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presence of air pollution accounted for less than 5% of the total variation in intraurban lung cancer mortality. In addition, the interpretation of geographic analysis must be guarded due to the introduction of potential biasdue toaggregation. The hypotbesisthatairpolhttion iscontributory to lung cancer cannot be tested until other, stronger individual risk factors for lung cancer can be better measured and controlled in studies of this association.

Geographic pattern of lung cancer in Japan and its environmental correlations. Minowa M, Stone BJ, Blot WJ. Department of Epidemiology, Institute of Public Health, Minato-kv. Tokyo 108. Jpn J Cancer Res, Gann 1988;79:1017-23.

Standardized lung cancer mortality ratios, 1969-1978, for basic administrative units of Japan were related to various environmental characteristics by multiple regression analysis. Elevated lung cancer mortality was demonstrated in the areas along the seacoast, particuhuly those with fishing ports, low socioeconomic status, and high level of air pollution. High mortality was also observed in coal mining areas and areas with shipyards. Data on tobacco expenditures provided partial adjustment for the effects of cigarette smoking on these correlations.

A comparative epidemiologic study on geographic distributions of cancers of the lung and the large intestine in Japan. Murata M, Takayama K, Fukuma S et al. Division of Epidemiology, Chiba Cance.r Center, Chiba 280. Jpn J Cancer Res, Gann 1988;79: 1005-16.

To examine what kinds of factors could have caused the geographic variation observed in lung cancer morbidity in Japan, a correlation study was performed comparing various regional traits. The same study was also conducted on huge intestinal cancer, aiming to distinguish the possible urban factors associated with both cancers. Lung cancer was highly correlated with industrialization-related factors such as localiza- tion of manufacturing industries, automobile traffic and air pollution, whereas colon cancer was correlated with the population density of workers in the tertiary industries such as services, tradeandgovemment. A multiple regression analysis could not detect any single factor with an exceptionally strong influence on either cancer. The present findings suggest that the hazardous environmental condition of urban areas has, to some extent, contributed to the recent increase of lung cancer cases in this country.

Lung cancer risks of underground miners: Cohort and case-control studies. Archer VE. Rocky Mountain Center for Occupational and Environ- mentalHealth.DepartmentofFamilyandPreventiveMedicine.Univer- sity of Utah, School of Medicine, Salt Luke City, UT. Yale J Biol Med 1988;61:183-93.

All underground mines have higher radon levels than are found in surface air. Ventilation is the primary method of controlling radon levels. Fourteen cohort and seven case-control studies done on under- ground miners are reviewed; they include many types of ore. Only five of the studies deal with more than 100 lung cancer deaths. Variations in the attributable risk are given. Some generalizations can be drawn from thesestudies: thelongerthcfollow-up, thegrcaterisdteattributablerisk, even though the relative risk is reasonably constant. The induction- latent period is quite variable but is shortened by high exposure rates, by cigarette smoking, and by increasing age at start of mining. The predominant histological type of lung cancer among miners changed from small-cell undifferentiated for short follow-up time to epidermoid afterlong follow-uptimcs. Withashort follow-uptime,amultiplicative interaction bctwecn smoking and radiation was indicated but, with long follow-up time, the two factors appear to be simply additive. This difference is probably due to theshortened latentperiod among cigarette smokers, not to synergism.

Mortality from lung cancer and chronic obstructive pulmonary disease in New Mexico, 1958-82. Samet JM, Wiggins CL, Key CR, Becker TM. New Mexico Tumor Registry, Cancer Center. University of New Men’co. School of Medi- cine, Albuquerque. NM 87131. Am J Public Health 1988;78: 1182-6.

We examined mortality from lung cancer and from chronic obstruc- tive pulmonary disease in Hispanic White., Other White., and Native American residents of New Mexico during the period 1958-82. Age- specific mortality was calculated by combining death certificate data with population estimates based on the 1960.1970, and 1980 censuses that were adjusted for inconsistencies in the designation of race and ethnicity. In Other Whites, age-adjusted mortality rates from lung cancer and from chronic obstructive pulmonary increased disease progressively in males and females. Mortality rates for both diseases also increased in Hispanics during the study period, but the most recent rates for Hispanics were well below those for Other Whites. Age- specific mortality rates for lung cancer declined for more recently born Hispanic women at older ages. In Native Americans, rates for both diseases were low throughout the study period and did not show consistent temporal trends.

Examination of the role of cigarette smoke in lung carcinogenesis using multistage models. Gaffncy M, Altshuler B. Department of CIinicaland Scientific Affairs, Pfizer Inc., New York, NY 10017. J Nat1 Cancer Inst 1988;80:925-3 1.

The widely used multistage model of Armitage and Doll is fit to the British physician lung cancer data of Doll and Hill under the assumption that cigarette smoke induces the initial and penultimate changes. It is shown that the best fit of this model in continuing smokers gives predictions not in accordance with incidence in ex-smokers and dose- response. A better global lit can be obtained by increasing the number of stages, but this de-emphasizes initiation and is inconsistent with the rise of incidence in nonsmokers. Thus, one should lood to other models. A two-stage model with clonal growth in which smoking initiates normal target cells and promotes the clonal growth of just the smoke- initiated cells is proposed. This model is shown to agree with the Doll andHi dataandthusit hasempiricalplausibilitythatshouldencourage biological studies of clonal growth in carcinogenesis.

Long-lasting effects of tobacco smoking on pulmonary drug-me- tabolizing enzymes: A case-control study on lung cancer patients. Petruz/elli S, Canms A.-M, Carrozzi L. CNR Institute of Clinical Physiology, Second Medical Clinic, University of Pisa, Pisa. Cancer Res 1988;48:4695-4700.

Lung tissue specimens wcrc taken during surgery from middle-aged men with either lung cancer (LC, n = 54) or a nonneoplastic lung disease (n = 20). Aryl hydrocarbon hydroxylase (AHH), 7-ethoxycoumarin O- deethylase (ECDE), epoxide hydrolase (EH), glutathione S-transferase (GST), and UDP-glucuronosyltransferase (UDPGT) activities and glu- tathionc and malondialdehyde contents were determined in 12,000 x g supcmatant fractions from nontumorous parenchymal tissues. Interin- dividual differences in enzyme activities ranged from 1 I- to 440-fold, and glutathione content varied by 17.fold; the values showed unimedal distributions. AHH, ECDE, EH, and UDPGT activities were signifi- cantly and positively correlated to each other; a significant negative correlation was found between GST and the other enzymes. A relation- ship bctwccn enzyme activity and number of cigarettes smoked (pack- years) was found only for GST. Ignoring detailed smoking histories in the 6-month period prcccding surgery, no difference was found in enzymcactivitiesorglutathionecontentbetweenLCandnonneopiastic lung disease patients or between smokers and nonsmokers. However, when the number of days since stopping smoking was considered, in smokers a significant increase was found for AHH. EH, and UDPGT activities and a significant decrease was found for GST activity, as compared to nonsmokers. LC patients who had smoked until the day

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bcforc surgery had higher activities of AHH, ECDE, EH, and UDPGT than nonsmokers, while GST activity was reduced by one-third. The activities of these enzymes returned to the basal level found in nonsmok- ers within 59 (AHH), 108 (EH). 67 (UDPGT), and 40 (GST) days. LC patients who were recent smokers (within 30 days prior to surgery) had significantly induced AHH and ECDE activities when compared with smoking nonneoplastic lung disease patients. These results show that pulmonary drug metabolism can be altered by tobacco smoking and that

these effects can last 40 to 108 days after cessation of smoking. These new findings should be considered in studies on the role of carcinogen- metabolizing enzymes in determining susceptibility to lung cancer.

Duration of exposure as a determinant of lung cancer risk in passive smokers. Hirayama T. Institute of Preventive Oncology. Tokyo 162. Environ Technol Lett 1988;9:731-2.

Age at first exposure to passive smoking (or age at fust marriage to smoking husbands) in non-smoking women in Japan was observed tobe about 8 years earlier than the age at fist exposure to active smoking (or age at start of smoking) and was identified as an important risk factor which determines the extent of lung cancer risk elevation in non- smoking women with smoking husbands in addition to the amount of husbands smoking.

Lung cancer and smoking in Shanghai. Gao Y-T, Blot WJ, Zheng W, Fraumeni JF, Hsu C-W. Narionul Cancer Insfitufe, National Institute of Health, Bethesda, MD 20892. Int J Epidemiol 1988;17:277-80.

A case-control study involving interviews with 733 male and 672 female incident lung cancer patients and 1495 population-based con- trols revealed that cigarette smoking is the dominant cause of lung canceramongmeninurbanShanghai.Alloftheprincipalcell typeswere affected, with clear trends of rising risk with increasing intensity and duration of smoking. Far fewer women smoked cigarettes, but the overall risk patterns resembled those among males. Among women, however, smoking accounted for only about one-quarter of all lung cancers and less than 10% of lung adenocarcinomas. The findings lay to rest any doubts about the health hazards of smoking Chinese cigarettes, although smoking is not responsible for the high rates of adenocarcinoma reported among Chinese women.

Dietary habits and lung cancer risk among Chinese females in Hong Kong who never smoked. Koo LC. Department of Community Medicine, University of Hong Kong, Hong Kong. Nutr Cancer 1988;11:155-72.

This describes a retrospective study in which 88 lung cancer patients and 137 district-matched controls were interviewed concerning the effects of diet on lung cancer risk among Hong Kong Chinese women who never smoked tobacco. Those in the lowest tertile of consuming fresh fruitor fresh fishandstatistically significantadjustedrelativerisks (RRs) of 2.4 and 2.8, respectively. The protective effects of diet, i.e., higher consumption of leafy green vegetables, carrots, tofu, fresh fruit, and fresh fish, were confined mostly to those with adenocarcinoma or large cell tumors. Only fresh fruit was found to positively, and smoked meats to negatively, affect the risk of squamous or small cell tumors. Foods high in vitamin C, retinal, and calcium seemed to exert larger effects.Subj~tsfromlargerhouseholdswereshowntobemorefrequent consumers of fresh vegetables, fruit, and fish. Because the lifetime weighted household size could be used as a surrogate index of past dietary quality, when it was combined with current dietary intakes of fresh fruit,theRRincreasedaseitherfactordecreasedinadose-response manner. The adjusted RR was 5.8 at the lowest level. Further testing of the validity of the lifetime weighted household size as an index of past dietary quality is needed.

Estimates of the proportion of lung cancer attributable to occupa- tional exposure. Simonato L, Vineis P, Fletcher AC. International Agency for Research on Cancer, F-69372 Lyon Cedex 08. Carcinogenesis1988;9:1159-65.

The proportion of lung cancer due to occupational exposure has been estimated by computing the attributable risk in the population (ARp) from various case-control studies. Different criteria have been used in including occupational exposures from published studies: (i) exposure to lung carcinogens according to a job-exposure matrix approach; (ii) occupations in which an increased risk of lung cancer has been estab- lished, (iii) occupations in which an increased risk of lung cancer has been suggested; and (iv) occupations associated with a statistically significant increase of lung cancer. Only studies in which the confound- ing effect of smoking was controlled for have been included. We found a wide variability of ARp estimates, mainly due to the different geographical locations of the studies, while they seem to be only moderately affected by the different criteria of inclusion of the relevant occupational exposures. Studies using job-exposure matrices gave ARpsrangingfrom0.6% to35%. Whenalistofrecognizedcarcinogenic exposures was used for the selection of the relevant occupations, the estimates varied between 2.4% and 40%. From the studies reviewed it alsoappears that tobacco smoking has a very limited confounding effect. Various limitations of the exercise are discussed.

ICRP publication 50: Lung cancer risk from indoor exposures to radon daughters. Smith H. J Can Assoc Radio1 1988;39: 144-7.

The review of the Task Group on radiogenic lung cancer leads to the following general conclusions. (1) A linear exposure-risk relationship is a good fit to be available epidemiological and experimental data on lung cancer from inhaled radon daughters, if exposures above about 500 WLM are excluded. (2) The appearance rate of radiation-induced lung cancer as a function of time is similar to the age-dependent distribution of the normal lung cancer rate in a comparable non-exposed population. (3)ConsequenUy,estimationoftheatvibutablelifetimeriskonthebasis of a relative risk concept seems to be more appropriate than an absolute risk model that assumes no temporal correlation with the normal lung cancer rate. (4) The relative lung cancer risk for adults is independent of the age at exposure and seems to be nearly equal for both sexes. For children and juveniles (age at exposure < 20 years), the relative lung cancer risk is probably somewhat higher than for adults. (5) With respect to bronchial cancer from inhaled radon daughters, the epidemiological and experimental findings suggest a more than additive influence of smoking. This influence can be approximated by a multiplicative model with respect to the age-specific lung cancer rate.

A retrospective look at Rn-induced lung cancer mortality from the viewpoint of a relative risk model. Puskin IS, Yang Y. Bioeffecfs Analysis Branch, Office of Radiation Programs, U.S. Environmental Protection Agency, Washington, DC 20460. Health Phys 1988:54:635-43.

The potential contribution to U.S. lung cancer deaths from 1930 to 1987 from indoor UzRn exposures is investigated from the standpoint of aconstantrelativeriskmodel.Basedonthismodel, whichassumesaRn risk proportional to the baseline lung cancer risk from other causes, the rate of Rn-induced lung cancer mortality has been increasing sharply since 1930. However, the estimated proportion of lung cancer deaths attributable to Rn has remained fairly constant. Applying the range of coefficients the U.S. Environmental Protection Agency employs in assessing therisk from indoorRn,it isestimatedthat8-25% ofallcurrent lung cancer deaths are ‘attributable to’ past Rn exposures. The major sources of uncertainty in the estimates are discussed.