Roles of transbronchial factors including cigarette smoke and asbestos for rapidly increasing lungcancer

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To investigate the causes of rapidly increasing lung cancer in Japan, we analysed both genetic changes and carcinogenic inhalants including smoking and asbestos. We examined primary lung cancers (9 in 1950s, 52 in 1970s and 60 1990s) in terms of asbestos deposition in the lung. Mean asbestos body concentrations (numbers per g of lung (dry)) were 559, 1804 and 563 in 1950s, 1970s and 1990 s, respectively. Statistically significant elevation in the concentration of 1970s was noted as compared to that of 1990s (p<0.005). Since the lung cancer incidence in Japan has been rising from 1950 to 1990, asbestos exposure is not thought to be a main cause of lung cancer increase. Further, we compared asbestos concentrations in the lung between primary and metastatic lung adenocarcinomas in 1970s. Also, we examined differentiation grades, LOH frequency (presented by FAL values) and p53 mutations in lung adenocarcinomas in 1990s, subclassified to 3 groups by asbestos body concentration (AB, numbers/dry g) : zero AB group (AB=0, n=21), low AB group (0<AB<1000, n=14 and high AB group (1000=<AB, n=l1). AB in primary cancers in 1970s was 2050 in males, significantly higher than that of metastatic cancers, 703, although the difference was not significant in females. In the three groups, well/moderate./poor. were 6/11/4, 6/8/0, 4/7/0 ; FAL values were 0.17, 0.07, 0.13 ; and p53 mutation frequencies were 3/19, 4/14, 5/11. Regardless of asbestos levels, well and moderatelydifferentiated carcinomas were predominant and FAL values were smaller than that for smokers (0.21, n=66). Interestingly, p53 mutation frequency was significantly more frequent in high AB group than in zero AB group (p =0.006).