Palli Domenico, Saieva Calogero, Grechi Daniele, Masala Giovanna, Zanna Ines, Barbaro Antongiulio, Decarli Adriano, Munnia Armelle, Peluso Marco
Molecular and Nutritional Epidemiology Unit, CSPO-Scientific Institute of Tuscany, Florence, Italy.
Int J Cancer. 2004 Mar;109(1):17-23. doi: 10.1002/ijc.11687.
Ozone (O(3)), the major oxidant component in photochemical smog, mostly derives from photolysis of nitrogen dioxide. O(3) may have biologic effects directly and/or via free radicals reacting with other primary pollutants and has been reported to influence daily mortality and to increase lung cancer risk. Although DNA damage may be caused by ozone itself, only other photochemical reaction products (as oxidised polycyclic aromatic hydrocarbons) may form bulky DNA adducts, a reliable biomarker of genotoxic damage and cancer risk, showing a seasonal trend. In a large series consisting of 320 residents in the metropolitan area of Florence, Italy, enrolled in a prospective study for the period 1993-1998 (206 randomly sampled volunteers, 114 traffic-exposed workers), we investigated the correlation between individual levels of DNA bulky adducts and a cumulative O(3) exposure score. The average O(3) concentrations were calculated for different time windows (0-5 to 0-90 days) prior to blood drawing for each participant, based on daily measurements provided by the local monitoring system. Significant correlations between DNA adduct levels and O3 cumulative exposure scores in the last 2-8 weeks before enrollment emerged in never smokers. Correlations were highest in the subgroup of never smokers residing in the urban area and not occupationally exposed to vehicle traffic pollution, with peak values for average concentrations 4-6 weeks before enrollment (r = 0.34). Our current findings indicate that DNA adduct formation may be modulated by individual characteristics and by the cumulative exposure to environmental levels of ozone in the last 4-6 weeks, possibly through ozone-associated reactive pollutants.
臭氧(O₃)是光化学烟雾中的主要氧化剂成分,主要来源于二氧化氮的光解。O₃可能直接和/或通过与其他主要污染物反应产生的自由基产生生物学效应,并且据报道会影响每日死亡率并增加肺癌风险。虽然臭氧本身可能会导致DNA损伤,但只有其他光化学反应产物(如氧化多环芳烃)可能形成大分子DNA加合物,这是一种可靠的遗传毒性损伤和癌症风险生物标志物,呈现出季节性趋势。在一项由意大利佛罗伦萨大都市区的320名居民组成的大型队列研究中,这些居民在1993年至1998年期间参与了一项前瞻性研究(206名随机抽样志愿者,114名交通暴露工人),我们调查了个体大分子DNA加合物水平与臭氧累积暴露评分之间的相关性。根据当地监测系统提供的每日测量数据,为每个参与者计算了采血前不同时间窗口(0 - 5至0 - 90天)的平均O₃浓度。在从不吸烟者中,发现登记前最后2 - 8周内DNA加合物水平与O₃累积暴露评分之间存在显著相关性。在居住在市区且未职业暴露于车辆交通污染的从不吸烟者亚组中相关性最高,登记前4 - 6周平均浓度的峰值(r = 0.34)。我们目前的研究结果表明,DNA加合物的形成可能受到个体特征以及登记前最后4 - 6周内环境臭氧累积暴露的调节,可能是通过与臭氧相关的反应性污染物。