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Lung cancer incidence among Northern Thai women is one of the highest in Asia (an annual age-adjusted incidence rate of 37.4 per 100,000), and the incidence rate significantly differs by geographical districts. Therefore, we conducted a comparative study of women living in the Sarapee area, which showed the highest (crude incidence rate, 40.9), and the Chom Tong area, which had one of the lowest incidence rates (8.5) in Chiang Mai Province, despite the two areas' geographical and cultural closeness. The women in this study were either family members of lung cancer patients or their neighbors. To find clues to the etiology of lung cancer, this study used various epidemiological and biochemical approaches: interviewing on lifestyle factors, duplicate meals, chemical examination of drinking water, biochemical analysis of sera, mutagenicity test of urine, and monitoring of fungi and bacteria in the living environment. We found that tobacco smoking (Khiyo, local cigars) was less frequently observed in Sarapee (high incidence), compared with Chom Tong (low incidence), and that the history of chronic benign respiratory diseases was the most distinct event among women in Sarapee, resulting in a significantly increased percentage of those with a history of both benign respiratory diseases and tobacco smoking. This population revealed increased levels of serum tumor necrosis factor (TNF)-alpha, an endogenous tumor promoter. Furthermore, significantly increased urine mutagenicity was found to be closely associated with history of benign respiratory disease in Sarapee. The fungus which was most commonly found in the air inside houses in Sarapee was identified as Microsporum canis. Additionally, significantly increased serum concentrations of a constituent of the fungus were found in Sarapee women, compared with those in Chom Tong. Our results suggest that tobacco (Khiyo) smoking alone may not be able to explain the very high incidence of female lung cancer in Northern Thailand, and that chronic benign respiratory disease, possibly caused by the infection of fungi such as M. canis, is likely to be involved in the etiology of female lung cancer in North Thailand.

The tumor promoter okadaic acid binds specifically to a particulate as well as a cytosolic fraction of various mouse tissues, e.g., skin, brain, lung and colon. The KD value was 21.7 nM for receptors in the particulate fraction and 1.0 nM for those in the cytosolic fraction of mouse skin. The specific binding of [3H]okadaic acid to the particulate fraction of mouse skin was inhibited dose-dependently by okadaic acid, but not okaidaic acid tetramethyl ether, an inactive compound, or by other tumor promoters, such as 12-O-tetradecanoylphorbol-13-acetate and teleocidin. The results suggest a new pathway of tumor promotion mediated through the okadaic acid receptor(s).