Cadmium (Cd) is one of the environmental risk factors for bone loss. The present study included 40 sewage workers occupationally exposed to Cd. Forty nonexposed men were included as a control group. Current smokers represented 65% and 47.5% of the exposed and control groups, respectively. The study aimed to investigate the hazard of occupational Cd exposure on bone health. This was achieved through measuring serum and urinary Cd, and calcium (Ca), in addition to serum osteoprotegerin (OPG) and estrogen receptor-α gene. Results showed significant elevation in serum Cd, OPG, and urinary Ca levels in the exposed compared to the controls. Bony aches and joint pain were more prevalent among the exposed workers. Serum and urinary Cd increased in exposed smokers relative to control smokers. Also, serum OPG levels showed significant rise among exposed smoker and nonsmoker compared to control smoker and nonsmoker groups. Serum Cd level increased significantly in PP and pp genotypes in exposed workers compared to controls, while elevated levels of serum OPG was observed in PP and Pp genotypes in exposed workers relative to controls. Urinary Cd exhibited significant rise in both PP and pp genotypes in exposed workers, while Ca excretion was elevated in pp genotype only. The study reflected an association of genetic predisposition and Cd exposure in progression of osteoporosis. Further research is needed to explain the mechanisms of Cd impact on bone. The role of smoking is important and hence smoking cessation programs are essential for sewage workers.

Dietary antioxidants are widely distributed in various types of our food. They are strongly associated with reduced risk of many chronic diseases such as atherosclerosis, cancer, and Alzheimer’s diseases. They include vitamins such as vitamins A, E, C, and carotenoids. Also, some minerals like; zinc, manganese, copper, iron, and selenium are essential for the activity of antioxidant enzymes. Furthermore, dietary polyphenols and flavonoids are considered as potent antioxidant compounds. Vegetables, fruits, and edible herbs are the richest sources of such antioxidants. Antioxidants reduce oxidative stress, either directly by reducing reactive species or indirectly by enhancing the body antioxidant defense mechanisms in different ways. These may include upregulating gene expression of some antioxidant enzymes via a nuclear factor erythroid 2 related factor2 pathway. Administration of a mixture of antioxidants is beneficial since they act synergistically in various phases. The aims of this review are to summarize the different antioxidants from dietary sources and their role in the prevention of different diseases.

Cigarette smoke contains harmful chemicals with hazardous adverse effects on almost every organ in the body of smokers as well as of nonsmokers exposed to environmental tobacco smoke (ETS). There has been increasing interest in the effects of passive smoking on the health of children. In order to detect the magnitude of passive smoking in children, parental questionnaires, measuring nicotine and cotinine body levels, and evaluating expired carbon monoxide (CO) concentrations, have been used. Passive smoking causes respiratory illness, asthma, poor growth, neurological disorders, and coronary heart diseases. Herein, we focused on the deleterious influences of passive smoking on immunity and liver. Besides, its effects on the concentrations of various biomarker levels related to the oxidant/antioxidant status were considered. Understanding these effects may help clinicians to counsel parents on smoking cessation and smoke exposure elimination. It may also help to develop interventions to improve the health of children. This review potentially demonstrated some nutraceuticals with a promising role in the prevention of smoking-related diseases.

Many studies proved the genotoxic effect of cadmium (Cd) exposure and highlighted the importance of the cytogenetic studies as a sensitive and effective means for early detection of Cd-induced mutagenicity. The relationship between occupational exposure to Cd and increased risk of cancer, particularly lung cancer, has been explored in number of epidemiological studies. The aim of this study is to assess the role of chromosomal abnormalities and sister chromatid exchange as sensitive indicators for the genotoxicity of occupational exposure to Cd. Cytogenetic studies was done for 40 workers (27 smokers and 13 non-smokers) exposed to Cd dust and fumes with 40 control subjects (28 smokers and 12 non-smokers) not exposed to Cd before. Both exposed and control groups were similar in age and other sociodemographic factors. Clinical examination, laboratory investigation including urinary and blood Cd, cytogenic analysis for detection of chromosomal aberrations and sister chromatid exchange and environmental study of the work places were done. Statistical analysis of cytogenetic studies revealed the presence of significant elevation of chromosomal aberrations and sister chromatid exchanges of the exposed group. Urinary and blood Cd of the exposed group were significantly higher than that of the control group. These abnormalities were not significantly affected with age, duration of exposure, smoking habits, blood and urinary Cd. In conclusion, the study adds more proof that Cd exposure has a genotoxic effect and highlighted the importance of using cytogenetic studies as a sensitive and effective means for early detection of Cd-induced mutagenicity

The presented study investigates the protective role of zinc (Zn) and selenium (Se) in attenuating benzene-induced toxicity in rats. Male Sprague—Dawley rats were injected with benzene (0.5 mL/kg body weight ip) and received a diet supplement containing Zn and Se. Several hematological and biochemical parameters (representing antioxidant status) were estimated. Histopathological examinations were performed. Results showed that food intake and body weight gain of benzene-injected rats were significantly lower than that of the control rats. Benzene-injected rats showed increased plasma malondialdehyde (MDA) and decreased activity of: glutathione peroxidase (GSH-Px), catalase, superoxide dismutase (SOD) enzymes, as well as reduced glutathione (GSH) when compared to the control group. Histopathological investigations revealed structural changes in benzene-injected rats’ liver. Supplementation with Zn and Se resulted in a significant decrease in MDA, elevation in GSH, GSH-Px, SOD and catalase levels. This study shows that Zn and Se supplementation can improve the activity of antioxidant enzymes in rats and decrease the histological anomalies induced by benzene toxicity as well.