Sorsa M, Husgafvel-Pursiainen K, Järventaus H, Koskimies K, Salo H, Vainio H
Institute of Occupational Health, Helsinki, Finland.
Mutat Res. 1989 Feb;222(2):111-6. doi: 10.1016/0165-1218(89)90024-4.
Tobacco smoke is highly genotoxic and produces chromosomal damage in several experimental systems. Active smokers have been shown to have an increased prevalence of somatic chromosome damage in their peripheral blood lymphocytes: this is seen in most cases as an increased sister-chromatid exchange (SCE) frequency and often also as increased structural chromosome aberrations (CAs). Among passive smokers, in association with exposure to environmental tobacco smoke, no such induction of chromosomal damage has been documented. In the present paper we report negative results on induction of chromosomal damage in 2 separate groups of intensive involuntary exposure to tobacco smoke, non-smoking restaurant personnel and newborn children of smoking mothers. While significant exposure in these groups is clearly seen in biochemical intake markers, e.g. cotinine and thiocyanate values in plasma, the conventional cytogenetic parameters, structural chromosome aberrations and sister-chromatid exchanges, are unable to detect the low exposures of involuntary smokers.
烟草烟雾具有高度的基因毒性，在多个实验系统中会导致染色体损伤。已有研究表明，主动吸烟者外周血淋巴细胞中体细胞染色体损伤的发生率增加：在大多数情况下，这表现为姐妹染色单体交换（SCE）频率升高，并且通常还表现为染色体结构畸变（CA）增加。在被动吸烟者中，与接触环境烟草烟雾相关的情况下，尚未有此类染色体损伤诱导的记录。在本文中，我们报告了两组分别因强烈非自愿接触烟草烟雾（非吸烟餐厅工作人员和吸烟母亲的新生儿）而导致染色体损伤诱导的阴性结果。虽然在这些人群中，通过生化摄入标志物（例如血浆中的可替宁和硫氰酸盐值）可以明显看出有显著接触，但传统的细胞遗传学参数，即染色体结构畸变和姐妹染色单体交换，无法检测到非自愿吸烟者的低暴露情况。
