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Background: Few studies have investigated occupational lung cancer risk in relation to specific histopathological subtypes., Methods: A case-control study was conducted to evaluate the relationship between lung cancer and occupation/industry of employment by histopathological subtype. A total of 2,998 male cases and 10,223 cancer controls, diagnosed between 1983 and 1990, were identified through the British Columbia Cancer Registry. Matched on age and year of diagnosis, conditional logistic regression analyses were performed for two different estimates of exposure with adjustment for potentially important confounding variables, including tobacco smoking, alcohol consumption, marital status, educational attainment, and questionnaire respondent., Results: For all lung cancers, an excess risk was observed for workers in the primary metal (OR = 1.31, 95% CI, 1.01-1.71), mining (OR = 1.53, 95% CI, 1.20-1.96), machining (OR = 1.33, 95% CI, 1.09-1.63), transport (OR = 1.50, 95% CI, 1.08-2.07), utility (OR = 1.60, 95% CI, 1.22-2.09), and protective services (OR = 1.27, 95% CI, 1.05-1.55) industries. Associations with histopathological subtypes included an increased risk of squamous cell carcinoma in construction trades (OR = 1.25, 95% CI, 1.06-1.48), adenocarcinoma for professional workers in medicine and health (OR = 1.73, 95% CI, 1.18-2.53), small cell carcinoma in railway (OR = 1.62, 95% CI, 1.06-2.49), and truck transport industries (OR = 1.51, 95% CI, 1.00-2.28), and large cell carcinoma for employment in the primary metal industry (OR = 2.35, 95% CI, 1.11-4.96)., Conclusions: Our results point to excess lung cancer risk for occupations involving exposure to metals, polyaromatic hydrocarbons and asbestos, as well as several new histopathologic-specific associations that merit further investigation.

The study of Xuan Wei fuel use and lung cancer mortality and also the interim case-control study suggested an association between domestic smoky coal use and Xuan Wei lung cancer. The collaborative studies of physical characterization, chemical analysis, and toxicology further substantiated this linkage. The Xuan Wei residents who used smoky coal inhaled extremely high concentrations of mostly submicron-sized particles, which can be inhaled and deposited effectively deep in the lung. These fine particles were composed mostly of organic compounds (72%), including mutagenic and carcinogenic organic compounds, especially in the aromatic and polar fractions. These residents were exposed to polycyclic aromatic compounds, such as benzo[a]pyrene, at comparable or higher levels than those measured in coke oven plants and other occupational environments (International Agency for Research on Cancer 1984). In comparison with wood and smokeless coal combustion emissions, the organic extracts of smoky coal emission particles showed much higher activity of genotoxicity and carcinogenicity. These results all point to a strong etiological link between the complex organic mixtures from smoky coal emissions and Xuan Wei lung cancer. This study and studies reported by other investigators (de Koning et al. 1984) suggested little association between indoor open-fire wood smoke and lung cancer. The less efficient lung deposition of the larger particles from wood combustion, as well as the lower concentrations of biologically active organic compounds, may contribute to the low rate of lung cancer in the wood-burning communes. As to the smokeless coal emissions, the lower particulate concentration and the lower organic content of the particles emitted may also contribute to the low lung cancer rate in the commune using this fuel. In conclusion, the complex organic mixtures from combustion emissions are genotoxic and carcinogenic in animal and in vitro assays. The magnitude of the cancer risks from the complex organic mixtures in man depends on the degree of the exposure, the types of the compounds contained in the mixtures, and the concentrations of these biologically active compounds present in the combustion emissions.

The growth rate of spherical pulmonary metastases was studied in 15 patients with osseous and soft tissue sarcoma. The median volume doubling time (Dt) was 25 days. The time from diagnosis of the primary tumor to occurrence of pulmonary metastases correlated directly with the length of Dt. No correlation between Dt and tumor histology was observed. The effect of therapy on the tumor growth curve was studied in 1 patient. The therapeutic implications derived from the quantitative evaluation of tumor growth rate are discussed.

A postmenopausal breast cancer patient with a measurable lung metastasis was treated with tamoxifen. The tumor doubling time of the pulmonary lesion was 140 days during spontaneous growth and 52 days during tamoxifen therapy, an almost threefold increase in tumor growth rate. This stimulation persisted fro 1 month after discontinuation of tamoxifen and was followed thereafter by a withdrawal regression lasting greater than 6 months. Awareness of the possible tumor growth enhancement with tamoxifen is of importance especially in view of its prolonged activity. Hormone withdrawal regression may occur following tamoxifen therapy, and a sufficient time interval should therefore elapse between cessation of tamoxifen and initiation of other therapeutic modalities.

Marked atypia (MA) is considered to represent a late stage in the sequence of cellular changes leading to carcinoma. In 1974 we undertook a sputum cytology (SC) survey of uranium workers (UW) and controls (Cancer 1980; 45:1273). Sixteen cases of MA (four with cells suspicious of malignancy) were diagnosed among the initial cohort of 292 male smokers; 11/172 (6.4%) underground UW; 4/78 (5%) surface UW; and 1/42 (2.4%) male controls. Follow up consisted of at least three yearly SC; in addition, selective segmental fiberoptic bronchoscopy was performed yearly for the first 3 years of observation. Three of the four-cases with marked atypia and suspicious malignant cells developed lung cancer. The remaining cases were followed for an average duration of 54 months; all 13 reverted to mild atypia or to normal cytologies. The high frequency of reversibility of MA will cause difficulties in interpreting results of chemoprevention trials if MA is used as the sole marker of effect. Chemoprevention trials should focus on differences in cancer incidence rates between treated and control groups at high risk of developing lung cancer and not on the reversibility of MA as the sole marker of effect.

Pulmonary lesions developed in three patients with an invasive hydatidiform mole. At open thoracotomy the modules were found to contain molar tissue. Therapy with twice-weekly methotrexate induced complete clinical and biologic remission of the disease in all three patients.