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EU project investigates dioxin effect on vitamin A metabolism


Contamination of foods by organohalogens, in particular dioxins (PCDD and PCDF) and dioxin-like PCBs (polychlorinated biphenyls) are a real health concern for the food industry, governments and consumers alike. Dioxins are produced in natural combustion processes; while PCBs, now prohibited, are synthetic chemicals used in many industrial products. A recent EU-funded research project, disseminated via Flair-Flow, set out to investigate the disruptive effects of organohalogen food residues on the vitamin A metabolism.

Several hundred dioxins and PCBs have been identified but only about 20-30 are of toxicological concern. The most toxic dioxin is TCDD (2,3,7,8-tetrachlorodibenzo-p-dioxin).

The highest concentrations of these compounds in foods are found in fish and fish products, followed by dairy and meat products. Once introduced in living organisms, they are slowly decomposed. They tend to concentrate in the liver and adipose tissues, in particular in animals and fish and finally in man.

Human studies have shown that dioxins and dioxin-like PCBs primarily affect the skin, the liver, and the nervous system but also have some effect on cancer development, disturbance in the immune system and on the growth and development of the foetus. Reports on the influence on vitamin A metabolism are also published but knowledge on the mechanism of the detrimental effects is incomplete.

The objective of the EU project was to provide a sound scientific basis for the vitamin A (i.e. retinoid) disruptive effects of organohalogen food residues and by that to quantify the real toxicological risk to consumers.

To meet the objective, scientists led by Dr. Abraham Brouwer at the Institute for Environmental Studies in Amsterdam, the Netherlands, studied the retinoid signalling pathway in mutated mice, the role of retinoid in early development, pathophysiology and neural development; organohalogen-induced alterations in metabolism; bioassays and biomarkers.

The results, according to the scientists, were quite surprising. They concluded that a significant part of the adverse developmental effects caused by organohalogens is mediated through disturbed processing of retinoid-controlled pathways.

The organohalogens at relatively high concentrations as tested in the laboratory induced a "functional hyper-vitaminosis A" with increased concentrations in plasma, liver and kidney, which can result in developmental abnormalities resembling the symptoms of excessive vitamin A intake.

The scientists recommended that further research should aim at investigating the possible effects of organohalogens at dietary intake levels.

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