Plasma proinflammatory cytokine response to surgical stress in elderly patients
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Oxford Univ Press
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The objective of this longitudinal study was to jointly assess DNA damage, apoptosis, inflammatory marker levels, and white blood cell (WBC) counts in physicians occupationally exposed to inhalation anesthetics during specializations. Thus, we aimed to identify a possible cause-effect relationship between occupational exposure to waste anesthetic gases (WAGs), which were measured, and genotoxic, cytotoxic, and immunotoxic effects. Nineteen medical residents were evaluated at four time points: before entering medical residency (baseline) and at the beginning, middle, and end of medical residency. Peripheral blood mononuclear cells (PBMCs) were investigated for DNA damage, which was detected via the comet assay, and for apoptosis, which was detected via an annexin marker (flow cytometry). High-sensitivity C-reactive protein and serum inflammatory cytokines were evaluated via flow cytometry, and total and differential WBCs were counted. In addition, the concentrations of the WAGs measured in the workplace during the study were evaluated via an infrared spectrophotometer. The WAG concentrations were far higher than the internationally recommended values. Compared with those at previous time points, we observed increased DNA damage (PaEuro...=aEuro....008) and apoptosis (PaEuro...=aEuro....001) in PBMCs from the middle to the end of medical residency. Significant increases (PaEuro...< aEuro....05) in the IL-8, IL-10, IL-12p70, IL-17A, IL-18, and IL-23 levels throughout medical residency were detected. There was no effect on the WBC count (PaEuro...< aEuro....05), and all the means were within the reference range values. Occupational exposure to high levels of WAGs induces DNA damage, apoptosis, and changes in serum inflammatory marker levels, but not in leukocyte counts, in physicians who work in surgical theaters lacking an adequate scavenging system during medical residency.
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occupational exposure, inhalation anesthetics, longitudinal study, inflammation mediators, cytotoxicity
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Mutagenesis. Oxford: Oxford Univ Press, 9 p., 2025.