Propelling plastics into the circular economy - weeding out the toxics first.

The Stockholm Convention bans toxic chemicals on its persistent organic pollutants (POPs) list in order to promote cleaner production and prevent POPs accumulation in the global environment. The original 'dirty dozen' set of POPs has been expanded to include some of the brominated diphenyl ether flame retardants (POP-BDEs). In addition to cleaner production, there is an urgent need for increased resource efficiency to address the finite amount of raw materials on Earth. Recycling plastic enhances resource efficiency and is part of the circular economy approach, but how clean are the materials we are recycling? With the help of a new screening method and detailed analyses, we set out to investigate where these largely obsolete BDEs were showing up in Dutch automotive and electronics waste streams, calculate mass flows and determine to what extent they are entering the new product chains. Our study revealed that banned BDEs and other toxic flame retardants are found at high concentrations in certain plastic materials destined for recycling markets. They were also found in a variety of new consumer products, including children's toys. A mass flow analysis showed that 22% of all the POP-BDE in waste electrical and electronic equipment (WEEE) is expected to end up in recycled plastics because these toxic, bioaccumulative and persistent substances are currently not effectively separated out of plastic waste streams. In the automotive sector, this is 14%, while an additional 19% is expected to end up in second-hand parts (reuse). These results raise the issue of delicate trade-offs between consumer safety/cleaner production and resource efficiency. As petroleum intensive materials, plastic products ought to be repaired, reused, remanufactured and recycled, making good use of the 'inner circles' of the circular economy. Keeping hazardous substances - whether they are well known POPs or emerging contaminants - out of products and plastic waste streams could make these cycles work better for businesses, people and nature.

Benserazide decreases central AADC activity, extracellular dopamine levels and levodopa decarboxylation in striatum of the rat.

In Parkinsonian patients treated with levodopa, peripheral decarboxylase inhibitors like carbidopa and benserazide are used to increase the central availability of levodopa. In experimental animal studies, this clinical situation is mimicked. However, at the dose used in many animal studies, both benserazide and carbidopa pass the blood brain barrier. In this study, we investigated to what extent their presence in brain inhibits striatal aromatic amino acid decarboxylase activity. At 50 mg/kg i.p., both carbidopa and benserazide decreased striatal decarboxylase activity. At 10 mg/kg i.p., only benserazide decreased the enzyme activity, but this did not change extracellular dopamine in striatum and allowed dopamine levels to increase after levodopa administration. In contrast, the inhibition of central decarboxylase activity by 50 mg/kg benserazide decreased striatal dopamine levels and prevented the levodopa-induced increase. Therefore, it is important to carefully consider the dose of the peripheral decarboxylase inhibitor used when the central effects of levodopa are studied.

Aerobic biodegradation studies of nonylphenol ethoxylates in river water using liquid chromatography-electrospray tandem mass spectrometry.

The aerobic biodegradation of nonylphenol ethoxylates (A9PEO) was kinetically investigated in a laboratory-scale bioreactor filled with riverwater, spiked at a concentration of 10 mg L(-1) nonionic surfactants. Analyses of the samples applying liquid chromatography-electrospray mass spectrometry (LC-ES-MS) after solid-phase enrichment revealed a relatively fast primary degradation of A9PEO with >99% degradation observed after 4 days. Contrary to the generally proposed degradation pathway of EO chain shortening, it could be shown that the initiating step of the degradation is omega-carboxylation of the individual ethoxylate chains: metabolites with long carboxylated EO chains are identified (A9PEC). Further degradation proceeds gradually into short-chain carboxylated EO with the most abundant species being AgPE2C. The oxidation of the nonyl chain proceeds concomitantly with this degradation, leading to metabolites having both a carboxylated ethoxylate and an alkyl chain of varying lengths (CAPEC). The identity of the CAPEC metabolites was confirmed by the fragmentation pattern obtained with LC-ES-MS/MS. Both A9PEC and CAPEC metabolites are still present in the bioreactor after 31 days. In the aerobic degradation pathway, A9PEO2 is formed only to a minor extent and is even further degraded in several days. The endocrine disruptor nonylphenol was not found as a metabolite in this study.

Evaluation in human volunteers of the potential anticarcinogenic activities of novel nutritional concepts: prebiotics, probiotics and synbiotics (the SYNCAN project QLK1-1999-00346).

Prebiotics is a recent novel food concept that includes food ingredients that are not digested in the human upper intestinal tract and hence arrive in the colon where they are selectively fermented by a limited number of colonic bacteria. Amongst these are bifidobacteria and lactobacilli, which are considered indicators of a well-balanced intestinal flora. Probiotics are bacteria that, while passing through the intestine, may exert specific beneficial effects on the host's physiology. In general, probiotics are members of the group of the lactic acid-producing bacteria. By means of a variety of experimental models it was demonstrated that prebiotic carbohydrates and probiotics consistently reduced processes of carcinogenesis and tumorigenesis. Synergistic chemopreventive actions were observed with combinations of the two, which together are called synbiotics. One of the most important causes of death in the ageing western population is colon cancer, which is typically associated with a western-style diet. On the basis of the available experimental data, an EU-funded research project (the SYNCAN project QLK1-1999-00346) was set up to evaluate whether synbiotics and prebiotics can be added to food without detriment to (and hopefully eventually improving) organoleptic properties. They are, as such, a good vector for importing nutritionally interesting properties into our diet.

MK801 influences L-DOPA-induced dopamine release in intact and hemi-parkinson rats.

In vivo microdialysis was used to investigate the influence of dizocilpine (MK801) on basal and levodopa (L-DOPA)-induced extracellular dopamine levels in striatum and substantia nigra of intact and 6-hydroxydopamine-lesioned rats. In lesioned rats, extracellular dopamine was decreased in striatum but not in substantia nigra. L-DOPA (25 mg/kg i.p. after benserazide 10 mg/kg i. p.) increased the dopamine levels in striatum and substantia nigra of intact and dopamine-depleted rats. This increase was significantly higher in dopamine-depleted compared to intact striatum. Pretreatment with MK801 (0.1 and 1.0 mg/kg i.p.) dose-dependently attenuated the L-DOPA-induced dopamine release in substantia nigra of intact rats. In dopamine-depleted striatum, MK801 enhanced L-DOPA-induced dopamine release. The present results indicate that the influence of MK801 on L-DOPA-induced dopamine release in striatum and substantia nigra depends on the integrity of the nigrostriatal pathway. In Parkinson's disease, NMDA receptor antagonists could be beneficial by enhancing the therapeutic efficacy of L-DOPA at the level of the striatum.

Neostigmine influences the L-dopa-induced extracellular dopamine levels in the striatum.

Using in vivo microdialysis in freely moving rats, we show that the addition to the dialysis perfusion fluid of the acetylcholinesterase inhibitor neostigmine influences the decarboxylation of levodopa (L-dopa). Continuous perfusion of neostigmine (10, 50 and 100 nM) in striatum attenuated the L-dopa-induced dopamine release in a dose-dependent manner. This effect suggests that changes in magnitude of drug responses may occur when an acetylcholinesterase inhibitor is included in the perfusion solution. Results obtained under these circumstances should be carefully interpreted concerning the pharmacological effects of other drugs when used concomitantly with neostigmine.