Abstract
Bladder cancer is almost certainly a product of the industrial revolution and the cigarette smoking that has accompanied it. Exposure to a chemical bladder carcinogen such as β naphthylamine, benzidine, or 4- diphenylaniline2 can be proved in only a small proportion of patients and only a handful obtain industrial diseases benefit after developing “Prescribed Industrial Disease C23.” None the less, the continued use of known carcinogenic substances in British industry for many years after their identification, the wide range of industries with a known or suspected increased risk of bladder cancer, and our ignorance of the carcinogenic potential of many materials used in current manufacturing should be a cause for continuing concern. The association between bladder cancer and cigarette smoking, first considered more than 30 years ago,1,3 has been confirmed only recently.4,5 The incidence of this cancer among workers in “at risk” industries has been shown to be increased if they smoke as well,6 and first degree relatives of bladder cancer patients may increase their familial risk if they smoke.7 Whether the increased tobacco consumption by young women in recent years will alter the current 3:1 male to female preponderance of this disease and whether young women can be persuaded to stop smoking for this reason remain to be seen. Whatever environmental causes may exist, it has been the molecular aetiology of bladder cancer that has attracted most recent attention. As Jones et al have explained, “chemical and physical carcinogens leave footprints of their activities on DNA because of the patterns of base changes they induce.”8 Chromosomes 1, 5, 9, 11, and 17 have shown non-random changes in bladder cancer, and allelic deletions of chromosomes 9 and 17 occur in over 60% of bladder tumours.9 Chromosome 9 aberrations have not been reported in …