Abstracts /Lung Cancer 12 (1995) 265-329

for >I0 im Uml, and 0.85 for >20 im Oml. These seemed to be independent of fibrc type. It has been shown that brief inhalation exposures to chrysotile fibre produces highly concentrated fibrc deposits on bifurcations of alveolar ducts, and that many ofthcsc fibres arc phagocytostd by the underlying type II cpitbelial cells within a few hours. Churg has shown that both chrysotile and amphibole fibres retained in the lungs of former miners and millers do not clear much with the years since last exposure. Thus, lung h~mours may be caused by that small fraction of the inhaled tibres that are retained in the interstitium below small airway bifurcations where clearance processes arc ineffective. By contrast, for mesothelioma, the (low) hlmour yields sccmcd to be. highly dependent upon tibre type. Combining the data from various studies by tibre type, the percentage of mesotheliomas was 0.6% for Zimbabwe (Rhodesian) chrysotile, 2.5% for the various amphiboles as a group, and 4.7% for Quebec (Canadian) chrysotile. This difference, together with the fact-that Zimbabwe chrysotile has 2 to 3 orders of magnitude less trcmolitc than Quebec chrysotile, provides support for the hypothesis that the mesotheliomas that have occurred among chrysotile miners and millers could be largely due tothcir cxposurcs to trcmolitc fibrcs. The cbrysotile tibres may be insufficiently biopersistcnt because of dissolution during trandccation from their sites of deposition to sites where more durable tibres can influence the transformation or progression to mesothelioma.

Effect of superoxide dismutasc and dietbylditbiocnrbamate on the induction of squamous cell carcinoma of lung with methylchol- anthrene in rats Liu M, Yu L, Shu Q. HubeiMedical Universi&, Wuhon 430071. Chin J Oncal 1994;16:269-72.

The squamous cell carcinoma of lung was induced with methylcholanthrcne (MCA) in iodized oil in Wistar rats. During the development of the cancer, the animals were given superoxide dismutase (SOD) or its inhibitor dicthyldithiocarbamcte (DDC). In DDC group, 3 out of 50 rats developed cancer and 4 devclopcd atypical hyperplasia of bronchial epithelium within 35 to 40 days. In SOD group, no cancer developed in all of the 52 rats, and only one had atypical hypcrplesia in the lungs. Only one of 42 control rats had cancer and 2 rats had atypical hypcrplasia of bronchial epithelium. The difference in cancer frequency betwan groups DDC and SOD was significant (P < 0.05). The results suggest that there is a synergism behveen DDC and MAC in the induction of lung cancer, while SOD can inhibit MCA-induced lung cancer development. The mechanism of the effect of SOD and DDC was discussed.

Primary carrb~olds of tbe lung3 - Asbestos dust-induced maligoaocies in tbe sense of occupational disease no. 4104 BeKV? Kraus T , Kirchner T , Raithcl HJ, Lehncrt G. Institut und Poliklinikfir Arbei6 Serial- und Umwelbnedizin. Universitaf Erlangen-Numberg, Schillerstrasse 25 u. 29. 91054 Erlangen. Arbeitsmad Sozialmed Umweltmed 1994;29:490-2.

According to the current list of occupational diseases asbestoscaused lung c.mccr cm be .acknowledgcd under certain conditions as occupational disease No. 4104. Aclmcrchamcterization ofthe term ‘lung cancer’ under histological aspects was not canicd out. The question is, whether rare epithclial malignancies of the lung such as carcinoids could also be classified as an oecupstional disease according to No. 4 104. There is no epidemiological evidence that exogenous factors especially asbestos dust exposure play an etiological role in the pathogcncsis of carcinoids. From a histogenetic point of view carcinoids of the lung have to be scparatcd from the common lung cancers as entity on their own. According to current scientitic knowledge carcinoids cannot bc regarded as occupational disease NO. 4104

Asthma and lung caocer by diesel exhaust Sagai M, lchinox T . Nat. Inst. for EnvironmenralSfudies, Tsubba, Iberaki 305. Jpn J Toxic01 Envtmn Health 1994;40:399-413.

Recently, diesel engine powered cars has been increasing steadily in Japan, because diesel engine is powerful and the fuel is less expensive. Diesel exhausts emit some 2 to 20 times more nitrogen dioxide and some 30 to 100 times more particles than do gasoline engine cars. The exhausts are main cause of air pollutants in urban area, and people are anxious about that the exhausts may cause lung diseases such as asthma and lung cancers. There are clinical and epidemiological studies on relationship between asthma and diesel exhausts.

However, it is not yet confined with experimenal study. Here, I will introduce recent experimental data that essential features of asthma such as chronic inflammation with eosinophil-infiltration, mucus hypersecretion and airway hypencsponsivcness has b&n caused by diesel exhaust particles, and that the active oxygcns generated from diesel exhaust particles may play an important role to cause asthmatic symptoms. The other hand, it is well established that diesel exhausts can cause lung tumors experimentally using F-344 rats. In this CBSC, it is considered that carcinogens contained in benzene extract-fraction of the diesel exhaust particles are important. However, it has been found that diesel exhaust particles washed out suffncicntly with organic solvent can also cause lung hlmors. Therefore, the significance of carcinogens in diesel exhaust particles on the actual carcinogenesis is also introduced.

Lung cancer and cignrette smoking in women: A case-control study in Barcelona (Spain) Agudo A, Bamadas A, Pallares C, Martinez I, Fabregat X, Rosello J et al. IREC, c. Jordi Joan 5, 08301 Mafaro. Int J Cancer 1994;59:165-9.

A cast-control shrdy on lung cancer and the habit of cigarette smoking was carried out in Barcelona (Spain). Cases were 103 women newly diagnosed with primary lung cancer in IO hospitals from the study area. Histologic confirmation was given in 101 cases, of which 53 were adcnowcinoma, I9 squamous-cell carcinoma, 9 small-cell carcinoma and 20 other types. Two controls per case were selected, matched by age, residence and hospital. Compared with the never-smokers, the odds ratios (OR), with corresponding 95% confidence intervals (Cl), were I.61 (0.4 to 6.9) for ex-smokers and 3.61 (I.6 to 8.3) for current smokers. The risk of lung cancer showed a good dose- response relationship with duration of the habit, average number of cigarettes smoked daily and cumulative cigarette consumption. The risk of lung cancer increased by 62% for each 10 packyears. Depth of inhalation also showed a remarkable effect independently of the intensity of the habit. Although mortality and incidence rates of lung cancer among women in Spain are lower than in other developed countries, the risk of lung cancer is that which would be expected according to the pattern of the smoking habit in Spanish women.

Lungcaocer mortality io a Freocb cohort of hard-metal workers Lasfargues G, Wild P, Moulin JJ, Hammon B, Rosmorduc B, Du Noycr CR et al. Medecine B.. C.H.R. U. de Tours, HopilalBretonneou. 3 7044 Tours Cedex. Am J Ind Med 1994;26:585-95.

A cohort mortality study ~8s carried out among workers of a plant producing hard metals using cobalt as a binder. This study was aimed at assessing possible lung cancer risks in relation with cobalt exposure. Seven hundred nine male workers with at least I year of employment were included in the cohort and followed for mortality from 1956 to 1989. Job histories were provided by the administration of the plant, whereas smoking habits were collected from medical records and by interview. The causes of deaths were ascertained from hospital and general practitioner records. The observed numbers of deaths (ohs) were compared with the expected based on national rates with adjustment for age, sex. and calendar time (standardiied mortality ratio; SMR). The overall mortality did not differ from that expected (obs = 75, SMR = 1.05), whereas mortality due to lung cancer was in significant excess (obs = IO, SMR = 2.13). This excess was higher among workers employed in the areas with the highest exposure (obs = 6, SMR = 5.03). No trend was observed, however, with duration of employment or time since tint employment. Smoking data were available for 81% of the workers and 69% of the deceased and showed that smoking alone does not account for these lung eanccr excesses, yet. bccausc of the small numbers involved, no tim, conclusion should bc drawn from this study.

Dietary cholesterol, fat, and lung cancer incidence among older women: The Iowa Women’s Flealtb Study (United States) Wu Y. Zheng W, Sellers TA, Kushi LH, Bostick RM, Potter JD Division of Epidemiologv University ofMinnesofa. 1300 Soulh Second Street. Minneapolis, MN 55454-101s. Cancer causes Control 1994;5: 395400.

To test the hypothesis that a high intake of dietary cholesterol and fat is associated with elevated risks of lung cancer, we analyzed data from a population-based, prospective, cohort study conducted among 41,837 postmenopausal Iowa (United States) women who completed, in 1986, a comprehensive mailed questionnaire including information on usual intake of