In an experiment involving 950 mice with a normal lifespan of 2-3 years, in laboratory conditions, regular benzpyrene application to the skin was started at 10, 25, 40 or 55 weeks of age. The incidence rate of malignant epithelial tumours among the survivors in each group increased steeply with time. This increase was associated directly with duration of exposure but, given duration, was independent of age at the start of exposure, as were the growth rates of already established tumours. In our experiment, although age per se was irrelevant, the cancer incidence rate increased approximately as a power of the duration of exposure to benzpyrene. This shows that the observed approximate power-law increase of most human adult cancer incidence rates with age could exist merely because age equals duration of exposure to background and spontaneous carcinogenic stimuli. Thus, no intrinsic effects of ageing (such as failing immunological surveillance or age related hormonal changes) whatever need to postulated to explain the vast increases in old age of the incidence rates of such human cancers. This result can greatly simplify speculation about mechanisms of carcinogenesis.

Smoking is a known cause of the outcomes COPD, chronic bronchitis (CB) and emphysema, but no previous systematic review exists. We summarize evidence for various smoking indices.

Smoking is a known lung cancer cause, but no detailed quantitative systematic review exists. We summarize evidence for various indices.

Overall evidence from 19 case-control studies of Alzheimer''s disease (AD) and smoking shows a highly significant (p < 0.001) negative association [ever/never smokers, relative risk (RR) 0.64, 95% confidence interval (CI) 0.54–0.76]. Some studies have apparent design faults but the association is clearly evident in those which do not (RR 0.60, 95% CI 0.46–0.78). A report of a positive relationship from a prospective study can be dismissed due to unreliability of AD diagnosis on death certificates, and other study weaknesses. Although more data are needed on dose response and to rule out possible confounding, the negative association is consistent with other data suggesting nicotine protects against AD.

In the latter part of a large hospital case-control study of the relationship of type of cigarette smoked to risk of various smoking-associated diseases, patients answered questions on the smoking habits of their first spouse and on the extent of passive smoke exposure at home, at work, during travel and during leisure. In an extension of this study an attempt was made to obtain smoking habit data directly from the spouses of all lifelong non-smoking lung cancer cases and of two lifelong non-smoking matched controls for each case. The attempt was made regardless of whether the patients had answered passive smoking questions in hospital or not. Amongst lifelong non-smokers, passive smoking was not associated with any significant increase in risk of lung cancer, chronic bronchitis, ischaemic heart disease or stroke in any analysis. Limitations of past studies on passive smoking are discussed and the need for further research underlined. From all the available evidence, it appears that any effect of passive smoke on risk of any of the major diseases that have been associated with active smoking is at most small, and may not exist at all.