- Email: [email protected]
SMOKING AND LUNG CANCER
950
cyclical response changes, including those underlying cyclical depressions, before the whole picture becomes clear. Center for the Study of Democratic
Institutions, Box 4068, Santa Barbara, California 93103, U.S.A.
ALEX COMFORT.
SMOKING AND LUNG CANCER
SIR,-Mr Manning (Sept. 14, p. 666) puts forward for
an
smoking. This analysis of secular trends leaves
open the possibility of the recorded increases in lung cancer are genuine although they are not associated with cigarette smoking: they might, for example, be attributed to environmental factors-such as atmospheric pollutionwhose impact on men and women was synchronous. However, certain details of the secular changes in the agedependence of the death-rates indicate that diagnostic error has made a large contribution to the apparent increase in lung cancer.1,2 Despite their many limitations,2 findings from necropsy series provide the best test we have of the genuineness, or otherwise, of the apparent secular increase in lung cancer. Doubting the genuineness of this increase and bearing in mind the frequent misdiagnosis of lung cancer, Willis3 argued that only fully proved necropsy records are of value in such contexts. From reviews of necropsy series, Passey and Holmes, and Rosenblatt and co-workers,5-’ were unable to confirm the reality of the supposed secular increases. The latter authors concluded that changes in clinical diagnosis-from drastic underdiagnosis at the beginning of the century5 to net overdiagnosis during the last decade or so 6-have been largely responsible for the apparent increase in the incidence of lung cancer. Mr Manning’s assertion that " there has been a secular change in lung-cancer incidence, as the recorded rate of increase differs between the sexes " assumes that proportionate errors in diagnosis must have been the same in the two sexes. This is improbable as the diseases with which lung cancer has been confused (mainly other respiratory disorders) are more frequent in men than in women. To return to Mr Manning’s hypothesis, the existence of a genetic association between a predisposition to smoke and a predisposition to lung cancer-as first proposed by Fisher 8-can scarcely be doubted. Thus, in Tokuhata
that
at
least
some
Burch, P. R. J. Lancet, 1972, ii, 132. Burch, P. R. J. ibid. 1973, ii, 102. Willis, R. A. Pathology of Tumours. London, 1960. Passey, R. D., Holmes, J. McD. Q. Jl Med. 1935, 4, 321. 5. Rosenblatt, M. B. Med. Counterpoint, 1969, 1, 29. 6. Rosenblatt, M. B., Teng, P. K., Kerpe, S., Beck, I. N.Y. St. J. Med. 1971, 71, 2189. 7. Rosenblatt, M. B., Teng, P. K., Kerpe, S. Prog. Clin. Cancer, 1973, 5, 71. 8. Fisher, R. A. Smoking: The Cancer Controversy. Edinburgh, 1959. 1. 2. 3. 4.
General Infirmary, Leeds LSI 3EX.
an
association at the ingenious hypothesis genetic level between smoking and lung cancer. He also assumes that a cigarette-associated increase in the incidence of lung cancer has occurred during the course of this century. However, his genetic theory does not require such an increase and the most reliable evidence fails to endorse it. The recorded age-specific and sex-specific death-rates from lung cancer in England and Wales, 1901 to 1970, have been analysed previously. 1,2 My analysis showed that the enormous secular increases,l and changes in the rates of increase2 were almost entirely synchronous in the two sexes. On the other hand, the secular increase in the rate of cigarette smoking by women lagged some 30 years behind that of men. In other words, the recorded increases in lung cancer, considered for men and women separately, are not associated in time with the increases in cigarette to account
and Lilienfeld’s 9 study, the frequency of smokers among the first-degree relatives of non-smoking lung-cancer probands was significantly higher (p ≃ 0.03) than among corresponding first-degree relatives of non-smoking and race, sex, age, and residence matched controls. This complication, coupled with the many anomalies 1-8 in the evidence, undermine the popular view that the association between cigarette smoking and lung cancer has a straightforward causal basis. P. R. J. BURCH.
SMOKING AND THE HEART
SIR,-A remark in the survey by Dr Ball and Dr Turner (Oct. 5, p. 822) about the need for methods to help man rid himself of the smoking habit reminded me of a curious incidental finding when I was engaged in exposing animals
methyl mercury compounds.1O I did indeed include it in footnote in the original version of the small piece which I wrote about these experiments, but this was subsequently
to a
cut out.
At that time I was an addicted cigarette smoker, but found quite consistently that for an hour or so after tending the animals, smoking was so distasteful that, if I inadvertently lit a cigarette, I forthwith stubbed it out. I have never experienced anything like this under any other circumstances and can only attribute it to a slight exposure to the vapours of methyl mercury compounds. These unfortunately are dangerously toxic substances. I am neither chemist nor pharmacologist, but I have wondered whether there is any chance that similar substances might be found with the same ability to produce aversion to smoking but without the toxic properties. Woodways, Little Baddow, Chelmsford CM3 4SZ.
R. R. BOMFORD.
PEAK-FLOW METER VERSUS PEAK-FLOW GAUGE
SiR,—The findings of Dr Campbell and his collaborators p. 199) coincide with our experience of the peakflow gauge. In October, 1973, we carried out a field
(July 27,
survey in a random population living in a rural area of the Netherlands. Besides other lung-function measurements, we measured the peak-flow rate with a Wright peak-flow meter. During this study of about 500 subjects a day, we learned of the release of the new peak-flow gauge and decided to include measurements with the gauge for a short trial, provided that the measurements with the gauge were always carried out after the measurements with the meter, in order not to disturb our own survey
protocol.
We compared the highest value of 3 measurements with the Wright peak-flow meter with the highest value of 2 measurements with the gauge in a random sample of 475 men and women. On average the readings of the meter were higher than those of the gauge. With the meter the mean peak-flow rate of the total group was 5118 litres per min. (s.D. 1015); with the gauge the mean of the same group was 489-0 litres per min. (s.D. 99-4). The mean of the individual differences between the reading of the meter and the reading of the gauge was 22 78 litres per min. (s.E. 2-05 litres per min.). The mean percentage difference was — 4 12 (s.E. 0-42), using the meter as reference measurement. In 342 subjects the difference between the instruments was smaller than 10% ; in 111 the difference fell between 10% and 20%; in 17 it was between 20% and 9. Tokuhata, G. K., Lilienfeld, A. M. J. natn. Cancer Inst. 1963, 30, 289. 10. Hunter, D., Bomford, R. R., Russell, D.Q. Jl Med. 1940, 35, 193.
cyclical response changes, including those underlying cyclical depressions, before the whole picture becomes clear. Center for the Study of Democratic
Institutions, Box 4068, Santa Barbara, California 93103, U.S.A.
ALEX COMFORT.
SMOKING AND LUNG CANCER
SIR,-Mr Manning (Sept. 14, p. 666) puts forward for
an
smoking. This analysis of secular trends leaves
open the possibility of the recorded increases in lung cancer are genuine although they are not associated with cigarette smoking: they might, for example, be attributed to environmental factors-such as atmospheric pollutionwhose impact on men and women was synchronous. However, certain details of the secular changes in the agedependence of the death-rates indicate that diagnostic error has made a large contribution to the apparent increase in lung cancer.1,2 Despite their many limitations,2 findings from necropsy series provide the best test we have of the genuineness, or otherwise, of the apparent secular increase in lung cancer. Doubting the genuineness of this increase and bearing in mind the frequent misdiagnosis of lung cancer, Willis3 argued that only fully proved necropsy records are of value in such contexts. From reviews of necropsy series, Passey and Holmes, and Rosenblatt and co-workers,5-’ were unable to confirm the reality of the supposed secular increases. The latter authors concluded that changes in clinical diagnosis-from drastic underdiagnosis at the beginning of the century5 to net overdiagnosis during the last decade or so 6-have been largely responsible for the apparent increase in the incidence of lung cancer. Mr Manning’s assertion that " there has been a secular change in lung-cancer incidence, as the recorded rate of increase differs between the sexes " assumes that proportionate errors in diagnosis must have been the same in the two sexes. This is improbable as the diseases with which lung cancer has been confused (mainly other respiratory disorders) are more frequent in men than in women. To return to Mr Manning’s hypothesis, the existence of a genetic association between a predisposition to smoke and a predisposition to lung cancer-as first proposed by Fisher 8-can scarcely be doubted. Thus, in Tokuhata
that
at
least
some
Burch, P. R. J. Lancet, 1972, ii, 132. Burch, P. R. J. ibid. 1973, ii, 102. Willis, R. A. Pathology of Tumours. London, 1960. Passey, R. D., Holmes, J. McD. Q. Jl Med. 1935, 4, 321. 5. Rosenblatt, M. B. Med. Counterpoint, 1969, 1, 29. 6. Rosenblatt, M. B., Teng, P. K., Kerpe, S., Beck, I. N.Y. St. J. Med. 1971, 71, 2189. 7. Rosenblatt, M. B., Teng, P. K., Kerpe, S. Prog. Clin. Cancer, 1973, 5, 71. 8. Fisher, R. A. Smoking: The Cancer Controversy. Edinburgh, 1959. 1. 2. 3. 4.
General Infirmary, Leeds LSI 3EX.
an
association at the ingenious hypothesis genetic level between smoking and lung cancer. He also assumes that a cigarette-associated increase in the incidence of lung cancer has occurred during the course of this century. However, his genetic theory does not require such an increase and the most reliable evidence fails to endorse it. The recorded age-specific and sex-specific death-rates from lung cancer in England and Wales, 1901 to 1970, have been analysed previously. 1,2 My analysis showed that the enormous secular increases,l and changes in the rates of increase2 were almost entirely synchronous in the two sexes. On the other hand, the secular increase in the rate of cigarette smoking by women lagged some 30 years behind that of men. In other words, the recorded increases in lung cancer, considered for men and women separately, are not associated in time with the increases in cigarette to account
and Lilienfeld’s 9 study, the frequency of smokers among the first-degree relatives of non-smoking lung-cancer probands was significantly higher (p ≃ 0.03) than among corresponding first-degree relatives of non-smoking and race, sex, age, and residence matched controls. This complication, coupled with the many anomalies 1-8 in the evidence, undermine the popular view that the association between cigarette smoking and lung cancer has a straightforward causal basis. P. R. J. BURCH.
SMOKING AND THE HEART
SIR,-A remark in the survey by Dr Ball and Dr Turner (Oct. 5, p. 822) about the need for methods to help man rid himself of the smoking habit reminded me of a curious incidental finding when I was engaged in exposing animals
methyl mercury compounds.1O I did indeed include it in footnote in the original version of the small piece which I wrote about these experiments, but this was subsequently
to a
cut out.
At that time I was an addicted cigarette smoker, but found quite consistently that for an hour or so after tending the animals, smoking was so distasteful that, if I inadvertently lit a cigarette, I forthwith stubbed it out. I have never experienced anything like this under any other circumstances and can only attribute it to a slight exposure to the vapours of methyl mercury compounds. These unfortunately are dangerously toxic substances. I am neither chemist nor pharmacologist, but I have wondered whether there is any chance that similar substances might be found with the same ability to produce aversion to smoking but without the toxic properties. Woodways, Little Baddow, Chelmsford CM3 4SZ.
R. R. BOMFORD.
PEAK-FLOW METER VERSUS PEAK-FLOW GAUGE
SiR,—The findings of Dr Campbell and his collaborators p. 199) coincide with our experience of the peakflow gauge. In October, 1973, we carried out a field
(July 27,
survey in a random population living in a rural area of the Netherlands. Besides other lung-function measurements, we measured the peak-flow rate with a Wright peak-flow meter. During this study of about 500 subjects a day, we learned of the release of the new peak-flow gauge and decided to include measurements with the gauge for a short trial, provided that the measurements with the gauge were always carried out after the measurements with the meter, in order not to disturb our own survey
protocol.
We compared the highest value of 3 measurements with the Wright peak-flow meter with the highest value of 2 measurements with the gauge in a random sample of 475 men and women. On average the readings of the meter were higher than those of the gauge. With the meter the mean peak-flow rate of the total group was 5118 litres per min. (s.D. 1015); with the gauge the mean of the same group was 489-0 litres per min. (s.D. 99-4). The mean of the individual differences between the reading of the meter and the reading of the gauge was 22 78 litres per min. (s.E. 2-05 litres per min.). The mean percentage difference was — 4 12 (s.E. 0-42), using the meter as reference measurement. In 342 subjects the difference between the instruments was smaller than 10% ; in 111 the difference fell between 10% and 20%; in 17 it was between 20% and 9. Tokuhata, G. K., Lilienfeld, A. M. J. natn. Cancer Inst. 1963, 30, 289. 10. Hunter, D., Bomford, R. R., Russell, D.Q. Jl Med. 1940, 35, 193.