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P R Burch

Publications and source records attributed to P R Burch.

At least 55 records · Page 3Linked to original sources
PubMed1981

Smoking, lung cancer and hypothesis testing.

It has been shown previously that the precipitator hypothesis of causation is able to account for certain key features of the epidemiological evidence that conflict with initiator and promoter hypotheses. The precipitator hypothesis states that the carcinogenic risk depends linearly in the average rate of smoking at an interval of tau years before death and that the 'doubling dose-rate', of D cigarettes per yr, is constant with respect to age from 35yr and above. In an earlier paper this hypothesis was tested by analysing secular trends in sex- and age-specific mortality from lung cancer recorded in England and Wales in relation to secular trends in cigarette consumption. The periods considered extended from 1950 up to 1975. The great majority of data failed to support the precipitator hypothesis but the well known errors in death certification were undoubtedly responsible for many anomalies. There were some indications of improved diagnostic accuracy towards the end of the period and hence it was considered important to update the analysis. This paper considers the trends over the recent period, 1974-5 to 1977-8. Unfortunately these newer data also appear to contain anomalies and they fail to support the precipitator hypothesis. In view of the difficulties confronting initiator and promoter hypotheses we have little alternative but to adopt Oldham's agnostic attitude "...we still do not know how cigarettes cause lung cancer, nor even, if we are particularly rigorous in our use of scientific logic, whether they do."

Age Factors↗
PubMed1981

Mammalian cell survival and radiation quality: analysis with allowance for delta tracks.

The RBE for mammalian cell survival is analysed in relation to the distribution of LET. Complex target theory is described, together with a procedure for applying LET distributions to experimental findings in order to estimate the modes of cellular inactivation. Track segment theory is shown to have previously unrecognised limitations. The stepwise method is adopted to calculate the LET distributions for the radiations (alpha-particles, deuterons and x-rays) used by Barendsen et al (1966) in their study of the survival of T1 cells of human origin. Satisfactory fits of theory to experiment are obtained. Three distinctive modes of cellular inactivation, with independent energy transfers (direct and indirect) to complex targets comprising 2, 4 adn 6 elements respectively, appear to be involved overall. At 'low dose', no contribution from the 2-transfer-mode can be discerned; only this mode is reparable. Saturation cross-sections (at high LET) for the 2- and 4-transfer-, but not the 6-transfer-mode, are oxygen-dependent. All three modes of inactivation might entail unrepaired double strand breaks and/or some form of mutation in DNA, at 1, 2 and 3 vulnerable sections, respectively.

Alpha Particles↗
PubMed1981

Limiting factors in the site distribution of dental caries.

From records of 32 067 dentate persons from low fluoride communities in South Yorkshire, England, clinical dental caries has been scored at the distal and mesial sites of permanent canines, first and second premolars, and first and second molars, in relation to age. For those teeth with distal or mesial caries or both, the average number of distal and mesial sites attacked per DF tooth is calculated. The ratio observed generally reaches a stable value as age increases and is lowest for mandibular canines (1.10 from 15 years of age and above) and highest for mandibular first molars (1.46 from 30 years and above). For second premolars--both maxillary and mandibular--the ratio reaches a maximum at 30-39 years, and then falls with increasing age. Because the ratio generally attains an effective ceiling with increasing age at a level well below 2, and because it is characteristic of the tooth-type, host factors would seem to be implicated. The data corroborate the authors' hypothesis that the site-specificity of dental caries is genetically-determined and that the timing of attacks in a given environment is governed largely by endogenous factors.

Adolescent↗