How diet, nutrition and physical activity affect bladder cancer risk. In total, we analysed 45 studies from around the world, comprising more than 7 million adults and nearly 37,000 cases of bladder cancer.
The urinary bladder is a membranous sac that functions as a receptacle to store urine excreted by the kidneys before it is discharged through the urethra. The bladder is lined with transitional epithelial cells, known as urothelial tissue.
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Our Expert Panel has reviewed the evidence on diet, weight, physical activity and the risk of bladder cancer.
There is strong evidence that:
There is some evidence that:
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> Download our 2018 bladder cancer report, with evidence matrices
In addition to the findings on diet, nutrition and physical activity outlined above, other established causes of bladder cancer include:
The risk of developing bladder cancer is between two and six times higher in smokers compared with non-smokers.
Infection from the parasitic worm schistosoma haematobium, causing schistosomiasis, is a major risk factor, especially for squamous cell carcinomas. This is a less common type of bladder cancer that occurs more frequently in countries with high parasitic infection rates (notably Africa and the Middle East).
People who work with metalworking fluids – such as sheet metalworkers and machine operators – have a significantly higher risk of bladder cancer, which increases with duration of employment. Exposure to aromatic amines and polyaromatic hydrocarbons (chemicals used in the plastic and chemical industries) has also been strongly associated with an elevated risk for this cancer.
We fund research on bladder cancer through our grant programme. Read about the latest findings and ongoing projects in our database of projects.
Dietary carcinogens, as well as those from tobacco smoke or other environmental sources, are often excreted in the urine, where the lining of the bladder is exposed to these agents.
Urothelial cell carcinomas start as superficial bladder carcinomas. The majority have low rates of progression, although they can occur at multiple sites. Low-risk lesions may never progress, but if they become invasive the prognosis can be poor.
The superficial lesion that carries the highest risk is carcinoma in situ, which progresses to invasive cancer in more than 50% of cases if it is not treated. These high-risk lesions are often found with multiple papillary tumours, but because they may involve different molecular changes, they are likely to have different pathways of development to low-risk lesions.
Squamous cell carcinoma may be caused by chronic inflammation, for instance from latent schistosomiasis, chronic infections or long-term catheter use.
Mutations in the p53 tumour suppressor gene, as well as abnormalities in chromosome 9, are common in invasive bladder cancer. Inherited mutations of two other genes, glutathione S-transferase (GSTM1) and NAT2 (n-acetyltransferase), also increase risk for bladder cancer. NAT2 is involved in detoxifying aromatic amines present in cigarette smoke, and a slow acetylation phenotype in both genes is estimated to be responsible for 20–46% of bladder cancers.
Full references and a summary of the mechanisms underpinning all the findings can be found in the bladder cancer report.
In 2018, World Cancer Research Fund International published Diet, Nutrition, Physical Activity and Cancer: a Global Perspective on behalf of AICR, WCRF and WKOF. This was the third in our series of major reports looking at the many ways in which our diets, and how active we are, affect our cancer risk. You can find out much more about bladder cancer by downloading a pdf of the relevant chapter in the 2018 report. Please note, however, that this webpage may have been updated since the report was published.
Selected findings from this report have been published in peer-reviewed journals. Details of the papers and links to the abstract in PubMed are below:
Fruits, vegetables, and bladder cancer risk: a systematic review and meta-analysis. Vieira AR, Vingeliene S, Chan DS, Aune D, Abar L, Navarro Rosenblatt D, Greenwood DC, Norat T. Cancer Med. 2015; 4(1): 136-46. Abstract