Search

Because of the more and more stringent regulations and customer demand, dishwasher detergent manufacturers are constantly improving the composition of the products towards better environmental performances. In order to quantify the pros and cons of these changes on the lifecycle of detergents, as compared to conventional products, the use of Life Cycle Assessment (LCA) is a meaningful opportunity. However, the application of the methodology is hampered by the lack of Characterisation Factors (CFs) relative to the specific chemical substances included in the detergents composition, which cannot be included in the impact assessment of the effluent discharge. In this study we have tackled this problem, taking advantage of the specific case of three dishwasher detergents produced by the Chemolux/McBride group: phosphate-based, eco-labelled and phosphate-free formulations. Nine CFs for freshwater ecotoxicity and seven CFs for human toxicity have been developed, using the USEtox methodology and data made available under the REACH regulation. As a result, the dishwasher effluent composition could be characterised by more than 95% for freshwater ecotoxicity whereas for human toxicity the percentage was less than 36%, due to the lack of adequate and reliable repeated dose toxicity studies. The main contributing substances to freshwater ecotoxicity were found to be sodium percarbonate and sodium triphosphate, the latter confirming the pertinence of phosphates banning in the detergent industry. Regarding human toxicity, zinc shows the highest contribution. Further comparison to previous studies and sensitivity analysis substantiated the robustness of these conclusions.

After ingestion, pharmaceuticals are excreted unchanged or metabolized. They subsequently arrive in conventional wastewater treatment plants and are then released into the environment, often without undergoing any degradation. Conventional treatment plants can be upgraded with post treatment, alternatively the removal of pharmaceuticals could be achieved directly at point sources. In the European project PILLS, several solutions for decentralized treatment of pharmaceuticals at hospitals were investigated at both pilot plant and full scale, and were then compared to conventional and upgraded centralized treatment plants using Life Cycle Assessment (LCA). Within the scope of the study, pharmaceuticals were found to have a comparatively minor environmental impact. As a consequence, an additional post treatment does not provide significant benefits. In the comparison of post treatment technologies, ozonation and activated carbon performed better than UV. These results suffer however from high uncertainties due to the assessment models of the toxicity of pharmaceuticals in LCA. Our results should therefore be interpreted with caution. LCA is a holistic approach and does not cover effects or issues on a local level, which may be highly relevant. We should therefore apply the precautionary ALARA principle (As Low As Reasonably Achievable) and not conclude that the effect of pharmaceuticals is negligible in the environment.

para-Phenylenediamine, a monocyclic arylamine, is a frequently used chemical and ingredient of oxidative hair coloring products. Thus exposure occurs predominantly via skin. Cyclooxygenases, the key enzymes in prostaglandin synthesis, exhibit manifold physiological and pathophysiologial functions in skin and skin cells such as keratinocytes. We studied if para-phenylenediamine impacts on the expression of enzymes in the cyclooxygenase pathway in human immortalized keratinocytes (HaCaT) as a model for keratinocytes. We analyzed COX-1, COX-2 and cPLA(2) steady state mRNA levels for 100-400 microM PPD after 2-24 h and found clear COX-2 induction for 400 microM PPD after 24 h, while cPLA(2) and COX-1 levels were increased dose-dependently between 8 and 24 h. Increased expression was accompanied by enhanced prostaglandin E(2) and F(2alpha) formation. Specific involvement of COX enzymes was confirmed by prostaglandin analysis in the presence of exogenous arachidonic acid and inhibition experiments using COX inhibitor NS-398. In addition, para-phenylenediamine-induced prostaglandin formation was completely inhibited in cells pre-stimulated with the anti-oxidant N-acetylcysteine. N-acetylation of PPD was observed in HaCaT yielding mono-acetyl-PPD (MAPPD) and di-acetyl-PPD (DAPPD). Further investigations of MAPPD and DAPPD and the generated auto-oxidation product Bandrowski's base (BB) found that these compounds were not able to impact on COX enzyme expression and activity. In sum, these results demonstrate that para-phenylenediamine, but not its generated acetylated derivatives or BB, induces COX expression and activity in human keratinocytes likely via oxidative processes.