To evaluate the importance of exposure to ambient air pollution for lung cancer risk, we conducted a case-control study in the vicinity of a nonferrous metal smelter. The smelter started operations in 1930 and had very high emissions during the early decades, particularly of arsenic and SO(2). Among subjects deceased 1961-1990 in the municipality where the smelter is located and who had not worked at the smelter, 209 male and 107 female lung cancer cases were identified and matched by sex and year of birth to 518 and 209 controls, respectively. Information on smoking habits, occupations and residences was collected by questionnaire to next-of-kin and from registry data. Living close to the smelter was associated with a relative risk (RR) for lung cancer of 1.38 [95% confidence interval (CI) 0.89-2.14] among men, adjusted for smoking and occupational exposures. No clear difference in risk was detected for men deceased 1961-1979 compared to men deceased 1980-1990 (RR point estimates 1.42 and 1.29, respectively). There appeared to be an increased risk especially for men exposed in the beginning of the operations (RR = 1.51, 95% CI 0.90-2.54), in particular combined with exposure duration shorter than 20 years (RR = 2.52, 95% CI 0.89-7.11). For women, however, no overall increased risk for lung cancer was observed. Although not significant, our findings thus indicated an increased risk of lung cancer among men living close to the nonferrous smelter. This increase appeared to concern primarily men exposed during the early years of operations, when emissions were very high.
The incidence of 5 polymorphisms of N-acetyltransferase-2 gene was evaluated in patients with lung cancer. A803G polymorphism is a factor of lung cancer resistance in tobacco smoking Caucasians in Novosibirsk. Opposite effects of NAT2 gene polymorphisms on the risk of lung cancer are possible.
Mice which were alive in Durham at the time of the Chernobyl nuclear accident presented a highly significant increase in the incidence of those which bore tumours. The comparison is based upon mice which were studied over the previous 4 years. In males and females the increase amounted to 19 and 100 per cent respectively. The most frequent neoplasms to increase were malignant tumours of the reticuloendothelial system and of the reticuloses, lymphosarcoma and reticulum cell sarcoma were prevalent in mice kept after Chernobyl. The incidence of reticuloses increased by 24 and 18 per cent in males and females respectively.
Cancer mortality of men with diagnosed asbestosis was studied in Finland. Of the 174 men registered as having asbestosis, 56 had died before 1977, whereas the number of expected deaths based on the Finnish male population was only 23.4. The respective figures for lung cancer were 19 observed and 2.1 expected. The mean age of these 19 lung cancer patients was 57.8 yr, and lung cancer was the cause of death (underlying cause) in 35% of all diseased men with asbestosis. The proportion of lung cancer mortality from all deaths among Finnish men 55-64 yr old is 10.8%, which is clearly lower than that among the men with asbestosis. No excess of other malignancies was found in Finland among workers with asbestosis.
During a 6-month period all lung cancer patients in a university hospital chest clinic were investigated for asbestos exposure by means of personal interview, bronchoalveolar lavage (BAL), roentgenograms, lung function testing, histology and measurement of fibre concentrations in lung tissue samples using scanning electron microscopy (SEM). About one-third of the patients (33%) were classified as having been exposed to asbestos on the basis of the interview. BAL was performed and AB counts were done in 51 patients. Fourteen (27%) BAL specimens had AB counts of 1 or more AB/ml, which is the conventional limit for non-trivial asbestos exposure. For a subgroup of 25 operated lung cancer patients fibre analysis was also available. In six cases (30%) the asbestos-containing samples had asbestos fibre concentrations equal to or more than 1 million fibres/g dry lung. In eight (32%) of the operated lung cancer patients histopathologically confirmed fibrosis was seen; five of these patients were in the two highest exposure classes. Pleural plaques on X-ray films were seen in six (24%) of the operated cases. With each indicator of exposure about 30% of lung cancer patients were found to have been exposed, confirming the "one-third rule"; however, when all the information was collated there were three cases (12%) in which exposure was most obvious according to the different parameters used in this study. In these three cases the cancer could well be attributed to asbestos. Anthophyllite was present in all asbestos-containing samples and anthophyllite was the main fibre type in 61% of these samples.
The aim of the study was to investigate the asbestos-associated risk of lung cancer according to histological type of cancer, lobe of origin, pulmonary concentration, and type of amphibole fibers and also to estimate the etiologic fraction of asbestos for lung cancer.
The pulmonary concentration of asbestos fibers in 113 surgically treated male lung cancer patients and 297 autopsy cases among men serving as referents was determined by scanning electron microscopy. The age- and smoking-adjusted odds ratios of lung cancer were calculated according to pulmonary fiber concentration for all lung cancer types, squamous-cell carcinoma, and adenocarcinoma and for the lower-lobe and the upper- and middle-lobe cancers.
The risk of lung cancer was increased according to the pulmonary concentration of asbestos fibers (f) of 1.0 to 4.99 x 10(6) f.g-1 [odds ratio (OR) 1.7] and > or = 5.0 x 10(6) f.g-1 (OR 5.3). The odds ratios associated with fiber concentrations of > or = 1.0 x 10(6) f.g-1 were higher for adenocarcinoma (OR 4.0) than for squamous-cell carcinoma (OR 1.6). The asbestos-associated risk was higher for lower lobe tumors than for upper lobe tumors. The risk estimates for anthophyllite and crocidolite-amosite fibers were similar, except for the risk of squamous-cell carcinoma. An etiologic fraction of 19% was calculated for asbestos among male surgical lung cancer patients in the greater Helsinki area.
Past exposure to asbestos is a significant factor in the etiology of lung cancer in southern Finland. The asbestos-associated risk seems to be higher for pulmonary adenocarcinoma and lower-lobe tumors than for squamous-cell carcinoma and upper-lobe tumors.
Epidemiologic studies of uranium miners and other underground miners have consistently shown miners exposed to high levels of radon to be at increased risk of lung cancer. More recently, concern has arisen about lung cancer risks among people exposed to lower levels of radon in homes. The current Canadian guideline for residential radon exposure was set in 1988 at 800 Bq/m(3). Because of the accumulation of a considerable body of new scientific evidence on radon lung cancer risks since that time, Health Canada sponsored a workshop to review the current state-of-the-science on radon health risks. The specific objectives of the workshop were (1) to collect and assess scientific information relevant to setting national radon policy in Canada, and (2) to gather information on social, political, and operational considerations in setting national policy. The workshop, held on 3-4 March 2004, was attended by 38 invited scientists, regulators, and other stakeholders from Canada and the United States. The presentations on the first day dealt primarily with scientific issues. The combined analysis of North American residential radon and lung cancer studies was reviewed. The analysis confirmed a small but detectable increase in lung cancer risk at residential exposure levels. Current estimates suggest that radon in homes is responsible for approximately 10% of all lung cancer deaths in Canada, making radon the second leading cause of lung cancer after tobacco smoking. This was followed by a perspective from an UNSCEAR (United Nations Scientific Committee on the Effects of Atomic Radiation) working group on radon. There were two presentations on occupational exposures to radon and two presentations considered the possibility of radon as a causative factor for cardiovascular disease and for cancer in other organs besides the lung. The possible contribution of environmental tobacco smoke to lung cancers in nonsmokers was also considered. Areas for future research were identified. The second day was devoted to policy and operational issues. The presentations began with a perspective from the U.S. Environmental Protection Agency, followed by a history of radon policy development in Canada. Subsequent presentations dealt with the cost-effectiveness of radon mitigation, Canadian building codes and radon, and a summary of radon standards from around the world. Provincial representatives and a private consultant were given opportunities to present their viewpoints. A number of strategies for reducing residential radon exposure in Canada were recognized, including testing and mitigation of existing homes (on either a widespread or targeted basis) and changing the building code to require that radon mitigation devices be installed at the time a new home is constructed. The various elements of a comprehensive national radon policy were set forth.