Does occupational exposure to anesthetic gases lead to increase of pro-inflammatory cytokines?

Chaoul, Mauricio M; Bráz, José Reinaldo Cerqueira; Lucio, Lorena M.C.; Golim, Márjorie de Assis; Braz, Leandro Gobbo; Braz, Mariana Gobbo

doi:10.1007/s00011-015-0881-2

Cited by 29 publications

(15 citation statements)

References 12 publications

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“…IL‐17A plays a key role in innate and adaptive immune responses, and this potent proinflammatory cytokine is associated with respiratory disorders . Interestingly, previous data revealed increased proinflammatory IL‐8 levels in young physicians exposed to waste anesthetic gases . Because both IL‐8 and IL‐17 are inflammatory cytokines that play roles in the human airways, the increases in levels of these two markers illustrate the relevant impact of waste anesthetic gas inhalation.…”

Section: Discussionmentioning

confidence: 95%

“…47 Interestingly, previous data revealed increased proinflammatory IL-8 levels in young physicians exposed to waste anesthetic gases. 48 Because for halogenated anesthetic and at 25 ppm for nitrous oxide (TWA during anesthetic administration). 49 These standards vary among countries, but formal regulation and safety measures are lacking in many developing nations, such as Brazil.…”

Section: F I G U R Ementioning

confidence: 99%

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High concentrations of waste anesthetic gases induce genetic damage and inflammation in physicians exposed for three years: A cross‐sectional study

et al. 2020

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This cross-sectional study analyzed the impact of occupational waste anesthetic gases on genetic material, oxidative stress, and inflammation status in young physicians exposed to inhalational anesthetics at the end of their medical residency.Concentrations of waste anesthetic gases were measured in the operating rooms to assess anesthetic pollution. The exposed group comprised individuals occupationally exposed to inhalational anesthetics, while the control group comprised individuals without anesthetic exposure. We quantified DNA damage; genetic instability (micronucleus-MN); protein, lipid, and DNA oxidation; antioxidant activities; and proinflammatory cytokine levels. Trace concentrations of anesthetics (isoflurane: 5.3 ± 2.5 ppm, sevoflurane: 9.7 ± 5.9 ppm, and nitrous oxide: 180 ± 150 ppm) were above international recommended thresholds. Basal DNA damage and IL-17A were significantly higher in the exposed group [27 ± 20 a.u. and 20.7(19.1;31.8) pg/mL, respectively] compared to the control group [17 ± 11 a.u. and 19.0(18.9;19.5) pg/mL, respectively], and MN frequency was slightly increased in the exposed physicians (2.3-fold). No significant difference was observed regarding oxidative stress biomarkers. The findings highlight the genetic and inflammatory risks in young physicians exposed to inhalational agents in operating rooms lacking adequate scavenging systems. This potential health hazard can accompany these subjects throughout their professional lives and reinforces the need to reduce ambient air pollution and consequently, occupational exposure. K E Y W O R D S genomic instability, indoor air pollution, inflammation, inhalation anesthetics, oxidative stress, work environment | 513 BRAZ et Al.

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Section: Discussionmentioning

confidence: 95%

Section: F I G U R Ementioning

confidence: 99%

High concentrations of waste anesthetic gases induce genetic damage and inflammation in physicians exposed for three years: A cross‐sectional study

et al. 2020

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“…The expression of the inflammatory gene IL‐6 appears to be a better marker of occupational exposure to WAGs than are the systemic levels of IL‐6; serum IL‐6 levels are not sensitive as IL‐6 gene expression, and IL‐6 was found in low amounts in the bloodstream. The levels of inflammatory IL‐8, which is associated with respiratory tract diseases (Díaz et al ., 2013), have been found to be augmented in medical personnel exposed to high concentrations of WAG even for relatively short period (Chaoul et al ., 2015). Interestingly, the serum levels and gene expression of the proinflammatory cytokine IL‐8 showed similar patterns in the studied anesthesia providers; however no statistically significant differences between control and exposed physicians were found when a stringent p value was applied.…”

Section: Discussionmentioning

confidence: 99%

Oxidative stress, DNA damage, inflammation and gene expression in occupationally exposed university hospital anesthesia providers

Souza

Vivo

Chen

et al. 2021

Environ and Mol Mutagen

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Considering the importance and lack of data of toxicogenomic approaches on occupational exposure to anesthetics, we evaluated possible associations between waste anesthetic gases (WAGs) exposure and biological effects including oxidative stress, DNA damage, inflammation, and transcriptional modulation. The exposed group was constituted by anesthesia providers who were mainly exposed to the anesthetics sevoflurane and isoflurane (10 ppm) and to a lesser degree to nitrous oxide (150 ppm), and the control group was constituted by physicians who had no exposure to WAGs. The oxidative stress markers included oxidized DNA bases (comet assay), malondialdehyde (high‐performance liquid chromatography [HPLC]), nitric oxide metabolites (ozone‐chemiluminescence), and antioxidative markers, including individual antioxidants (HPLC) and antioxidant defense marker (ferric reducing antioxidant power by spectrophotometry). The inflammatory markers included high‐sensitivity C‐reactive protein (chemiluminescent immunoassay) and the proinflammatory interleukins IL‐6, IL‐8 and IL‐17A (flow cytometry). Telomere length and gene expression related to DNA repair (hOGG1 and XRCC1), antioxidant defense (NRF2) and inflammation (IL6, IL8 and IL17A) were evaluated by real‐time quantitative polymerase chain reaction. No significant differences (p > .0025) between the groups were observed for any parameter evaluated. Thus, under the conditions of the study, the findings suggest that occupational exposure to WAGs is not associated with oxidative stress or inflammation when evaluated in serum/plasma, with DNA damage evaluated in lymphocytes and leucocytes or with molecular modulation assessed in peripheral blood cells in university anesthesia providers. However, it is prudent to reduce WAGs exposure and to increase biomonitoring of all occupationally exposed professionals.

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“…A delayed or inadequate immune response can lead to prolonged disease, while an excessive or under-regulated response can lead to autoimmunity. Oxidative stress and in ammation are strongly connected and either one can lead to the other (Costa et al 2014;Chaoul et al 2015). In ammatory cells produce soluble mediators, such as cytokines, which also recruit cells to the site of tissue damage by releasing ROS and further intensifying the in ammatory process (Ferguson 2010).…”

Section: Discussionmentioning

confidence: 99%

Effect of inhaled anesthetics gases on cytokines and oxidative stress alterations for the staff health status in hospitals

Alrasheedi¹,

Alqasoumi

Emara

2020

Preprint

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Abstract Background Waste anesthetic gases are few amounts of inhalational anesthesia that escape during its administration. Waste anesthetic gases such as sevoflurane and nitrous oxide can induce toxic effects among health team members working in hospitals. The objective of this study was to identify the harmful effects of upon the waste anesthetic gases exposure on oxidative stress and cytokines of health team members working in hospitals. Methods This study involved a control group and waste anesthetic gases exposure group. The exposed group was divided into six subgroups (Surgeons; Surgeon's assistants; Anaesthesiologists; Anesthesiologists' assistants; Nurses and Workers). Serum fluoride, tumor necrosis alpha, interleukin 2 and plasma malondialdehyde, catalase, glutathione peroxidase and superoxide dismutase activities were measured. Results A significant elevation was detected in fluoride, tumor necrosis alpha and interleukin 2 levels in anesthesia specialists and anesthesia assistances as compared with the surgeon, surgeon assistants, nurses and workers groups. On the other hand; a significant elevation in levels of malondialdehyde and a significant decline in levels of glutathione peroxidase, catalase and superoxide dismutase in surgeon group as compared with other exposed groups. However, a significant elevation was detected in serum interleukin 4 level among anesthesia specialists as compared with exposed groups. Conclusions Exposure to waste anesthetic gases explained a high prevalence of morbidity among operating room personnel which was observed in the present study due to exposure to oxidative stress and cytokines storm. Oxidative stress and inflammatory cytokines are responsible for induction or progression of some diseases. The studied groups (anesthesia specialists and anesthesia assistances) had exposure to high levels of waste anesthetic gases and were more risky to its toxic effects. Accordingly, an education program should be focusing on how to manage these gases to reduce its toxic effects on health staff, and continuous effort evaluating the safety of anesthesia in various aspects is required.

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Does occupational exposure to anesthetic gases lead to increase of pro-inflammatory cytokines?

Abstract: Our findings suggest an increase of the pro-inflammatory IL-8 (p<0.05) in medical personnel exposed to high concentrations of anesthetic gases, even for a relatively short period.

Cited by 29 publications

References 12 publications

High concentrations of waste anesthetic gases induce genetic damage and inflammation in physicians exposed for three years: A cross‐sectional study

High concentrations of waste anesthetic gases induce genetic damage and inflammation in physicians exposed for three years: A cross‐sectional study

Oxidative stress, DNA damage, inflammation and gene expression in occupationally exposed university hospital anesthesia providers

Effect of inhaled anesthetics gases on cytokines and oxidative stress alterations for the staff health status in hospitals

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