Impact of low- and high-risk operators handling irinotecan on the blood contamination of health care workers in oncology day care units.

INTRODUCTION: Health care workers handling antineoplastic drugs (ADs) are at risk of mutagenicity and adverse reproductive effects. Despite protective equipment and AD handling guidelines, AD levels are still detected in caregivers in oncology units. This study attempted to assess blood contamination by irinotecan and its metabolites in all health care workers in oncology day hospital units according to activities specific to each employment category. METHODS: The study was performed at two different hospitals: a university hospital and a comprehensive cancer centre. Forty-four participants were categorized according to their daily activity as a high-risk operator (29 nurses/ward aides and 5 cleaning staff) and a low-risk operator (7 doctors and 3 secretaries). The collected blood samples were subjected to UHPLC-MS/MS. The plasma and red blood cell (RBC) levels of irinotecan and its metabolites (SN-38; APC) were determined using a validated analytical method detection test. RESULTS: Two hundred sixty-four assay results were collected (132 plasma results and 132 RBC results). The comparison between low- and high-risk operator-contaminated workers was not significant (18.33% positive results in low-risk operators vs. 25.98% positive results in high-risk operators; P = 0.22). This homogeneity showed overall contamination within the unit. Positive results were obtained in 21.43% of physicians, 11.11% of secretaries, 25.86% of nurses/ward aides and 26.67% of cleaning staff. These results could be explained by the lack or failure of personal and collective protective equipment. A lack of protection and inadequate decontamination procedures can result in surface contamination. CONCLUSIONS: This study evaluated blood contamination with irinotecan and its metabolites in health care workers from day hospital care units. Among the 24.24% of contaminations observed in care units, the difference between low- and high-risk operator contamination was not significant (P = 0.22). The impact on blood contamination found is the same between low- and high-risk caregivers. This implies that the protective precautions associated with the handling of anticancer drugs must therefore be followed by all staff, including those believed to be at low risk of exposure.

Impact of after-treatment devices and biofuels on diesel exhausts genotoxicity in A549 cells exposed at air-liquid interface.

Using an air-liquid interface (ALI) device in dynamic conditions, we evaluated the efficiency of fuel after-treatment strategies (diesel oxidation catalysis, DOC, and diesel particulate filter, DPF, devices) and the impact of 7% and 30% rapeseed methyl esters (RME) blending on oxidative stress and genotoxicity induced in A549 lung cells after 3h exposure to whole Diesel exhausts. Oxidative stress was studied using assays of ROS production, glutathione level, catalase and superoxide-dismutase (SOD) activities. No oxidative stress and no clear differences on cytotoxicity patterns between biodiesel and standard Diesel exhausts were found. A weak but significant genotoxicity (8-oxodGuo adducts) and, for standard Diesel only, a DNA damage response (DDR) as evidenced by ƔH2AX foci, remained after DOC+DPF flowing. All together, these data could contribute to the improvement of the after treatment strategies and to health risk assessment of current diesel exhausts.

Effects of alcohol consumption on biomarkers of oxidative damage to DNA and lipids in ethanol-fed pigs.

Chronic alcohol consumption is known to result in tissue injury, particularly in the liver, and is considered a major risk factor for cancers of the upper respiratory tract. Here we assessed the oxidative effects of subchronic ethanol consumption on DNA and lipids by measuring biomarkers 8-oxo-7,8-dihydro-2'-deoxyguanosine (8-oxodG) and malondialdehyde (MDA), respectively. Physiological responses of pigs (n = 4) administered ethanol in drinking water for 39 days were compared with those of water-fed pigs (n = 4). Alcoholisation resulted in serum ethanol concentration of 1.90 g L(-1) and in a moderate but significant increase in alanine aminotransferase activity, an index of liver injury. However, between the alcoholised and control groups there were no significant differences in the levels of 8-oxodG (8-oxodG per 10(6) 2'deoxyguanosine) from leucocytes (2.52 ± 0.42 Vs 2.39 ± 0.34) or from target organs, liver, cardia and oesophagus. Serum MDA levels were also similar in ethanol-fed pigs (0.33 ± 0.04 µM) and controls (0.28 ± 0.03 µM). Interestingly, levels of 8-oxodG in cardia were positively correlated with those in oesophagus (Spearman correlation coefficient R = 1, P < 0.0001). Our results suggest that alcohol consumption may not cause oxidative damage to DNA and lipids as measured by 8-oxodG and MDA, respectively. The duration of alcoholisation and the potential alcohol-induced nutritional deficiency may be critical determinants of ethanol toxicity. Relevant biomarkers, such as factors involved in sensitization to ethanol-induced oxidative stress are required to better elucidate the relationship between alcohol consumption, oxidative stress and carcinogenesis.