Background. Exposure to lead (Pb) has been associated with endocrine, hematological, gastrointestinal, renal and neurological problems in humans. However, effects on the thyroid gland are controversial. Objectives. The aim of the present study was to assess thyroid function in foundry workers occupationally exposed to Pb and the mechanism of oxidative-antioxidant imbalance. Methods. Thyroid function parameters and markers of oxidative stress were examined in 59 adult males who had been occupationally exposed to Pb. The results were then compared to those of 28 male subjects who had no history of Pb exposure or thyroid abnormalities and served as a control group. Results. Mean blood lead levels (16.5±1.74 μg/dl) were significantly higher among the exposed workers compared to those of the control group (12.8±1.16 μg/dl, (p <0.001)). The exposed group had significantly increased free triiodothyronine (FT3), free thyroxine (FT4) and significantly decreased thyroid stimulating hormone (TSH) (1.77±0.44 μIU/ml), whereas the control group had a TSH level of 2.61±0.94 μIU/ml (p< 0.0001). A state of oxidative stress was indicated by the significant increase in mean levels of malondialdehyde (MDA) and significant decrease in glutathione (GSH) (p < 0.0001). There was a significant positive correlation (r=0.358, p <0.05) between blood lead levels (BLL) and duration of employment, while BLL showed a significant negative correlation with TSH (r =−0.486, p <0.001), and GSH (r =−0.336, p <0.05). Of the occupationally exposed workers, 32.76% had elevated thyroid hormones. The results showed a significant positive relationship between GSH and TSH (β coefficient=0.274, p < 0.05), MDA with FT3 (β coefficient=0.355, p < 0.05) and FT4 (β coefficient = 0.491, p < 0.0001) among exposed workers. Conclusions. Workers exposed to Pb dust proved to be at risk for hyperthyroidism, which was found to have a significant role in oxidative–antioxidant imbalance present among workers with increasing duration of exposure. Participant Consent. Obtained Ethics Approval. This study was approved by the Ethical Committee of the National Research Centre in Egypt (NRC) under the registration number 15225. Competing Interests. The authors declare no competing financial interests.

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Autism Spectrum Disorder (ASD) is considered a multifaceted neurodevelopmental disorder. The last two decades showed an increase in its prevalence until reached about 1 in 54 children. Autistic symptoms may be exacerbated when the interaction of the genetic and the environmental risk factors occur, suggesting that gene-environment interaction could be a mechanism underlying the aetiology of ASD. Aluminium is a known neurotoxic metal that has known health effects in humans. Glutathione-S-transferase (GST) genes and their enzymes play a major role in the detoxification of many toxic metals. Data were collected from 76 children aged 2-8 years diagnosed with ASD and 30 sex and age matched healthy children. The aim of this study was to investigate the association of polymorphisms in the two GST genes (GSTM1 and GSTT1) with mean aluminium concentrations (as, gene-environment interaction) and oxidative status markers (GST enzyme, malondialdehyde and nitric oxide) among the studied groups. The study started at December 2019 and last for one year at the clinics of National Research Centre, Egypt. The results of this study showed that the null GSTM1 and GSTT1 genotype is the most common type in ASD and that genotype may predispose ASD children to decreased antioxidant status (GST enzyme activity) which in term lead to mal detoxification of aluminium. There is marked increase in aluminium concentrations in hair of ASD children and oxidative markers (increase in MDA and NO) leading to oxidative damage that may play an important role in children autistic status. The study recommends adding antioxidant supplements to daily diet of ASD children to improve their antioxidant status and in term improving management of patients with autism spectrum disorders. Further studies are needed to describe other GST gene polymorphisms.

Assessment of noise effects were carried out in four working sites at the airport besides control sites. The average noise level in the exposure sites was 106.5 dB compared with 54 dB at the control sites. The study comprised a group of 200 male workers exposed to aircraft noise and 110 male workers not exposed to noise as control group. All workers had full general medical examination after filling specially formulated questionnaire. Hearing impairment, raised blood pressure, headaches, disturbed sleep, and symptoms of anxiety were more prominent among the exposed workers than the control. Symptoms of upper respiratory tract were reported among night shifters of both groups with high tendency for smoking. Thus, night-shift workers at CIA work under more than one stressor. Hypertension and smoking might act as intermediate factors on the causal pathway of complaints, making aircraft noise and night shift acting as two synergistic stressors. Airport workers are in need for aggressive hearing conservation programs. Organization of the working hours schedule is mandatory to avoid excessive noise exposure.

Altered miRNAs were associated with cigarette smoking. The study aimed to examine the gene expression level of plasma let-7a among healthy smokers and compared it with the non-smokers. Forty subjects were recruited for the present study and classified into 21 smokers and 19 non-smokers, age, and sex were matched. The software that used to design functional primers was MIRprimer. Quantitative real-time PCR was employed to compare the relative expression of plasma let-7a. Results showed that the level of let-7a was down-regulated in smokers to 0.34fold (p = 0.006) that of the non-smokers. Plasma let-7a showed an area under curve (AUC) of 0.749 with sensitivity 43% and specificity 100%. In conclusion, plasma let-7a was significantly down-regulated in the smokers, and it might be considered a candidate biomarker to discriminate between smokers and non-smokers.