Economically feasible strategy for confirmation of pharmaceuticals in hospital effluent using screening analysis.

The contamination of aquatic systems by pharmaceuticals has received considerable attention in recent decades, because these substances are increasingly detected in the environment. This is due to the abundant use of pharmaceuticals by the population and, consequently, their constant introduction into aquatic systems through domestic, industrial, and hospital wastewaters. Hospital effluents have highly complex compositions and present potential toxicity towards the environment. In this work, a screening methodology was developed to evaluate the occurrence of pharmaceutical products in hospital wastewater, using a viable, easy, and economical strategy employing commercial pharmaceutical compounds for screening analysis. Six samplings of hospital wastewater were carried out monthly (from winter until summer). The samples were filtered and pre-concentrated/extracted using solid phase extraction (SPE). The pharmaceuticals screening procedure required the construction of two databases, one for each ionization mode (positive and negative), which contained information that allowed the identification of the presence of these pharmaceuticals in the studied samples. Commercial pharmaceutical compounds were used as analytical standards. Based on this strategy and, using liquid chromatography coupled to high resolution mass spectrometry, it was possible to screen 110 pharmaceuticals and, from these, to confirm the presence of 38 pharmaceuticals in analyzed samples. These results indicate the analytes that should be taken into account in the further development of quantitative methods for pharmaceutical analysis.

Imiquimod-Induced Psoriasis-Like Skin Lesions Do Not Accelerate Atherosclerosis in Low-Density Lipoprotein Receptor-Deficient Mice.

Psoriasis is a chronic inflammatory skin disorder associated with several comorbidities, including atherosclerosis. Disease mechanisms that may affect both psoriasis and atherosclerosis include activation of T helper 1 and T helper 17 cells. Imiquimod application is an established mouse model of psoriasis-like skin inflammation. The cardiac glycoside digoxin inhibits the master transcription factor of T helper 17 differentiation, retinoid acid receptor-related orphan nuclear receptor γt, and attenuates IL-17-dependent pathologies in mice. We investigated whether cyclic imiquimod-induced psoriasis-like skin inflammation affects atherosclerosis in low-density lipoprotein receptor-deficient mice and whether digoxin modifies either disease. Topical imiquimod application increased ear thickness, keratinocyte proliferation, and accumulation of CD3+ T cells in the skin of low-density lipoprotein receptor-deficient mice. Also, imiquimod affected the mice systemically with induction of splenomegaly as well as increased plasma levels of IL-17A and serum amyloid A. Overall, imiquimod reduced atherosclerosis in the aortic arch en face, but it did not affect atherosclerosis in the aortic root. Digoxin significantly reduced the imiquimod-induced ear thickening, had divergent effects on imiquimod-induced systemic inflammation, and did not affect atherosclerosis. In conclusion, cyclic imiquimod applications can be used for long-term induction of psoriasis-like skin lesions, but they attenuate atherosclerosis in low-density lipoprotein-deficient mice. In this model, digoxin reduces skin inflammation, but it has no effect on atherosclerosis.