Abstract
An extension of the follow-up period from 1985 to 1990 for two quinquennial intakes of rubber workers (newly engaged at a large tyre factory in the Midlands between 1950 and 1960) was undertaken to assess bladder cancer morbidity. This gave the opportunity of examining more closely the spatial departmental distribution of cases on a factory plan: and to contrast this with that exhibited by rubber workers employed before 194 9, when two carcinogenic antioxidants (NONOX ‘S’ and AGERITE RESIN) were in use then withdrawn at the end of that year. Both these latter agents were contaminated by approximately 2500 ppm of betanaphthylamine (BNA), a recognised potent human bladder carcinogen, exposure to which had almost doubled the incidence of bladder tumours in the exposed workforce.
Some residual concerns about a small excess of bladder tumour incidence still being extant for workers engaged for the first time after January 1950 remained, although the dangerous products had been withdrawn in 1949. It became clear, however, that those men joining within the single intake year of 1950 may have inherited a small ‘spillover of risk’ from the pre-end of 1949 situation. Nevertheless, by 1951 any residual risk had dissipated entirely. Having now been followed to the end of 1990, the relevant post 1951 intake groups show no excess of bladder cancer morbidity, thus adding further reassurance that a ‘reversal effect’ had been demonstrated.
Most of this population under study, however, continued to be exposed to another common antioxidant in use both pre and post 1950. This antioxidant also contained trace residual amounts of BNA (20-50 ppm); but no excess of bladder tumours was detected on subsequent follow-up of the workforce. The antioxidant concerned was phenyl beta-naphthylamine (PBNA).
The background evidence which has perhaps unjustly maligned PBNA as a potential urinary tract carcinogen is examined, and some relevant background occupational hygiene data are presented.
The overall conclusion to be drawn is that exposure to, and use of, the antioxidant PBNA did not increase the incidence of bladder tumours in the workforce so exposed, at the factory studied and under normal operating conditions of rubber manufacturing. Despite concerns about residual trace contamination of PBNA by BNA, and the somewhat disturbing finding that PBNA itself can dephenylate in vivo reforming BNA, there is little supporting evidence from other sources that its widespread use in modem rubber processing enhances the incidence of urothelial tract tumours.
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