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  • Considering the on going debate


    Considering the on-going debate on mesothelioma urban risk, attributable to asbestos exposure sources related to the presence of asbestos contaminated materials in building and to traffic [20,[45], [46], [47], [48]], we analysed the sex ratio of the cases in urban and rural areas. We tested the hypothesis that there is a “urban risk”, regardless of occupational exposure risk, if there is a higher number of female cases in urban areas, compared to the rural ones. A recent study investigated long-term trends in MPM incidence in urban and rural areas in the United States. The purpose of that study was to determine whether variation in ambient asbestos concentration might influence MPM risk in females, using female mesothelioma incidence to evaluate the background risk of mesothelioma [49]. In the present paper the sex-ratio (male/female cases) did not differ in municipalities at different degrees of population density used as a proxy of urban rate, with respect to rural ambient. The lower value found in the North-Western municipalities of “medium density” class, could be, partially, explained by the presence of a number of female cases in Grugliasco and Sarnico textile industries. The higher value found in the “low density of population” municipal class of Sardinia, still has no explanation.
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    Introduction Gliomas represent the majority of primary intracranial tumors; approximately 80% of malignant Rottlerin tumors arise from the glial cells of the brain [1]. Mortality from glioma is high with only 5% survival at 5 years in glioblastoma multiforme (GBM), the most aggressive and common subtype of glioma (WHO Grade IV) [1]. Gliomas occur more frequently in males, and in Caucasians when compared to other racial groups [2]. Genetic susceptibility [3], as well as rare Mendelian disorders including neurofibromatosis, tuberous sclerosis, and Li-Fraumeni syndrome also contributes to disease [[4], [5], [6]]. A history of chicken pox, allergies, or atopic disease has a protective association with glioma suggesting that the immune response may play a role in glioma development [7,8]. A prolonged adolescent growth phase is positively associated with glioma risk [9], as is a higher BMI during adolescence [10], and a later age at menarche in women [11,12]. The only known environmental risk factor is ionizing radiation [13]. The role of diet in glioma including trace elements such as selenium is poorly studied. Selenium (Se) is an essential trace element obtained through diet that plays a critical role in reproduction, thyroid hormone metabolism, DNA synthesis, and protection from oxidative damage and infection [14]. Se is naturally present in many foods and is also available as a dietary supplement. Concentrations of Se in foods vary with Se in the soil in which food is produced [14]. Toenail concentrations of Se offer a useful measure of dietary exposure and reflect long-term dietary intake [15]. In the brain, Se and the selenoproteins play a central role in brain function and neuroprotection [[16], [17], [18], [19]]. Se stores in the body reflect not only diet but GI absorption and tissue uptake, and vary according to alcohol consumption and cigarette smoking which may deplete Se stores in the body by contributing to oxidative stress [20]. Epidemiologic studies have suggested a protective association between Se and cancer risk though data are inconsistent [21]. A Cochrane meta-analysis of prospective observational studies showed lower cancer incidence among patients with higher Se exposure for cancers of the prostate, gastric cardia, bladder, and lung, but not for breast or colon [21]. In contrast, randomized clinical trials have not found evidence that Se supplementation is associated with risk reduction for primary liver cancer, non-melanoma skin cancer, basal cell carcinoma, squamous cell carcinoma, prostate cancer, lung, bladder, or colorectal cancer, and with cancer-related mortality; it is speculated that supplementation may not reduce cancer in persons already replete for Se as would apply to the majority of persons in the US [21]. Two studies have examined Se levels and brain tumor risk in human populations. One small study (N = 22) found no difference in Se levels in cerebrospinal fluid of patients with glioma as compared to patients with benign tumors of the brain (meningioma), or diagnosed with hydrocephalus, arterial malformation, aneurysm, or headaches [22]. Another study examined serum levels of Se in patients with malignant brain tumors (n = 139) compared to healthy adult individuals (n = 294) and found lower Se serum levels in the glioma patients [23]; however, as concentrations of Se in blood reflect recent Se intake [24], Se in the serum of cases may have reflected recent changes in diet related to the glioma diagnosis.