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煤厂的煤烟颗粒有机溶剂（硝基甲烷和二氯甲烷）和水相二种类型的抽提物都能有效增强、加速Ｕｄｅｎｆｒｉｅｎｄ反应体系中脱氧核糖（ｄＲ）羟化降解，并呈现一定的剂量一效应关系。用脱氧腺苷（ｄＡ）替代，也能获此结果。而燃油厂的油烟颗粒则无上述作用。经ＥＳＲ测定，燃煤厂的煤烟颗粒自由基ｇ值为２００１６；燃油厂的油烟颗粒自由基ｇ值为２１００８，前者接近于半醌自由基，后者为类似于大气飘尘中性质完全不同的宽谱、稳定自由基。提示煤烟的诱变性和致癌性与其对ＯＨ生成的加速作用及其对ＤＮＡ造成的氧化损伤有一定关系。
Coal plant soot particulate organic solvents (nitromethane and methylene chloride) and aqueous two types of extracts can be effectively enhanced to speed up the U denfriend reaction system deoxyribose (dR) hydroxylation and rendering A certain dose-effect relationship. This result was also obtained using deoxyadenosine (dA) instead. Fuel oil soot particles do not have the above effect. By ESR measurement, coal-fired plant soot particle g value of 2 0016; fuel oil fume particle free radical g value of 2 1008, the former close to semi-quinone free radicals, the latter is similar to the atmospheric fly ash A completely different nature of the broad spectrum, stable free radicals. It is suggested that the mutagenicity and carcinogenicity of soot are related to the accelerating effect of OH and its oxidative damage to DNA.