Over the years, neurotoxicity and cognitive dysfunction have separately been associated with endogenous formaldehyde and reduction of acetylcholine signals. However, a limited number of studies have shown a relationship between cholinergic neurotransmitter and formaldehyde exposure. Therefore, the aim of this study was to assess the neurological effect on workers from melamine-dish preparation workshop, who were exposed to formaldehyde. A total of 35 formaldehyde-exposed workers were compared with 32 control employees from the food industry. Occupational exposure to formaldehyde was conducted using the National Institute of Occupational Safety and Health 3500 methods. Using the Ellman method, acetylcholinesterase (AChE) as a biomarker for neurotoxicity was analyzed in blood erythrocyte. The effects of alcohol dehydrogenase III (ADH3) and Mn-superoxide dismutase (Mn-SOD) polymorphism were used to survey the level of AChE activity. In this study, it was found that exposure to airborne formaldehyde increased from 0.024 to 0.74 ppm and the median personnel exposure was 0.057. Induction of AChE activity was observed in formaldehyde-exposed workers as compared with the control group (p < 0.01), while AChE activity increased in 64 % of the exposed subjects. Spearman's correlation (p < 0.02) was used to evaluate the association between AChE activity and occupational exposure to formaldehyde. Exposed subjects containing ADH3 genotype had higher AChE than others. The findings of this study suggest that the neurotoxic effect of formaldehyde depends on the AChE activity, which is affected by metabolism. It can be concluded that cholinergic signal reduction in cases of cognitive dysfunction could be associated with endogenous formaldehyde.

Treatment using cytotoxic drugs is considered to be the most common treatment for cancers. However, the widespread use of these drugs on the health status of the staff at the oncology department has become a great concern. Due to challenges of sampling and analysis of cytotoxic drugs, the aim of this study was to development a novel practical method called Needle trap devices (NTD) for sampling and analysis of personal exposure to cyclophosphamide drug. The sampler consisted of a stainless steel hyper needle gauge 21 of length 9 cm packed with Carboxen 1000 for adsorbing cyclophosphamide. A total of 41 samples of staff's air breathing zone in different wards of the oncology department were taken with the sampler. Samples were analyzed by gas chromatography coupled with electron capture detector (ECD). Linear range concentration was 212-1062 μg/m(3), and LOD and LOQ were 100 and 191 μg/m(3), respectively. The mean inter-day and intra-day coefficient variations for standards within linear range concentration were 8.9 and 4.8 %, respectively. Detectable levels of cyclophosphamide were measured in 31.7 % of air samples. The developed method is user-friendly, quick, and precise for sampling of airborne cyclophosphamide. The results showed that some staff of the oncology department were exposed to the carcinogenic drug and their health were at risk. Since carcinogens do not have a threshold and oncology staffs with their continuous exposure might be at risk, therefore, proper work practice and adequate control measures are essential to ensure their wellbeing.

Background: Chlorophenols (CPs) and related phenoxyacetic acids (PAs) are pesticide groups contaminated with highly toxic 2, 3, 7, 8-tetrachlorodibenzo-p-dioxin (TCDD) during production. PAs and CPs exposure is associated with risk of cancer, but the situation regarding lung cancer has not been clearly defined. We proposed a meta-analysis of published researches to evaluate relationship between chronic exposure to PAs and CPs in pesticide production workplaces and the risk of lung cancer. Materials and Methods: After searching PubMed, Scopus, Scholar Google, Web of Sciences until August 2013, the association between chronic PAs and CPs exposure in production workplace and lung cancer was studied in 15 cohort studies. The standardized mortality rate (SMR) and 95% confidence intervals (CI) were collected from the papers. We used random or fixed-effects models, Egger test, funnel plot and meta regression in our analysis. Results: Five papers with six reports were included in the final analysis. The standardized mortality rate for lung cancer from the random model was 1.18 (95% CI: 1.03-1.35, p=0.014) with moderate heterogeneity. Publication bias was not found for included studies in meta-analysis (p=0.9). Conclusions: Our findings has strengthen the evidence of lung cancer from chronic exposure to chlorophenol related compounds (PAs, CPs).

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