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induce lung cancers. In the context of this study, samples of pulmonary tissue from 34 deceased persons from the Bergen area (Norway) were analysed by atomic absorption spectrometry with regard to their content of chromium and nickel. The deceased comprised 21 men and 13 women. In 15 cases, death resulted from lung cancer; in the other 19 deceased, there was no indication of a malignant disease of the airways. The concenuations of nickel found in the lung tissue do not differ between patients with lung cancer and patients with healthy lungs. On the other hand, the concentration of chromium in the pulmonary tissue in the patients who had died of lung cancer and who had all been inhalative smokers, are higher (statistically signiticant) than in the nonsmokers or in those with healthy lungs. An accumulation of these two metals in the tumor matrix could not be detected. Both the average nickel and the average chromium concentrations were higher in the persons who had probably been exposed occupationally. Considering the present state of scientific knowledge, the aspects relevant to expert reports which result from the analyses of metals in the pulmonary tissue are discussed.

Pathobiilogy of lung tumors induced in hamsters by 4-(metbylni- trosamino)-1-(3-pyridyl)-1-butanone and the modulating effect of hyperoxia Schuller HM, Witschi H-P, Nylen E, Joshi PA, Cornea E, Becker IU. Eqwimenml Oncology Laboratory, Dep&menr of Parhobiology, Colle&!e of Veterinary Medicine, University of Tennessee. Knoxville, TN 37901- 1071. Cancer Res 199050: 1960-5.

Neuroendocrine lung cancer is among the most common types of lung cancers in smokers. We have recently shown that exposure of hamsters to N-nitrosodiethylamine and hyperoxia causes a high inci- denceof this tumor type. In this study, we show that the tobacco-specific

niuosamine 4-(methylrtibosamino)-I-(3-pyridyl)-l-bumtorte also causes nemoendocrine lung tumors in hyperoxic hamsters. Animals main- tained in ambient air while being treated with 4-(methylnitrosamino)- I-(3-pyridyl)-1-butanone developed pulmonary adenomas composed of Clara cells and alveolar type II cells. Pathogenesis experiments pmvideevidence for the tumors caused by 4-(methylniaosamino)-l-(3- pyridyl)-1-butanone in ambient air being derived from Clara cells. In the hypemxic hamsters, the neumendocrine carcinogettesis appears to involve two stages: (a) transformation of focal alveolar type II cells into nemoendocrine cells and (b) development of nemoendocrine lung tumors from such foci.

Mortality of a cohort of men in a silicosis register: Further evidence of an association with lung cancer Ng TP, Ghan SL, Lee J. Department of Communify, Occupational and FamilyMedicine,National UniversifyofSingapore, Lower KentRidge, Singupore0511. AmJIndMed 1990,17:163-71.

Lung cancer mortality from 1980 to 1986 was studied in a cohort of 1,419 men in a silicosis register who had no previous exposure to asbestos and polyaromatic hydrocarbons. The 28 deaths from lung cancerwerestatisticallyinexcessofexpected(SMR2.03;95%CI 1.35. 2.93). Excess risks of lung cancer were found in both underground workers (SMR 3.41; 95% CI 1.10-7.97; based on 5 deaths) and surface workers (SMR 1.87,95% CI 1.18-2.81; based on 23 deaths). All lung cancerdeathsweresmokers.TherewasanincreaseinSMRswithlonger latency periods and years of exposure, with the greatest risk found in those who had worked for 30 or more years after more than 30 years since fmt exposed (SMR 3.07, based on 16 deaths). The risk for lung cancer was higher in those with tuberculosis (SMR 2.52; 95% CI 1.52- 3.94) and showed an increasing trend with severity of silicosis, from category I to 3 and from category A to C, with highest risk in those with tuberculosis and category 3 (SMR 4.44 based on 3 deaths) or tubercu- losis and category C (SMR 7.63 based on 7 deaths). Most of the excess lung cancer risk in silicotics is due to smoking, but a synergistic effect between smoking and silic&ilicosis on the risk of lung cancer is aIs.0

likely. In particular, a possible role of silicosis and tuberculosis as the fibrotic seedbed for malignant gmwth in the lung is strongly supported.

Chronic ethanol intake and reduction of lung tumours from ure- thane in strain A mice Kristiansen E, Clemmensen S, Meyer 0. Institute of Toxicology, Na- tional Food Agency. 19, Morkhoj Bygade, DK-2860 Soborg. Food Chem Toxicol 199&28:35-S.

Combinations of ethanol and urethane were added to the drinking- water of female strain A/Ph mice for 12 wk, at the end of which the animalswerekilled.Urethaneconcenuationswere0,2OO,5OOand 1000 ppm and ethanol concentrations, 0, 5, 10 and 20% (v/v). All possible combinations of these urethane and ethanol concentrations were tested. Urethane induced primary lung adenomas in all treated mice in a dose- dependent manner. An average of 71 i 15 tumours/mouse were found, when the animals were killed, after treatment with 1000 ppm urethane for 12 wk. Ethanol alone did not alter the background incidence of tumours and produced only marginal hepatotoxicity. The tumour yields induced by urethane treatment were greatly reduced by simultaneous treatment with ethanol. The effect of ethanol was independent of urethane dose. When the concentrations of ethanol in the drinking- water were 20 arid 10% the incidences of lung adenomas induced by urethane were reduced by about two-thirds and one-half, respectively. The effect of 5% ethanol, if any, was not statistically significant.

Radiobiological aspects in a long-term epidemiological study of malignant lung neoplasm Sevc J, Placek V, Tomasek L, Kunz E, Horacek J. Cenfrum Hygieny Zareni, Insritut Hygieny a Epidemiologic, Praha. Rat Lek 1989;41:415- 22.

After 33 years of observation on the average in a prospective study in miners of uranium mines, with daily cumulated uptake of radon daughters of 220 WLM, the observed frequency of a malignant lung neoplasm exceeded the expected neoplasm rate almost five-fold. An additional annual risk of the neoplasm for 1 WLM (Working Level Months) in the whole cohort of smokers and non-smokers was 21 10 WLM-’ and the coefftcient of relative risk was 1.4% for 1 WLM. In the

lowest dose cohorts up to 99 WLM however, both coefficients of risk were now twice higher due to the increment of lung neoplasm a long latency period. The level of risk of the lung neoplasm was influenced by age at the time of irradiation, the mode of dose accumulation and there was also a different degree of simultaneous inhibition (sterilization) effect of irradiation and a decrease of carcinogenic effect with the time period after the irradiation. The first significant excess of the observed neoplasm rate in the lungs above the expected rate was in the 6th year after entering the risk, the maximal excess was in the 22nd year and from 33rd year the observed and expected rates were not different. The mean time period from the entry into the risk to the time of death was 20.3 f 7.0 years.

Multiple malignant cancer tumours in patients with occupational bronchial cancer Fatkova R. Zavodni Usfav Narodniho Zdravi Uranoveho Prumyslu. Pribrom. Prac Lek 1989;41:41 l-4.

In the years 1975-1987 the Clinical Oncology Ward of the Plant Institute of National Health in Uranium Industry at Pribram examined 1076 patients with occupational bronchogenic cancer. In 40 patients (3.7%) there were also other malignant turnours. Duplicate neoplasms were demonstrated in 35 patients, triplicate tumours in five patients. The mean age at the time of establishing the diagnosis of bmnchogenic cancer in patients with multiple malignant tumours was 59.6 f 7.8 years.Sevenpatientsunderwentoperationonbmnchogeniccancer,five of them having metachronic duplicate turnours, two patients with triplicate turnours. In December 31st 1988 three patients still survive.

Bronchogenic cancer in miners of Czechoslovak uranium mines Patina V, Vich Z, Smetana J. Zavodni Ustav Narodniho zdrovi Ura- noveho Prumyslu, Pribram. F’rac Lek 1989:41:387-9.

The authors analyzed a cohort of miners in uranium mines affected by lung cancer having been reported in the years 1962-1985 as ati