Binková B, Lewtas J, Misková I, Lenícek J, Srám R
Laboratory of Genetic Ecotoxicology, Institute of Experimental Medicine of the Academy of Sciences of the Czech Republic, Prague.
Carcinogenesis. 1995 May;16(5):1037-46. doi: 10.1093/carcin/16.5.1037.
The effect of personal exposure to air pollution on DNA adducts in humans was analyzed in a group (n = 30) of women working outdoors (up to 8 h/day) as postal workers or gardeners in the city of Teplice, Czech Republic (Northern Bohemia), where winter inversions may result in high levels of air pollution from coal combustion. Ten of these women were followed up during the next winter season by repeated personal exposure monitoring and analysis of the DNA adducts in their white blood cells (in four sampling periods). Personal exposure monitoring for respirable particles (< 2.5 microns) was conducted for the 24 h period prior to collection of blood and urine. Particle extracts were analyzed for carcinogenic polycyclic aromatic hydrocarbons (PAH). Urine samples were collected for cotinine analysis to control for exposure to tobacco smoke. DNA isolated from white blood cells was analyzed by 32P-postlabeling with the butanol enrichment procedure. There were 21 non-smokers and nine light smokers in the pilot study (November 1992) and only non-smokers in the follow-up study (winter season 1993/94). In both studies high personal exposure variability between the individuals sampled on the same day was observed. In the pilot study we found a significantly higher (P < 0.05) level of DNA adducts in the 14 non-smoking women sampled on November 24, when their exposure to carcinogenic PAH was also significantly higher (P < 0.05), compared with seven non-smoking women sampled on November 26. We also found a significant correlation (r = 0.541, P < 0.016) between individual exposure to carcinogenic PAH and DNA adducts for the group of non-smokers (n = 21). No significant difference in DNA adduct levels was found between non-smokers and smokers. In the follow-up study, during one sampling period the ambient and personal air monitors exhibited a significantly elevated exposure to respirable particles and carcinogenic PAH. Analyzing data from the follow-up study, a significant effect of personal exposure on DNA adduct levels and their relationship with short-term exposure to carcinogenic PAH was found. The results suggest that DNA adduct levels in white blood cells reflect a short-term environmental exposure.
在捷克共和国北部波希米亚州的特普利采市,对一组(n = 30)户外工作(每天工作时长可达8小时)的女性进行了研究,分析个人暴露于空气污染对人体DNA加合物的影响。这些女性为邮政工作人员或园艺工人,当地冬季逆温可能导致煤炭燃烧产生的高水平空气污染。其中10名女性在接下来的冬季通过重复的个人暴露监测以及对她们白细胞中DNA加合物的分析(在四个采样期)进行随访。在采集血液和尿液前的24小时内,对可吸入颗粒物(< 2.5微米)进行个人暴露监测。对颗粒物提取物进行致癌多环芳烃(PAH)分析。采集尿液样本进行可替宁分析,以控制烟草烟雾暴露情况。从白细胞中分离出的DNA通过丁醇富集程序的32P后标记法进行分析。在初步研究(1992年11月)中有21名非吸烟者和9名轻度吸烟者,在随访研究(1993/94年冬季)中只有非吸烟者。在两项研究中,均观察到同一天采样的个体之间存在高度的个人暴露变异性。在初步研究中,我们发现11月24日采样的14名非吸烟女性的DNA加合物水平显著更高(P < 0.05),此时她们对致癌PAH的暴露也显著更高(P < 0.05),相比之下,11月26日采样了7名非吸烟女性。我们还发现非吸烟组(n = 21)中个体对致癌PAH的暴露与DNA加合物之间存在显著相关性(r = 0.541,P < 0.016)。非吸烟者和吸烟者之间未发现DNA加合物水平有显著差异。在随访研究中,在一个采样期内,环境和个人空气监测器显示对可吸入颗粒物和致癌PAH的暴露显著升高。分析随访研究的数据发现,个人暴露对DNA加合物水平有显著影响,以及它们与短期致癌PAH暴露的关系。结果表明,白细胞中的DNA加合物水平反映了短期环境暴露。