Bladder cancer incidence

Ouellet-Hellstrom R, Rench JD. 1996. Bladder cancer incidence in arylamine workers. J Occup Environ Med 38(12) 1239-1247. 

Susceptibility to bladder cancer in humans has been linked to the slow acetylator phenotype of the polymorphic NAT2 AT-acetyltrans-ferase gene. In a study from China, a 25-fold increase in bladder cancer incidence and a 17-fold increase in bladder cancer mortality were determined in 1972 benzidine-exposed workers. In the Asian population the slow acetylator phenotype occurs significantly less often than in Caucasian populations, but an association between those who contracted bladder cancer and phenotype has yet to be determined for this group. Other, more recent data have suggested that the acetylation rate may not be an important risk factor for developing bladder cancer. ... 

A bladder cancer incidence study was conducted among workers exposed to ortho-toluidine at a plant manufacturing rubber chemicals in New York State, United States. The study was initiated at the request of the union representing workers at the plant, who had noted a number of bladder cancers among workers in a department where an... 

Table 4. Air and urine levels and haemoglobin adduct levels measured in 1990 among chemical workers employed at a plant where excess bladder cancer incidence was observed...

Vitamin E supplement nse was inversely associated with bladder cancer incidence or mortahty in two large cohorts. - ... 

A toxic component of braken fern, perhaps either quercetin (105) or ptaquiloside, a glucoside (106), has a mixed history of carcinogenicity. It is sometimes impHcated in an increased incidence of bladder cancer in animals and esophageal cancer in humans. Multiple other dietary components seem to either promote or interfere with its action, and the significance of braken fern in human carcinogenesis remains unproven. 

An update of a previous study (Axelson et al. 1978), Axelson (1986) evaluated an expanded cohort of 1,424 men (levels of trichloroethylene exposure inferred from measured urinary metabolite concentrations) and found a significant increase in incidences of bladder cancer and lymphomas, and a lower than expected incidence of total cancer mortality. A further update of this work (Axelson et al. 1994) expanded the cohort to include 249 women, tracking cancer morbidity over 30 years, and found no correlation between exposure concentration or exposure time and cancer incidence at any site. The highest standardized incidence ratio noted in this study was 1.56 (95% Cl of 0.51-3.64) for 5 cases of non-Hodgkin s lymphoma observed in men. Although four of these cases occurred in persons exposed for at least 2 years, and 3 cases had a latency of 10 years or more, urinary levels of TCA showed that 4 of the 5 cases were exposed to the lowest levels of trichloroethylene (urinary levels of TCA 0-49 mg/L). The study authors mentioned that a urinary TCA level below 50 mg/L corresponds to a trichloroethylene exposure concentration of about 20 ppm. The study authors concluded that "this study provides no evidence that trichloroethylene is a human carcinogen, i.e., when the exposure is as low as for this study population."... 

Historically, bladder tumors have been associated with exposures in the aniline dye industry. However, conclusive evidence for any one particular exposure could not be obtained in these studies since the workers were exposed to many chemicals within the same work area. For example, Case et al. (1954) investigated the incidence of bladder tumors among British workers in the chemical dye industry. In addition to aniline, the workers were exposed to other aromatic amines, including a- and P-naphthylamine, benzidine, and auramine. Although exposures could not be quantified, there was insufficient evidence to suggest that aniline was a cause of bladder cancers. More recent studies indicate that P-naphthylamine, 4-aminodiphenyl, 4-nitrodiphenyl, 4,4-diaminodiphenyl, or o-toluidine may be involved in increased cancers in the dye industry (Ward et al. 1991 Benya and Cornish 1994). 

Cancer. No studies were available regarding eaneer in humans or animals after inhalation exposure to chloroform. Epidemiology studies suggest an association between chronic exposure to chlorinated drinking-water sources and increased incidences of colon cancer (Young et al. 1981), pancreatic cancer (Ijsselmuiden et al. 1982) and bladder cancer (Cantor et al. 1978 McGeehin et al. 1993 Zierler et al. 

Toxicology. 4-Aminodiphenyl exposure is associated with a high incidence of bladder cancer in humans. 

Meigs JW, Marrett LD, Ulrich FU, et al Bladder tumor incidence among workers exposed to benzidine a thirty year follow-up. J Natl Cancer Inst 76 1-8, 1986... 

There are no reports in which DCB exposure has been conclusively linked to cancer in humans. However, DCB exposure may have been a factor in some cases of bladder cancer attributed to benzidine, because these substances are often produced together, and DCB also bears a close structural similarity to benzidine. A British plant handling 3,3 -dichlorobenzidine had a site incidence of bladder cancer 2-3 times that predicted for males employed between 1972 and 1987 the cause of this apparent excess could not be identified because of potential exposure to many other chemicals. Since that time, the incidence of bladder cancer appears to have fallen to background levels and has been attributed to an alteration in hygiene standards. ... 

Percivall Pott made one of the first observations of a health risk related to occupational exposure. In 1775, he noted that chimney sweeps had a higher incidence of cancer of the scrotum. A century later, in 1895, it was observed that workers in the aniline dye industry were more likely to develop bladder cancer. 

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