Oxidative stress and chromosomal aberrations in an environmentally exposed population

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Abstract

We investigated the effect of the seasonal variability of environmental air pollutants on oxidative stress and cytogenetic biomarkers in a group of 59 city policemen working in Prague, Czech Republic. The studied group was monitored in February and May 2007. The exposure to environmental pollutants (carcinogenic polycyclic aromatic hydrocarbons, c-PAHs, including benzo[a]pyrene, B[a]P, and particulate matter of aerodynamic diameter < 2.5 μm, PM2.5) was measured by personal and/or stationary monitors. Levels of c-PAHs were significantly higher in winter than spring, while exposure to PM2.5 was higher in May than in February 2007. We did not observe any significant difference between the two seasons for any biomarker of oxidative stress (8-oxo-7,8-dihydro-2′-deoxyguanosine, 8-oxodG, 15-F2t-isoprostane, 15-F2t-IsoP, protein carbonyl levels) or any cytogenetic parameter, including the genomic frequency of translocations (FG/100), the percentage of aberrant cells (%AB.C.) or the number of acentric fragments (ace). Analyses of associations between oxidative stress biomarkers and cytogenetic parameters showed a negative relationship between protein oxidation and FG/100, as well as protein oxidation and ace. We further analyzed the effect of air pollution on all subjects regardless of the season. Data from stationary monitors showed that 8-oxodG levels were significantly increased by exposure to PM2.5 over a 2-day period before sampling and by exposure to B[a]P over a 28-day period, days 57–84 before sampling. 15-F2t-IsoP levels were increased after exposure to B[a]P over both 2-day and 3-day periods preceding sample collection and after exposure to c-PAHs over a 2-day period before sampling. %AB.C. was significantly affected by exposure to B[a]P over a 14-day period, days 57–70 before sampling. In summary, our results indicate that the exposure to environmental pollutants affects urinary excretion of 8-oxodG, lipid peroxidation and the frequency of chromosomal aberrations.

Introduction

Air pollution is a significant factor negatively affecting the inhabitants of both developed and developing countries. Many studies have dealt with the health effects of polluted air. A recent review indicates that long-term exposure to particulate matter (PM) of aerodynamic diameter < 2.5 μm (PM2.5) increases the risk of nonaccidental mortality by 6% for each 10 μg/m3 increase in the concentration of pollutants, irrespective of age, gender or geographic location [1]. Exposure to polluted air is also associated with a higher incidence of various diseases, including cardiovascular and pulmonary disorders, as well as cancer [1], [2], [3], [4], [5], [6], [7], [8], [9], [10]. Negative effects of exposure to air pollutants are particularly deleterious for children and adolescents, in whom they may affect the development of lung function [3]. PM2.5 consists of respirable particles of dust, soot, liquid and aerosol with various chemicals bound to them. Of many chemicals adsorbed to respirable particles carcinogenic polycyclic aromatic hydrocarbons (c-PAHs) are regarded as one of the most important [11]. c-PAHs are metabolized into reactive intermediates that may bind to DNA and form PAH–DNA adducts, thus causing mutations and increasing cancer risk [12].

There are also other mechanisms underlying the effect of c-PAHs on genetic material. Polycyclic aromatic hydrocarbons (PAHs) may induce oxidative stress when metabolized by aldo-keto reductases to o-quinones [13]. These compounds may enter redox cycles and cause oxidative damage to macromolecules by the formation of reactive oxygen species (ROS). Chromosomal aberrations (CA) are another result of the exposure of cells to PAHs. CA, either unstable (e.g. breaks) or more serious stable translocations, which are conserved in the genome and may lead to changes in the expression of various genes, including oncogenes, may be formed by two different mechanisms. The production of ROS as a result of PAH metabolism and their interaction with DNA may induce strand breaks [14], [15]. If double strand breaks are formed and then processed by DNA repair mechanisms (homologous repair or nonhomologous end-joining repair), CA may result [16]. Another pathway leading to CA is initiated by PAH–DNA adducts. The adducts do not form double strand breaks directly, but as byproducts of repair mechanisms [17], [18].

Oxidative stress, caused by ROS, is defined as an imbalance between the levels of pro-oxidants and antioxidants. It may arise from endogenous and exogenous sources. While endogenous sources include natural processes, e.g. cellular metabolism or inflammation, exogenous sources arise from the environment, diet or life style. Oxidative stress affects all cellular macromolecules: DNA, lipids, as well as proteins [19]. It changes their function, causing mutations or disseminating oxidative stress to other molecules.

Measuring the levels of molecules modified or induced by oxidative stress has proved to be a useful approach to identify health risks in the environment [20]. Stable CA detected by fluorescence in situ hybridization (FISH) were repeatedly shown to be a sensitive biomarker of exposure to c-PAHs (e.g. [21], [22]). The advantage of FISH is its ability to detect the type of CA that are long lasting, transfer through many cell cycles, affect the expression of target genes and thus are directly related to cancer initiation.

In the present study we analyzed the levels of oxidative stress markers (8-oxo-7,8-dihydro-2′-deoxyguanosine, 8-oxodG; 15-F2t-isoprostane, 15-F2t-IsoP, protein carbonyls) and the frequency of chromosomal aberrations in a group of 59 city policemen working in Prague, Czech Republic. We collected the samples in February and May 2007, two seasons that might differ in the levels of air pollution. We investigated the seasonal variability of the biomarkers and their associations with levels of c-PAHs and PM2.5 in the ambient air. Due to the possible effect of ROS on the frequency of CA, we further analyzed the associations between the biomarkers of oxidative stress and CA. We hypothesized that exposure to higher concentrations of ambient air pollutants (PM2.5, c-PAHs) in winter season will be associated with both elevated levels of oxidative stress markers and higher frequency of cytogenetic parameters. We also expected oxidative stress markers to be positively correlated with cytogenetic parameters.

Section snippets

Subjects and sampling

The study population consisted of 59 city policemen (39 non-smokers, 20 smokers) living and working in the city center of Prague, Czech Republic, spending more than 8 h outdoors. The study subjects were followed in two seasons with supposedly different levels of air pollutants, in February and May 2007. Each participant completed a questionnaire on his personal medical history and life-style. All participants signed an informed consent form and could cancel their participation at any time during

Results

The average age (±standard deviation, SD) of subjects enrolled in our study was 33.0 ± 5.6 years. The average cholesterol concentration was 5.1 ± 0.8 mmol/l, levels of LDL-cholesterol reached 3.2 ± 0.6 mmol/l, HDL-cholesterol 1.4 ± 0.2 mmol/l and triglycerides 1.3 ± 0.9 mmol/l. These parameters were followed because they may affect levels of oxidative stress markers. High-fat diet results in increased levels of plasma lipids; at the same time high fat diet was shown to be associated with increased oxidative

Discussion

In our study we investigated the effect of environmental pollution on biomarkers of oxidative stress and cytogenetic parameters in a group of 59 city policemen in two seasons with different levels of air pollutants. We also studied possible associations between oxidative stress and cytogenetic biomarkers.

Our data indicate that there is no significant difference between the levels of the studied biomarkers in the two seasons despite differences in the concentrations of ambient air pollutants at

Conflict of interest statement

The authors have no conflict of interest to disclose.

Acknowledgement

The study was supported by the Czech Ministry of the Environment (SP/1b3/8/08).

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