Dec 6, 1986 - Of course, the stereotypes that I have invented are as foolish as those of general practitioners paraded by Dr Nicholas L Bishop (1 November, p.
BRITISH MEDICAL JOURNAL
VOLUME 293
the problems of "diagnosis by therapeutic trial," specifically the risks of exposing the patient to potential adverse reactions from inappropriate therapy or the possibility of missing another treatable diagnosis. A number of infections in patients with AIDS may present in a similar manner to P carinii pneumonia.' Consequently, the authors' management approach may lead to patients with essentially untreatable conditions such as cytomegalovirus pneumonia being placed at risk of drug related reactions. Leucopenia, rashes, and fever will occur in up to 65% of patients with AIDS treated with co-trimoxazole.2 Alternatively, there may be an inappropriate delay in diagnosing other treatable infectious agents such as tuberculosis, which is being increasingly recognised in AIDS.3 An alternative method of diagnosing P carinii pneumonia and of reducing the demand for bronchoscopy would be the examination of induced sputum stained with methenamine silver or Giemsa stains. This has been shown in two studies to have a sensitivity greater than 55%4 5 and this experience is now being confirmed in other centres. TIMoTY MCDONNELL Division of Pulmonary and Critical Care Medicine, University of Colorado Health Sciences Center, Denver, CO 80262, USA 1 Stover DE, White DA, Romano PA, Yellene RA, Robeson WA. Spectrum of pulmonary diseases associated with the acquired immune deficiency syndrome. Amj Med 1985;78:429-37. 2 Kovacs JA, Hiemenz JW, Macher AM, et al. Pneumocystis carinii pneumonia: a comparison between patients with the acquired immunodeficiency syndrome and patients with other immunodeficiencies. Anm Intem Med 1984;100:663-7 1. 3 Rieder HL, Snider DE. Tuberculosis and the acquired immunodeficiency syndrome. Chest 1986;90:469-70. 4 Pitchenik AE, Ganjei P, Torres A, Evans DA, Rubin E, Baier H. Sputum examination for the diagnosis of Pneumocystis carinii pneumonia in the acquired immunodeficiency syndrome. Am RevRespirDis 1986;133:226-9. 5 Bigby TD, Margolskee D, Curtis JL, et al. The usefulness of induced sputum in the diagnosis of Pneumocystis carinii pneumonia in patients with the acquired immunodeficiency syndrome. Am Rev RespuDis 1986;133:515-8.
What is a good GP? SIR,-Someone once asked me to write an article about how to get the best from the local radiology department. I was a bit of a wag in those days and started off by saying that radiologists can usually be classified into one of two types. The first, younger and tenser, will as soon wiggle a catheter up your circle of Willis as look at you, while the other, older and slower, reports his two views of the duodenal cap with one eye on Yachting Weekly and the other on the clock. I quite quickly realised that this approach might prejudice the reader against any further comments on radiologists, or anything else for that matter. So I decided to go and talk to some real radiologists and asked them how general practitioners could best use their services. Of course, the stereotypes that I have invented are as foolish as those of general practitioners paraded by Dr Nicholas L Bishop (1 November, p 1152), which I imagine had the same effect on many of his readers. He talked about communication but clearly sees this as a one way process, with tablets of radiological stone tumbling down the mountainside to the arid wastes of general practice below. A good GP, it seems, is one who does what the specialist tells him. Although Dr Bishop might not be expected to be familiar with the primary care literature on investigation and referral rates (although he clearly feels free to make pejorative comments about those with high referral rates), he should be aware of studies which examine the use of x ray facilities by general
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practitioners. Several of these suggest that GPs use such investigations as the barium meal as wisely as their hospital colleagues.'2 Although he talks about the costs of tests, this is only one factor in the cost-benefit analysis which would enable the value of an investigation in the overall management of an individual patient to be measured. Many of the other factors lie outside the x ray department, and Dr Bishop needs to talk to general practitioners and to understand something of general practice if he is to appreciate their importance. I worked at Dr Bishop's hospital 12 years ago and since then have cherished the hope that the gulf which existed between general practitioners and specialists might have narrowed or, at least, been bridged from time to time. It is disappointing to read an article in a series on good practice among family doctors which perpetuates this divide.
RoGER JomNS Southampton S02 ISE 1 Haines AP, Ashleigh R, Bates R, Kreel L. The use of barium meals by general practitioners and hospital doctors. J R Coil GenPraci 1980;30:97-100. 2 Conry BG, McLean AM, Farthing MJG. General practice and teaching hospital use of barium meal examinations in the City and Hackney Health District. Postgrad Med J7 1986;62: 273-275.
Does breathing other people's tobacco smoke cause lung cancer? SIR,-We have been interested in the role of passive smoking in office workers and its relation to the symptoms of "building sickness." We investigated 206 randomly sampled office workers with a doctor administered questionnaire which included questions on active and passive smoking and found the following results. Fifty one (25%) were current smokers, and 155 (75%) current non-smokers. Of the non-smokers, 57 (37%) were not passively exposed to cigarette smoke at home and work, 70 (45%) were passively exposed to smoke at work only, 8 (5%) were exposed at home only, and 20 (13%) were exposed at both home and work. We were able to confirm positively non-smoking in %% of the non-smokers with a combination of serum thiocyanate and exhaled breath carbon monoxide measurements. In our workers therefore passive exposure to the cigarette smoke of others was much more likely to occur at work than at home. If this is applicable in a more general population then the relative risks of lung cancer obtained by Professor Nicholas J Wald and his colleagues may well have underestimated the risks of passive smoking. In general there is more choice in whom you live with than in whom you share working space with. Now that the risks of passive smoking are becoming clearer all workers should have the right to work in an area without exposure to cigarette smoke. P SHERwoOD BURGE A S ROBERTSON Solihull Hospital, Solihull, West Midlands B91 3JL
SIR,-Professor Nicholas J Wald and colleagues (8 November, p 1217) make out a strong case for a weak but significant association between the risk of lung cancer in non-smokers and the smoking state of people with whom they lived, generally the spouse. They adjust for some recognised biases and conclude that breathing other people's tobacco smoke does cause lung cancer. They add: "Other potential sources of bias are unlikely to have distorted the estimate of risk," but they do not consider alternatives to the causal interpretation.
The case-control and prospective epidemiological studies they review yield associations but they do not bear on the all important problem ofcausation. Among alternative interpretations is Fisher's genetic hypothesis' of the association between active smoking and lung cancer, coupled with the possibility that assortative mating results in a tendency for people genetically predisposed to lung cancer to marry smokers rather than nonsmokers. Of course, if the association between active smoking and lung cancer has a genetic and not a causal basis then it is most unlikely that passive smoking causes the cancer because active smokers are also "passive smokers." In practice, it has been extremely difficult to discriminate reliably between causal and genetic hypotheses, which in any case are not mutually exclusive. In principle the randomised controlled intervention trial offers one of the few ways of doing so, although even that is not entirely free of complications.2 Two such trials have been carried out that bear on our present problem: the Whitehall study2 and the multiple risk factor intervention trial.3 The similarity in the design of the two trials in so far as smoking intervention is concerned enables us to pool the results for lung cancer. In the combined intervention, low smoking groups some 56 cases of lung cancer were recorded out of 7142 men at entry (0 78%); in the normal care, relatively high smoking groups 53 cases were found out of 7169 at entry (O 74%). This is, perhaps, the most direct epidemiological evidence actually to bear on the causal/genetic issue, and, although it is strikingly consistent with Fisher's genetic hypothesis, numbers are insufficient to reject the causal alternative. Nevertheless, the conclusion of Professor Wald and his colleagues that passive smoking causes lung cancer would appear to fall into the "not proven" category.
PHIIP R J BURCH University Department of Medical Physics, General Infirmary, Leeds LS1 3EX 1 FisherRA. Smoking. The cancer conavvey. Some auenptsto assess the evidence. Edinburgh: Oliver and Boyd, 1959. 2 Rose G, Hamilton PJS, Colwell L, Shipley MJ. A randomised controlied trial of anti-smoking advice: 10-year results. J Epidemiol Communit Healh 1982;36:102-8. 3 MRFIT Research Group. Multiple risk factor intervention trial: risk factor changes and mortality results. JAMA 1982;248: 1465-77.
SIR,-Professor Nicholas J Wald and colleagues (8 November, p 1217) agree with me' and others2 (Doll R, 14th UICC Conference, Budapest 1986) that self reported non-smokers have a 20-500/o excess risk of lung cancer if married to a smoker. Some time ago I pointed out that this excess may come mainly from bias due to misclassification of smokers coupled with concordance of smoking habit between spouses.3 Professor Wald and colleagues consider this bias to be relatively unimportant. My own conclusion, based on three recent studies designed to measure it, differs greatly. In the first study 1775 representative British men and women interviewed at home answered questions on smoking and the use of other nicotine products; 1537 provided saliva for cotinine estimation4 (table I). Of 808 self reported non-smokers, 11 (1-4%) with cotinine values greater than 100 lkg/l were considered "regular" smokers and a further nine (1-1%) with values greater than 30 Lg/I were considered "occasional" smokers. Gotinine values among self reported non-smokers were higher (p
