@misc{oai:repo.qst.go.jp:00062943,
 author = {Zhang, Wei and Chun, Yan Wang and Minamihisamatsu, Masako and Luxin, Wei and Sugahara, Tsutomu and Hayata, Isamu and 張 偉 and 王 春燕 and 南久松 眞子 and 早田 勇},
 month = {Dec},
 note = {Chromosome aberration frequencies have increasingly been used for the study of various occupational and environmental exposures. Factors related to environmental mutagens influence translocation yield. Smoking has impact on the translocation yield and is most influential factor among the environmental mutagens to increase cancer incidence. In order to know how environmental mutagens affect the induction of translocations caused by smoking we analyzed translocations in the lymphocytes of smokers and nonsmokers in a large city, Beijing, a high natural background radiation area (HBRA) and in this control area (CA), remote villages in the south of China (Zhang et al., J. Radiat. Res., 45: 441-446, 2004; Zhang et al., Carcinoge. Teratge. Mutage., 20: 41-43,2008). The results of our analyses are reviewed in this presentation.
Studied residents in Beijing have lived there for longer than 40 years and people in HBRA and CA have lived there for several generations. The level of natural radiation in HBRA is 3-5 times higher than those in CA and in Beijing. The residents in HBRA and CA mainly smoke the shredded tobaccos through a water pipe instead of the cigarette which is common in Beijing. Individual radiation dose was measured with a pocket dosimeter (Aloka PDM-10) put on the body for 24 hours and/or estimated from the dose rate measured by a NaI scintillation survey meter (Aloka TCS-166) in their homes. Peripheral blood was from 10, 11, and 7 smokers in Beijing, HBRA and CA, respectively. Their ages were around 60 years old. Peripheral lymphocytes were cultured for 48 hours with PHA and colcemid, and harvested according to our standard method for biodosimetry (Hayata et al., J. Radiat. Res. 33: Supple, 231-241, 1992). Chromosome painting was performed using Biotin-labeled whole chromosome painting probes specific to chromosome 1,2 and 4 (Cambio, UK), representing 22.71% and 22.34% of the human genome in male and in female, respectively. The frequencies of translocations per 1000 cells were scaled to genome-equivalent frequencies by the formula reported by Lucas et al. (Int. J. Radiat. Biol. 62: 53-63, 1992). The number of metaphases analyzed was totally 321,795(3,973 per subject). Statistical analysis was performed by Mann-Whitney U test.
Genome equivalent frequencies of translocations in 1,000 lymphocytes per subject were 10.6+/-3.1, 11.3+/-3.4, and 13.4+/- 3.4 in smokers and 9.6 +/-5.0, 11.7 +/- 4.7, and 9.1 +/-3.8 in nonsmokers in Beijing, HBRA and CA, respectively. CA smokers showed the highest average value among six groups. There was a statistically significance difference (p<0.05) in the frequencies of translocation between CA nonsmokers and CA smokers, and between Beijing nonsmokers and CA smokers, respectively. But no other possible comparisons between groups showed significant difference.
There is discrepancy in the results of the studies on the effects of smoking to the chromosomal translocations in the peripheral lymphocytes. Majority of the studies (Littlefield et al., Radiat Res. 150: 237-249, 1998; Sram et al., Mutat. Res.593: 50-63, 2006; Sigurdson et al., Mutat. Res. 652: 112-121, 2008, and etc.) observed increased translocation frequencies due to smoking. In contrast, Okladnikova et al. (Radiat. Pror. Dosimetry 113; 3-13, 2005). Did not find a significant relationship of chromosome aberrations (stable and unstable) and smoking. Whitehouse et al.,(Int. J. Radiat. Biol. 81: 139-145, 2005) reported that lifestyle factors such as smoking did not appear to have a significant effect on translocation yield. But they also reported that there is suggestion that the translocation yield might increase with smoking status in two age groups (30-39y and 60-69y), and that occurs only when heavy smoker are compared with non-smokers. Ikeda et al. (Mutat. Res. 626: 15-25, 2007)reported that genotoxic effects in the lung of gpt delta transgenic mice decreased when low-dose-rate radiation was given together with 4-(methylnitroamino)-1-(3-pyridyl)-1-butanone(NNK), the most carcinogenic tobacco-specific nitrosamine. They suggested that NNK induced adaptive response that eliminated the cells bearing radiation induced double strand breaks in DNA. In the present study, we detected increase of the frequency of translocations caused by smoking in CA but not in HBRA nor in Beijing. The effect of smoking on chromosome aberrations seems to be suppressed by the environmental mutagens including the elevated level of natural radiation in HBRA and ever-existed continuous air pollution in Beijing., The 3rd Asian Chromosome Colloquium},
 title = {Effect of smoking on the chromosome aberrations induced by environmental mutagens},
 year = {2008}
}