Leanness and lung-cancer risk
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121 Leanness and lung-cancer risk Knekt P, Heliovaan M, Rissanen A, Aromaa A, Seppanen R, Teppo L et al. Research Institure for Socral Security, P.O. Box 78. SF-00381 Helsnki. Int J Cancer 1991;49:208-13. Body mass index (weightieight2) was studied for its prediction of lung cancer in Finnish men examined by the Social Insurance Instiu~- tion’s Mobile Clinic and followed up by the Finnish Cancer Registry. Among 25,994 participants aged 20 to 75 years and free from cancer at Ihe start of rhe study, 504 lung-cancer were diagnosed during a maxi- mum follow-up of I9 years. There was a significant inverse gradient between body mass index and the incidence of lung cancer. Thts association was not due to confoundmg by age, smoking, social class, self-percened general health, hlstory of suess symptoms, chronic cough or chest X-ray lindings, although these factors correlated with body mass index and were also significantly predictive of lung cancer. After adjustmem for these factors, the relative risks of lung cancer were I .O, 1.4, 1.5 and 1.8 (p for trend < 0.001) from the blghesl to the lowest quartiles of body mass index. The association was noted among current smokers, but it was most obvrous among men who had never smoked, the relawe nsk of lung cancer between the lowest and highest quartiles of body mass index being 7.6 (95% confidence mterval = 2.0 to 29.4). The inverse gradient persisted throughout tie entire follow-up period, and was most dlstmcr after the first 10 years of follow-up, the relawe risks for the quartiles of body mass index bcmg 1.O, I .9,2.3 and 2.6 (p < 0.001). The present study shows that the thinner the man, the more liable he IS to develop lung cancer. Leanness, or some factor or cluster of factors closely correlated LO iI, may play an aetiological role in lung cancer. Long cancer in lifelong non-smokers Capewell S, Sankaran R, Lamb D, McIntyre M, Sudlow MF. Depan- men! of MedGze, Royal Infirmary. Edmburgh. EH3 9YW. Thorax 1991;46:565-8. The Edinburgh Lung Cancer Group registered 3070 new patients with lung cancer in the five years 1981-5 from a calchment population of 95oooO. After review only 74 (2%) were classified as lifelong non- smokers. They differed significantly from the 2996 smokers with lung cancer in that far more were female (77% v 26%) and their mean age was higher (75.4 v 68.0 years). More were m the worst Kamofsky performance categories and fewer patients underwem surgery. The stages of disease were simdarly distributed in the two groups and the five year survival was equally poor (5%). Hwological cell type was determmed m 59 of the 74 paL,enls. All histological cell types were present. More non-smokers had adcnocarcinoma than smokers (42% v 13~~)andfewerhadsquamouscellcarcinoma(32%v49%)orsmallcell carcinoma (15% v 24%). Lung cancer in lifelong non-smokers is uncommon and the diagnosis should therefore always be questioned. Squamous cell carcinoma of the lung in a nonsmoking, nonirradi- ated patient with juvenile laryngotracheal papillomatosis: Evi- dence of human papillomavirus-11 DNA in both carcinoma and papillomas Guillou L, Sahli R, Chaubert P. Monnier P, Cuttat J-F, Costa J. lnstilur Universiraire de Pathoiogie, 25, rue du Bugnon, 1011 Lausanne. Am J Surg Pathol 1991;15:891-8. Malignant transformation of laryngeal juvenile papillomatosis most often occurs m patients wth previous radiation therapy or smokmg hw_ories. We report the case of a 35.year-old, nonsmoking, nonirradi- atedmanwhodevelopedsquamouscellcarcinomaof thelungwitha33- year history of laryngotracheal juvenile papillomatosis. Postmortem examination showed pulmonary cavitating papdlomatosis and chest wall, vertebrae, and peribronchial lymph node involvement by tumor. Molecular studies (Southern blot, polymerase chain reaction) showed extrachromosomal human papillomavirus- I1 (HPV 11) DNA in both carcinoma and two laryngotmcheal squamous cell papillomas, includ- mgoneexcised20yeanpreviously. Ourobservation isanalogoustothe previously reported cases of spontaneous (not related to irradiation or smoking) malignant transformation of juvenile laryngolracheal papil- lomatosis. Although HPVl I viral infection likely played a role in the malignant transformation, other less likely factors, such as drugs given for Ueatment and radiography performed throughout the illness, should be considered. Repeated pulmonary infecdons and rhe host immune response are additional consideradons. Fluorescence detection of benzo[a]pyrene-DNA adducts in human long Weston A. Bowman ED. Laboratory of Human Carcinogenesis, %a- tional Cancer Institute, Notional lnsrirutes of Health, Berhesda, MD 20892. Carcinogenesis 1991;12:1445-9. Improved techniques are described for the specific identification of benzo[alpyrene,-diolepoxide (BPDE)-DNA adducts in human tissues. Immunoaffinity chromarography, synchronous fluorescence spectros- copy and second-derivative synchronous fluorescence spectroscopy have previously been used 10 detect BPDE-DNA adducts in human placenta. Here we report how these methods, together with HPLC and the generation of complete fluorescence excitation-emission matrices, have been used to idenufy unequivocally BPDE-DNA adducts in samples of human lung. BPDE nucleolide adducts were isolated with immunoaffinily chromatography columns bearing antibodies raised against the (f)antl-7,8-dial-9,10-epoxlde-deoxyguanosine adduct of benzola] pyreoe. These adducts were hydrolyzed to teuahydrotetrols and Ihe hydrolysis products SubJected to HPLC. The major product Isolated by HPLC. benzo(a] pyrene-7,10/8$texrahydroleuol, was de- tenomed by fluorescence spectroscopy. using rhis method, levels of BPDE-DNA adducts in the range of 1 40 in 108 nucleoGdes were measured in 6 out of 25 samples, with a lower detection limit of one adduct in IO’nucleottdes. The data may also indicate thatadducl levels show regional variation in different parts of the same lung. Carcinoma of the long in Ontario gold miners: Possible aetiological factors Kusiak RA, Springer J. Ritchie AC, Muller J. He&h and Safery Sfudies Unit, Onrario MinistryofLabour,400UniversityAvenue. Toronlo, Ont. M7A 177. Br J Ind Med 1991:48:808-17. A cohon of 54128 men who worked in Ontario mines was observed for monalily between 1955 and 1986. Most of these men worked tn nickel, gold, or uranium mines; a few worked in silver, iron, lead/zinc, or other ore mines. If mortality that occurred after a man had started to mine uranium was excluded, an excess of carcinoma of the lung was foundamong the 13603 Ontariogold miners in the study (standard&d monalityratio(SMR) 129,95%confidenceinlerval(95%CI) 115-145) and in men who began to mine nickel before 1936 (SMR 141,95% Cl 105-184). Theexcessmortality from lungcancerm thegold mmerswas confined to men who began gold minmg before 1946. No increase in the mortality from carcmoma of the lung was evident in men who began mininggoldafterrheendof 1945, in men who beganmining nickelafter 1936, or in men who mined ores other than gold, nickel, and uranium. In the gold mines each year of employment before the end of 1945 was associated with a 6.5% increase in mortality from lung cancer 20 or more years after the miner began working the mines (95% CI 1.6. 11.4%); each year of employment before the end of 1945 in mines m which the host rock contained 0. I % arsenic was associated with a 3.1% increase in lung cancer 20 years or more after exposure began (95% CT I. I-5. I %); and each working level month of exposure to radon decay products was associated with a 1.2% increase in mortality from lung cancer five or more years after exposure began (95% CI 0.02.2.4%). A comparison of two models shows that the excess of lung cancer mortahtyinOntanogoldminersisasscciated withexpcwreto highdust concentrations before 1946, with exposure to arsenic before 1946, and with exposure to radon decay products. No association between the increased incidence of carcmoma of the lung in Ontariogold miners and exposure to mineral fibre could be detected. It is concluded that the excess of carcinoma of the lung m Ontario gold miners is probably due to exposure to arsenic and radon decay products.
Transcript of Leanness and lung-cancer risk
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Leanness and lung-cancer risk Knekt P, Heliovaan M, Rissanen A, Aromaa A, Seppanen R, Teppo L et al. Research Institure for Socral Security, P.O. Box 78. SF-00381 Helsnki. Int J Cancer 1991;49:208-13.
Body mass index (weightieight2) was studied for its prediction of lung cancer in Finnish men examined by the Social Insurance Instiu~- tion’s Mobile Clinic and followed up by the Finnish Cancer Registry. Among 25,994 participants aged 20 to 75 years and free from cancer at Ihe start of rhe study, 504 lung-cancer were diagnosed during a maxi- mum follow-up of I9 years. There was a significant inverse gradient between body mass index and the incidence of lung cancer. Thts association was not due to confoundmg by age, smoking, social class, self-percened general health, hlstory of suess symptoms, chronic cough or chest X-ray lindings, although these factors correlated with body mass index and were also significantly predictive of lung cancer. After adjustmem for these factors, the relative risks of lung cancer were I .O, 1.4, 1.5 and 1.8 (p for trend < 0.001) from the blghesl to the lowest quartiles of body mass index. The association was noted among current smokers, but it was most obvrous among men who had never smoked, the relawe nsk of lung cancer between the lowest and highest quartiles of body mass index being 7.6 (95% confidence mterval = 2.0 to 29.4). The inverse gradient persisted throughout tie entire follow-up period, and was most dlstmcr after the first 10 years of follow-up, the relawe risks for the quartiles of body mass index bcmg 1 .O, I .9,2.3 and 2.6 (p < 0.001). The present study shows that the thinner the man, the more liable he IS to develop lung cancer. Leanness, or some factor or cluster of factors closely correlated LO iI, may play an aetiological role in lung cancer.
Long cancer in lifelong non-smokers Capewell S, Sankaran R, Lamb D, McIntyre M, Sudlow MF. Depan- men! of MedGze, Royal Infirmary. Edmburgh. EH3 9YW. Thorax 1991;46:565-8.
The Edinburgh Lung Cancer Group registered 3070 new patients with lung cancer in the five years 1981-5 from a calchment population of 95oooO. After review only 74 (2%) were classified as lifelong non- smokers. They differed significantly from the 2996 smokers with lung cancer in that far more were female (77% v 26%) and their mean age was higher (75.4 v 68.0 years). More were m the worst Kamofsky performance categories and fewer patients underwem surgery. The stages of disease were simdarly distributed in the two groups and the five year survival was equally poor (5%). Hwological cell type was determmed m 59 of the 74 paL,enls. All histological cell types were present. More non-smokers had adcnocarcinoma than smokers (42% v 13~~)andfewerhadsquamouscellcarcinoma(32%v49%)orsmallcell carcinoma (15% v 24%). Lung cancer in lifelong non-smokers is uncommon and the diagnosis should therefore always be questioned.
Squamous cell carcinoma of the lung in a nonsmoking, nonirradi- ated patient with juvenile laryngotracheal papillomatosis: Evi- dence of human papillomavirus-11 DNA in both carcinoma and papillomas Guillou L, Sahli R, Chaubert P. Monnier P, Cuttat J-F, Costa J. lnstilur Universiraire de Pathoiogie, 25, rue du Bugnon, 1011 Lausanne. Am J Surg Pathol 1991;15:891-8.
Malignant transformation of laryngeal juvenile papillomatosis most often occurs m patients wth previous radiation therapy or smokmg hw_ories. We report the case of a 35.year-old, nonsmoking, nonirradi- atedmanwhodevelopedsquamouscellcarcinomaof thelungwitha33- year history of laryngotracheal juvenile papillomatosis. Postmortem examination showed pulmonary cavitating papdlomatosis and chest wall, vertebrae, and peribronchial lymph node involvement by tumor. Molecular studies (Southern blot, polymerase chain reaction) showed extrachromosomal human papillomavirus- I1 (HPV 11) DNA in both carcinoma and two laryngotmcheal squamous cell papillomas, includ- mgoneexcised20yeanpreviously. Ourobservation isanalogoustothe previously reported cases of spontaneous (not related to irradiation or
smoking) malignant transformation of juvenile laryngolracheal papil- lomatosis. Although HPVl I viral infection likely played a role in the malignant transformation, other less likely factors, such as drugs given for Ueatment and radiography performed throughout the illness, should be considered. Repeated pulmonary infecdons and rhe host immune response are additional consideradons.
Fluorescence detection of benzo[a]pyrene-DNA adducts in human long Weston A. Bowman ED. Laboratory of Human Carcinogenesis, %a- tional Cancer Institute, Notional lnsrirutes of Health, Berhesda, MD 20892. Carcinogenesis 1991;12:1445-9.
Improved techniques are described for the specific identification of benzo[alpyrene,-diolepoxide (BPDE)-DNA adducts in human tissues. Immunoaffinity chromarography, synchronous fluorescence spectros- copy and second-derivative synchronous fluorescence spectroscopy have previously been used 10 detect BPDE-DNA adducts in human placenta. Here we report how these methods, together with HPLC and the generation of complete fluorescence excitation-emission matrices, have been used to idenufy unequivocally BPDE-DNA adducts in samples of human lung. BPDE nucleolide adducts were isolated with immunoaffinily chromatography columns bearing antibodies raised against the (f)antl-7,8-dial-9,10-epoxlde-deoxyguanosine adduct of benzola] pyreoe. These adducts were hydrolyzed to teuahydrotetrols and Ihe hydrolysis products SubJected to HPLC. The major product Isolated by HPLC. benzo(a] pyrene-7,10/8$texrahydroleuol, was de- tenomed by fluorescence spectroscopy. using rhis method, levels of BPDE-DNA adducts in the range of 1 40 in 108 nucleoGdes were measured in 6 out of 25 samples, with a lower detection limit of one adduct in IO’ nucleottdes. The data may also indicate thatadducl levels show regional variation in different parts of the same lung.
Carcinoma of the long in Ontario gold miners: Possible aetiological factors Kusiak RA, Springer J. Ritchie AC, Muller J. He&h and Safery Sfudies Unit, Onrario MinistryofLabour,400UniversityAvenue. Toronlo, Ont. M7A 177. Br J Ind Med 1991:48:808-17.
A cohon of 54128 men who worked in Ontario mines was observed for monalily between 1955 and 1986. Most of these men worked tn nickel, gold, or uranium mines; a few worked in silver, iron, lead/zinc, or other ore mines. If mortality that occurred after a man had started to mine uranium was excluded, an excess of carcinoma of the lung was foundamong the 13603 Ontariogold miners in the study (standard&d monalityratio(SMR) 129,95%confidenceinlerval(95%CI) 115-145) and in men who began to mine nickel before 1936 (SMR 141,95% Cl 105-184). Theexcessmortality from lungcancerm thegold mmerswas confined to men who began gold minmg before 1946. No increase in the mortality from carcmoma of the lung was evident in men who began mininggoldafterrheendof 1945, in men who beganmining nickelafter 1936, or in men who mined ores other than gold, nickel, and uranium. In the gold mines each year of employment before the end of 1945 was associated with a 6.5% increase in mortality from lung cancer 20 or more years after the miner began working the mines (95% CI 1.6. 11.4%); each year of employment before the end of 1945 in mines m which the host rock contained 0. I % arsenic was associated with a 3.1% increase in lung cancer 20 years or more after exposure began (95% CT I. I-5. I %); and each working level month of exposure to radon decay products was associated with a 1.2% increase in mortality from lung cancer five or more years after exposure began (95% CI 0.02.2.4%). A comparison of two models shows that the excess of lung cancer mortahtyinOntanogoldminersisasscciated withexpcwreto highdust concentrations before 1946, with exposure to arsenic before 1946, and with exposure to radon decay products. No association between the increased incidence of carcmoma of the lung in Ontariogold miners and exposure to mineral fibre could be detected. It is concluded that the excess of carcinoma of the lung m Ontario gold miners is probably due to exposure to arsenic and radon decay products.
