In the first place, causes of bladder cancer are multifactorial and it is a disease of the elderly with a peak at around 60 to 70 years. In the U.S. the male to female ratio is about 3 to 1.
Moreover, in the last few years more women developed bladder cancer due to the increase of numbers of women who started to smoke in the past decades. Significantly, the lag period for developing bladder cancer from exposure to cigarette smoke is 19 plus minus 3 years.
The relative risk ratio for both whites and blacks is about 1.6 every year of exposure. This means that in 5 years of smoking the risk is 8-fold in comparison to non-smokers to develop bladder cancer.
Occupational risks of developing bladder cancer
In general, occupational risks are common: exposure to aniline with dye workers, working with organic chemicals such as aryl amines, aniline, dye, rubber and paint leads to an increased risk of bladder cancer. Exposure to diesel fumes or exhaust from cars in urban areas has no link to bladder cancer. Specifically, chronic abuse of phenacetin in the past, particularly in the Swiss watch industry, was linked to bladder cancer.
Notably, there were initial suggestions in animal models that dietary sweeteners might promote bladder cancer development when carcinogens were given at the same time. But four well controlled studies in humans could not show any bladder cancer from cyclamate and saccharin. It is interesting that many people still hold on to the fears that were generated by the popular press generated from these poorly conducted animal experiments despite the proof that diet sweeteners are safe from a cancer perspective.
Cigarette smoking can cause bladder cancer
Certainly, the strongest association that is reported in the literature is that between cigarette smoking and bladder cancer. Indeed, study after study shows an association between the amount of cigarettes smoked, the duration of years of exposure and bladder cancer risk. The more and the longer people smoke, the more the carcinogens attack the very susceptible bladder lining leading sooner or later to changes in the cell structure.
The end result is what physicians call a “transitional cell carcinoma”, just a fancy name for “bladder cancer”. It is important to realize that 95% of bladder cancers are of this pathological type (Ref. 1 and 2).
Causes Of Bladder Cancer
Chronic bilharziasis
It must be remembered that chronic bilharziasis (also called “schistosomiasis”) leads to chronic bladder irritation and bladder ulcerations, followed by the development of papillomatous masses in the bladder. These often turn into bladder cancer. This is not a problem in the U.S., but is very common in other countries such as in African countries, also in Brazil, Venezuela, some Caribbean islands, China, the Philippines, Laos and Cambodia.
A point often overlooked is that the bladder cancer producing effect from having bilharziasis is as strong as exposure to cigarette smoking. If a patient with bilharziasis smokes as well, the bladder cancer causing effect certainly can get more pronounced.
Recurrent bladder infections can cause bladder cancer
Another key point is that patients with bladder infections, particularly when these are chronic recurrent, have a higher risk for bladder cancer. Researchers have investigated the cause for this. In this case they found that bacteria in chronic bladder infections produce nitrates and nitrosurea. To clarify, these are carcinogens that are responsible for the development of bladder cancer. This type of mechanism leads to a different histological type of bladder cancer, called “squamous cell carcinoma”, which is only found in about 3% of all bladder cancers.
A minority of bladder cancer cases is caused by genetic factors, partially because of chromosomal breaks, chromosomal deletions or alterations. There are also familial genetic syndromes, where patients younger than 45 years of age come down with bladder cancer.
There is a suggestion that milk and vitamin A protects from the development of bladder cancer.
References
1. Cancer: Principles&Practice of Oncology. 5th edition, volume 1. Edited by Vincent T DeVita, Jr. et al. Lippincott-Raven Publ., Philadelphia,PA, 1997.
2. Cancer: Principles &Practice of Oncology, 4th edition, by V.T. De Vita,Jr.,et al. J.B. LippincottCo.,Philadelphia,1993.Chapter 34, page 1054 (data from text arranged as a table).
3. M Simoneau et al. Oncogene 2000 Dec 19(54): 6317-6323.
4. G Dalbagni , HW Herr Urol Clin North Am 2000 Feb 27(1): 137-146.
5. HW Herr J Clin Oncol 2001 Jan 1;19(1): 89-93.
6. DA Corral, CJ Logothetis World J Urol 1997; 15(2): 139 – 143.
7. PM Dodd et al. J Clin Oncol 1999 Aug;17 (8): 2546- 2552.
8. B. Sears: “The age-free zone”.Regan Books, Harper Collins, 2000.
9. Conn’s Current Therapy 2004, 56th ed., Copyright © 2004 Elsevier
10. Ferri: Ferri’s Clinical Advisor: Instant Diagnosis and Treatment, 2004 ed., Copyright © 2004 Mosby, Inc
