1, man-made glass fibers People have studied the carcinogenicity of man-made glass fibers in humans extensively, but there is insufficient evidence that lung cancer is associated with exposure to mineral wool insulation fibers, glass filament (mineral wool) fibers (marsh et al., 2001; iarc, 2002; kj aerheim et al., 2002). The available evidence concludes that glass wool fibers and long glass wool fibers have no carcinogenic effect (iarc, 2002). Other man-made fibers such as heat-resistant ceramic fibers can cause seedlings in animal tests, but there are insufficient data on carcinogenicity in humans. 2. Silica and other mineral dusts There has been a consensus on the high prevalence of lung cancer in silicosis patients (iarc, 1997a; steenland and stayner, 1997). Many workers in the foundry, pottery processing, ceramic industries, silicon-nickel mines, brick factories and rock processing industries develop silicosis due to exposure to crystalline silica. Therefore, many scholars have used this as a study subject. Some of the studies have shown an increased risk of lung cancer, but not many of the positive studies have shown this increased risk. Precise dose-one effect analyses have shown a linear relationship, however there is no evidence for a threshold value (steenland et al., 2001). Evidence on the carcinogenic effects of non-crystalline silica is also insufficient. Several studies have attempted to assess the risk of talc exposure, but their results indicate that workers exposed to talc contaminated with asbestos fibers have an increased risk of lung cancer, while exposure to uncontaminated talc does not appear to have a carcinogenic effect. There is insufficient evidence whether other ore products such as coal products are carcinogenic (iarc, l997b). 3. mixtures of polycyclic aromatic hydrocarbons Polycyclic aromatic hydrocarbons (pahs) are a group of chemical tableaux produced when organic materials are not burned sufficiently. They are widely distributed in the human living environment; food and smoking are the two main sources of people’s exposure to pahs. People are exposed to pahs to varying degrees in certain occupational settings. These compounds exist in complex mixtures, so that an assessment of the carcinogenicity of single pahs substances is not possible. Industrial or occupational settings that produce pahs are aluminum manufacturing, gas industry, coke manufacturing, steel manufacturing, tar distillation, roof and chimney sweeping (boffetta et al., 1997). Increases in lung cancer have been found in several other industries, such as petroleum extraction, wood protection, paving, black soot end production, and graphite electrode manufacturing. Exhaust fumes from cars and other engines are important sources of pahs mixtures, which contribute to atmospheric pollution. Epidemiological data confirm that the risk of lung cancer is increased by /0 50% in people exposed to diesel engine exhaust at work (lipsett and campleman, 1999). Exhaust data from other engines, such as gasoline engines, have not reached similar conclusions (iarc, 1989a). 4. mineral oil and carbon black A study of workers exposed to petroleum and other mineral oils showed no effect on metal workers, but positive results for printing workers (tolbert, 1997). The best evidence for newspaper printing inks and metal waste fluids suggests that high exposure to ionizing radiation increases the risk of developing lung cancer. Both atomic bombing survivors and patients treated with radiation therapy have a somewhat increased risk of lung cancer above the loorad cumulative exposure rr of 1. The association of high doses of lonizing radiation with small cell lung cancer is substantially higher than that with other tissue types of lung cancer. Studies of nuclear industry workers exposed to relatively low doses did not find an increased risk of lung cancer. Radioactive radium and its decay products can emit a-particles, and miners exposed to its underground work have an increased risk of lung cancer (lare, 2001). The magnitude of this risk is based on cumulative exposure, and the younger the age of exposure the longer the exposure, the greater the risk. Convergent analysis of 11 cohort studies found a clear linear relationship, with an approximately 6% increase in lung cancer risk for each additional year of exposure (lubin 6.3.6 Other chemicals Workers exposed to chloromethyl ether and bis(chloromethyl) ether have an increased risk of lung cancer, particularly small cell lung cancer (iarc, 1987; blair and kazerouni 1997). Dichlorodiethyl sulfide, or mustard gas, was used during World War I. Soldiers and workers in manufacturing plants who were exposed to mustard gas had an increased risk of lung cancer. Workers exposed to inorganic strong acids, especially sulfuric acid, which is used in electroplating, metalworking, battery manufacturing, and the chemical industry, have an increased risk of lung cancer. An increased risk of lung cancer has also been reported in workers exposed to formaldehyde, vinyl chloride and acrylonitrile, but in studies of these chemicals, no causal relationship between them and lung cancer has been established. An increased risk of lung cancer in workers exposed to dioxins has also been reported, but the increase was small (iarc, 1997e) and inconclusive.