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CIGARETTE SMOKING, TAR CONTENT, AND DEATH-RATES FROM LUNG CANCER IN AUSTRALIAN MEN
1252 PLASMA VITAMIN A AND ZINC CONCENTRATIONS IN PATIENTS
I
I
Each sample represents
6 CIRRHOTIC
mean
of two
samples collected on successive days.
plasma-vitamin-A in addition to the characteristically low plasma-zinc concentrations. Unexpectedly, liver stores of vitamin A (!Jog. per g.) were not depressed during the course of the deficiency.1 It seems that zinc is necessary for the mobilisation of vitamin A from the liver. Although the exact mechanism is unknown, we have found that zinc deficiency in rats depressed the concentration of serumtransport-protein for vitamin A (retinol-binding protein).2 We suggested that zinc may be involved in the occurrence of night blindness in patients with liver disease. In some patients with liver disease as well as other clinical conditions in which both plasma vitamin A and zinc are depressed, vitamin-A supplementation alone may be ineffective in restoring the plasma-vitamin-A to normal. We suggest that such patients may exhibit low plasma-vitamin-A concentrations because of insufficient metabolisable zinc. In such cases, zinc supplementation may be beneficial. Trace Element Research Laboratory and Gastroenterology-Hepatology
Section,
14% were over 24 mg., by 1974 18% were under 12 mg. and none of the sixty-one brands tested exceeded 24 mg. Over the 5-year period, the proportion of brands under 19 mg. rose from 33% to over 90%. Thus high-tar cigarettes have virtually disappeared from the market and there is a useful selection of low-tar brands available. Retrospective sales figures are not readily available, but in the 1974 survey it was found that one low-tar brand (8 mg.) was the sixth best-selling brand in Melbourne. This represents a considerable market force. Although the tar content of most Australian cigarettes before 1969 is not published, preliminary tests in 1967 at Roswell Park Memorial Institute showed six out of ten popular brands with a wet-tar content over 35 mg.5 The general level of tar content of Australian cigarettes in the early 1960s was considerably higher than that found in 1969, paralleling the findings in the U.S.A. and U.K.6,7 Age-specific lung-cancer death-rates have been provided by the Australian Bureau of Census and Statistics Victorian Office. The accompanying figure shows the death-rates per 1000 males from 1950 to 1973. It is difficult to discern the trend in the 50-54-year agegroup as the rates are relatively low. However, the 55-59 5. Victorian Cancer News, no. 34, 1967. 6. Kiefer, J. E., Tovey, G. P. in Tobacco and Tobacco Smoke (edited by E. L. Wynder and D. Hoffman); p. 572. New York, 1967. 7. Todd, G. F. in Proceedings of XI International Cancer Congress, Florence, 1974 (in the press).
J. CECIL SMITH, JR.
ELLEN D. BROWN Veterans Administration Hospital, STEVEN C. WHITE 50 Irving Street North West, Washington D.C. 20422, U.S.A. JAMES D. FINKELSTEIN.
CIGARETTE SMOKING, TAR CONTENT, AND DEATH-RATES FROM LUNG CANCER IN AUSTRALIAN MEN
SIR,—In Australia, during the past decade, there has been an anti-smoking health-education programme. For 6 years, in some States, this has included considerable publicity aimed at encouraging smokers to use low rather than high-tar brands of cigarettes. Australian national smoking-rates for males and females were measured in 1974. Results were based on 6637 interviews conducted with people selected by a national probability sample. In men, as age increased, the proportion of current cigarette smokers fell from 46 % among 20-29-year-olds to 31 % of those 60 or over. The proportion of ex-smokers increased with age, reaching 39% in those aged 60 or more. 80% of those aged 60 or more had given up more than 5 years ago, as against 61 % in the 50-59, 51 % in the 30-49, and 21 % in the 20-29-year-old age-groups. Since 1969 brands representing at least 95% of cigarettes sold have been tested for dry-tar content by the method described by Forbes et al.4 Testing in 1969 and 1971 was done at Monash University, Melbourne; in 1972 and 1974 it was done at the University of Waterloo, Ontario, Canada. The number of brands in the low (under 12 mg. per cigarette) and low intermediate tar (13-18 mg.) range has increased. Whereas in 1969 only 4% of the forty-nine brands tested were under 12 mg. of tar per cigarette and 1.
Smith, J. Cecil, Jr., McDaniel, E. G., Fan, F. F., Halsted, J. A. Science, 1973, 181, 954. 2. Smith, J. E., Brown, E. D., Smith, J. Cecil, Jr. J. Lab. clin. Med. 1974, 84, 692. 3. Halsted, J. A., Smith, J. Cecil, Jr. Gastroenterology, 1974, 67, 193. 4. Forbes, W. F., Robinson, J. C., Stanton, M. Cancer, 1969, 23, 910.
Age-specific male lung-cancer death-rates, Australia,
1950-73.
1253 and 60-64-year age-groups show
a reduction in death-rate since 1970 and 1971, respectively, instead of the continued upward trend seen in the older men. There is not yet any change in the trend of total male lung-cancer death-rates, either crude or age-adjusted. Although both crude lung-cancer death-rates and the age-adjusted rates have continued to rise, the recent fall in the rates for 55-59 and 60-64 years is a noteworthy change in trend, particularly if it persists with time and spreads
other age-groups.
to
The existence of a substantial population in this age group which gave up smoking 5 or more years ago, plus the steady reduction in tar content of cigarette smoke, provides an acceptable explanation for the fall in deathThe largest changes in tar rates in men aged 55-64. content are relatively recent, so it may be that the increased number of ex-smokers is the more important factor. Anti-Cancer Council of Victoria, 412 Albert Street,
NIGEL GRAY DAVID HILL.
East Melbourne, Australia 3002.
CHROMOSOME POLYMORPHISM AND PRENATAL DIAGNOSIS SIR,-In studies of amniotic-cell cultures for the prenatal diagnosis of chromosomal abnormalities a 46,XY karyotype always indicates a male fetus. However, a 46,XX karyotype does not always represent a female fetus, since there is a possibility of admixture of maternal cells during sampling.! The fact that polymorphism of homologous chromosomes is not uncommon2 suggested an approach for differentiating fetal from maternal karyotypes. Polymorphism of homologues can readily be demonstrated by various staining methods. For example, C-band staining best reveals the qh polymorphism of chromosomes 1, 9, and 16. For other polymorphic bands on the autosomes, Q-band staining appears to be the best method, whereas G-band staining is the least helpful. With Q-band staining, the polymorphism is manifested in very bright bands (polymorphic Q-bands) near the centromeres of chromosomes 3, 4, 13, and 22, or in very bright satellites on one or more In addition, a qh polyacrocentric chromosomes. chromosomes in 1, 9, and 16 may also be well morphism
visualised. Because of our findings in a study of parent-child chromosomal polymorphism difference, Q-band staining now is carried out routinely in our laboratory on peripheralblood cultures of both parents in each case in which amniocentesis is to be performed. In 109 families studied (a child and both parents or an amniotic sample and both parents), it was found that on the basis of chromosomal polymorphism the fetal (or child) karyotype could be distinguished from that of the mother in 101 out of 109 families. In 2 families there were no distinguishing bands in the child or in either parent. In 6 families, the chromosomes of the child and the mother could not be differentiated because their polymorphic bands were similar. Our experience suggests that routine examination of peripheral-blood cultures of the parents for chromosomal polymorphism is a valuable supplementary procedure in prenatal diagnosis. Michael J. Connell Foundation Medical Genetics Fund, and Health, Education and Welfare, MCH project 422. Childrens Hospital of Los Angeles and University of Southern California, P.O. Box 54700, Los Angeles, California 90054, U.S.A.
Nadler,
Case 1.—A 60-year-old woman was admitted to hospital semiconscious. The history given by her companion was of a sore throat for four days and severe headaches for three. In the past 24 hours she had become very drowsy. On examination she had blotchy, generalised purpura especially over the trunk and had slight neck stiffness. Her B.P. was 60/0 mm. Hg and
temperature 38.5OC. Meningococcal septicaemia was suspected and cerebrospinal fluid and blood-cultures were obtained. Intravenous penicillin and hydrocortisone were administered but she died five hours after admission. The post-mortem findings were typical of meningococcal septicaemia with bilateral adrenal haemorrhage. The brain and meninges appeared normal but there was evidence of a severe pharyngitis. The blood and pharyngeal cultures yielded a profuse growth of Neisseria meningitidis Group C. C.S.F. and brain cultures were sterile. Cells and protein in the c.s.F. were normal and the peripheral white-blood-cell count was 6500 per c.mm. Group-C meningococcal antigen was detected in the serum but not in the C.S.F. with c.i.E. Case 2.-A thirteen-month-old girl was admitted to hospital at 6 A.M. on a Saturday morning. According to the parents, the child had been hot, irritable, anorexic, and had not slept during Friday night. On examination she had tachypnoea, pulse 60 per minute, and a temperature of 38°C. By 10 A.M. she had developed a widespread erythematous rash which gradually faded only to be
replaced by
purpura.
was
suspected
The prognosis when meningococcal capsular antigens are detected by C.I.E. in serum is said to be generally worse than when none is detectable. 2,3 These two cases support this theory and underline the fact that, while C.I.E. is sometimes of little use in the actual diagnosis of meningococcal disease, it does have its value in detecting those patients having a more severe form of the disease and who therefore need more careful management. to
We thank Dr R. Lancaster and Dr D. R. Harvey for permission describe patients admitted under their care. Department of Bacteriology, St. Mary’s Hospital Medical R. C. SPENCER School,
M. A. SAVAGE.
London W2 1PG.
GENITOURINARY MEDICINE SIR,--The executive committee of the Renal Association have noted with some concern the proposal that the specialty known as " venereology or sexually-transmitted diseases " be renamed " genitourinary medicine". They feel that this name is unfortunate since it may lead to confusion with renal medicine and especially urology.
particularly important when posts are advertised, that already an advertisement for an appointWe ment to this specialty has appeared under urology. obviously have no say in what the specialty is called, and This is and we
note
to
draw attention
Department of Nephrology, St. Bartholomew’s Hospital,
O. ALFI A. DERENCSENYI G. DONNELL. (edited by H. Harris
Meningococcal septicaemia
and cerebrospinal fluid and blood-cultures were obtained as were nose and throat swabs. Antibiotics were administered and the child made a successful recovery. Neisseria meningitidis Group C was isolated from the blood and throat cultures. The c.s.F. was sterile with no increased cells or protein and the peripheral W.B.C. was 19,400 per c.mm. with a neutrophil leucocytosis. Group-C meningococcal antigen was not detectable using C.I.E. in either c.s.F. or serum.
I write merelv
H. L. Advances in Human Genetics and K. Hirschhorn), 1972, 3, 11. 2. Evans, H. J. Br. med. Bull. 1973, 29, 196. 1.
C.I.E. IN MENINGOCOCCAL INFECTION SIR,--We should like to report two cases of group-C meningococcal septicaemia in which counterimmunoelectrophoresis (C.I.E.) was used in an attempt to detect meningococcal capsular antigen in conjunction with standard The C.1.E. was performed using the basic methods. method originally described by Dorff.l
London EC1A 7BE.
to
this possible confusion. W. R. CATTELL,
Secretary, the Renal Association. 1. 2. 3.
Dorff, G. H., Coonrod, J. D., Rytel, M. W. Lancet, 1971, ii, 578. Hoffman, R. T., Edwards, E. A. J. infect. Dis. 1972, 126, 636. Ferstenfeld, J. E., Rytel, M. W. J. Am. med. Ass. 1974, 227, 1301.
I
I
Each sample represents
6 CIRRHOTIC
mean
of two
samples collected on successive days.
plasma-vitamin-A in addition to the characteristically low plasma-zinc concentrations. Unexpectedly, liver stores of vitamin A (!Jog. per g.) were not depressed during the course of the deficiency.1 It seems that zinc is necessary for the mobilisation of vitamin A from the liver. Although the exact mechanism is unknown, we have found that zinc deficiency in rats depressed the concentration of serumtransport-protein for vitamin A (retinol-binding protein).2 We suggested that zinc may be involved in the occurrence of night blindness in patients with liver disease. In some patients with liver disease as well as other clinical conditions in which both plasma vitamin A and zinc are depressed, vitamin-A supplementation alone may be ineffective in restoring the plasma-vitamin-A to normal. We suggest that such patients may exhibit low plasma-vitamin-A concentrations because of insufficient metabolisable zinc. In such cases, zinc supplementation may be beneficial. Trace Element Research Laboratory and Gastroenterology-Hepatology
Section,
14% were over 24 mg., by 1974 18% were under 12 mg. and none of the sixty-one brands tested exceeded 24 mg. Over the 5-year period, the proportion of brands under 19 mg. rose from 33% to over 90%. Thus high-tar cigarettes have virtually disappeared from the market and there is a useful selection of low-tar brands available. Retrospective sales figures are not readily available, but in the 1974 survey it was found that one low-tar brand (8 mg.) was the sixth best-selling brand in Melbourne. This represents a considerable market force. Although the tar content of most Australian cigarettes before 1969 is not published, preliminary tests in 1967 at Roswell Park Memorial Institute showed six out of ten popular brands with a wet-tar content over 35 mg.5 The general level of tar content of Australian cigarettes in the early 1960s was considerably higher than that found in 1969, paralleling the findings in the U.S.A. and U.K.6,7 Age-specific lung-cancer death-rates have been provided by the Australian Bureau of Census and Statistics Victorian Office. The accompanying figure shows the death-rates per 1000 males from 1950 to 1973. It is difficult to discern the trend in the 50-54-year agegroup as the rates are relatively low. However, the 55-59 5. Victorian Cancer News, no. 34, 1967. 6. Kiefer, J. E., Tovey, G. P. in Tobacco and Tobacco Smoke (edited by E. L. Wynder and D. Hoffman); p. 572. New York, 1967. 7. Todd, G. F. in Proceedings of XI International Cancer Congress, Florence, 1974 (in the press).
J. CECIL SMITH, JR.
ELLEN D. BROWN Veterans Administration Hospital, STEVEN C. WHITE 50 Irving Street North West, Washington D.C. 20422, U.S.A. JAMES D. FINKELSTEIN.
CIGARETTE SMOKING, TAR CONTENT, AND DEATH-RATES FROM LUNG CANCER IN AUSTRALIAN MEN
SIR,—In Australia, during the past decade, there has been an anti-smoking health-education programme. For 6 years, in some States, this has included considerable publicity aimed at encouraging smokers to use low rather than high-tar brands of cigarettes. Australian national smoking-rates for males and females were measured in 1974. Results were based on 6637 interviews conducted with people selected by a national probability sample. In men, as age increased, the proportion of current cigarette smokers fell from 46 % among 20-29-year-olds to 31 % of those 60 or over. The proportion of ex-smokers increased with age, reaching 39% in those aged 60 or more. 80% of those aged 60 or more had given up more than 5 years ago, as against 61 % in the 50-59, 51 % in the 30-49, and 21 % in the 20-29-year-old age-groups. Since 1969 brands representing at least 95% of cigarettes sold have been tested for dry-tar content by the method described by Forbes et al.4 Testing in 1969 and 1971 was done at Monash University, Melbourne; in 1972 and 1974 it was done at the University of Waterloo, Ontario, Canada. The number of brands in the low (under 12 mg. per cigarette) and low intermediate tar (13-18 mg.) range has increased. Whereas in 1969 only 4% of the forty-nine brands tested were under 12 mg. of tar per cigarette and 1.
Smith, J. Cecil, Jr., McDaniel, E. G., Fan, F. F., Halsted, J. A. Science, 1973, 181, 954. 2. Smith, J. E., Brown, E. D., Smith, J. Cecil, Jr. J. Lab. clin. Med. 1974, 84, 692. 3. Halsted, J. A., Smith, J. Cecil, Jr. Gastroenterology, 1974, 67, 193. 4. Forbes, W. F., Robinson, J. C., Stanton, M. Cancer, 1969, 23, 910.
Age-specific male lung-cancer death-rates, Australia,
1950-73.
1253 and 60-64-year age-groups show
a reduction in death-rate since 1970 and 1971, respectively, instead of the continued upward trend seen in the older men. There is not yet any change in the trend of total male lung-cancer death-rates, either crude or age-adjusted. Although both crude lung-cancer death-rates and the age-adjusted rates have continued to rise, the recent fall in the rates for 55-59 and 60-64 years is a noteworthy change in trend, particularly if it persists with time and spreads
other age-groups.
to
The existence of a substantial population in this age group which gave up smoking 5 or more years ago, plus the steady reduction in tar content of cigarette smoke, provides an acceptable explanation for the fall in deathThe largest changes in tar rates in men aged 55-64. content are relatively recent, so it may be that the increased number of ex-smokers is the more important factor. Anti-Cancer Council of Victoria, 412 Albert Street,
NIGEL GRAY DAVID HILL.
East Melbourne, Australia 3002.
CHROMOSOME POLYMORPHISM AND PRENATAL DIAGNOSIS SIR,-In studies of amniotic-cell cultures for the prenatal diagnosis of chromosomal abnormalities a 46,XY karyotype always indicates a male fetus. However, a 46,XX karyotype does not always represent a female fetus, since there is a possibility of admixture of maternal cells during sampling.! The fact that polymorphism of homologous chromosomes is not uncommon2 suggested an approach for differentiating fetal from maternal karyotypes. Polymorphism of homologues can readily be demonstrated by various staining methods. For example, C-band staining best reveals the qh polymorphism of chromosomes 1, 9, and 16. For other polymorphic bands on the autosomes, Q-band staining appears to be the best method, whereas G-band staining is the least helpful. With Q-band staining, the polymorphism is manifested in very bright bands (polymorphic Q-bands) near the centromeres of chromosomes 3, 4, 13, and 22, or in very bright satellites on one or more In addition, a qh polyacrocentric chromosomes. chromosomes in 1, 9, and 16 may also be well morphism
visualised. Because of our findings in a study of parent-child chromosomal polymorphism difference, Q-band staining now is carried out routinely in our laboratory on peripheralblood cultures of both parents in each case in which amniocentesis is to be performed. In 109 families studied (a child and both parents or an amniotic sample and both parents), it was found that on the basis of chromosomal polymorphism the fetal (or child) karyotype could be distinguished from that of the mother in 101 out of 109 families. In 2 families there were no distinguishing bands in the child or in either parent. In 6 families, the chromosomes of the child and the mother could not be differentiated because their polymorphic bands were similar. Our experience suggests that routine examination of peripheral-blood cultures of the parents for chromosomal polymorphism is a valuable supplementary procedure in prenatal diagnosis. Michael J. Connell Foundation Medical Genetics Fund, and Health, Education and Welfare, MCH project 422. Childrens Hospital of Los Angeles and University of Southern California, P.O. Box 54700, Los Angeles, California 90054, U.S.A.
Nadler,
Case 1.—A 60-year-old woman was admitted to hospital semiconscious. The history given by her companion was of a sore throat for four days and severe headaches for three. In the past 24 hours she had become very drowsy. On examination she had blotchy, generalised purpura especially over the trunk and had slight neck stiffness. Her B.P. was 60/0 mm. Hg and
temperature 38.5OC. Meningococcal septicaemia was suspected and cerebrospinal fluid and blood-cultures were obtained. Intravenous penicillin and hydrocortisone were administered but she died five hours after admission. The post-mortem findings were typical of meningococcal septicaemia with bilateral adrenal haemorrhage. The brain and meninges appeared normal but there was evidence of a severe pharyngitis. The blood and pharyngeal cultures yielded a profuse growth of Neisseria meningitidis Group C. C.S.F. and brain cultures were sterile. Cells and protein in the c.s.F. were normal and the peripheral white-blood-cell count was 6500 per c.mm. Group-C meningococcal antigen was detected in the serum but not in the C.S.F. with c.i.E. Case 2.-A thirteen-month-old girl was admitted to hospital at 6 A.M. on a Saturday morning. According to the parents, the child had been hot, irritable, anorexic, and had not slept during Friday night. On examination she had tachypnoea, pulse 60 per minute, and a temperature of 38°C. By 10 A.M. she had developed a widespread erythematous rash which gradually faded only to be
replaced by
purpura.
was
suspected
The prognosis when meningococcal capsular antigens are detected by C.I.E. in serum is said to be generally worse than when none is detectable. 2,3 These two cases support this theory and underline the fact that, while C.I.E. is sometimes of little use in the actual diagnosis of meningococcal disease, it does have its value in detecting those patients having a more severe form of the disease and who therefore need more careful management. to
We thank Dr R. Lancaster and Dr D. R. Harvey for permission describe patients admitted under their care. Department of Bacteriology, St. Mary’s Hospital Medical R. C. SPENCER School,
M. A. SAVAGE.
London W2 1PG.
GENITOURINARY MEDICINE SIR,--The executive committee of the Renal Association have noted with some concern the proposal that the specialty known as " venereology or sexually-transmitted diseases " be renamed " genitourinary medicine". They feel that this name is unfortunate since it may lead to confusion with renal medicine and especially urology.
particularly important when posts are advertised, that already an advertisement for an appointWe ment to this specialty has appeared under urology. obviously have no say in what the specialty is called, and This is and we
note
to
draw attention
Department of Nephrology, St. Bartholomew’s Hospital,
O. ALFI A. DERENCSENYI G. DONNELL. (edited by H. Harris
Meningococcal septicaemia
and cerebrospinal fluid and blood-cultures were obtained as were nose and throat swabs. Antibiotics were administered and the child made a successful recovery. Neisseria meningitidis Group C was isolated from the blood and throat cultures. The c.s.F. was sterile with no increased cells or protein and the peripheral W.B.C. was 19,400 per c.mm. with a neutrophil leucocytosis. Group-C meningococcal antigen was not detectable using C.I.E. in either c.s.F. or serum.
I write merelv
H. L. Advances in Human Genetics and K. Hirschhorn), 1972, 3, 11. 2. Evans, H. J. Br. med. Bull. 1973, 29, 196. 1.
C.I.E. IN MENINGOCOCCAL INFECTION SIR,--We should like to report two cases of group-C meningococcal septicaemia in which counterimmunoelectrophoresis (C.I.E.) was used in an attempt to detect meningococcal capsular antigen in conjunction with standard The C.1.E. was performed using the basic methods. method originally described by Dorff.l
London EC1A 7BE.
to
this possible confusion. W. R. CATTELL,
Secretary, the Renal Association. 1. 2. 3.
Dorff, G. H., Coonrod, J. D., Rytel, M. W. Lancet, 1971, ii, 578. Hoffman, R. T., Edwards, E. A. J. infect. Dis. 1972, 126, 636. Ferstenfeld, J. E., Rytel, M. W. J. Am. med. Ass. 1974, 227, 1301.