PCB's

Hoe kan ontkend worden dat de implantaten niet schadelijk zijn voor het immuunsysteem en waarom wordt niet de moeite genomen dit te onderzoeken, terwijl in een bloedonderzoek van een patiënt die erg ziek is door gescheurde implantaten, een véél te hoge pcb-waarde werd gemeten. (Dit onderzoek vond plaats op eigen initiatief van de patiënt.)

PCB's: 4 maal de maximale referentiewaarde (mag zijn 1-4ng/ml) deze was 16ng/ml

Deze patiënte was/is vegetarisch en heeft nooit vis gegeten, dat de hoge pcb waarde zou kunnen verklaren.

Hexaan: 2 maal de maximale referentiewaarde (mag zijn 2.8-7.9mg/ml) deze was 16.4 mg/ml

Xyleen: ruim 3 maal de maximale referentiewaarde (mag zijn 1-2.9mg/ml) deze was 9.2 mg/m l

Exposure to dioxin and dioxin-like substances; A major public health concern 

Polychlorinated biphenyls: human health aspects

Humans may be exposed to PCBs by inhaling contaminated air and ingesting contaminated water and food. In 1978, the estimated dietary intake of PCBs by adults in the USA was 0.027 µg/kg body weight per day, but it declined to 0.0005 µg/kg body weight per day in 1982-1984 and <0.001 µg/kg body weight per day for the period 1986 - 1991.

Dioxins and their effects on human health

Extensive stores of PCB-based waste industrial oils, many with high levels of PCDFs, exist throughout the world. Long-term storage and improper disposal of this material may result in dioxin release into the environment and the contamination of human and animal food supplies. PCB-based waste is not easily disposed of without contamination of the environment and human populations. Such material needs to be treated as hazardous waste and is best destroyed by high temperature incineration.

Safety evaluation of certain food additives and contaminants 

Polychlorinates Dibenzodioxins

Polychlorinated Dibenzofurans

Coplanar polychlorinated Biphenyls

Maximum levels set for dioxins and PCB's in feed and food 

Questions and answers on Dioxins and PCBs

What is the problem with dioxins and PCBs?

Dioxins and PCBs are toxic chemicals that can provoke serious health effects such as cancer, hormone disruption, reduced ability to reproduce, skin toxicity and immune system disorders. They are not soluble in water and are highly soluble in fat. This means that they bind to sediment and organic matter in the environment and are absorbed in animal and human fatty tissue. In addition they are not biodegradable so they are persistent and bio-accumulate in the food chain. This means that once released into the environment, via air or via water, they pile up in the fat tissue of animals and humans, causing toxicological damage over time.

What are the WHO-TEQs, used to set the maximum limits for dioxins and dioxin-like PCBs?

The EU maximum levels set for dioxins and dioxin-like PCBs are based on the World Health Organisation (WHO) toxic equivalents (TEQs), which are used to express the toxicological concentrations of these chemicals and enable risk assessments to be carried out.

European Commission - Dioxins and PCBs

The dietary exposure to dioxins and dioxin-like PCBs exceeds the Tolerable Weekly Intake (TWI) or the Tolerable Daily Intake (TDI) for a considerable part of the European population: the Scientific Committee on Food (SCF) of the EU adopted on 30 May 2001 an opinion on the Risk Assessment of dioxins and dioxin-like PCBs in food. The Committee established a group TWI for dioxins and dioxin-like PCBs of 14 pg Toxic Equivalent (WHO-TEQ) /kg bodyweight. This TWI is in line with the provisional Tolerable Monthly Intake of 70 pg/kg bodyweight/month established by the Joint FAO/WHO Expert Committee on Food Additives (JECFA) at its fifty-seventh meeting (Rome, 5-14 June 2001) and concurs with the lower end of the range TDI of 1-4 pg WHO-TEQ/kg body weight, established by the World Health Organisation (WHO) Consultation in 1998. Representative recent dietary intake data indicate that the average dietary intakes of dioxins and dioxin-like PCBs in the EU is in the range of 1.2-3 pg/kg bodyweight and day which means that a considerable part of the European population would still exceed the TWI or TDI.

Eur-lex.europa -  PCB's 2004.

Eur-lex.europa -  PCB's 2007

What measures have been taken at EU level in the past 10 years to tackle contamination by dioxin/PCB?

De effecten van perinatale blootstelling aan PCB's op de immuunrespons 

Blootstelling aan PCB’s zou in deze gevallen een risico kunnen vormen als het functioneren van het immuunsysteem ook wordt aangetast door andere factoren, zoals vroegtijdige geboorte, chronische ziekten of andere aandoeningen.

De meeste chloorkoolwaterstoffen worden aangetroffen in dierlijke producten zoals vis, vlees, en melkproducten. Het is dus aannemelijk dat deze producten het meest bijdragen aan de hoeveelheid PCB’s waar mensen aan worden blootgesteld (Covaci et al., 2002).

ABSTRACT PCBs and PCB metabolites have been suggested to cause cytotoxicity by inducing oxidative stress, but the effectiveness of antioxidant intervention after exposure has not been established. Exponentially growing MCF-10A human breast and RWPE-1 human prostate epithelial cells continuously exposed for 5 days to 3 microM PCBs [Aroclor 1254 (Aroclor), PCB153, and the 2-(4-chlorophenyl)-1,4-benzoquinone metabolite of PCB3 (4ClBQ)] were found to exhibit growth inhibition and clonogenic cell killing, with 4ClBQ having the most pronounced effects. These PCBs were also found to increase steady-state levels of intracellular O(2)(*-) and H(2)O(2) (as determined by dihydroethidium, MitoSOX red, and 5-(and 6)-carboxy-2',7'-dichlorodihydrofluorescein diacetate oxidation). These PCBs also caused 1.5- to 5.0-fold increases in MnSOD activity in MCF-10A cells and 2.5- to 5-fold increases in CuZnSOD activity in RWPE-1 cells. Measurement of MitoSOX red oxidation with confocal microscopy coupled with colocalization of MitoTracker green in MCF-10A and RWPE-1 cells supported the hypothesis that PCBs caused increased steady-state levels of O(2)(*-) in mitochondria. Finally, treatment with either N-acetylcysteine (NAC) or the combination of polyethylene glycol (PEG)-conjugated CuZnSOD and PEG-catalase added 1 h after PCBs significantly protected these cells from PCB toxicity. These results support the hypothesis that exposure of exponentially growing human breast and prostate epithelial cells to PCBs causes increased steady-state levels of intracellular O(2)(*-) and H(2)O(2), induction of MnSOD or CuZnSOD activity, and clonogenic cell killing that could be inhibited by a clinically relevant thiol antioxidant, NAC, as well as by catalase and superoxide dismutase after PCB exposure.  >>

ABSTRACT Polychlorinated biphenyls (PCBs) are environmental chemical contaminants believed to adversely affect cellular processes. We investigated the hypothesis that PCB-induced changes in the levels of cellular reactive oxygen species (ROS) induce DNA damage resulting in cytotoxicity. Exponentially growing cultures of human nonmalignant breast epithelial cells (MCF10A) were incubated with PCBs for 3 days and assayed for cell number, ROS levels, DNA damage, and cytotoxicity. Exposure to 2,2',4,4',5,5'-hexachlorobiphenyl (PCB153) or 2-(4-chlorophenyl)benzo-1,4-quinone (4-Cl-BQ), a metabolite of 4-chlorobiphenyl (PCB3), significantly decreased cell number and MTS reduction and increased the percentage of cells with sub-G1 DNA content. Results from electron paramagnetic resonance (EPR) spectroscopy showed a 4-fold increase in the steady-state levels of ROS, which was suppressed in cells pretreated with catalase. EPR measurements in cells treated with 4-Cl-BQ detected the presence of a semiquinone radical, suggesting that the increased levels of ROS could be due to the redox cycling of 4-Cl-BQ. A dose-dependent increase in micronuclei frequency was observed in PCB-treated cells, consistent with an increase in histone 2AX phosphorylation. Treatment of cells with catalase blunted the PCB-induced increase in micronuclei frequency and H2AX phosphorylation that was consistent with an increase in cell survival. Our results demonstrate a PCB-induced increase in cellular levels of ROS causing DNA damage, resulting in cell killing.  >>

ABSTRACT This paper attempts to clarify the most common measures available for the fire and electrical engineer in the prevention of polychlorinated biphenyl (PCB) hazards. It points out the risks and the potential for making large risks involved in the use of transformers and capacitors more manageable. The focus in solving the PCB problem is on priority. This should be reflected in the agenda of the workshop: it should discuss not only transformers and capacitors as such, but deal more with questions concerning waste disposal, getting correct information to people on substances containing PCBs and on the proper and nonpanicky handling of such substances. The PCB issue does not lend itself to any black and white solution. Instead, a number of different aspects have to be taken into account. Any solutions arrived at are therefore always compromises between risk evaluation and cost effectiveness. Reduction of PCB risks does not have to result, for example, in an increase in fire risks. It is preferable to move step by step and avoid making irretractable decisions. Alternatives available for replacing PCB-filled devices or the widely used method of refilling PCB-filled transformers with silicone oils are not discussed. Refilling is not dealt with because its capacity to reduce the fire risk sufficiently in locations where these transformers are usually found in northern Europe is not known with certainty. >>

ABSTRACT This study examined the influence of lactational and in utero exposure to polychlorinated biphenyls (PCBs) on plasma PCB levels in children.

Plasma PCB levels were measured in 173 children at 3.5 years, of whom 91 were breast-fed and 82 were formula-fed in infancy.

Median plasma PCB levels were 3.6 times higher in breast-fed children (0.75 microgram/L) than in their formula-fed peers (0.21 microgram/L). Breast-feeding period and breast-milk PCB levels were important predictors for PCB levels in the breast-fed group. For children in the formula-fed group, PCB levels were significantly related to their material plasma PCB levels.

PCB levels in Dutch preschool children are related to transfer of maternal PCBs; therefore, strategies should be aimed at reducing maternal PCB body burden. >>.

In recent years, there has been growing concern about the potential long-term neurobe-havioral effects of perinatal polychlorinated biphenyl (PCB) exposure. We have addressed this issue in a series of studies at the Harlow Primate Laboratory. Offspring of rhesus monkeys (Macaca mulatto) exposed to commercial PCB mixtures (Aroclor 1016 or Aroclor 1248) were tested on two-choice discrimination-reversal learning at 1.5 years of age and on delayed spatial alternation, a spatial learning and memory task, at four to six years of age. Deficits in performance were observed on both tasks. The deficit observed on delayed spatial alternation in Aroclor 1248-exposed monkeys was quite dramatic. The monkeys were tested for 80 test sessions, but were never able to achieve control levels of performance. This effect was observed when the monkeys were four to six years of age (young adulthood), even though they had not been exposed to PCBs since they were weaned at four months of age. The pattern of effects on both discrimination-reversal learning and delayed spatial alternation was suggestive of damage to the prefrontal cortex  >>

Numerous studies have examined the relationship between organochlorines and breast cancer, but the results are not consistent. In most studies,organochlorines were measured in serum, but levels in breast adipose tissue are higher and represent cumulative internal exposure at the target site for breast cancer. Therefore, a hospital-based case-control study was conducted in Ontario, Canada to evaluate the association between breast cancer risk and breast adipose tissue concentrations of several organochlorines. Women scheduled for excision biopsy of the breast were enrolled and completed a questionnaire. The biopsy tissue of 217 cases and 213 benign controls frequency matched by study site and age in 5-year groups was analyzed for 14 polychlorinated biphenyl(PCB) congeners, total PCBs, and 10 other organochlorines, including p,p′-1,1-dichloro-2,2-bis(p-chlorophenyl)ethylene. Multiple logistic regression was used to assess the magnitude of risk. While adjusting for age, menopausal status, and other factors, odds ratios (ORs) were above 1.0 for almost all organochlorines except five pesticide residues. The ORs were above two in the highest concentration categories of PCB congeners 105 and 118, and the ORs for these PCBs increased linearly across categories (Ps for trend≤0.01). Differences by menopausal status are noted especially for PCBs 105 and 118, with risks higher among premenopausal women, and for PCBs 170 and 180, with risks higher among postmenopausal women. Clear associations with breast cancer risk were demonstrated in this study for some PCBs measured in breast adipose tissue. >>