Environmental exposure, chlorinated drinking water, and bladder cancer

Abstract

Environmental and/or occupational factors have been proposed to play a critical role in urological malignancies and, in particular, in bladder cancer. Epidemiological studies have demonstrated with sufficient evidence that factors such as smoking and exposure to aromatic amines, paints and solvents, leather dust, inks, some metals, polycyclic aromatic hydrocarbons, combustion products, or diesel exhaust fumes are associated with the development of bladder cancer. Candidates with an uncertain potential for inducing this type of cancer include dietary factors, specifically fats and cholesterol, and the exposure to contaminants in drinking water. This chapter will describe and discuss the respective literature on environmental and occupational factors linked to carcinogenesis in bladder cancer. For several reasons, the potential effects of tea and coffee consumption will also be considered. A solid epidemiological evaluation of environmental and occupational factors linked to carcinogenesis has to meet many challenges: the number of confounding factors is often large, exposure needs to be determined retrospectively, and elevation of the attributable risk is low in most cases. In view of the long-term exposure of the vast majority of the population to, for instance, drinking- water contaminants, however, the impact of even small elevations of risk warrants evaluation. This complex task needs comprehensive approaches on a large scale including modern analytical, molecular biological and epidemiological methods.

A Meta-Analysis of Tea Consumption and the Risk of Bladder Cancer

“…After a closer examination, 10 studies were excluded due to lack of information [35,36,37,38,39,40,41,42,43,44]. In addition, another study was abandoned for duplicated data [34].…”

“…We identified 28 studies on the risk of bladder cancer and tea consumption between 1980 and March 2012 [11,12,13,14,21,22,23,24,25,26,27,28,29,30,31,32,33,34,35,36,37,38,39,40,41,42,43,44]. After a closer examination, 10 studies were excluded due to lack of information [35,36,37,38,39,40,41,42,43,44].…”

Chloroacetic acid triggers apoptosis in neuronal cells via a reactive oxygen species-induced endoplasmic reticulum stress signaling pathway

“…However, the effects and underlying mechanisms of CA-induced neurotoxicity remain 42 unknown. In the present study, we found that CA (0.5-2.0 mM) significantly increased LDH release, 43 decreased the number of viable cells (cytotoxicity) and induced apoptotic events (including: increases 44 in the numbers of apoptotic cells, the membrane externalization of phosphatidylserine (PS), and cas- 45 pase-3/-7 activity) in Neuro-2a cells. CA (1.5 mM; the approximate to LD 50 ) also triggered ER stress, 46 which was identified by monitoring several key molecules that are involved in the unfolded protein 47 responses (including the increase in the expressions of p-PERK, p-IRE-1, p-eIF2a, ATF-4, ATF-6, CHOP, 48 XBP-1, GRP 78, GRP 94, and caspase-12) and calpain activity.…”

Glucuronidation and UGT isozymes in bladder: new targets for the treatment of uroepithelial carcinomas?

“…The reason for this broad range seems to be due to the amount of exposure to bladder carcinogens [3]. Disinfection of drinking water via chlorination forms byproducts including trihalomethanes such as chloroform, bromodichloromethane, chlorodibromomethane and bromoform [4]. These chlorinated byproducts have been shown to be carcinogenic in several animal studies [5–7].…”