Gloves represent an essential feature for hand protection because it is a requirement in the professional framework to comply with both hand hygiene standards and the principles of good laboratory practice. Despite their wide use, there is a knowledge gap regarding their composition, including phthalates. The purpose of the present study was to develop two orthogonal methods, GC–MS and HPLC–DAD, for the screening of plasticizers in gloves. Performances of these two methods were compared in terms of ease of use, number of analyzed plasticizers, and sample preparation. The two methods were validated and applied for the identification and quantification of plasticizers in ten gloves made with different materials (vinyl, nitrile, latex, and neoprene). Results revealed the presence of three main ones: DEHP, DEHT, and DINP. Additionally, the contents of plasticizers were extremely variable, depending on the glove material. As expected, the results point out a predominant use of plasticizers in vinyl gloves with an amount that should be of concern. While DEHP is classified as a toxic substance for reproduction 1B, it was, however, quantified in the ten different glove samples studied. This study provides new data regarding the plasticizers’ content in protective gloves, which could be useful for risk assessment.

Plasticizers are chemicals in high demand, used in a wide range of commercial products. Human are exposed through multiple pathways, from numerous sources, to multiple plasticizers. This is a matter of concern, as it may contribute to adverse health effects. The vascular system carries plasticizers throughout the body and therefore can interact with the endothelium. The aim of the study was to evaluate the in vitro toxicity on endothelial cells by considering the individual and the mixture effects of bis-(2-ethylhexyl) phthalate (DEHP), diisononyl phthalate (DINP) or bis-(2-ethylhexyl) terephthalate (DEHT). In this study, their cytotoxicity on HMEC-1 cells was evaluated on cell function (viability, cell counting, total glutathione and intracellular adenosines) and mitochondrial function (mitochondrial respiration). Results showed cellular physiological perturbations induced with all the condition tested, excepted for DEHT. Plasticizers induced a cytotoxicity by targeting mitochondrial respiration, depleting mitochondrial ATP production and increasing glycolytic metabolism. Additionally, delayed effects were observed between the cellular and the mitochondrial parameters. These results suggest that endothelial cells could go through a metabolic adaptation to face plasticizer-induced cellular stress, to effectively maintain their cellular processes. This study provides additional information on the adverse effects of plasticizers on endothelial cells.

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