Genotoxic Effects Of Occupational Exposure Research Articles

Genotoxic effects of occupational exposure to glass fibres - A human biomonitoring study

As part of a large human biomonitoring study, we conducted occupational monitoring in a glass fibre factory in Slovakia. Shopfloor workers (n = 80), with a matched group of administrators in the same factory (n = 36), were monitored for exposure to glass fibres and to polycyclic aromatic hydrocarbons (PAHs). The impact of occupational exposure on chromosomal aberrations, DNA damage and DNA repair, immunomodulatory markers, and the role of nutritional and lifestyle factors, as well as the effect of polymorphisms in metabolic and DNA repair genes on genetic stability, were investigated.The (enzyme-modified) comet assay was employed to measure DNA strand breaks (SBs) and apurinic sites, oxidised and alkylated bases. Antioxidant status was estimated by resistance to H2O2-induced DNA damage. Base excision repair capacity was measured with an in vitro assay (based on the comet assay).Exposure of workers to fibres was low, but still was associated with higher levels of SBs, and SBs plus oxidised bases, and higher sensitivity to H2O2. Multivariate analysis showed that exposure increased the risk of high levels of SBs by 20%. DNA damage was influenced by antioxidant enzymes catalase and glutathione S-transferase (measured in blood). DNA repair capacity was inversely correlated with DNA damage and positively with antioxidant status. An inverse correlation was found between DNA base oxidation and the percentage of eosinophils (involved in the inflammatory response) in peripheral blood of both exposed and reference groups. Genotypes of XRCC1 variants rs3213245 and rs25487 significantly decreased the risk of high levels of base oxidation, to 0.50 (p = 0.001) and 0.59 (p = 0.001), respectively.Increases in DNA damage owing to glass fibre exposure were significant but modest, and no increases were seen in chromosome aberrations or micronuclei. However, it is of concern that even low levels of exposure to these fibres can cause significant genetic damage.

Induction of genotoxicity and mutagenic potential of heavy metals in Thai occupational workers

Heavy metals are widely used in many industries in Thailand and found in the environment. Occupational exposure to heavy metals is often chronic and caused by environmental contaminations, potentially leading to mutations and cancer. Although the genotoxic effects of occupational exposure to multiple heavy metals have been extensively studied, the findings regarding their genotoxicity are conflicting. In this study, we focused on investigating the genotoxic effects of certain heavy metals mixtures, including lead (Pb), copper (Cu), zinc (Zn), and tin (Sn), to which workers are exposed in the manufacturing industry. The cytokinesis-blocked micronucleus (CBMN) assay in peripheral blood lymphocytes was performed, and DNA damage was assessed by measuring tumour-associated protein levels and 8-hydroxy-2′-deoxyguanosine (8-OHdG) generated by oxidative stress that causes cytotoxicity. The occupational exposure group included 110 workers exposed to heavy metal mixtures and 105 matched control subjects. We found statistically significant differences in the blood Pb, Sn, and Cu levels between the exposed workers and the control subjects (p < 0.001). Analysis of micronuclei (MN) in peripheral blood lymphocytes revealed a significantly increased frequency of MN in exposed workers compared with that in control subjects (p<0.05). Non-smoking exposed workers were selected for 8-OHdG formation and mutant p53 tests, and significant differences in the mean plasma 8-OHdG concentration (p < 0.001) were found between the occupational exposure and the control group, but no differences were found in the levels of mutant p53. Thus, chronic exposure to different heavy metals causes genotoxic effects in humans. Furthermore, the CBMN assay and 8-OHdG formation can be used as surrogate biomarkers to identify and monitor groups with higher carcinogenic risk in the early stages of toxicity. In summary, our results indicate that mixtures of heavy metals (Pb, Sn, and Cu) in manufacturing industries pose an elevated health risk due to DNA damage.

Assessment of DNA Damage in Lymphocytes of RadiationWorkers at Al-Tuwaitha Site using Nuclear Division Index and Hypoxanthine guanine phosphoribosyl transferase (HPRT)

Radiation of its different types is one of the major well known mutagens and carcinogens. Ionizingradiation (IR) imposes risks to human health and the environment. Man is exposed to different types of radiation of which those used in diagnosis of diseases, treatment of cancer and occupationally exposed to ionizing radiation . Radiation exposure induces damage on normal cells.IR at low dosesand low dose rates has the potency to initiate carcinogenesis. Genotoxic environmental agents such as IR trigger a cascade of signal transduction pathways for cellular protection. Iraqi radiation workers in radioactive waste treatment and management at Al-Tuwaithasite.This study included 30 Iraqi radiation workers in radioactive waste treatment and management at Al-Tuwaitha site , 20 were non-smokers and 10 smokers, aged (25 - 55 year), as well as 20 male blood samples, aged (26 - 54 year) which are 13 were non-smokers and 7 smokers as control. Three cytogenetic parameters were studied to determine genotoxic effects of occupational exposure of low ionizing radiation doses in peripheral blood lymphocytes of from radiation workers at radioactive waste treatment and management at Al-Tuwaitha site in Baghdad .Investigations were carried out by using Hypoxanthine guanine phosphorribosyl transferase (HPRT) mutation assay were performed on peripheral blood lymphocytes for workers and control groups.

Genotoxic effects of occupational exposure to benzene in gasoline station workers.

Benzene, a hazardous component of gasoline, is a genotoxic class I human carcinogen. This study evaluated the genotoxic effects of occupational exposure to benzene in gasoline stations. Genotoxicity of exposure to benzene was assessed in peripheral blood leucocytes of 62 gasoline station workers and compared with an equal numbers of matched controls using total genomic DNA fragmentation, micronucleus test and cell viability test. An ambient air samples were collected and analyzed for Monitoring of benzene, toluene, ethyl benzene and xylene (BTEX) in work environment and control areas. DNA fragmentation, micronucleus and dead cells percent were significantly higher in exposed workers than controls. Level of benzene, Toluene, Ethyl benzene and xylene in the work environment were higher than the control areas and the permissible limits. Gasoline station workers occupationally exposed to benzene are susceptible to genotoxic effects indicated by increased DNA fragmentation, higher frequency of micronucleus and decreased leukocytes viability.

Immunological and genotoxic effects of occupational exposure to α-cypermethrin pesticide.

The aim of this work has been to find out the occupational oxidative stress, immunological and genotoxic health hazards among α-cypermethrin (CYP) pesticide-exposed workers. A cross-sectional study was performed including 200 workers divided into 3 groups according to the level of exposure: highly exposed group (50 workers), moderately exposed group (50 workers) and unexposed group (100 workers). All workers were subjected to detailed laboratory investigation for gene P53 mutations, immunological parameters as a cluster of differentiation into 3 percentage (CD3%), CD4% and CD8% in addition to peripheral blood total leukocytic and platelet counts that were measured. Spectrophotometer technique was used for detection of superoxide dismutase (SOD), catalase (CAT), glutathione (GSH) and glutathione peroxidase (GPx). Air samples were collected with a High Volume Small Surface Sampler for measurement of α-cypermethrin level. A highly exposed group to the α-cypermethrin had lower CD4/CD8 as compared to an unexposed group with statistically significant difference. As regards gene mutation, exons 5a and 6 were more frequent among the highly exposed group as compared to no mutation among moderately exposed and unexposed groups with significant difference. As regards antioxidants; SOD, CAT, GSH and GPx were higher among the unexposed group as compared to the highly and moderately exposed group with statistically significant difference. Significant negative correlation was found between working years and antioxidant parameters. Repeated exposure to α-CYP may lead to gene mutations, immunological disturbances and oxidative stress. Strict safety precautions are required not only for workers but also for public users. Int J Occup Med Environ Health 2017;30(4):603-615.

Nuclear anomalies in exfoliated buccal cells in Pakistani cotton weavers.

Cotton workers in small weaving household factories (power looms) in Pakistan are typically exposed to high levels of cotton dusts. Working in the textile manufacturing industry has been classified as a possible human carcinogen (group 2B) by the International Agency for Research on Cancer. The study set out to determine potential cytotoxic and genotoxic effects of occupational exposure to cotton dusts in exfoliated buccal cells of exposed cotton workers. Nuclear anomalies reflecting cytotoxic and genotoxic effects were evaluated in a representative sample of 51 exposed male cotton weavers and in the same number of age-matched male non-exposed subjects applying the micronucleus cytome assay. Nuclear anomalies reflecting cytotoxicity (karyolysis, karyorrhexis, condensed chromatin and pyknosis) were significantly elevated in exposed cotton workers. The frequency of micronucleated cells increased significantly with increasing years of work in power looms (odds ratio = 1.043 per year; 95% confidence interval: 1.012-1.076, P = 0.007). Results were consistent with the typical inflammatory pattern and injury in epithelia due to unprotected occupational exposure to cotton dusts and other toxic, allergic and infectious substances in the working areas of the cotton industry. Occupational exposure in power looms induces cytotoxic effects and, upon chronic exposure, DNA damage. This may eventually result in typical obstructive patterns of pulmonary symptoms and in a clinical condition called byssinosis in exposed cotton workers. Long exposure may lead to chronic inflammation and cumulative damage of DNA in buccal stem cells that may indicate an increased risk of oropharyngeal cancer.

Chromosomal Abnormalities among Petrol Station Workers Occupationally Exposed to Benzene

It is known that the vast majority of malignancies are the result of genetic and environmental interactions. Fuel (diesel and petrol) constitutes a complex mixture of benzene, toluene and xylene and other monocyclic, aromatic, aliphatic and polycyclic aromatic hydrocarbons; benzene being the most hazardous because of its carcinogenic potency. This study aims to evaluate the genotoxic effects of occupational exposure to benzene through cytogenetic analysis at low levels of exposure also to investigate the possibility of liver and kidney affections. The studied group comprised 40 workers from 3 different petrol stations occupationally exposed to benzene and 20 control subjects. The two studied groups were matched regarding age and sex. Results show significant difference between exposed workers and control group in chromosomal abnormalities regarding mitotic index, gap, isogap and break. Regarding period of exposure, the frequency of different types of chromosomal aberrations was relatively high during first few years of exposure and decrease with Original Research Article El Mahdy et al.; BJAST, 7(5): 502-513, 2015; Article no.BJAST.2015.168 503 increasing duration. Regarding liver function tests, levels were within normal ranges but higher in workers with statistically significant difference between exposed workers and control group and they were significantly correlated with the duration of exposure (p value= .05). Occupational exposure to mutagenic and carcinogenic agents creates a significant impact on the health status of gasoline station attendants. Identification and prevention of possible health problems related to such exposure would help in maintaining good health of workers; prevent reduction in working capacity and loss of working hours besides reducing the cost of medical care for affected workers. Further studies are needed to assess DNA status in the lymphocytes that might be a predictor of future cancer risks and might help to prevent further deterioration in the health of these workers.

Genotoxic effects of occupational exposure to lead and influence of polymorphisms in genes involved in lead toxicokinetics and in DNA repair

Lead is still widely used in many industrial processes and is very persistent in the environment. Although toxic effects caused by occupational exposure to lead have been extensively studied, there are still conflicting results regarding its genotoxicity. In a previous pilot study we observed some genotoxic effects in a population of lead exposed workers. Thus, we extended our study analysing a larger population, increasing the number of genotoxicity endpoints, and including a set of 20 genetic polymorphisms related to lead toxicokinetics and DNA repair as susceptibility biomarkers. Our population comprised 148 workers from two Portuguese factories and 107 controls. The parameters analysed were: blood lead levels (BLL) and δ-aminolevulinic acid dehydratase (ALAD) activity as exposure biomarkers, and T-cell receptor (TCR) mutation assay, micronucleus (MN) test, comet assay and OGG1-modified comet assay as genotoxicity biomarkers. Lead exposed workers showed markedly higher BLL and lower ALAD activity than the controls, and significant increases of TCR mutation frequency (TCR-Mf), MN rate and DNA damage. Oxidative damage did not experience any significant alteration in the exposed population. Besides, significant influence was observed for VDR rs1544410 polymorphism on BLL; APE1 rs1130409 and LIG4 rs1805388 polymorphisms on TCR-Mf; MUTYH rs3219489, XRCC4 rs28360135 and LIG4 rs1805388 polymorphisms on comet assay parameter; and OGG1 rs1052133 and XRCC4 rs28360135 polymorphisms on oxidative damage. Our results showed genotoxic effects related to occupational lead exposure to levels under the Portuguese regulation limit of 70μg/dl. Moreover, a significant influence of polymorphisms in genes involved in DNA repair on genotoxicity biomarkers was observed.

Evaluation of genotoxic effects of lead in pottery-glaze workers using micronucleus assay, alkaline comet assay and DNA diffusion assay

We investigated genotoxic effects of occupational exposure to lead acetate in pottery-glaze ceramic workers. The study was carried out in 30 exposed workers and 30 matched controls, to whom several biochemical parameters-the blood lead (B-Pb; range: exposed, 41.68-404.77; controls, 12-52) and cadmium (B-Cd) level, the activity of delta-aminolevulinic acid dehydratase (ALAD), erythrocyte protoporphyrin (EP), the level of vitamin B(12) and folate in serum-were measured. The genotoxic effects were evaluated by the alkaline comet assay, the DNA diffusion assay and micronucleus test in peripheral blood lymphocytes. Subjects exposed to lead had significantly higher B-Pb level and, consequently, increased values of tail intensity (TI), frequency of apoptotic and necrotic cells, and frequency of micronuclei (MN). In contrast, their activity of ALAD, the level of vitamin B(12) and folate in serum were significantly lower compared to controls. Poisson regression analysis showed a significant correlation of profession, duration of exposure, smoking, level of cadmium in blood, ALAD and EP with primary DNA damage. A majority of primary damage repairs in a short period after exposure to a genotoxic agent. In addition, the influence of gender and level of vitamin B(12) and folate in serum MN frequency in exposed group was observed. In this study, DNA diffusion and micronucleus test showed higher influence of tested parameters to DNA damage. The results indicate a need for concomitant use of at least two different biomarkers of exposure when estimating a genetic risk of lead exposure.

Genotoxic effect of occupational exposure to cadmium

Many studies proved the genotoxic effect of cadmium (Cd) exposure and highlighted the importance of the cytogenetic studies as a sensitive and effective means for early detection of Cd-induced mutagenicity. The relationship between occupational exposure to Cd and increased risk of cancer, particularly lung cancer, has been explored in number of epidemiological studies. The aim of this study is to assess the role of chromosomal abnormalities and sister chromatid exchange as sensitive indicators for the genotoxicity of occupational exposure to Cd. Cytogenetic studies was done for 40 workers (27 smokers and 13 non-smokers) exposed to Cd dust and fumes with 40 control subjects (28 smokers and 12 non-smokers) not exposed to Cd before. Both exposed and control groups were similar in age and other sociodemographic factors. Clinical examination, laboratory investigation including urinary and blood Cd, cytogenic analysis for detection of chromosomal aberrations and sister chromatid exchange and environmental study of the work places were done. Statistical analysis of cytogenetic studies revealed the presence of significant elevation of chromosomal aberrations and sister chromatid exchanges of the exposed group. Urinary and blood Cd of the exposed group were significantly higher than that of the control group. These abnormalities were not significantly affected with age, duration of exposure, smoking habits, blood and urinary Cd. In conclusion, the study adds more proof that Cd exposure has a genotoxic effect and highlighted the importance of using cytogenetic studies as a sensitive and effective means for early detection of Cd-induced mutagenicity.

Évaluation du risque génotoxique chez les infirmiers manipulant les cytostatiques

The aim of this study is to assess the genotoxic effect of occupational exposure to antineoplastic drugs on oncology nurses in order to propose a strategy for adequate safety. The study included 20oncology nurses from the Farhat Hached university hospital-Sousse (Tunisia) exposed to antineoplastic drugs compared to 20controls. The two groups were paired according to sex, age, and smoking habits. The genotoxic risk assessment was carried out by the micronucleus test and chromosomal abnormalities. The search for the clinical effects of cytostatic drugs was based on a questionnaire. Determination of the level of the exposure to cytostatic was performed by calculation of the index of the exposure to these drugs. The median age of nurses was 36years. Afemale prevalence (80%) was noted. The exposed period to cytostatic was 6.1 years. The middle index of cytostatic contact calculated for the whole of the nurses, was of 1.5. However this index becomes higher (>3) in nurses working at day care. Asignificant increase in frequencies rates for both micronucleus (9.40‰ vs 4.35‰) and chromosome abnormalities (1.85% vs 0.30%) were noted in exposed group more than controls. In conclusion, application of genotoxic tests may be useful to detect cytogenetic damage related to occupational exposure to a potentially cancerogenic environment. Results of the present biomonitoring study emphasize the need for developing safety programs.

Genotoxic effects of occupational exposure measured in lymphocytes of waste-incinerator workers

Workers of solid-waste incinerators are exposed to a variety of pollutants such as dioxins, polycyclic aromatic hydrocarbons and heavy metals. It has been shown that the emissions and the fly ash produced by incineration have mutagenic properties. To our knowledge, no studies have been conducted in which genotoxic effects were investigated in exposed workers. Therefore, we monitored DNA damage by means of the single-cell gel electrophoresis (SCGE) and micronucleus (MN) assays in lymphocytes of individuals ( n = 23) who were temporarily (1–11 months) conducting maintenance works of an incinerator and in unexposed controls ( n = 19). Additionally, we measured the urinary concentrations of selected metals (Cr, Mn, Ni, As) with atomic absorption resonance. We found no differences in the levels of DNA migration and in the MN frequencies between different exposure groups and controls. Likewise, we also failed to find differences in the metal concentrations. Taken together, our results indicate that incinerator workers at the site investigated here have no increased health risks due to DNA damage.

CHROMOSOMAL ABERRATIONS AND OXIDATIVE STRESS INDICATORS IN PAINTERS,IS POWDER COATING SAFER?

Background: There are different and diverse groups of paints, the potential toxicity of which depends on the types of pigments, resins and solvents used in their manufacture. Numerous recent evidences support the role of oxidative stress in the pathophysiologyof genotoxicity induced by the exposure to solvent based paints. Indeed powder coatings were considered as safer than other types of paintings. Recently however health problems when handling or using a powder coating may arise through exposure to hazardous substances, which may be contained in the coatings, or to the powdercoating itself. Objectives: to evaluate the genotoxic effects of occupational exposure to paints and the possible role of oxidative stress in the pathogenesis of chromosomal aberrations, and to compare these effects between workers exposed to solvent based paints and workers exposed to powder coatings (dry paints) which are considered as a safer alternative to solvent based paints. Subjects: The study population consisted of 65 males divided into 34 exposed and 31 control groups. The exposed group was comprised of all workers exposed to paint in the painting unit of a small scale factory inCairo involved in furniture production and painting. The exposed workers were further subdivided into two subgroups, group 1 (n=23) comprised workers occupationally exposed to solvent based paints, and group 2 (n=11) comprised workers exposed to dry powder coating type of painting. Methods: every individual was subjected to detailedoccupational and medical history, cytogenetic chromosomal analysis and laboratory investigations to evaluate the level of oxidative stress indicators, malondialdehyde (MDA), Peroxynitrile (PN) and Total Sulphydril Groups (SHG). Results: The chromosomal aberrations and oxidative stress (higher MDA and PN and lower SHG) were significantly higher in the painters group compared to the control. The mean level of all aberrations except separation was highest in group 1 (solvent based painters) compared to group 2 (powder dry painters) and control group, and the difference washighly significant between group 1 and group 2 for all aberrations. The mean level of aberrations was higher in group 2 compared to the control group, but the difference was not significant for all except for break/ gap type aberrations. Oxidative stress was evident in group 1compared to group2 and the control group. On the other hand, oxidative stress was more evident in group 2 compared to the control and the difference was statistically significant. Conclusion: Our study confirms other studies that claim the role of oxidative stress in the pathophysiology of genotoxicity in painters especially those exposed to solvent based paints. The higher level in the chromosonmal aberrations and oxidative stress indicators in the dry powder coating exposed workers compared to the control, indeed raises suspicion that powder coatings is a “Safer Alternative to Solvent Based Paints”. Adopting safe working procedures will definitely reduce therisks to a minimum.

Genotoxic effects of occupational exposure to chemotherapeutic agents among healthcare personnel as revealed by comet assay in the peripheral blood

Genotoxic effects of occupational exposure to chemotherapeutic agents among healthcare personnel as revealed by comet assay in the peripheral blood

DNA damage in workers occupationally exposed to pesticide mixtures

Pesticides are used in agriculture to protect crops but represent at the same time a potential risk to farmers and environment. The aim of this work is the evaluation of 54 subjects occupationally exposed to pesticides and 30 subjects as a control group using the quantification of DNA damage level by means of the alkaline Comet assay and the evaluation of repair processes. Damage index Comet assay (DICA) and damage index repair assay (DIRA) were studied in 27 pesticide applicator workers, 27 non-pesticide applicators and controls. Our results show that both exposed groups revealed significant increase in DICA when compared with controls (P < 0.0001), as well as in DIRA (P < 0.0001). However, the spraying group exhibited a marginally significant difference in DICA (P = 0.05) when years of exposure are considered and a significant difference (P < 0.05) when the personal protective equipment used by individuals was taken as a comparison factor. The influence of confounding factors on the genotoxic effects of occupational exposure to pesticides was investigated and no significant differences were observed considering age, gender, smoking and alcohol consumption in relation to DICA and DIRA. Since DNA damage is an important step in events leading from carcinogen exposure to cancer disease, our study highlights the potential health risk associated with agrochemical exposure in developing countries with vast cultivated areas, such as Argentina.

Assessment of DNA Damage in Japanese Nurses Handling Antineoplastic Drugs by the Comet Assay

To clarify genotoxic effects of occupational exposure to antineoplastic drugs in Japan, we examined DNA damage, assessed by the comet assay, in 121 female nurses and 46 female clerks working at three hospitals in the northeast of Japan. The comet assay is considered to be a sensitive and rapid method for DNA strand break detection in individual cells, and tail length and tail moment are used as the comet parameters. Concerning the basal characteristics, the 46 control subjects had higher rates of smoking and coffee-drinking habits and lower hemoglobin than the 121 nurses (p<0.05). The log-transformed tail length in the nurses was significantly longer than that in the control subjects after adjusting for possible covariates such as age and smoking habit (p<0.05). Also, the log-transformed tail length was significantly longer, in the 57 nurses who had handled antineoplastic drugs in the last six months, than that in the 46 control subjects (p<0.05); but, no significant difference in tail length or tail moment was seen between the two nurse groups with and without experience of handling hazardous drugs (p>0.05). These results suggest that Japanese nurses who have worked at hospitals using antineoplastic drugs may have a potential risk of DNA damage. To minimize this risk in Japan, use of biological safety cabinet and appropriate protective equipment, in addition to staff education and training, should be implemented in the healthcare environment.

Micronucleus induction and FISH analysis in buccal cells and lymphocytes of nurses administering antineoplastic drugs

A genotoxic effect for antineoplastic drugs, in particular micronucleus induction, has been shown in several studies. The aim of our study was to assess genotoxic effects in nurses administering different mixtures of antineoplastic drugs in an oncology hospital by evaluating the frequency of micronuclei in exfoliated buccal cells and blood lymphocytes by use of the standard micronucleus (MN) test and by identifying, by means of FISH analysis with centromeric probes, the mechanism of micronucleus induction (clastogenic or aneugenic). The study group comprised 23 nurses, 10 of whom worked in the day-care hospital and 13 in the ward. Twenty healthy subjects were selected as controls. Pan-centromeric FISH analysis was performed on lymphocytes from a selected group of nurses (12/23 subjects) characterized by higher MN frequencies as observed by standard Giemsa staining. A significant increase of micronucleus frequency compared with controls was found in exfoliated buccal cells of both groups of nurses: day-care hospital nurses 0.92 versus 0.45 ( p = 0.034) and ward nurses 0.94 versus 0.45 ( p = 0.051). An increase, although not statistically significant, of mean MN frequency was also found by the MN standard test on lymphocytes of the day-care hospital nurses (10.9 versus 7.5; p = 0.056), while no differences were found in ward nurses (8.15 versus 7.5; p = 0.56). We found that the administration of antineoplastic drugs by nurses in ward units induced a higher frequency of FISH MN+ (43% of subjects) than in the day-care hospital (20%). This was associated with the micronucleus size percentage. This finding could be correlated with the different compositions of administered mixtures of antineoplastic drugs: in ward units the mixtures contained drugs, such as vinorelbine, that were absent in the mixtures administered in the day-care hospital. Our results show genetic damage induced by administration of antineoplastic drugs, particularly in exfoliated buccal cells. This result suggests the useful application of this non-invasive sampling to evaluate genotoxic effects of occupational exposure to mixtures of inhalable chemicals at low doses.

Genotoxic risk assessment of pathology and anatomy laboratory workers exposed to formaldehyde by use of personal air sampling and analysis of DNA damage in peripheral lymphocytes

A study was conducted to evaluate the genotoxic effect of occupational exposure to formaldehyde on pathology and anatomy laboratory workers. The level of exposure to formaldehyde was determined by use of passive air-monitoring badges clipped near the breathing zone of 59 workers for a total sampling time of 15 min or 8 h. To estimate DNA damage, a chemiluminescence microplate assay was performed on 57 workers before and after a 1-day exposure. Assessment of chromosomal damage was carried out by use of the cytokinesis-blocked micronucleus assay (CBMN) in peripheral lymphocytes of 59 exposed subjects in comparison with 37 controls matched for gender, age, and smoking habits. The CBMN assay was combined with fluorescent in situ hybridization with a pan-centromeric DNA probe in 18 exposed subjects and 18 control subjects randomized from the initial populations. Mean concentrations of formaldehyde were 2.0 (range <0.1–20.4 ppm) and 0.1 ppm (range <0.1–0.7 ppm) for the sampling times of 15 min and 8 h, respectively. No increase in DNA damage was detected in lymphocytes after a one-workday exposure. However, the frequency of binucleated micronucleated cells was significantly higher in pathologists/anatomists than in controls (16.9‰ ± 9.3 versus 11.1‰ ± 6.0, P = 0.001). The frequency of centromeric micronuclei was higher in exposed subjects than in controls (17.3‰ ± 11.5 versus 10.3‰ ± 7.1) but the difference was not significant. The frequency of monocentromeric micronuclei was significantly higher in exposed subjects than in controls (11.0‰ ± 6.2 versus 3.1‰ ± 2.4, P < 0.001), while that of the acentromeric micronuclei was similar in exposed subjects and controls (3.7‰ ± 4.2 and 4.1‰ ± 2.7, respectively). The enhanced chromosomal damage (particularly chromosome loss) in peripheral lymphocytes of pathologists/anatomists emphasizes the need to develop safety programs.

Evaluation of genotoxicity in a group of workers from a petroleum refinery aromatics plant

Petroleum refinery workers are potentially exposed to a wide range of petroleum-derived hydrocarbons and chemical substances used in the manufacturing of petroleum derivatives. Benzene, toluene and xylene (BTX) are produced by distillation in the aromatics units and used as raw materials for petrol and petrochemical products. The aim of this study was to evaluate the genotoxic effects of occupational exposure to BTX in a petroleum refinery in the North of Portugal. The exposed group consisted of 48 workers from the aromatics plant and the control group consisted of 30 persons matched for various confounding factors. Chromosome aberrations (CA), micronuclei (MN), and DNA damage (evaluated by means of the comet assay) were measured in peripheral blood leukocytes. t, t-Muconic acid ( t, t-MA), hippuric acid (HA) and methylhippuric acid (MHA) concentrations were measured in urine samples collected at the end of the workshift. The results suggest that occupational exposure to toluene and xylene is very low. A statistically significant increase in t, t-MA excretion was found in the exposed group although t, t-MA levels were found to be lower than the biological exposure index (BEI). Significant increases were found for CA, MN and comet tail length (TL) in the exposed group ( p < 0.05). No association was found between tobacco smoking and the effect biomarkers analysed. A positive association was found between CA and MN with age in the control group ( p < 0.05).

Genotoxic effects of occupational exposure to lead and cadmium

This study was designed to assess genotoxic damage in somatic cells of workers in a Polish battery plant after high-level occupational exposure to lead (Pb) and cadmium (Cd), by use of the following techniques: the micronucleus (MN) assay, combined with in situ fluorescence hybridization (FISH) with pan-centromeric probes, analysis of sister chromatid exchanges (SCEs), and the comet assay. Blood samples from 44 workers exposed to lead, 22 exposed to cadmium, and 52 unexposed persons were used for SCE and MN analysis with 5′-bromodeoxyuridine (BrdU) or cytokinesis block, respectively. In parallel, the comet assay was performed with blood samples from the same persons for detection of DNA damage, including single-strand breaks (SSB) and alkali-labile sites (ALS). In workers exposed mostly to lead, blood Pb concentrations ranged from 282 to 655 μg/l, while the range in the controls was from 17 to 180 μg/l. Cd concentration in lead-exposed workers fell in the same range as for the controls. In workers exposed mainly to cadmium, blood Cd levels varied from 5.4 to 30.8 μg/l, with respective values for controls within the range of 0.2–5.7 μg/l. Pb concentrations were similar as for the controls. The incidence of MN in peripheral lymphocytes from workers exposed to Pb and Cd was over twice as high as in the controls ( P<0.01). Using a combination of conventional scoring of MN and FISH with pan-centromeric probes, we assessed that this increase may have been due to clastogenic as well as aneugenic effects. In Cd- and Pb-exposed workers, the frequency of SCEs as well as the incidence of leukocytes with DNA fragmentation in lymphocytes were slightly, but significantly increased ( P<0.05) as compared with controls. After a 3 h incubation of the cells to allow for DNA repair, a clear decrease was found in the level of DNA damage in the controls as well as in the exposed workers. No significant influence of smoking on genotoxic damage could be detected in metal-exposed cohorts. Our findings indicate that lead and cadmium induce clastogenic as well as aneugenic effects in peripheral lymphocytes, indicating a potential health risk for working populations with significant exposures to these heavy metals.