaponica ) were fed different doses of Arochlor 1260 for 25 days to evaluate chemical stress in relation to accumulation, compartmentation and the release of PCBs into blood circulation. Total PCBs were determined in blood and liver. EROD, BROD, PROD, aldrin epoxidase and cytochrome P-450 were measured in the liver microsomal fraction, and the somatic liver index was calculated. In blood and liver, the principal congeners found (153, 138, 180 and 170) were the most persistent ones. Statistically significant correlations were found between liver monooxygenase activity, PCB levels in blood and dose. Evaluation of PCBs in blood can be proposed as a tool to predict induction of liver monooxygenases.

Comparison of clinical picture between Yusho/Yucheng cases and occupational pcb poisoning cases

Literature review on clinical picture was made on two food poisoning episodes of Yusho and Yucheng in comparison with occupational PCB exposures. It was found that the dose-response relationship is quite different between Yusho/Yucheng patients and workers occupationally exposed to PCBs, when PCB levels in blood were taken as a common indicator of exposure intensity; the clinical manifestations were much severer in the former than in the latter, even when blood PCB levels were comparable. This conclusion is in support of the suggestions that chemicals such as polychlorinated dibenzofurans should have played an important role in the etiology of Yusho and Yucheng.

Abnormally high polychlorinated biphenyl levels in striped dolphins ( Stenella coeruleoalba) affected by the 1990–1992 Mediterranean epizootic

PCB concentrations and total lipid content were determined in the blubber and liver of striped dolphins affected by the 1990 morbillivirus epizootic in the Mediterranean Sea, and in the blubber of striped dolphins from the same area sampled with a biopsy dart in 1987–1989 and 1991. PCB levels were found to be significantly higher in the individuals that succumbed to the epizootic than in the ‘healthy’ population sampled before or after the event. Although recent mobilization of lipid reserves was found to have occurred in some of the diseased dolphins, this had little effect on their PCB blubber concentrations and cannot explain the observed difference with the healthy individuals. Three hypotheses are put forward to explain the apparent link between high PCB levels and mortality caused by the epizootic: (i) depressed immunocompetence caused by PCBs leading to an increase in individual susceptibility to the morbillivirus infection, (ii) mobilization of fat reserves leading to increased PCB levels in blood which, in turn, may produce a liver lesion capable of increasing the individual's susceptibility to the morbillivirus infection, and (iii) previous existence of an unspecific hepatic lesion producing impairment of the liver function which, in turn, could lead to an increase both in tissue PCB concentrations and in individual susceptibility to the morbillivirus infection.

Subchronic Dietary Exposure to Aroclor 1254 in Rats: Accumulation of PCBs in Liver, Blood, and Adipose Tissue and Its Relationship to Induction of Various Hepatic Drug-Metabolizing Enzymes

Female F344/NCr rats were exposed continuously (7-84 days) or discontinuously (7 days exposure/21 days control diet or 28 days exposure/56 days control diet) to various dietary concentrations (1-100 ppm) of Aroclor 1254. There were dose- and time-dependent increases in PCB levels in liver, blood, and adipose tissue. Following removal of the rats from diet containing Aroclor 1254, there was a relatively rapid decrease in PCB levels, particularly in rats exposed to higher concentrations of Aroclor 1254. In parallel with the alterations in PCB levels observed, the rats showed striking dose- and time-dependent increases in hepatic levels of CYP1A1 and CYP1A2, as determined by various methods [RNA analysis, immunochemical detection, or measurement of the O-dealkylation of methoxyresorufin (CYP1A2) or ethoxyresorufin (CYP1A1)]. In rats removed from the Aroclor 1254 diet, catalytic activity for CYP1A1 as well as RNA levels for both CYP1A1 and CYP1A2 rapidly diminished. In contrast to the high levels of induction of CYP1A1 and CYP1A2 observed, limited induction (<5-fold) of epoxide hydrolase, quinone oxidoreductase, and aldehyde dehydrogenase was detected, even in rats exposed to the highest concentration of Aroclor (100 ppm) for up to 84 days. Furthermore, induction of these non-CYP hepatic drug-metabolizing genes exhibited distinctly different concentration-response curves. The ratios of hepatic CYP1A1 activity to hepatic PCB burden were similar for rats exposed continuously to Aroclor in the diet for 7, 28, or 84 days, and for rats exposed discontinuously (7 days Aroclor/21 days control diet or 28 days Aroclor/56 days control diet). Thus, hepatic PCB levels alone appeared to be reasonably predictive of CYP1A1 levels under a variety of modes of exposure. When the ratio of CYP1A1 activity to adipose or blood PCB concentration was determined, similar ratios were observed for rats exposed continuously for 7, 28, or 84 days. However, lower ratios were observed for rats discontinuously exposed to Aroclor in the diet. These results have important implications with respect to: (a) employing PCB levels in various tissues to predict biological effects, and (b) determining different concentration-response curves for the various biological effects induced by PCBs.

Increase in the human blood PCB levels promptly following ingestion of fish containing PCBs.

Increase in the human blood PCB levels promptly following ingestion of fish containing PCBs.