Induction of sister chromatid exchanges in traffic policemen exposed to vehicular exhaust

In urban areas there is an explosive growth of population and the number of automobiles. The ever-increasing vehicular traffic density is posing continued threat to the ambient air quality. Traffic policemen as a group of workers are exposed occupationally to the pollutants from vehicular exhaust. Sister chromatid exchanges (SCEs) as a biomarker of the pollutant's effect, were analyzed in peripheral blood lymphocytes of 85 traffic policemen and 60 control subjects. There was a significant increase in the mean SCEs+/-S.D./cell in the exposed group (9.31+/-5.29) when compared to the controls (4.18+/-1.85). Thus the present study concludes that vehicular exhaust might induce cytogenetic damage in traffic police. Further, the more pronounced frequency of SCEs observed in the smoking traffic policemen than in the non-smoking group suggests the joint effect of smoking and vehicular exhaust.     

A note on urine trans, trans muconic acid level among a sample of Thai police: implication for an occupational health issue

Benzene exposure is of particular concern because recent research indicating that benzene exposure can result in chronic toxicity, therefore, monitoring for benzene exposure among at-risk workers is recommended. In exposure- and risk-evaluation, the monitoring of benzene by peripheral biomarker has several advantages over technical assessment of exposure. For this purpose, the urine trans, trans muconic acid (ttMA)e level is accepted as a useful monitoring tool for early diagnosis of dangerous exposure. Apart from the industrial workers, there are other occupations with high risk for benzene exposure. In this study, we study another at-risk occupation, the police. Thirty-nine urine samples were obtained from 39 Thai police working close to traffic in an urban area. All 39 samples were analyzed for ttMA level and compared to 10 other controls. The average urine ttMA level for the control and exposed group were < 0.05 mg/gCr and was 0.79 +/- 1.43 mg/gCr, respectively. Significant higher urine ttMA acid level among the police were observed (p <.05). Working in the air pollution in the urban area can be health hazard for the police. Exposure to the benzene from automobile exhaust can be an important occupational problem for these police.     

Chromosomal aberrations in peripheral lymphocytes of train engine drivers.

Studies of Swedish railway employees have indicated that railroad engine drivers have an increased cancer morbidity and incidence of chronic lymphatic leukemia. The drivers are exposed to relatively high magnetic fields (MF), ranging from a few to over a hundred microT. Although the possible genotoxic potential of MF is unclear, some earlier studies have indicated that occupational exposure to MF may increase chromosome aberrations in blood lymphocytes. Since an increased level of chromosomal aberrations has been suggested to predict elevated cancer risk, we performed a cytogenetic analysis on cultured (48 h) peripheral lymphocytes of Swedish train engine drivers. A pilot study of 18 engine drivers indicated a significant difference in the frequency of cells with chromosomal aberrations (gaps included or excluded) in comparison with seven concurrent referents (train dispatchers) and a control group of 16 office workers. The engine drivers had about four times higher frequency of cells with chromosome-type aberrations (excluding gaps) than the office workers (P < 0.01) and the dispatchers (P < 0.05). Seventy-eight percent of the engine drivers showed at least one cell per 100 with chromosome-type aberrations compared with 29% among the dispatchers and 31% among the office workers. In a follow-up study, another 30 engine drivers showed an increase (P < 0.05) in the frequency of cells with chromosome-type aberrations (gaps excluded) as compared with 30 referent policemen. Sixty percent of the engine drivers had one or more cells (per 100 cells) with chromosome-type aberrations compared with 30% among the policemen. In conclusion, the results of the two studies support the hypothesis that exposure to MF at mean intensities of 2-15 microT can induce chromosomal damage.     

Exposure to environmental polycyclic aromatic hydrocarbons: influences on cellular susceptibility to DNA damage (sampling Kosice and Sofia)

The aim of this study was to investigate a possible influence of occupational exposure to carcinogenic environmental polycyclic aromatic hydrocarbons (c-PAHs) on cellular susceptibility to the induction of the DNA damage. Monitoring was performed and blood samples were collected from two groups of male subjects: occupationally exposed and matched controls. The group exposed to c-PAHs (average age of 35.1 years) consisted of 52 policemen from Košice and 26 policemen and 25 bus drivers (51 altogether) from Sofia. The control group (average age of 36.4 years) consisted of 54 unexposed subjects from Košice and 24 from Sofia. In the investigated groups 52.5% of exposed subjects and 45.3% of control were current smokers. A challenging dose of X-rays (3 Gy) and an alkaline version of the single cell gel electrophoresis (SCGE) assay, known as Comet assay, were used to evaluate levels of induced DNA damage and repair kinetics in isolated human blood lymphocytes. DNA damage detected in lymphocytes prior to or after irradiation did not differ significantly between exposed and unexposed subjects. A significant decrease in repair efficiency due to exposure to PAHs was observed in the exposed individuals from Košice and Sofia, when analysed separately or together. A negative influence of tobacco smoking on the efficiency of DNA repair was observed. Statistically significant differences were found between subgroups stratified according to education level in Sofia: the half times for DNA repair declined with the increasing level of education. These results confirm that environmental exposure to c-PAHs can alter the ability of blood lymphocytes to repair DNA damage and, as a result could potentially lead to effects that are hazardous to human health.     

Health outcomes of road-traffic pollution among exposed roadside workers in Rawalpindi City,Pakistan

To document ill-health effects of air pollution on the local inhabitants, we analyzed the self-reported health issues associated with the inhalation of road traffic on daily basis. For this purpose, a revised version of ALS-DLD-78S questionnaire was administered, comprising the personal information and details related to the clinical history of the surveyed population (i.e. n = 580). Five dependent (outcome) variables, including chest pain, redness of eyes, shortness of breath, eye-tearing, and skin-itching were taken into account. The results revealed that ～80% of the surveyed population were directly or indirectly exposed to road traffic, and the incidence of chest pain among exposed individuals was estimated to increase with age (odds ratio (OR) = 6.49; 95% confidence interval (CI) = 1.46–28.81), especially among cardiac patients (OR = 13.87; 95%-CI = 3.28–58.61). However, the shortness of breath was predominantly observed among those who reported to have asthmatic symptoms (OR = 32.84; 95%-CI = 15.59–69.15) and cardiovascular symptoms (OR = 13.8: 95%-CI = 3.63–52.41). In case of itching, the population along the roadside were more vulnerable to exposure (OR = 5.79; 95%-CI = 2.81–11.93). While, exposure to traffic exhaust could be attributed to ～3.13% rise in the incidences of redness of eyes among general population, the outcomes of this survey show that daily exposure to traffic pollution is an important health concern for the urban population in general, as well as for various occupational groups in particular, working in outdoor environment.     

Biomonitoring of exposure to urban air pollutants: analysis of sister chromatid exchanges and DNA lesions in peripheral lymphocytes of traffic policemen

In order to elucidate the health effects of occupational exposure to traffic fumes, a few biomarkers of early genetic effect were investigated in Rome traffic policemen. One hundred and ninety healthy subjects engaged in traffic control (133 subjects) or in office work (57 subjects) participated the study. For all subjects, detailed information on smoking habits and other potential confounders were recorded by questionnaires. Average exposure of the study groups to benzene and other aromatic hydrocarbons was evaluated in a parallel exposure survey. All workers were genotyped for the following metabolic polymorphisms: CYP1A1 (m1, m2, and m4 variants), CYP2E1 (PstI and RsaI), NQO1 (Hinf1), GSTM1 and GSTT1 (null variants). In this paper, the results of the analysis of sister chromatid exchanges (SCE) in peripheral lymphocytes, and DNA damage by alkaline (pH 13) comet assay in mononuclear blood cells are reported. No statistically significant difference in the frequency of SCE or high frequency cells (HFC) was observed between traffic wardens and office workers (controls), despite the significantly higher exposure to benzene of the former (average group exposure 9.5 versus 3.8microg/m(3), 7h TWA). Conversely, both SCE per cell and HFC were highly significantly (P<0.001) increased in smokers compared to nonsmokers, showing a significant correlation (P<0.001) with the number of cigarettes per day. Multiple regression analyses of data, with metabolic polymorphisms, smoking habits, alcohol consumption, age, gender, and family history of cancer as independent variables, showed that smoking habits, and possibly the CYP2E1 variant genotypes, were the main factors explaining the variance of both SCE and HFC. Within smokers, an association of borderline significance between the CYP1A1 variant genotypes and increased SCE (P=0.050) and HFC (P=0.090) was found. This effect was mainly observed in light smokers (<15 cigarettes per day). The analysis of DNA damage by comet assay did not highlight any statistically significant difference between the exposed and control workers. Moreover, no significant model explaining tail moment variance was obtained by multiple regression analysis using the independent variables shown above. On the whole, these results indicate that exposure to moderate air pollution levels does not result in a detectable increase of genetic damage in blood cells. This evidence does not rule out any possibility of adverse effects, but strongly suggests that in urban residents life-style related factors, such as tobacco smoking, give the prevailing contribution to individual genotoxic burden.     

Chromosomal aberrations in lymphocytes of employees in transformer and generator production exposed to electromagnetic fields and mineral oil

The objective was to study the risk of cytogenetic damage among high voltage laboratory workers exposed to electromagnetic fields and mineral oil. This is a cross sectional study of 24 exposed and 24 matched controls in a Norwegian transformer factory. The exposure group included employees in the high voltage laboratory and in the generator soldering department. Electric and magnetic fields and oil mist and vapor were measured. Blood samples were analyzed for chromosomal aberrations in cultured lymphocytes. In addition to conventional cultures, the lymphocytes were also treated with hydroxyurea and caffeine. This procedure inhibits DNA synthesis and repair in vitro, revealing in vivo genotoxic lesions that are repaired during conventional culturing. In conventional cultures, the exposure group and the controls showed similar values for all cytogenetic parameters. In the DNA synthesis- and repair-inhibited cultures, generator welders showed no differences compared to controls. Among high voltage laboratory testers, compared to the controls, the median number of chromatid breaks was doubled (5 vs. 2.5 per 50 cells; P<0.05) the median number of chromosome breaks was 2 vs. 0.5 (P>0.05) and the median number of aberrant cells was 5 vs. 3.5 (P<0.05). Further analysis of the inhibited culture data from this and a previous study indicated that years of exposure and smoking increase the risk of aberrations. We conclude that there was no increase in cytogenetic damage among exposed workers compared to controls in the conventional lymphocyte assay. In inhibited cultures, however, there were indications that electromagnetic fields in combination with mineral oil exposure may produce chromosomal aberrations.     

Influence of PAHs in ambient air on chromosomal aberrations in exposed subjects: international study - EXPAH

The aim of this study was to determine the influence of carcinogenic polycyclic aromatic hydrocarbons (c–PAHs) in complex mixtures in ambient air on DNA damage (chromosomal aberrations) in occupationally exposed subjects measured as percent of aberrant cells (% AB.C.).

There were in total 203 exposed subjects and 150 respective controls in the whole project, allocated in three different European cities – Kosice (Slovakia), Prague (Czech Republic) and Sofia (Bulgaria). The studied population from Kosice (Slovakia) consisted of 106 subjects. From these 51 were exposed policemen and 55 were controls. The Czech population comprised 52 exposed policemen and 50 controls. In Bulgaria, there were two equally numerous exposed groups: 50 policemen and 50 professional bus drivers together with 45 controls. According to personal monitoring, policemen and bus drivers in the Bulgarian capital Sofia were exposed to the highest levels of c-PAHs amongst the exposed subject groups in the cities (45.3 ± 25.9 ng/m³ in policemen resp. 36.1 ± 31.6 ng/m³ in bus drivers in Sofia, 26.8 ± 39.8 ng/m³ for policemen in Kosice and 11.9 ± 11.2 ng/m³ for policemen in Prague), compared to the respective controls (24.9 ± 17.7 ng/m³ for controls in Sofia, 7.9 ± 3.8 ng/m³ for controls in Kosice and 6.2 ± 3.6 ng/m³ for controls in Prague).

We observed the following frequency of % AB.C. scored by conventional method: 2.60 ± 2.64 in exposed policemen and 2.14 ± 1.61 in controls in Kosice (p = n.s.); 2.33 ± 1.53 in exposed policemen and 1.94 ± 1.28 in controls in Prague (p = n.s.); 3.04 ± 1.64 in exposed policemen, respectively, 3.60 ± 1.63 in exposed bus drivers and 1.79 ± 0.77 in the control group in Sofia (p < 0.05, respectively, p < 0.05).

According to data from multiple regression analysis, and group comparison of smokers versus nonsmokers in Sofia also cigarette smoking (p = 0.055) and the age (p = 0.020) seem to play an important role within the aberrant cell formation in addition to the occupational c-PAHs exposure (p = 0.000). Smoking status was the modifying factor for % AB.C. in Kosice (p = 0.020) after multiple regression approach was employed.

In summary, we can say that subjects occupationally exposed to higher levels of c-PAHs in ambient air in Sofia are at greater genotoxic risk compared to those working indoors.     

Genotoxic damage in mine workers exposed to diesel exhaust, and the effects of glutathione transferase genotypes

This study was performed in an Estonian shale-oil mine with the purpose to develop and apply a number of biomarkers for occupational diesel-exhaust exposure monitoring. Increased breathing-zone exposures to exhaust from operators of diesel-powered trucks in the mine was confirmed in the environmental monitoring part of the study, showing a 7.5-fold higher exposure to particle-associated 1-nitropyrene (1-NP) in 50 underground workers compared with 42 surface workers [P.T.J. Scheepers, D. Coggon, L.E. Knudsen, R. Anzion, H. Autrup, S. Bogovski, R.P. Bos, D. Dahmann, P. Farmer, E.A. Martin, V. Micka, V. Muzyka, H.-G. Neumann, J. Poole, A. Schmidt-Ott, F. Seiler, J. Volf, I. Zwirner-Baier, Biomarkers for occupational diesel exhaust exposure monitoring (BIOMODEM)-a study in underground mining, Toxicol. Lett. 134 (2002) 305-317; P.T.J. Scheepers, V. Micka, V. Muzyka, R. Anzion, D. Dahmann, J. Poole, R.P. Bos, Exposure to dust and particle-associated 1-nitropyrene of drivers of diesel-powered equipment in underground mining, Ann. Occp. Hyg. 47 (2003) 379-388]. Analysis of DNA damage by the Comet assay on frozen blood samples was performed on the total study group and showed significantly higher levels (p=0.003) in underground workers (smokers) driving diesel-powered excavation machines (median 155 on a scale from 0 to 400, among 47 persons), compared with surface workers who smoked (median of 90, among 46 persons). The level of DNA damage in underground smokers was significantly higher (p=0.04) than in non-smokers. Samples from 2 of the 3 sampling weeks had significantly lower DNA damage compared with the third week, probably due to timely processing and freezing. These samples also showed significant differences (p<0.001) between underground workers (median 145, among 41 persons) and surface workers (median 60, among 30 persons). An HPLC method was developed for the analysis of (32)P-postlabelled 1-NP-DNA-adducts, and was applied to a sub-sample of 20 workers. No significant differences between surface and underground workers were found in this sub-sample with respect to the minor, unidentified adducts that had similar chromatographic properties to 1-NP adducts, and smoking did not have any effect on adduct levels. No significant effects of the genotypes of GSTM1, GSTP1 and GSTT1 on DNA-adducts and on DNA damage as measured by the Comet assay were found in the total study group. The study confirms an increased level of DNA damage in workers exposed to exhaust from truck-driving in the mine. However, the results of the environmental and biological monitoring of 1-NP did not correlate, suggesting that inhalation exposure to diesel exhaust is not reflected by an increase in 1-NP-DNA-adduct levels and/or that factors other than occupational exposure to diesel exhaust are primary determinants of these DNA-adduct levels.     

Chromosome aberrations in workers of nuclear-power plants

The frequencies of chromosome aberrations in 135 workers from nuclear-power plants were compared with those in 135 age-matched controls. A total of 135,000 cells was scored. The frequencies of dicentric chromosome were 1.67 × 10⁻³ in the exposed group and 0.49 × 10⁻³ in the control group and those of chromosome-type deletion were 3.33 × 10⁻³ and 1.10 × 10⁻³, respectively. The frequencies of all types of chromosome aberrations in the exposed subjects were higher than those in the control group, but no significant trend of dose-dependent increase was observed when only the exposed group were considered. Poisson regression analysis, with both exposed and control included, showed that there was a significant association of chromosome aberration with radiation dose and the duration of work, but not with age, smoking habit and alcohol intake. It was also found that recent exposure to radiation, within the last 5 years, had contributed more to the observed chromosome aberration than earlier exposure.     

急性臭氧暴露对大鼠肺部细胞遗传毒性的影响*

目的: 探讨不同浓度臭氧急性暴露对大鼠肺部细胞的遗传毒性的影响。方法: 36只wistar大鼠随机分为对照组(过滤空气暴露)、臭氧暴露组(0.12 ppm、0.5 ppm、1.0 ppm、2.0 ppm、4.0 ppm)共6组,每组6只。以不同浓度的臭氧对大鼠进行动态染毒4 h后,取肺组织并分离单细胞,采用酶联免疫吸附法检测8-羟基脱氧鸟苷(8-OHdG),利用彗星实验、微核试验和DNA-蛋白质交联实验进行DNA和染色体损伤分析。结果: 与对照组相比,肺组织中8-OHdG含量从臭氧暴露浓度为0.12 ppm起即显著增加,在0.5 ppm时达到最高值。随着臭氧暴露浓度升高,彗星拖尾率逐渐上升,且存在明显的剂量-效应关系;DNA-蛋白质交联率有先升高后下降的趋势,且在2.0 ppm时达到最大值;而肺部细胞微核率尽管呈现出上升趋势,但与对照组相比无显著性差异。结论: 急性臭氧暴露在较低浓度(0.12 ppm)时即可导致大鼠肺部细胞的DNA损伤;而在较高浓度(4 ppm)时却未见显著的染色体损伤。     

Serum pneumoproteins and biomarkers of exposure to urban air pollution: a cross-sectional comparison of policemen and foresters

Very few biomarkers are available for the non-invasive detection of effects of urban air pollution on the respiratory tract. The objective was to evaluate whether Clara cell protein (CC16) and surfactant-associated protein-A (SP-A), two pulmonary secretory proteins, were useful in the detection of effects of urban air pollutants on the pulmonary epithelium. These proteins were determined in the serum of 53 policemen working in Brussels, Belgium, and a control group of 59 foresters working in the countryside. Except for ozone (O₃), annual concentrations of the main air pollutants (PM₁₀, NO₂, CO, SO₂ and benzene) were significantly higher in Brussels than in the country. The proportion of smokers was lower in urban policemen compared with foresters, but they smoked on average a similar number of cigarettes per day as confirmed by their urinary excretion of cotinine. Muconic acid, a marker of benzene exposure, was significantly higher in urban policemen than in foresters, in both smokers and non-smokers. Multiple regression analysis showed that the type of work, smoking habits and time spent outdoors and in a car were significant determinants of benzene uptake. Tobacco smoking impaired lung function to a similar extent in urban policemen and foresters. The serum levels of SP-A were significantly increased in smokers but were not different between policemen and foresters. Serum CC16 was significantly reduced by tobacco smoking and slightly decreased in policemen compared with foresters. Interestingly, the reduction of serum CC16 was more pronounced in the subgroup of traffic compared with survey policemen, the latter being also less exposed to benzene. The results suggest that serum pneumoproteins and especially serum CC16 could be useful in the detection of chronic effects of urban air pollutants on the respiratory epithelium of populations particularly at risk.     

Serum pneumoproteins and biomarkers of exposure to urban air pollution: a cross-sectional comparison of policemen and foresters.

Very few biomarkers are available for the non-invasive detection of effects of urban air pollution on the respiratory tract. The objective was to evaluate whether Clara cell protein (CC16) and surfactant-associated protein-A (SP-A), two pulmonary secretory proteins, were useful in the detection of effects of urban air pollutants on the pulmonary epithelium. These proteins were determined in the serum of 53 policemen working in Brussels, Belgium, and a control group of 59 foresters working in the countryside. Except for ozone (O(3)), annual concentrations of the main air pollutants (PM(10), NO(2), CO, SO(2) and benzene) were significantly higher in Brussels than in the country. The proportion of smokers was lower in urban policemen compared with foresters, but they smoked on average a similar number of cigarettes per day as confirmed by their urinary excretion of cotinine. Muconic acid, a marker of benzene exposure, was significantly higher in urban policemen than in foresters, in both smokers and non-smokers. Multiple regression analysis showed that the type of work, smoking habits and time spent outdoors and in a car were significant determinants of benzene uptake. Tobacco smoking impaired lung function to a similar extent in urban policemen and foresters. The serum levels of SP-A were significantly increased in smokers but were not different between policemen and foresters. Serum CC16 was significantly reduced by tobacco smoking and slightly decreased in policemen compared with foresters. Interestingly, the reduction of serum CC16 was more pronounced in the subgroup of traffic compared with survey policemen, the latter being also less exposed to benzene. The results suggest that serum pneumoproteins and especially serum CC16 could be useful in the detection of chronic effects of urban air pollutants on the respiratory epithelium of populations particularly at risk.     

DNA damage in humans exposed to environmental and dietary polycyclic aromatic hydrocarbons

The paper describes recent research on human DNA damage related to environmental and dietary polycyclic aromatic hydrocarbon (PAH) exposures. The study populations either represent general populations of large geographical regions, or their exposure situation may have relevance to the general population. In Silesia, Poland, and Northern Bohemia, Czech Republic, where coal-based industry and domestic heating are the major sources of PAHs, significant differences have been observed in white blood cell DNA adducts and cytogenetic biomarkers between environmentally exposed and rural control populations, and significant seasonal variations of DNA damage have been detected. Bus drivers, traffic policemen and local residents have been involved in biomarker studies in Copenhagen, Athens, Genoa and Cairo, and differences have been measured in the level of DNA damage of urban and rural populations. Burning of smoky coal in unvented homes in Xuan Wei region, China, causes high PAH exposure of residents, which has been reflected in DNA adduct levels in different tissues. Indoor wood burning in open fireplaces did not increase human DNA adduct levels. Oil-well fires left burning in Kuwait after the Persian Gulf war created an unprecedented environmental pollution. However, insignificant environmental PAH levels were measured several miles from these fires. Aromatic and PAH-DNA adduct levels in white blood cells of US Army soldiers were lower during their deployment in Kuwait, than in Fulda, Germany, where they were stationed before and after serving in Kuwait. The contribution of dietary PAH exposure to blood cell DNA adduct levels had been demonstrated in studies in which volunteers consumed heavily charbroiled beef. Environmental tobacco smoke did not cause detectable changes, as measured by 32P-postlabelling, in DNA adduct levels in non-smokers. In the reviewed studies, observed DNA adduct levels were generally in the range of 1 to 10 adducts, and not higher than 40 adducts in 108 nucleotides. Typically, 1.5 to 3-fold differences have been detected in DNA adduct levels between the exposed and control groups.     

Effects of polycyclic aromatic hydrocarbons (PAHs) in environmental pollution on exogenous and oxidative DNA damage (EXPAH project): description of the population under study

The EXPAH project was a molecular epidemiology study whose aims were to evaluate the hypothesis that polycyclic aromatic hydrocarbons (PAHs) are a major source of genotoxic activities of organic mixtures associated with air pollution. Biomarkers of exposure, effects and susceptibility, and oxidative DNA damage were measured in three PAH-exposed populations from Prague (Czech Republic), Kosice (Slovakia) and Sofia (Bulgaria). Control populations were included from each city. In total 356 individuals were enrolled. A questionnaire was used to determine life style/dietary factors. Ambient air exposure was measured by stationary monitoring, and personal exposure monitoring was also carried out. The characteristics of the population are described in this paper together with their personal exposure to carcinogenic PAHs (c-PAHs). The dose of c-PAH exposure was found to vary between the occupationally exposed (e.g. policemen and bus drivers) and the control populations in each country, and also varied from country to country.     

Long-term cytogenetic effects in children prenatally-exposed to radiation as a result of the accident at the Chernobyl Atomic Energy Station

Forty-two children exposed to ionizing radiation in prenatal period and 15 children of control group were examined in the remote terms after the accident using the method of differential G-staining of chromosomes in lymphocytes of peripheral blood. It was found that the average group rate of aberrant cells and chromosome aberrations was reliably higher in the children exposed in utero compared to control. Long-term cytogenetic consequences of the pre-natal exposure were characterized by prevalence of aberrations of a chromosome type, mainly stable chromosome lesions. At chronic exposure to low doses of ionizing radiation the increase in the rate both stable and unstable chromosome aberrations.     

Repair competence assay in studies of the influence of environmental exposure to c-PAHs on individual susceptibility to induction of DNA damage

Previous results from studies performed in three European cities suggested a decrease in DNA repair efficiency observed in lymphocytes of subjects occupationally exposed to environmental carcinogenic polycyclic aromatic hydrocarbons (c-PAHs). The aim of this study was to investigate whether a relationship between exposure to environmental c-PAHs and cellular vulnerability to the induction of DNA damage and its repair is confirmed in a pooled group of subjects from Prague, Košice and Sofia. The investigated pool consisted of 144 subjects occupationally exposed to environmental c-PAHs, who were municipal policemen or bus drivers. A control group of 115 matched individuals consisted of males unexposed at work to c-PAHs. The repair efficacy was evaluated by a comparison of the DNA damage detected by the single cell gel electrophoresis (SCGE) immediately after challenging the cells with X-ray irradiation, with residual damage (RD) being measured after an incubation period of 60 min. A stochastic concept for a mechanism of the interaction between DNA and various genotoxic exposures, was applied to analyze a relationship between exposure and biological effect in the studied sample. The outcome of the study confirms that the exposure to environmental c-PAHs or smoking cigarettes, significantly decreases DNA repair efficiency (repair efficiency in the pooled group of exposed individuals was 61.8 ± 11.8% versus 67.9 ± 9.9 in control, p < 0.001, and repair efficiency in group of smoking individuals was 63.0 ± 11.5% versus 65.9 ± 11.1 in nonsmokers, p < 0.005). The repair efficiency can be affected by a genetic polymorphism, such as subjects with a homozygous mutation in polymorphic CYP1A1_(Val/Val) enzyme, or slow NAT2 acetylators, who showed a considerably lower DNA repair efficiency (i.e. average repair efficiency in subgroups of fast acetylators was for the control subgroup 68.1% versus 66.5% in exposed subjects, while in the case of subgroups of slow acetylators, for the control group was 68.0% versus significantly less in the exposed subjects, 60.6%, p < 0.05). Smoking habits, or the diet's vitamin content, significantly affected the process. The results obtained confirm a potential value of the method as a biomarker of susceptibility in molecular epidemiology or preclinical studies, aimed at predicting susceptibility to various genotoxic exposures (environmental, occupational, therapeutic). To conclude, the research proved the influence of environmental c-PAHs, genotypes, and life styles on DNA damage and on its repair efficiency. Even low exposure to environmental c-PAHs altered DNA repair abilities of the subjects, which may result in an increased cancer risk. The findings confirm that c-PAHs should become pollutants that are subject to regulation.     

Cytogenetic biomonitoring of carpet fabric workers using micronucleus frequency, nuclear changes, and the calculation of risk assessment by repair index in exfoliated mucosa cells

The micronucleus (MN) assay in exfoliated buccal cells is a minimally invasive method for monitoring genetic damage in human populations and is used as an indicator of genotoxic exposition, as it is associated with chromosome aberrations. In this study, we evaluated MN frequencies and other nuclear changes (NCs), such as karyorrhexis (KR), karyolysis (KL), broken egg (BE), and binucleus in buccal mucosa cells of 50 carpet fabric workers (25 smokers and 25 nonsmokers) and 50 healthy control subjects (25 smokers and 25 nonsmokers). Microscopic observation of 2000 cells per individual was performed in both workers and control subjects. In both the control group and the exposed group, for each person a repair index (RI) was calculated via the following formula: (KR+KL)/(BE+MN). The results showed a statistically significant increase in the frequency of MN in buccal epithelial cells of exposed group compared with control group. There is a significant difference between worker and control groups (p<0.001) for RI. We believe that the calculation of RI values, in addition to nuclear changes, presents a new approach in risk assessment in relation to occupational exposure.     

Serum pneumoproteins and biomarkers of exposure to urban air pollution: a cross-sectional comparison of policemen and foresters

Very few biomarkers are available for the non-invasive detection of effects of urban air pollution on the respiratory tract. The objective was to evaluate whether Clara cell protein (CC16) and surfactant-associated protein-A (SP-A), two pulmonary secretory proteins, were useful in the detection of effects of urban air pollutants on the pulmonary epithelium. These proteins were determined in the serum of 53 policemen working in Brussels, Belgium, and a control group of 59 foresters working in the countryside. Except for ozone (O₃), annual concentrations of the main air pollutants (PM₁₀, NO₂, CO, SO₂ and benzene) were significantly higher in Brussels than in the country. The proportion of smokers was lower in urban policemen compared with foresters, but they smoked on average a similar number of cigarettes per day as confirmed by their urinary excretion of cotinine. Muconic acid, a marker of benzene exposure, was significantly higher in urban policemen than in foresters, in both smokers and non-smokers. Multiple regression analysis showed that the type of work, smoking habits and time spent outdoors and in a car were significant determinants of benzene uptake. Tobacco smoking impaired lung function to a similar extent in urban policemen and foresters. The serum levels of SP-A were significantly increased in smokers but were not different between policemen and foresters. Serum CC16 was significantly reduced by tobacco smoking and slightly decreased in policemen compared with foresters. Interestingly, the reduction of serum CC16 was more pronounced in the subgroup of traffic compared with survey policemen, the latter being also less exposed to benzene. The results suggest that serum pneumoproteins and especially serum CC16 could be useful in the detection of chronic effects of urban air pollutants on the respiratory epithelium of populations particularly at risk.     

Investigating DNA damage in tannery workers occupationally exposed to trivalent chromium using comet assay

DNA damage of peripheral lymphocytes in 60 workers occupationally exposed to trivalent chromium [Cr(III)] in a tannery was studied using comet assay. The urinary and blood chromium levels were detected as a biomarker of internal exposure. The 90 subjects were divided into three groups: (i) exposure group I included 30 tannery workers highly exposed to chromium from tanning department; (ii) exposure group II included 30 tannery workers with moderate chromium exposure from finishing department; (iii) control group included 30 individuals without exposure to physical or chemical genotoxic agents. No significant difference was found among the three groups for age and smoking. The results showed that the medians of blood and urinary Cr of two exposure groups were significantly higher than those of control group (P<0.01). And the medians of blood and urinary Cr of exposure group I were significantly higher than those of exposure group II (P<0.05 or P<0.01). The medians of mean tail length (MTL) of the three groups were 5.33 (2.90-8.50), 3.43 (2.31-8.29) and 2.04 (0.09-3.83) microm, respectively; The medians of mean tail moment (MTM) of the three groups were 6.28 (2.14-11.81), 3.41 (1.25-11.07) and 0.53 (0.13-3.29), respectively. The MTL and MTM of two exposure groups were significantly higher than those of control group (P<0.01). The MTL and MTM of exposure group I were significantly higher than those of exposure group II (P<0.01). The results of the present investigation suggest that occupational exposure to trivalent chromium can lead to a detectable DNA damage of human peripheral lymphocytes. Moreover, DNA damage was associated with chromium levels in blood. DNA damage may serve as a valuable effective biomarker and total chromium in blood may serve as a useful internal exposure biomarker in the population occupationally exposed to trivalent chromium.