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A method for determining plasma paroxonase activity using an auto-analyser is described. Frequency distributions for British and Indian subjects show bimodality. A study of 40 British families confirms the presence of a genetic polymorphism with regard to plasma paroxonase activity. Two phenotypes can be defined, controlled by two alleles at one autosomal locus. The frequency of the low activity phenotype is less in the Indian population than in the British population. Malay, Chinese, and African subjects fail to show obvious bimodality.

Thirty-eight healthy white British Caucasian subjects were hydroxylator phenotyped with sparteine and acetylator phenotyped with sulphadimidine. The results showed that there was no significant difference in the mean sparteine metabolic ratio between eight rapid acetylator extensive hydroxylators and 27 slow acetylator extensive hydroxylators.

There is an association between exposure to aromatic amines and the development of bladder cancer. Aromatic amines such as are known to occur in tobacco smoke are polymorphically acetylated. One hundred bladder cancer patients have been acetylator phenotyped. Only three of them were non-smokers at the time of diagnosis. This new series, together with four previous series (each with its own control), have been statistically analysed together. The results show a significant association between the slow acetylator phenotype and bladder cancer. The slow acetylator phenotype is associated about 39% more with bladder cancer than is the rapid acetylator phenotype. This association can be interpreted in one of two ways: (1) rapid acetylators may be protected against developing bladder cancer because they are better able to render amines non-carcinogenic by acetylation, or (2) slow acetylators have greater survival with bladder cancer than rapid acetylators. Further evidence will be required to differentiate between these alternatives.