Context: Bladder cancer (BC) is a significant health problem, and understanding the risk factors for this disease could improve prevention and early detection. Objective: To provide a systematic review and summary of novel developments in epidemiology and risk factors for BC. Evidence acquisition: A systematic review of original articles was performed by two pairs of reviewers (M.G.C., I.J., F.E., and K.P.) using PubMed/Medline in December 2017, updated in April 2018. To address our primary objective of reporting contemporary studies, we restricted our search to include studies from the last 5 yr. We subdivided our review according to specific risk factors (PICO [Population Intervention Comparator Outcome]). Evidence synthesis: Our search found 2191 articles, of which 279 full-text manuscripts were included. We separated our manuscripts by the specific risk factor they addressed (PICO). According to GLOBOCAN estimates, there were 430 000 new BC cases and 165 000 deaths worldwide in 2012. Tobacco smoking and occupational exposure to carcinogens remain the factors with the highest attributable risk. The literature was limited by heterogeneity of data. Conclusions: Evidence is emerging regarding gene-environment interactions, particularly for tobacco and occupational exposures. In some populations, incidence rates are declining, which may reflect a decrease in smoking. Standardisation of reporting may help improve epidemiologic evaluation of risk. Patient summary: Bladder cancer is common worldwide, and the main risk factors are tobacco smoking and exposure to certain chemicals in the working and general environments. There is ongoing research to identify and reduce risk factors, as well as to understand the impact of genetics on bladder cancer risk. Bladder cancer remains an important health problem requiring evolving understanding of disease risk factors and the ability to improve early detection. We present the most contemporary data, which have been researched extensively. Tobacco smoking and environmental carcinogen exposures remain the predominant causative agents. Our knowledge of gene-environment interactions is becoming more detailed.
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