Abstracts/Lung Cancer IO (1993) 123-150 125

Epidemiology, Dow Chemical Company. IBO3 Building, Midland, MI 48674. Am 1 Ind Med 1992;22:69-83.

Cohort mortality and nested casa-control shtdies were conducted involving 2,901 mm employed 1 year or more bdween 1940 and 1986 at any of four California facilities of P major chemical company. Employeesexperienced fewerdeaths fi-omeachofthemajorcausesthnn were expected ba.xd on U.S., Gxlifomia, and local county mortality rate.Respintorycpncerw~signifiuntlyelevstedinonesocioecooomic category comprised of operators (SMR = 157, 95% CI = 109-220). The 34 cases who died from respiratory cancer nod 136 matched controls. all of whom were operators, were included in a nested case- control study. Departments in which subject&ad woked were. grouped into 13 worL~gnmentorproductcptegoriesbynn industrial hygienist without knowledge of case-control status. Smoking habits and other occupational exposurea were asc&ained by telephone interview from subjectsorsurmg~te-re+ondesponders. Asexpected, cunmtcigarettesm&inoking w~stmnglyrelatcdtorespintory-~. ARe.radjustmmtforsmoking, cases were. significantly more likely than controls to have ever worked in one of the 13 work areas (supervision, services, and business support). However, no dose- response relationship was evident with duration of employment in this work prep and the aeputmeats involved were associated with plant security and not chemical production. Results weresimilrutienn IS-yearlateacyperiodwsassumsd. These findings suggest that the excess of rwpiratory cancer mortality among operators was most likely due to differences in cigarette smoking or other factors not ascertained, rather than to * specific occupational exposure.

Dietary intake and risk of lung - in women who never smoked Candelon EC, Stockwell HG, Armstrong AW, F’inkha PA. Depr. of Epi&miology/Biostatktics. College of Public Health, Uniwmiry of South Florida, Tampa, FL 33612~3&75. Nutr Cancer 1992; 17963-70.

A casee-colltrol shuly ~98 conducted to examine the influarce of dietary factors on the risk of developing lung cancer among women who have never smoked cigarettes. This study included 124 cases of histologically confirmed urcinoIM of the lung and 263 community- basal controls. Dietary data werscollected utilizing the reduced version of the National Cancer Institute (Block) food frequency questionnaire. The results of this analysis. adjusted for age, education, and total caloriea. indicated a stmnn motective effect associated with total

q&tile of vege&le consumption experienced the greatest risk with an odds ratio (OR) of 0.2, [confidence inte& (CI) 0.1~3.51. The effect of alI vegeteblea wmbii was gmater than that of green end yellowvsgstnblssllane(bighestquMileOR0.4, ClO.2-0.7). Similarly, the protective effect of total carotene (highest quartile OR 0.3, CI 0. I- 0.6)wssomwhatgmaterthanthatofBamteneaIone@ighestqutile ORO.4,CIO.2-0.8). Retiwlintakcwasnotassociatedwithadecmased risk of lung cancer in our populatiw. llwe was an inverse association bshueeDlung-risk~dviEpminCiahle,vrhichwnsnotsignificnnt, although a statistiully significant trend was noted.

ormpstionrl exposure to c&tdliae silica and lung cawer Pairon JC, Jawand MC, Bignon I, Bmchwd P. ConsvUotion & Patbologk Profuss., Service de Pneumokgie. C. H. I., 40, Awue & l&dun, 94010 Creteil Ceder. Arch Md Pmf Med Tnv Sear Sot 1992;53: 257-74.

Cristallii silica is an ubiquitous miner& pmmt either es e nahuel contaminant (ores...) or as an industrial material (abrasives...). Its fibrogenic propsrcies have beea msponsible for a large pmpo&m of occupational respiratory di-. Some recat data have raised the hypothesis of a carcinogenic effect. These data have bkn recently reviewed by the International Agency for Reamrcb on Cancer: the expsrCspmpossdtocl~ifysiliuinthegroupU~Mycrrcinogaic to human). Howeva accordiig to some controvnsial discwnia~~ and new~ts,sfurtber~nisll~ussful.‘Ihcresultsofinvitro studies have sugssstsd some weak gmotoxic effect while result8 of in vivostudiesconfirmsda~~ce~t.Theovonll~daniologicrl dataMmorecontilsing.Ia&ed,tbeonin~ iah-shdie.

problem of associated confounding parameters (tobacco, other minerals, metals, organic compounds, etc.). Finally, it appears that non-asbestos pneumoconiosis (rather than pure silicosis) is associated with * lung cancerexcess.‘Ibeprecise~~smsofthisexeess~iIlnquire~~er studies. Prescat data suggest that the control of the tibrogeaic risk will be efficient to control P potential carcinogenic risk. The data also underline that efforts must be pursued in order to control tobacco consumption.

Lung tumor incidence after intrabronchial arbninistration of the nonionic contrast agent met&amide Baker DG, Alford BA, Feldman PS. DeputmmrofRadiology, Virginia Univ. Health Science Ctr., Box 383, Chorlottesvilk, VA 22908. Invest Radio1 1992;27:525-8.

Ration&and Objediw. Metrimmide hasbeen used for examination ofthegastrointestinaltrPctMdtrscheobmnchialtreeofinfPmls. Contrast agents may enter the lungs during such examinations. The current shuly wasuadertPkentodeterrninewhethertherewould~~y l~terpulmowy effects when metrizamide was administered to the lungs of weanling mice. Merh&. One hundred fifty mice (18-21 days old). divided into groups, received either 75 L of metrizamide, using the manufacturer’s diluent (190 mg iodiie [I]/mL), or saline solution administered to tbe lungs by Injection into the trachea. The mice were observed for the duration of their lives. Moribund animals were killed. At death, all animals underwent necropsy. The lungs were fixed in formahn, and histologic sections were examined for pathologic changes. Resulrs. The incidence of lung hlmors was increased (P < .05) in the lungs of mice receiving metrilamide compared with those receiving saline. Eighteen percent of the lung tumors in tbe metrizunide-treated mice were lymphomas. a histologic type not found in the saline-treated controls. Conclurionr. A hypothesis proposing that metriamide may be an rnitiator of carcinogenic transformation rather than e carcinogen was developed.

Martin G, Steyn K, Yach D. Ewential Health Rutwch Group, South ~a~Mal.Rwca~Cowteil,Pam~ki. SAfrMedJ 1992:82:241- 5.

The opinions of P representative sample of adult South Africans about the et&&s of smoking on health and their attitudes tmwld tob&%a control measues were surveyed by - of an interviewer-administeaecl questionnaire. Sweaty-five per cat of the nspotwJezds were bleck and 55,3 % were femele. More than 50% of blacks and Asians (61.7% end 53,296) were non-smokers, whereas 52.1% of ‘colacrrds’ were c-t smokers and 23.8% of whites en- smokers. The majority of smokers (68.5 I) acknowledged the hermfel effectsofdirrctsmokinOIldelugsr~~geofnw-Mdeexamdters (79,796 end 77% respectively) shared this view. A similar trend was observed in beliefs about passive smoking. Seventy-five per cent of participants felt that tobacco sales to minors should be benned end 55.8% thou&t that texes on tobacco ~rcxhuzts should be imxased.

cmnpmies tium spcmsariog spotting evmts. Most rtiespkdfa~ts felt thst tobacco advertising should be banned ora television (59.7%). radio (60,1%). inaew~pers(58,4%),onbillboprds(58,7%)~d~cineme~ (59,316). The nrsults indicate that in the main the public supports the inhuductior~ of the -ma ptqwxed in the dnR Tobacco Products Control Act and evea moan extensive legislation to control tobecco amsunption. This augurs well for future strategies aimed at tobacco coahul in South Africa.

~re~andl~cancwinmmnw&ngwanen Bmwn.wn RC, Alavmja MCR. Hack ET, Lay TS. DCDPHP. Missouri Depaimeni of Health. 201 Bvsinrss Loqp m Wur. Columbia. MO 6.5203. Am J Public Halth 1992; 82: 1525-30.

Objeuiw. ‘fhec.euseoflttng wtweremongnotwmokereare not CISUIY undastood. To fwtherevahute ths relation bshvsso pssive

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&ltildradon 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