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Passive smoking and protection of nonsmokers at the workplace
LUNG CANCER --a&Lung Cancer 10 (1994) 395-430
Abstracts Prevention Lung cancer incidence rate for male ex-smokers according to age at cessiition of smoking Sobue T, Yamaguchi N. Suzuki T. Fujimoto I, Matsuda M. Doi 0 et al. 77~sCenrer for Adult Di.waws, l-l-3 Nokomichi, Higoshittnri-ku. Osaka 537. Jpn J Cancer 1993;84:601-7. Lung cancer incidence rate after the cessation of smoking was assessed for male ex-smokers according to the age at cessation, using the results from a case-control sNdv for ex-smoker versus continuing smoker, and the lung cancer incidence rate function for continuing smoker estimated from Japan Vital Statistics and the ‘Six-prefectural Cohort Study’ in Japan. Tbis hospiral-based case-control study consisted of776 lung cancer cases (553 current smokers and 223 ex-smokers) and 772 controls (490 current smokers and 282 ex-smokers) who started smoking at ages 18-22. The odds ratio ofdeveloping lung cancer for exsmokers compared to continuing smokers according to years since the cessation of smoking was estimated for four age groups (5564.6069. 65-74 and 70-79). Given that thz number of years since cessation of smoking is the same, reduction of the odds ratio appeared to be greater for the younger age group than for the older age group, mtlecting the shorter period of exposure for the younger age group. Lung cancer incidence rate (per 100,000) was assumed to be expressed by the following function; 1.7x10‘5x(age-24.3)1s for continuing smokers and rate among ex0.15x 10.sx(age)* for nonsmokers. Lung cancer incidence smokers according to years since cessation was then estimated to be the above function multiplied by the odds ratio from the case-control study for each age group. In conttast to the greater reduction of the odds ratio among younger ex-smokers, reduction of the incidence rate, in terms of rate difference, was considerably greater for older ex-smokers due to a high incidence rate of lung cancer for older continuing smokers. This indicates that the absolute ma_tiNde of reductton of the lung cancer incidence rate after cessation ofsmoking is gmter for older ax-smokers. although the relative ma&tiNde of reduction is greater for younger exsmokers.
The glutatbione S-tramferase polymorphism as a marker for susceptibility to lung carcinoma Nazar-Stewart V. Motulsky AG. Eaton DL. White E. Homung SK, L.eng Z-T et al. Department of Epidemiology, Sch. of Public Health/ Community Med., University of Washington. Seottk, Cancer Res 1993;53:2313-8.
WA 98195.
Glutathione S-transferase (GST) enzymes detoxify carcinogens in tobacco smoke. Interindividual variation in GST function may be related to differences in risk for smoking-related cancer. Leukocytes from 50% of Caucasians lack GST activity toward tram-stilbene oxide (TSO), due to a deletion of the gene for the GST-enzyme. Presence of GST-TSO activity in leukocytes has been associated with low risk for lung cancer among cigarette smokers. We sought to determine whether GSTactivityinlung tissueisdeterminedbythesamegenepolymorphism
and whether it is associated with risk for lung cancer. Subjects were cigarette smokers, identified at the time of lung resection or autopsy in Seattle hospitals. Uninvolved lung tissue was obtained fmm 35 patients with lung carcinoma and 43 control patients and assayed for GSTactivity with TSO, for the presence of the GST-gene product with an immunological assay, and for tbe GST-gene with Southern blotting. Mailed questionnaires were used to collect information on subjects’ smoking histories and exposures which might alter enzyme activity. Interindividual results from tits three assays correlated well. Smokers with high GST-TSO enzyme activity present in their lung tissue had a lower risk for lung carcinoma than did smokers with no or low activity (relative risk = 0.30; 95% confidence interval, 0.11-0.79), as did smokers with GST- antigen identified in lung tissue versus those with no antigen (relative risk = 0.30: 95 % confidence interval, 0.1 I-0.79). Smokers with both maternal and paternal copies of GST- DNA (n = 7) had a lower cancer risk than smokers lacking GST- DNA (n = 30; relative risk = 0.35: 95% contidence interval, 0.06- 2.10). High GSTactivity appeared to be associated with a greeter decrease in lung cancer risk among 38 heavy cigarette smokers (relative risk = 0.15; 95% confidence interval. 0.03-0.64) than among 38 light smokers (relative risk = 0.61; 95 46confidence interval, 0.14-2.60). Presence or absence and number of copies of the GST- gene appear to determine activity of the GST-enzyme in lung. Smokers with the GST-etuyme have approximately one-third of the risk for lung carcinoma of smokers without the enzyme.
Passive smoking and protection of nommokers at the workplace Kaiker U. Gesuttdheitsomt, Broubochrtrosse 18-22,6@WFrat@urt/M. 1, Arbeitsmed Sozialmed Pnventivmed 1993;28: 138-42 + 147-9. In Germany 36 % of the male and 28 I of the female employ= are exposed to passive smoking at their working place. Envimnmental tobacco smoke contains dozens of carcinogens and is supposed to cause more cancer diseases than other airborne pollutants like asbestos, arsenic, benzene, vinylchloride. In 199 I during two public information campaigns organ&d by the Public Health Service of Frankfurt on the Main 942 persons were asked about their opinion about passivesmoking and protection against environmental tobacco smoke. More than50% oftbemanswered, that therewerenosmoking reglementationa at all at their wotking place. More rhao70% felt bothered by envimnmental tobacco smoke (>90% of the nonsmokers (NS) and >30% of the smokers (S) as well). More than 75 46complained about bad air ( > 80 96 NS and about 40% S), and more than 60% of them complained about smoke in hair and clothes ( > 70 % NS and 1l-24 96S). Asked about their recommendations on protection against involuntary environmental tobacco smoke nonsmokers as well as smokers preferted common decision (unanimity or majority) or specid regulations (different times and/or places), very seldom total permission or complete prohibition was proposed. 50-8045 of the nonsmoker and the smoker unanimously suggested total smoking prohibition in floors, elevatorsand bathrooms. In their immediate working place, during conferences and in the restroom nonsmokers preferred smoking prohibition, whereas smokers
Abstracts/Lung suggested common decision or special smoking rooms or smoking breaks. Not only the nonsmokers, but also the smokers themselves felt bothered by passive smoking. Both of them agreed in the necessitiy for regulanons against involuntary environmental tobacco smoke and they preferred spectal regulations instead of acomplete smoking permission. Those smoking regulations are mandatory, because of 500-1200 lung cancer diseases by passtve smoking per year in the Federal Republic of Germany where 36 % of the male and 28 R of the female employees are expostxl to env~ronmentai tobacco smoke at their working stte and should be protected agamst toxic and carcinogenic substances in the smoke. CARET, the beta-carotene and retinal eficacy trial to prevent lung cancer in high-risk populations Omen0 GS. Fred Hutchinson Cancer Retearch Ct., Seattle, WA 98195. Public He&h Rev 1991;199’2;19:205-8. Background: CARETisamuiti-centercoikborabon.withpartitipan~ recruited in Seattle. Portland, San Francisco, Irvine, Baltimoreand New Haven. Methods: CARET is a two-armed double-blind randomized chemoprevention trial to test the hypothesis that oral administration of kta-carotene 30 mg/day plus retinyl paimitate 25,000 [U/day will decrease the incidence of lung cancer in high-risk populations: heavy smokers and askstos-exposed workers who have smoked. The agents combine anti-oxidant and nuclear tumor suppressor mechamsma. Fastidious monitoring for possibleside effects is facilitated by inclusion of a Vanguard population (cootinued from pilot studies). Results: As of 3 1 July 199 I, 8 129 participants had been randomized into the Trial, of the 18,000 needed. Efficacy results are expected in 1998. Conclurion: The Tnal demonstrates the movemeot of environmental epidemiology mto intervennonist research to preveot adverse health effects. Risk of male lung cancer attributed to coal combustion indoors in sbangbai Tao X, Hong C-J, Yu S, Zhu H. School of Public Health, Shanghai Medical Uni&rsiry. Shanghai 20(1032. Public Health Rev 1991;1992; 19: 127-34. Lungcancerisoow theleadingcauaeofdeathamongaii malecancers in Shanghai. Besides the smoking habit, the indoor air pollution from coal comb&on may also make some coottibutioo. The purpose of our study is to explore the risk of long cancer death in male residents who live in coal-using families. Stratified by two extreme. levels of ambieo:nt sulphur dioxide (SO?) and inhaiable particulate (IP) concentrations, 4 areas were chosen in the city proper: Area A (low SO,, low IP); Area B (high SO*, low IP); Area C (low SO,. high IP) and Area D (high SOz, high IP). Withio each oftheseareas, two neighboring residential groups were chosen, one of which coal as fitel (group I), with the other using coal gas or iiquitied petroleum gas as fuel (group 0). The percentages of smokers and the ambient environmcot of the two chosen groups within each area are comparable. Total persoo-years observed is 117,039 from I January 1978 to 31 Decemkr 1987 for ail males in the 8 groups. The mortalities (per 100,000 person years) of male lung cancer in the 8 groups are as follows: AO-22.33. Al-37.64; BO-27.14, 81-30.72; CO41.77, Cl-54.99; D0-49.97. Dl-78.11. The result shows that male lung cancer mortalityin tbe coal-using group is higher than that in thecoai-gas-usinggroupwithin eacharea. Mantel-Haenszel’s Relative Risk (RRMH) of male lung cancer in coal-using groups is 1.44 stratified by ambient SO, and IP and smoking levels. Attributable Risk Percent (AR%) to coal-using is 30.40%. and Population Attributable Risk Percent (PAR%) IS 17.92%. Screening for lung cancer reexamined: A reinterpretation of the Mayo Lung f%ject randomized bial on hmg cancer screening Strauss GM, Gleason RE. Sugarbaker DJ. Division of Hematology-
Cancer 10 (1994) 395-430
Oncology, Brigham and Women’s Hospital, Bosron, MA 02115. Cheast 1993; IO3:Suppl.: 337s-41.S. In the 1970s. three randomized trials, each involvingapproximately 10,000 male subjects, were carried out to determine the value of luog cancer screening in cigarette smokers. These studies have been widely ioterpretedasprovidingstroogevideocethatscreeningdoesootcootnbute to decreased death rates, and, accordingly. the American Cancer Society tirmly recommends against lung cancer screening. No randomized trial, however, has evaluated screening for lung cancer in women, who currently comprise 39% of the lung cancer population. The trials perfotmed at Memorial-Sloan Kettering and at Johns Hopkins were designed so that subjects were randomized to either a single screen (annuaichestx-rayaiona)oraduaiscreen(a~uaicht?st x-rayandevery4-month sputum cytology) group. While the results of both revealed no difference in mortality bztweeo the groups. thti stud& were designed to examine the value of sputum cytology, and no conclusion regarding the efficacy of chest x-rays can be inferred. in the Mayo Lung Project, patients were randomized to a screened group in which a cheat x-ray and sputum cytology were obtained every 4 months or to a control group in which an annual chest x-ray and cytology were simply recommended. The results indicate that after 6 years, more lung cancers were detected among the 4,618 men in the screened group (206 cases, 4.46%) than in the 4,593 men in the control group (160 cases, 3.48%). Thz screened group showed a superiority over the control subjects m resectability rate (46 46vs 32 46)and S-year survival (33 46vs I.546). However, the number of cancer deaths was slightly greater in the screened (122) than in the control group (115). and, consequently. the mortality rates were not significantly different among the groups. An ‘overdiagnosis bias’ has been suggested to account for the increased number of lung cancers detected in the screened vs the control population in the Mayo Lung Project. This explanation is statistically plaus~bie. but, given the status of lung cancer as the most lethal of malignancies, is biologically unlikely. An alternative hypothesis is that chance alone might have accounted for the observed 0.98% difference in lung cancer detection rates. Were this the case, then 46 additional cases would have been de&ted in the control group had this chance event oo1 occurmd. If it wereasaumed that these 46 lung cancer cases had achieved the spme 15 96 5-year survival as was observed in the actual control subjects, there would have been 154, oot 115. lung cancer deatha among the control subjecxts, compared to 122deathsintheacreeoedpopulatioo. adiffereoce that would approach statistical significance (p=O.O52). Baaed oo favorable survival rate.s observed in the Memorial study and in the scre~~nedgroup in the Mayo Lung Project, as well as this hypothetical analysis of relative mortality in the Mayo study, we conclude there. is iosufficieotevidenceto lirmlyrecommeodagainatlungcancerscrmoing. Further investigation is needed, in both male and female cigarette smokers, to resolve this question.
Epidemiology and etiology Polymorphimns of the CYPI Al and glutathione S-tramferase genes associated with susceptibility to lung cancer in relation to cigarette dose in a Japwese population Nakacbi K, Imai K, Hayaahi S-I, Kawajiri K. Departmenr of Epidemiology, Saitama Cancer Ctr. Research Inst., 818 Komuro, Ina. Saitama 362. Cancer Res 1993:53:2994-g. An aaac&atioa.of lung cancer susceptibility with an MspI restriction site polymorphism of the CYPlAl gene was reported in our previous study. This polymorphism has been subsequently found to be. closely linked to another iaoleucine-valine (Ile-Val) polymorphism, which resulted in an Ile-Vai amino acid replacement in the heme-binding region of P4501Al. We report here that genetic risk for squamous cell carcinoma of the lung was associated with thesa two polymorphisms of
Abstracts Prevention Lung cancer incidence rate for male ex-smokers according to age at cessiition of smoking Sobue T, Yamaguchi N. Suzuki T. Fujimoto I, Matsuda M. Doi 0 et al. 77~sCenrer for Adult Di.waws, l-l-3 Nokomichi, Higoshittnri-ku. Osaka 537. Jpn J Cancer 1993;84:601-7. Lung cancer incidence rate after the cessation of smoking was assessed for male ex-smokers according to the age at cessation, using the results from a case-control sNdv for ex-smoker versus continuing smoker, and the lung cancer incidence rate function for continuing smoker estimated from Japan Vital Statistics and the ‘Six-prefectural Cohort Study’ in Japan. Tbis hospiral-based case-control study consisted of776 lung cancer cases (553 current smokers and 223 ex-smokers) and 772 controls (490 current smokers and 282 ex-smokers) who started smoking at ages 18-22. The odds ratio ofdeveloping lung cancer for exsmokers compared to continuing smokers according to years since the cessation of smoking was estimated for four age groups (5564.6069. 65-74 and 70-79). Given that thz number of years since cessation of smoking is the same, reduction of the odds ratio appeared to be greater for the younger age group than for the older age group, mtlecting the shorter period of exposure for the younger age group. Lung cancer incidence rate (per 100,000) was assumed to be expressed by the following function; 1.7x10‘5x(age-24.3)1s for continuing smokers and rate among ex0.15x 10.sx(age)* for nonsmokers. Lung cancer incidence smokers according to years since cessation was then estimated to be the above function multiplied by the odds ratio from the case-control study for each age group. In conttast to the greater reduction of the odds ratio among younger ex-smokers, reduction of the incidence rate, in terms of rate difference, was considerably greater for older ex-smokers due to a high incidence rate of lung cancer for older continuing smokers. This indicates that the absolute ma_tiNde of reductton of the lung cancer incidence rate after cessation ofsmoking is gmter for older ax-smokers. although the relative ma&tiNde of reduction is greater for younger exsmokers.
The glutatbione S-tramferase polymorphism as a marker for susceptibility to lung carcinoma Nazar-Stewart V. Motulsky AG. Eaton DL. White E. Homung SK, L.eng Z-T et al. Department of Epidemiology, Sch. of Public Health/ Community Med., University of Washington. Seottk, Cancer Res 1993;53:2313-8.
WA 98195.
Glutathione S-transferase (GST) enzymes detoxify carcinogens in tobacco smoke. Interindividual variation in GST function may be related to differences in risk for smoking-related cancer. Leukocytes from 50% of Caucasians lack GST activity toward tram-stilbene oxide (TSO), due to a deletion of the gene for the GST-enzyme. Presence of GST-TSO activity in leukocytes has been associated with low risk for lung cancer among cigarette smokers. We sought to determine whether GSTactivityinlung tissueisdeterminedbythesamegenepolymorphism
and whether it is associated with risk for lung cancer. Subjects were cigarette smokers, identified at the time of lung resection or autopsy in Seattle hospitals. Uninvolved lung tissue was obtained fmm 35 patients with lung carcinoma and 43 control patients and assayed for GSTactivity with TSO, for the presence of the GST-gene product with an immunological assay, and for tbe GST-gene with Southern blotting. Mailed questionnaires were used to collect information on subjects’ smoking histories and exposures which might alter enzyme activity. Interindividual results from tits three assays correlated well. Smokers with high GST-TSO enzyme activity present in their lung tissue had a lower risk for lung carcinoma than did smokers with no or low activity (relative risk = 0.30; 95% confidence interval, 0.11-0.79), as did smokers with GST- antigen identified in lung tissue versus those with no antigen (relative risk = 0.30: 95 % confidence interval, 0.1 I-0.79). Smokers with both maternal and paternal copies of GST- DNA (n = 7) had a lower cancer risk than smokers lacking GST- DNA (n = 30; relative risk = 0.35: 95% contidence interval, 0.06- 2.10). High GSTactivity appeared to be associated with a greeter decrease in lung cancer risk among 38 heavy cigarette smokers (relative risk = 0.15; 95% confidence interval. 0.03-0.64) than among 38 light smokers (relative risk = 0.61; 95 46confidence interval, 0.14-2.60). Presence or absence and number of copies of the GST- gene appear to determine activity of the GST-enzyme in lung. Smokers with the GST-etuyme have approximately one-third of the risk for lung carcinoma of smokers without the enzyme.
Passive smoking and protection of nommokers at the workplace Kaiker U. Gesuttdheitsomt, Broubochrtrosse 18-22,6@WFrat@urt/M. 1, Arbeitsmed Sozialmed Pnventivmed 1993;28: 138-42 + 147-9. In Germany 36 % of the male and 28 I of the female employ= are exposed to passive smoking at their working place. Envimnmental tobacco smoke contains dozens of carcinogens and is supposed to cause more cancer diseases than other airborne pollutants like asbestos, arsenic, benzene, vinylchloride. In 199 I during two public information campaigns organ&d by the Public Health Service of Frankfurt on the Main 942 persons were asked about their opinion about passivesmoking and protection against environmental tobacco smoke. More than50% oftbemanswered, that therewerenosmoking reglementationa at all at their wotking place. More rhao70% felt bothered by envimnmental tobacco smoke (>90% of the nonsmokers (NS) and >30% of the smokers (S) as well). More than 75 46complained about bad air ( > 80 96 NS and about 40% S), and more than 60% of them complained about smoke in hair and clothes ( > 70 % NS and 1l-24 96S). Asked about their recommendations on protection against involuntary environmental tobacco smoke nonsmokers as well as smokers preferted common decision (unanimity or majority) or specid regulations (different times and/or places), very seldom total permission or complete prohibition was proposed. 50-8045 of the nonsmoker and the smoker unanimously suggested total smoking prohibition in floors, elevatorsand bathrooms. In their immediate working place, during conferences and in the restroom nonsmokers preferred smoking prohibition, whereas smokers
Abstracts/Lung suggested common decision or special smoking rooms or smoking breaks. Not only the nonsmokers, but also the smokers themselves felt bothered by passive smoking. Both of them agreed in the necessitiy for regulanons against involuntary environmental tobacco smoke and they preferred spectal regulations instead of acomplete smoking permission. Those smoking regulations are mandatory, because of 500-1200 lung cancer diseases by passtve smoking per year in the Federal Republic of Germany where 36 % of the male and 28 R of the female employees are expostxl to env~ronmentai tobacco smoke at their working stte and should be protected agamst toxic and carcinogenic substances in the smoke. CARET, the beta-carotene and retinal eficacy trial to prevent lung cancer in high-risk populations Omen0 GS. Fred Hutchinson Cancer Retearch Ct., Seattle, WA 98195. Public He&h Rev 1991;199’2;19:205-8. Background: CARETisamuiti-centercoikborabon.withpartitipan~ recruited in Seattle. Portland, San Francisco, Irvine, Baltimoreand New Haven. Methods: CARET is a two-armed double-blind randomized chemoprevention trial to test the hypothesis that oral administration of kta-carotene 30 mg/day plus retinyl paimitate 25,000 [U/day will decrease the incidence of lung cancer in high-risk populations: heavy smokers and askstos-exposed workers who have smoked. The agents combine anti-oxidant and nuclear tumor suppressor mechamsma. Fastidious monitoring for possibleside effects is facilitated by inclusion of a Vanguard population (cootinued from pilot studies). Results: As of 3 1 July 199 I, 8 129 participants had been randomized into the Trial, of the 18,000 needed. Efficacy results are expected in 1998. Conclurion: The Tnal demonstrates the movemeot of environmental epidemiology mto intervennonist research to preveot adverse health effects. Risk of male lung cancer attributed to coal combustion indoors in sbangbai Tao X, Hong C-J, Yu S, Zhu H. School of Public Health, Shanghai Medical Uni&rsiry. Shanghai 20(1032. Public Health Rev 1991;1992; 19: 127-34. Lungcancerisoow theleadingcauaeofdeathamongaii malecancers in Shanghai. Besides the smoking habit, the indoor air pollution from coal comb&on may also make some coottibutioo. The purpose of our study is to explore the risk of long cancer death in male residents who live in coal-using families. Stratified by two extreme. levels of ambieo:nt sulphur dioxide (SO?) and inhaiable particulate (IP) concentrations, 4 areas were chosen in the city proper: Area A (low SO,, low IP); Area B (high SO*, low IP); Area C (low SO,. high IP) and Area D (high SOz, high IP). Withio each oftheseareas, two neighboring residential groups were chosen, one of which coal as fitel (group I), with the other using coal gas or iiquitied petroleum gas as fuel (group 0). The percentages of smokers and the ambient environmcot of the two chosen groups within each area are comparable. Total persoo-years observed is 117,039 from I January 1978 to 31 Decemkr 1987 for ail males in the 8 groups. The mortalities (per 100,000 person years) of male lung cancer in the 8 groups are as follows: AO-22.33. Al-37.64; BO-27.14, 81-30.72; CO41.77, Cl-54.99; D0-49.97. Dl-78.11. The result shows that male lung cancer mortalityin tbe coal-using group is higher than that in thecoai-gas-usinggroupwithin eacharea. Mantel-Haenszel’s Relative Risk (RRMH) of male lung cancer in coal-using groups is 1.44 stratified by ambient SO, and IP and smoking levels. Attributable Risk Percent (AR%) to coal-using is 30.40%. and Population Attributable Risk Percent (PAR%) IS 17.92%. Screening for lung cancer reexamined: A reinterpretation of the Mayo Lung f%ject randomized bial on hmg cancer screening Strauss GM, Gleason RE. Sugarbaker DJ. Division of Hematology-
Cancer 10 (1994) 395-430
Oncology, Brigham and Women’s Hospital, Bosron, MA 02115. Cheast 1993; IO3:Suppl.: 337s-41.S. In the 1970s. three randomized trials, each involvingapproximately 10,000 male subjects, were carried out to determine the value of luog cancer screening in cigarette smokers. These studies have been widely ioterpretedasprovidingstroogevideocethatscreeningdoesootcootnbute to decreased death rates, and, accordingly. the American Cancer Society tirmly recommends against lung cancer screening. No randomized trial, however, has evaluated screening for lung cancer in women, who currently comprise 39% of the lung cancer population. The trials perfotmed at Memorial-Sloan Kettering and at Johns Hopkins were designed so that subjects were randomized to either a single screen (annuaichestx-rayaiona)oraduaiscreen(a~uaicht?st x-rayandevery4-month sputum cytology) group. While the results of both revealed no difference in mortality bztweeo the groups. thti stud& were designed to examine the value of sputum cytology, and no conclusion regarding the efficacy of chest x-rays can be inferred. in the Mayo Lung Project, patients were randomized to a screened group in which a cheat x-ray and sputum cytology were obtained every 4 months or to a control group in which an annual chest x-ray and cytology were simply recommended. The results indicate that after 6 years, more lung cancers were detected among the 4,618 men in the screened group (206 cases, 4.46%) than in the 4,593 men in the control group (160 cases, 3.48%). Thz screened group showed a superiority over the control subjects m resectability rate (46 46vs 32 46)and S-year survival (33 46vs I.546). However, the number of cancer deaths was slightly greater in the screened (122) than in the control group (115). and, consequently. the mortality rates were not significantly different among the groups. An ‘overdiagnosis bias’ has been suggested to account for the increased number of lung cancers detected in the screened vs the control population in the Mayo Lung Project. This explanation is statistically plaus~bie. but, given the status of lung cancer as the most lethal of malignancies, is biologically unlikely. An alternative hypothesis is that chance alone might have accounted for the observed 0.98% difference in lung cancer detection rates. Were this the case, then 46 additional cases would have been de&ted in the control group had this chance event oo1 occurmd. If it wereasaumed that these 46 lung cancer cases had achieved the spme 15 96 5-year survival as was observed in the actual control subjects, there would have been 154, oot 115. lung cancer deatha among the control subjecxts, compared to 122deathsintheacreeoedpopulatioo. adiffereoce that would approach statistical significance (p=O.O52). Baaed oo favorable survival rate.s observed in the Memorial study and in the scre~~nedgroup in the Mayo Lung Project, as well as this hypothetical analysis of relative mortality in the Mayo study, we conclude there. is iosufficieotevidenceto lirmlyrecommeodagainatlungcancerscrmoing. Further investigation is needed, in both male and female cigarette smokers, to resolve this question.
Epidemiology and etiology Polymorphimns of the CYPI Al and glutathione S-tramferase genes associated with susceptibility to lung cancer in relation to cigarette dose in a Japwese population Nakacbi K, Imai K, Hayaahi S-I, Kawajiri K. Departmenr of Epidemiology, Saitama Cancer Ctr. Research Inst., 818 Komuro, Ina. Saitama 362. Cancer Res 1993:53:2994-g. An aaac&atioa.of lung cancer susceptibility with an MspI restriction site polymorphism of the CYPlAl gene was reported in our previous study. This polymorphism has been subsequently found to be. closely linked to another iaoleucine-valine (Ile-Val) polymorphism, which resulted in an Ile-Vai amino acid replacement in the heme-binding region of P4501Al. We report here that genetic risk for squamous cell carcinoma of the lung was associated with thesa two polymorphisms of