Strom S S, Wu S, Sigurdson A J, Hsu T C, Fueger J J, Lopez J, Tee P G, Spitz M R
Department of Epidemiology, University of Texas M.D. Anderson Cancer Center, Houston 77030, USA.
J Natl Cancer Inst Monogr. 1995(18):29-33.
Mexican-Americans have lower age-adjusted lung cancer incidence rates than non-Hispanic whites and African-Americans. Since 87% of lung cancers are attributed to tobacco exposure, this difference could be explained partly by lower prevalence of cigarette smoking. However, only a fraction of exposed individuals will develop smoking-related cancer, and genetically determined differences in modulation of environmental exposures could also explain some of this ethnic risk differential in lung cancer incidence in the United States. However, little research on genetic susceptibility has been focused on Hispanic populations in the United States.
We are conducting a case-control study of lung cancer in a high-risk group (African-Americans) and a low-risk group (Mexican-Americans) to evaluate ethnic differences in mutagen sensitivity by an in vitro assay that quantifies mutagen-induced chromosome breaks in short-term lymphocyte cultures.
In the 174 Mexican-Americans (67 lung cancer case patients and 107 control subjects) accrued to date, all measures of cigarette smoking (intensity, duration, nicotine and tar contents, depth of inhalation, and type of cigarette) were significant predictors of lung cancer risk. There were significantly higher risks associated with mutagen sensitivity (defined as > or = 1 break/cell) for both former smokers (odds ratio [OR] = 4.5; 95% confidence interval [CI] = 0.9-21.9) and current smokers (OR = 2.6; 95% CI = 0.6-11.1). Mutagen sensitivity also appeared to be implicated in risk in patients who were less than 55 years old at diagnosis (OR = 15.0; 95% CI = 1.0-228.9) and in those with lower cigarette exposure (OR = 11.0; compared with an OR of 1.7 for the heaviest smokers). The overall OR for mutagen sensitivity adjusted for age, sex, and pack-years of smoking was 2.9 (95% CI = 0.8-9.9). Neither current smoking status nor years of exposure shifted the sensitivity profile of case patients and control subjects.
Although this study showed higher percentages of nonsmokers among Mexican-Americans than our previously reported data for African-Americans, the Mexican-American case patients were heavier smokers than the African-American case patients. The prevalence of mutagen sensitivity for Mexican-Americans was 64.1% in case patients and 26.2% in control subjects. In African-Americans, mutagen sensitivity was previously reported to be 55.3% in case patients and 24.6% in control subjects. These preliminary data do not support our a priori hypothesis that a lower prevalence of mutagen sensitivity in Mexican-Americans would account for the lower incidence of lung cancer. Mutagen sensitivity, however, is only one of an array of potential susceptibility markers that we are evaluating in this unique population.
墨西哥裔美国人经年龄调整后的肺癌发病率低于非西班牙裔白人和非裔美国人。由于87%的肺癌归因于烟草暴露,这种差异部分可由较低的吸烟率来解释。然而,只有一小部分暴露个体才会罹患与吸烟相关的癌症,而且在环境暴露调节方面由基因决定的差异也可能解释美国肺癌发病率方面的部分种族风险差异。然而,针对美国西班牙裔人群的遗传易感性研究较少。
我们正在对一个高危组(非裔美国人)和一个低危组(墨西哥裔美国人)进行肺癌病例对照研究,通过一种体外试验来评估诱变敏感性方面的种族差异,该试验可量化短期淋巴细胞培养中诱变剂诱导的染色体断裂情况。
在迄今招募的174名墨西哥裔美国人(67例肺癌患者和107名对照者)中,所有吸烟指标(强度、持续时间、尼古丁和焦油含量、吸入深度以及香烟类型)都是肺癌风险的显著预测因素。既往吸烟者(比值比[OR]=4.5;95%置信区间[CI]=0.9 - 21.9)和当前吸烟者(OR = 2.6;95% CI = 0.6 - 11.1)诱变敏感性(定义为≥1个断裂/细胞)相关风险均显著更高。诱变敏感性似乎也与诊断时年龄小于55岁的患者(OR = 15.0;95% CI = 1.0 - 228.9)以及吸烟暴露较少的患者(OR = 11.0;与重度吸烟者的OR值1.7相比)的风险有关。经年龄、性别和吸烟包年数校正后的诱变敏感性总体OR值为2.9(95% CI = 0.8 - 9.9)。当前吸烟状态和暴露年限均未改变病例患者和对照者的敏感性特征。
尽管本研究显示墨西哥裔美国人中不吸烟者的比例高于我们之前报道的非裔美国人数据,但墨西哥裔美国病例患者比非裔美国病例患者吸烟更重。墨西哥裔美国人病例患者中诱变敏感性的患病率为64.1%,对照者中为26.2%。在非裔美国人中,之前报道病例患者诱变敏感性患病率为55.3%,对照者中为24.6%。这些初步数据不支持我们的先验假设,即墨西哥裔美国人诱变敏感性患病率较低可解释其较低的肺癌发病率。然而,诱变敏感性只是我们在这个独特人群中正在评估的一系列潜在易感性标志物之一。