Lung cancers associated with Thorotrast exposure: High incidence of small-cell carcinoma and...
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126 Abstracts/Lung Cancer IO (1993) 123-150 618). identified tbmugh the Missoori Camcar Registry for the period 19% thmogb 1991, incloded 432 lifetime ncmsmo~ and 186 ox- smokers who bad stopped at least 15 years before diagnosis or who h.4 smoked for less than 1 pack-year. Control subjects (II = 1402) wee selected from driver’s Ii- nod Medicarefiles. Rewlts. No im-ead risk of lung caocer was associated with childhood passive smoke exposwe. Adulthood aoalyses showsd ao iocreased lung cancer risk for lifetime noosmokers with exposure of more thao 40 pack-years from all housebold members (odds ratio [OR] = 1.3; 95% cootidence iotewal Icily= l.O,l.g)orfmmspousesonly(OR= 1.3;95%CI= 1.0, 1.7). When the time-weighted product of pack-years and average hours exposed per day was coosia, .30% excess risk wan shown at the highest qwtile of exposore amoog lifetime ooosmokcrs. Conclurions. Ours sod other recent studies supesst P small but coo&eat iocreased risk of long cancer from passive smokiog. C!ompr&eosive actions to limit smokiog in public places and worksites are well-advised. EtY~oCWholtItiff~ insmokingprevalenceonmod&oflung cancer suscqtibility Sellers T.A. Bailey-Wilson JE, Potter JD, Rich SS, Rothschild I-I, ELstonRC. DivitionofEp~ology,SdtwlofPublieHoalh, Univmiry of Minnesota. 1300 South Second Street, Minneapolis. MN X5454. &net Epidemiol 1992;9:261-71. Data 011337 long cancer families were eoalyzed to determioe PprnmteR from a segregationaoalysis. Previous results suggested that, after allowiog for PII individual’s pack-years of tobacco exposure, Meadelian codomimmt inheritawe of no allele that produced no earlier sgeofoasetprovidedagwdfittothe&tn.Inthepresentstudy,thedPts were split into two groups of familiw probe& age 60 and over (born before.WWI) and pmbsods yoooger than age 60. This patitioo of the data bv we of tbe orobaod was done to swarate families in which there likely to smoke - prediated*on the koown iocrease ‘of smoking prevalexe aRer World War I. For the younger proband families (those with ~areats more likely to smoke), only Mead&o codomioaet inheritawe adequately fit the data. The hypotheses of DO major type, enviro-tal transmission, and Memielinn domimmt or recessive iohwitaocewemrejected. Ineontrssttooorearlierfindings,tbeestima ofpopullltioosupfeptibilityiDcressedfrom28% iothetotal datato6OW in this subset. In the older pmksod families (those with parents Less likely to smoke), the no rmjor typeand eawimnmea tal hypotheses were reimted; tiutber. nooe of the Meodelisn models could be. distinguished. estimated. It huther suggests thatsusceptibilityto lung cancer occurs as P timction of susceptibility to the etTecta of tobacco smoking. ltesi<ildradon apoeureand luql cawer: Evidmce of an inverse asaociBtioo in wll&i@m state Neuberger JS, Frost FJ, GemId KB. Dept. of Pmwuiw Medicine. Univ. OfKmsw Medid Sdwol, R&bow BlHd. at 3%h. Konsav City. KS 66103. J Environ Health 1992;55:23-5. Relationship of the type of tobacco and inhalation pattern to pulmonary and total mortality Lange P, Nyboe J, Appleyard M, J- G, S&o&r P. Copenhagen Ciry Hemi Study, Rigshospimk, Dept. 7123. Tagemvj 20. DK-2200 Copmha~en N. Eur Reapir J 1992;S:lll l-7. Data from The Copmhweo City Heart Stodv, a orosoective bfiolwco and &lotion &I total mmtalitv. ?be st& from the genemt~poput.tion. -There were 2,9s8 plaio cisprette smokers, 3,222 filter cigarctts smokers, 1,578 smokers of chemotslcigers, 433 malepipe smokers nod 773 sobjects smoking more thao one type of tobacco. From 1976 until the end of 1989, 2,765 subjects died. Lug -was considered as meio death caose in 268. Chronic obstwtive pulmonarydisease (COPD) was considered as the nvincPuscia94cPsessndmfinorcontributoty~~ofderthin195 cases (COPD related mortality). Current smokers had. higher risk of total mortalitycompeted to lifstimnoosmokers: the relative riska(RR) ranged betwea 1.2 for male pipe smokers aod 2.4 for female plain cigarette smokers. With regud to lung ceocer mortality, the RR nmged betwee 4. I for male pipe smokers sod 7.9 for female plaio cigarette smokers. Eveo higher RR veloea wen estimated for COPD related mortality. In both sexes, the RR for the iovestigated end-points were lower in cheroot/cigar smokers nod in pipe smokers thao io cigawte smokers, but those differences were mukedly diminished after ao adjustmentfor the iohalatioo habit. The p-t shadysubstantiates the view thattobacco smokiog iocmwes polmooary sod total mortality. The small differetlces be4wea the vuioos type8 of tobacco are p&ably cawed by diffaeot inhalation pattems. Lung cancers associated with Tbomtrast exposure: High incidence of small~l carci- and implhtions for estimation of radon risk Ishikawa Y, Mori T, Kate Y, Tsochiya E, M&inami R, Sugaoo H, Kitagawa T. Harwe11 Laboratory. Biodical Research Departmem. AEA Environment and Enera. Honve-II OKll ORA. lnt J Caocer 1992;52:570-4. The widely accepted concept that the alpha-emitting mdionoclide mdoo (mRo, %o) induces bmg caocers io humans has been based on the excess of loon tomows obsewed io ondermmmd impotiaot qua&o of whether radon is the only urcinoge& factor because. such mioem are also heavily exposed to mine dusts in&diig silicates, d&e1 exkawt. etc. in their working envimnment. Patieots to whom Tbomtmst was administeredcontimmosly exhale radon (poRo) derived from wTh deposits in the body sod therefore provide a good model for lung carcinogenesis by radon witboot coocomitaot dust exposure. We therefore investigated 1uog-caoce.riocideace in our epidemiological follow-up series, analysieg the histological types of 11 lung caocers which were found among 359 Tborotmst autopsy cases nod maswing radioactivity in the breathof living Thorotrastpatients. The study revealed that, while. the proportion of small-cell lung caocers considered to be related to alpha-particles was sigoificaotly iocreased, tbe overall hmg ullcer incidence was not significantly higher tbao in cootmls, io spite of tbe high level of PoRnio the patients’ bmath. This result suggests that mdoo in the long does iodwe caocers @rticularly small-cell urcinomas) but that the induction rate is not as high as expected from risk factors associated with miniog. Thus, oxwas lung caocers amoog the mioers might be related to the combioed effects of exposure to radon sod mine dusts, sod not solely to radon. Es~teoflifcrimcexcLIIIungaaoerliskdlKtopanda~htua UpomlreiIlKolm C!hangSY.HaCW,L.eaBH. HeahhPhysicdqammu, KO~dfO#tiC Energy Reumch hut, PO Bar 7. L&&k Science Town. Taejon 305- 353. Rediat Pmt Dosim 1992;42:127-32. Lifetime excess Itug - risk doe to =%I deoghters exposure in Korea wan e&mated by modified mletive risk projection model mggmted in the BEIR IV report. Age-specific long cancer risk and lifetime baseline risk of lug - mortality under all causes of
Transcript of Lung cancers associated with Thorotrast exposure: High incidence of small-cell carcinoma and...
126 Abstracts/Lung Cancer IO (1993) 123-150
618). identified tbmugh the Missoori Camcar Registry for the period 19% thmogb 1991, incloded 432 lifetime ncmsmo~ and 186 ox- smokers who bad stopped at least 15 years before diagnosis or who h.4 smoked for less than 1 pack-year. Control subjects (II = 1402) wee selected from driver’s Ii- nod Medicare files. Rewlts. No im-ead risk of lung caocer was associated with childhood passive smoke exposwe. Adulthood aoalyses showsd ao iocreased lung cancer risk for lifetime noosmokers with exposure of more thao 40 pack-years from all housebold members (odds ratio [OR] = 1.3; 95% cootidence iotewal Icily= l.O,l.g)orfmmspousesonly(OR= 1.3;95%CI= 1.0, 1.7). When the time-weighted product of pack-years and average hours exposed per day was coosia, .30% excess risk wan shown at the highest qwtile of exposore amoog lifetime ooosmokcrs. Conclurions. Ours sod other recent studies supesst P small but coo&eat iocreased risk of long cancer from passive smokiog. C!ompr&eosive actions to limit smokiog in public places and worksites are well-advised.
EtY~oCWholtItiff~ insmokingprevalenceonmod&oflung cancer suscqtibility Sellers T.A. Bailey-Wilson JE, Potter JD, Rich SS, Rothschild I-I, ELstonRC. DivitionofEp~ology,SdtwlofPublieHoalh, Univmiry of Minnesota. 1300 South Second Street, Minneapolis. MN X5454. &net Epidemiol 1992;9:261-71.
Data 011337 long cancer families were eoalyzed to determioe
PprnmteR from a segregation aoalysis. Previous results suggested that, after allowiog for PII individual’s pack-years of tobacco exposure, Meadelian codomimmt inheritawe of no allele that produced no earlier sgeofoasetprovidedagwdfittothe&tn.Inthepresentstudy,thedPts were split into two groups of familiw probe& age 60 and over (born before. WWI) and pmbsods yoooger than age 60. This patitioo of the data bv we of tbe orobaod was done to swarate families in which there
likely to smoke - prediated*on the koown iocrease ‘of smoking prevalexe aRer World War I. For the younger proband families (those with ~areats more likely to smoke), only Mead&o codomioaet inheritawe adequately fit the data. The hypotheses of DO major type, enviro-tal transmission, and Memielinn domimmt or recessive iohwitaocewemrejected. Ineontrssttooorearlierfindings,tbeestima ofpopullltioosupfeptibilityiDcressedfrom28% iothetotal datato6OW in this subset. In the older pmksod families (those with parents Less likely to smoke), the no rmjor typeand eawimnmea tal hypotheses were reimted; tiutber. nooe of the Meodelisn models could be. distinguished.
estimated. It huther suggests that susceptibility to lung cancer occurs as P timction of susceptibility to the etTecta of tobacco smoking.
ltesi<ildradon apoeureand luql cawer: Evidmce of an inverse asaociBtioo in wll&i@m state Neuberger JS, Frost FJ, GemId KB. Dept. of Pmwuiw Medicine. Univ. OfKmsw Medid Sdwol, R&bow BlHd. at 3%h. Konsav City. KS 66103. J Environ Health 1992;55:23-5.
Relationship of the type of tobacco and inhalation pattern to pulmonary and total mortality Lange P, Nyboe J, Appleyard M, J- G, S&o&r P. Copenhagen Ciry Hemi Study, Rigshospimk, Dept. 7123. Tagemvj 20. DK-2200 Copmha~en N. Eur Reapir J 1992;S:lll l-7.
Data from The Copmhweo City Heart Stodv, a orosoective
bfiolwco and &lotion &I total mmtalitv. ?be st&
from the genemt~poput.tion. -There were 2,9s8 plaio cisprette smokers, 3,222 filter cigarctts smokers, 1,578 smokers of chemotslcigers, 433 male pipe smokers nod 773 sobjects smoking more thao one type of tobacco. From 1976 until the end of 1989, 2,765 subjects died. Lug -was considered as meio death caose in 268. Chronic obstwtive pulmonary disease (COPD) was considered as the nvincPuscia94cPsessndmfinorcontributoty~~ofderthin195 cases (COPD related mortality). Current smokers had. higher risk of total mortality competed to lifstimnoosmokers: the relative riska (RR) ranged betwea 1.2 for male pipe smokers aod 2.4 for female plain cigarette smokers. With regud to lung ceocer mortality, the RR nmged betwee 4. I for male pipe smokers sod 7.9 for female plaio cigarette smokers. Eveo higher RR veloea wen estimated for COPD related mortality. In both sexes, the RR for the iovestigated end-points were lower in cheroot/cigar smokers nod in pipe smokers thao io cigawte smokers, but those differences were mukedly diminished after ao adjustment for the iohalatioo habit. The p-t shady substantiates the view that tobacco smokiog iocmwes polmooary sod total mortality. The small differetlces be4wea the vuioos type8 of tobacco are p&ably cawed by diffaeot inhalation pattems.
Lung cancers associated with Tbomtrast exposure: High incidence of small~l carci- and implhtions for estimation of radon risk Ishikawa Y, Mori T, Kate Y, Tsochiya E, M&inami R, Sugaoo H, Kitagawa T. Harwe11 Laboratory. Biodical Research Departmem. AEA Environment and Enera. Honve-II OKll ORA. lnt J Caocer 1992;52:570-4.
The widely accepted concept that the alpha-emitting mdionoclide mdoo (mRo, %o) induces bmg caocers io humans has been based on the excess of loon tomows obsewed io ondermmmd
impotiaot qua&o of whether radon is the only urcinoge& factor because. such mioem are also heavily exposed to mine dusts in&diig silicates, d&e1 exkawt. etc. in their working envimnment. Patieots to whom Tbomtmst was administered contimmosly exhale radon (poRo) derived from wTh deposits in the body sod therefore provide a good model for lung carcinogenesis by radon witboot coocomitaot dust exposure. We therefore investigated 1uog-caoce.r iocideace in our epidemiological follow-up series, analysieg the histological types of 11 lung caocers which were found among 359 Tborotmst autopsy cases nod maswing radioactivity in the breath of living Thorotrast patients. The study revealed that, while. the proportion of small-cell lung caocers considered to be related to alpha-particles was sigoificaotly iocreased, tbe overall hmg ullcer incidence was not significantly higher tbao in cootmls, io spite of tbe high level of PoRn io the patients’ bmath. This result suggests that mdoo in the long does iodwe caocers @rticularly small-cell urcinomas) but that the induction rate is not as high as expected from risk factors associated with miniog. Thus, oxwas lung caocers amoog the mioers might be related to the combioed effects of exposure to radon sod mine dusts, sod not solely to radon.
Es~teoflifcrimcexcLIIIungaaoerliskdlKtopanda~htua UpomlreiIlKolm C!hangSY.HaCW,L.eaBH. HeahhPhysicdqammu, KO~dfO#tiC Energy Reumch hut, PO Bar 7. L&&k Science Town. Taejon 305- 353. Rediat Pmt Dosim 1992;42:127-32.
Lifetime excess Itug - risk doe to =%I deoghters exposure in Korea wan e&mated by modified mletive risk projection model mggmted in the BEIR IV report. Age-specific long cancer risk and lifetime baseline risk of lug - mortality under all causes of
