Lymphocyte DNA damage in elevator manufacturing workers in Guangzhou, China

AIMS: To study the effect of smoking, passive smoking, alcohol drinking, and occupational exposure to low level of benzene on DNA strand breaks in elevator manufacturing workers in Guangzhou, China. METHODS: Three hundred and fifty-nine workers (252 men and 107 women) of a modern elevator manufacturing factory, 205 were from production departments and 154 from managerial department. Information on the workers' health conditions, smoking, passive smoking, alcohol consumption and occupational exposure history was collected by personal interview. Lymphocyte DNA damage was measured by the Comet assay. RESULTS: None of the women smoked and 20.6% of the men were daily smokers. In non-smokers, the prevalence of passive smoking at work was 25% for men and 11.2% for women, and at home, 37.8 and 48.6%, respectively. Smoking significantly increased tail moment (P<0.001). Daily smokers had the largest tail moment (geometric mean, 95% CI) (0.93 microm (0.81-0.94)), followed by occasional smokers (0.76 microm (0.59-0.95)), ex-smokers (0.70 microm (0.58-0.85)), and never smokers (0.56 microm (0.53-0.60)). Tail moment increased significantly with daily tobacco consumption (cigarettes per day) (r=0.26, P<0.001) after adjusting for age, gender, occupational exposure, passive smoking, and drinking. Analysis of covariance (ANCOVA) showed that smoking (P<0.001), passive smoking at home (P=0.026), occupational exposure (P<0.001), male gender (P<0.001), and age (P=0.001) had independent effects on tail moment, whereas passive smoking at work and alcohol drinking had no significant effect. CONCLUSIONS: Smoking, passive smoking at home, male gender, age and occupational exposure independently increased lymphocyte DNA strand breaks. The presence of excess DNA damage under low level of occupational exposure to benzene or other solvents suggest that the current allowance concentrations may not be safe to prevent genotoxicity.     

Increased lymphocyte DNA strand breaks in rubber workers

OBJECTIVE: To study the effect of occupational exposure to rubber processing, smoking, and alcohol drinking on lymphocyte DNA damage. SUBJECTS AND METHODS: Of 371 employees (197 men and 174 women) from a rubber factory in Guangzhou, 281 were rubber processing workers from five production sections and 90 were managerial workers. Information on occupational exposure, smoking, and drinking was collected by interviews. Blood samples were taken in the morning by venipuncture. DNA damages were measured by the Comet assay. Possible DNA-protein crosslinks were broken down by proteinase K. Tail moment, measured by Komet 4.0 image analysis software, was the measure of DNA damage. RESULTS: The rubber processing workers had larger tail moment than the managerial workers (Geometric mean, 95%CI) [1. 77microm (1.64-1.90) versus 1.52microm (1.36-1.71), P=0.04]. Both smoking [1.93microm (1.74-2.13) versus 1.59microm (1.47-1.71), P=0. 003] and alcohol drinking [2.21microm (1.87-2.62) versus 1.63microm (1.53-1.74), P<0.001] increased tail moment. Tail moment differed significantly among job categories (F=3.21, P=0.008), the largest was observed in mixers. In the non-smoking and non-drinking workers, rubber processing workers had larger tail moment than managerial workers after adjusting for age (P=0.033). General linear model analysis showed that after adjusting for each other, occupational exposure (P=0.027), smoking (P=0.012), and alcohol drinking (P=0. 013) was associated with larger tail moment, whereas age and gender had no effect. CONCLUSIONS: Occupational exposure to rubber processing, smoking, and alcohol drinking can cause DNA damage.     

Lymphocyte DNA damage in bus manufacturing workers

To study the effect of occupational exposure, smoking, and drinking on lymphocyte DNA damage in bus manufacturing workers, 346 employees (106 women and 240 men) from six job categories (welders, mechanics, painters, and assembling, auxiliary and managerial workers) in a bus manufacturing factory in Guangzhou were included. Significant differences of tail moment among the six job categories were found (P=0.003) with adjustment for age and gender. Smoking increased tail moment significantly (3.14 (2.89-3.40) versus 2.79 microm (2.63-2.97), P=0.023). Analysis of covariance showed that occupational exposure (P=0.001) and smoking (P=0.019) had significant effect on tail moment after adjusting for all factors, whereas age and gender had no effect on DNA damage. Stratified analysis showed that painters (P=0.002), auxiliary workers (P=0.011), and mechanics (P=0.044) had larger tail moments than managerial workers after adjusting for age, gender, smoking, and drinking.     

Genotoxic evaluation of workers employed in pesticide production

Pesticides are widely used throughout the world in agriculture to protect crops and in public health to control diseases. Nevertheless exposure to pesticides can represent a potential risk to humans. Pesticide manufacturing unit workers are prone to possible occupational pesticide exposure. Therefore, this study was performed to evaluate the genotoxic effect of pesticide exposure in these workers. In the present investigation 54 pesticide workers and an equal number of control subjects were assessed for genome damage in blood lymphocytes utilizing the chromosomal aberration analysis and the buccal epithelial cell by adopting the micronucleus test. The results suggested that pesticide workers had a significantly increased frequency of chromosomal aberrations when compared with controls (mean+/-S.D., 8.43+/-2.36 versus 3.32+/-1.26; P<0.05). Similarly, the pesticides exposed workers showed a significant increase in micronucleated cells compared with controls (1.24+/-0.72 versus 0.32+/-0.26; P<0.05). Analysis of variance revealed that occupational exposure to pesticides had a significant effect on frequency of micronuclei (P<0.05), whereas smoking, age, gender and alcohol consumption had no significant effect on genetic damage (P>0.05). However, no association was found between years of exposure, smoking, age, gender, alcohol consumption and higher levels of genetic damage as assessed by the chromosomal aberration assay (P>0.05). Our findings indicate that occupational exposure to pesticides could cause genome damage in somatic cells.     

Increased lymphocyte DNA strand breaks in rubber workers

Objective: To study the effect of occupational exposure to rubber processing, smoking, and alcohol drinking on lymphocyte DNA damage. Subjects and Methods: Of 371 employees (197 men and 174 women) from a rubber factory in Guangzhou, 281 were rubber processing workers from five production sections and 90 were managerial workers. Information on occupational exposure, smoking, and drinking was collected by interviews. Blood samples were taken in the morning by venipuncture. DNA damages were measured by the Comet assay. Possible DNA-protein crosslinks were broken down by proteinase K. Tail moment, measured by Komet 4.0 image analysis software, was the measure of DNA damage. Results: The rubber processing workers had larger tail moment than the managerial workers (Geometric mean, 95%CI) [1.77 μm (1.64–1.90) versus 1.52 μm (1.36–1.71), P=0.04]. Both smoking [1.93 μm (1.74–2.13) versus 1.59 μm (1.47–1.71), P=0.003] and alcohol drinking [2.21 μm (1.87–2.62) versus 1.63 μm (1.53–1.74), P<0.001] increased tail moment. Tail moment differed significantly among job categories (F=3.21, P=0.008), the largest was observed in mixers. In the non-smoking and non-drinking workers, rubber processing workers had larger tail moment than managerial workers after adjusting for age (P=0.033). General linear model analysis showed that after adjusting for each other, occupational exposure (P=0.027), smoking (P=0.012), and alcohol drinking (P=0.013) was associated with larger tail moment, whereas age and gender had no effect. Conclusions: Occupational exposure to rubber processing, smoking, and alcohol drinking can cause DNA damage.     

Aromatic DNA adduct levels in coke oven workers: correlation with polymorphisms in genes GSTP1, GSTM1, GSTT1 and CYP1A1

The aim of this study was to use DNA adducts levels, detected by 32P-postlabelling, as a biomarker to assess human exposure to polycyclic aromatic hydrocarbons (PAHs) from a coke oven plant and explore the possible association between CYP1A1 MspI, GSTP1, GSTM1 and GSTT1 genotypes, and smoking status on bulky DNA adduct formation. A large amount of inter-individual variation in adduct level was observed among workers with the same job and the same smoking habits. No significant differences were observed in DNA adduct levels between the coke oven workers and control group. Smokers in the control group had significantly higher DNA adducts than the non-smokers in the same group (35.13+/-21.11 versus 11.18+/-8.00, per 10(8) nucleotides, P=0.003). In this group, the correlation between the level of DNA adducts and the cigarettes smoked was strongly significant (r=0.70, P<0.0005), but no correlation was found among the coke oven workers. Among non-smokers there was a significant difference between the control group and the coke oven workers (11.18+/-8.00 versus 24.62+/-15.20, per 10(8) nucleotides, P=0.03). These results suggests that tobacco smoke could behave as a confounding factor for evaluation of DNA adducts arising from occupational exposure. The levels of DNA adducts in smokers not occupationally exposed to PAHs is dependent on the polymorphisms CYP1A1 MspI in the 3' non-coding region (49.04+/-22.18 versus 25.85+/-15.87, per 10(8) nucleotides, P<0.05), but no effect was observed for the GST genotypes studied.     

Formation of 8-nitroguanine in tobacco cigarette smokers and in tobacco smoke-exposed Wistar rats

Our previous studies have shown that 8-nitroguanine (8-NO(2)-G) could serve as a specific biomarker of DNA damage induced by gaseous nitrogen oxides (NO(x)) exposure. To evaluate the effect of tobacco cigarette smoking on the DNA damage in peripheral lymphocytes of cigarette smoke ones, we randomly collected and determined the level of 8-NO(2)-G in DNA extracted from peripheral lymphocyte of 15 each of light-smoking healthy volunteer (L-S, less than one pack per day), moderate-smoking healthy volunteers (M-S, one to two pack per day for 5-10 years), heavy-smoking healthy volunteers (H-S, over two packs per day for 10 years), lung cancer patients with heavy smoking (cancer H-S) and non-smoking healthy controls. Both of the mean level of the 8-NO(2)-G levels in peripheral lymphocyte (0.90+/-1.0, 1.23+/-1.14, 1.43+/-0.79, 3.62+/-1.38 ng per microg DNA) and serum nitrite (38.99+/-9.58, 46.70+/-9.38, 55.46+/-10.45, 70.1+/-18.54 microM) of L-S, M-S, H-S and cancer H-S groups were higher than that of non-smoking healthy controls (0.02+/-0.04 and 18.96+/-4.31 for 8-NO(2)-G level and serum nitrite, respectively). Furthermore, in animal experiment, a dose-dependent increase in 8-NO(2)-G was observed in rat lung and peripheral lymphocyte DNA of Wistar rats after tobacco cigarette smoke exposure twice a day, for 1 month. The level of 8-NO(2)-G is 0.17+/-0.41, 1.65+/-3.15, 23.50+/-20.75 and 37.58+/-17.55 ng per microg lung DNA for rat exposed with tobacco cigarette smoke from 0, 5, 10, 15 cigarettes per day, respectively. It was also found that count of peripheral lymphocytes and nitrite concentration in serum of rat increased after the tobacco smoke exposure. It is postulated that tobacco cigarette smoking could induce DNA damage (8-NO(2)-G formation) by exo- and endogenous NO(x).     

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.     

Analysis of chromosome damage in circulating lymphocytes of radiological workers affected by thyroid nodules

The aim of our study was to assess whether or not thyroid nodularity in combination with occupational exposure to low levels of ionising radiation would be correlated with chromosome damage in peripheral lymphocytes. Conventional chromosome-aberration analysis was performed on a group of 92 hospital workers with or without thyroid nodules. On the basis of measurements of their exposure levels, the workers were classified into a low (mean total level=0.03 mSv), medium (mean total level=1.04 mSv) or high (mean total level=8.60 mSv) exposure category. Our results indicate that among workers with thyroid nodules, the high-exposed workers showed significantly higher levels of both total (2.35+/-0.34 per 100 cells) and chromosome-type aberrations (1.46+/-0.20 per 100 cells) than medium-exposed (0.98+/-0.42 and 0.68+/-0.25 per 100 cells, respectively) or low-exposed workers (1.11+/-0.29 and 0.58+/-0.17 per 100 cells, respectively). Workers without thyroid nodules had comparable frequencies of chromosome aberrations among the three exposure categories. To our knowledge, this is the first study revealing a slight, but significant increase of chromosome damage in peripheral lymphocytes from hospital workers who developed thyroid nodules under conditions of occupational exposure to radiation well below the threshold limit for the workplace. The existence of a possible association between chromosome aberrations and development of thyroid nodularity will be discussed.     

Cadmium exposure in tobacco workers: possible renal effects.

Cadmium is a nephrotoxic metal widely used in industry and the main source of Cd in general population is smoking. Considering that the source of Cd in cigarettes is the tobacco leaf, the exposure to Cd was evaluated in workers employed at a tobacco leaf processing factory. Blood and urinary Cd levels were measured by flameless atomic absorption spectrometry in 87 workers and 35 controls. Urinary enzymes, total protein, albumin and uric acid were also determined to investigate the possible nephrotoxic effects of Cd. Blood Cd levels were significantly higher in workers (1.63 +/- 1.95 microg/L) than in controls (0.91 +/- 1.15 microg/L) (p = 0.044). The increase observed in urinary Cd levels of workers was non significant (0.56 +/- 0.5 microg/g creatinine in workers and 0.46 +/- 0.5 microg/g creatinine in controls). Both in workers and in controls, subjects smoking >10 cigarettes/day showed significantly increased blood Cd levels compared to non-smokers (p = 0.000 and p = 0.011, respectively). In workers, urinary alkaline phosphatase (ALP), gamma glutamyl transferase (GGT), total protein, and uric acid were observed to be significantly increased (p = 0.013, p = 0.000, p = 0.000, p = 0.025, respectively), ALP, GGT and total protein being positively correlated with Cd in urine. In conclusion, the workers in the tobacco leaf processing factory were found to be exposed to Cd compared to the general population. The increase in the urinary enzymes and proteins suggests that an exposure to Cd affects kidney functions even below the toxic limits generally accepted.     

溴氰菊酯致大鼠DNA损伤及对肝功能的影响

目的：研究溴氰菊酯（DM）对大鼠外周血淋巴细胞DNA的损伤作用及对肝脏功能的影响。方法：32只雌性Wistar大鼠随机分成4组,染毒剂量分别为0,3．125,6．250,12．500mg／kg,连续灌胃染毒10天。DNA损伤采用单细胞凝胶电泳（彗星实验）进行评价,并测定丙氨酸氨基转移酶（ALT）以反映肝功能变化。结果：染毒组大鼠外周淋巴细胞的尾DNA％（Tail DNA％）、尾矩（Tail Moment）和Olive尾矩（Olive Tail Moment）均高于对照组（P〈0．05）,差别有统计学意义。各染毒组与对照组的肝功能差异均无统计学意义。结论：DM可导致外周血淋巴细胞DNA损伤。     

Cytogenetic monitoring by use of the micronucleus assay among hospital workers exposed to low doses of ionizing radiation

The aim of this study was to assess occupationally induced chromosomal damage in a large population of hospital workers exposed to low doses of ionizing radiation. We used the cytokinesis-block micronucleus (CBMN) assay in the peripheral lymphocytes of 132 exposed workers compared with 69 controls matched for gender, age and smoking habits. The CBMN assay was combined with fluorescence in situ hybridization with a human pan-centromeric DNA probe in 32 exposed subjects and 30 controls randomly chosen from the initial populations. Occupational dosimetry records were collected over the last 10-year period and revealed very low exposure levels. The average binucleated micronucleated cell rate (BMCR) was significantly higher in the exposed subjects than in the controls (14.9 per thousand+/-8.1 versus 11.8 per thousand+/-6.5; P=0.011). About one-third of the micronuclei were centromere-negative in the exposed and control groups. BMCR significantly positively correlated with donor age in the exposed population; this correlation was at the border of significance in the control group. In the two groups, BMCR was significantly greater in females than in males, and the significant correlation between age and BMCR was observed in the female population, but not in the male one. No effect of smoking habits emerged. Univariate analysis revealed a possible influence of familial cancer history and diagnostic medical radiation dose (estimated from examinations reported in the questionnaire) on BMCR. Multiple regression analysis, taking into account all the previous confounding factors, showed that only occupational exposure status, gender and age had a significant effect on BMCR. In conclusion, the present study shows that chromosomal damage leading to micronucleated lymphocytes is more frequent in hospital workers exposed to ionizing radiation than in controls, despite the very low levels of exposure.     

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 15min or 8h. 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 <0.1-20.4ppm) and 0.1ppm (range <0.1-0.7ppm) for the sampling times of 15min and 8h, 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 per thousand+/-9.3 versus 11.1 per thousand+/-6.0, P=0.001). The frequency of centromeric micronuclei was higher in exposed subjects than in controls (17.3 per thousand+/-11.5 versus 10.3 per thousand+/-7.1) but the difference was not significant. The frequency of monocentromeric micronuclei was significantly higher in exposed subjects than in controls (11.0 per thousand+/-6.2 versus 3.1 per thousand+/-2.4, P<0.001), while that of the acentromeric micronuclei was similar in exposed subjects and controls (3.7 per thousand+/-4.2 and 4.1 per thousand+/-2.7, respectively). The enhanced chromosomal damage (particularly chromosome loss) in peripheral lymphocytes of pathologists/anatomists emphasizes the need to develop safety programs.     

GSTM1 [corrected] deletion modifies the levels of polycyclic aromatic hydrocarbon-DNA adducts in human sperm

DNA adducts measured in tissues are promising markers for identifying damage in organs that could be a target for carcinogens. Polymorphisms in genes involved in polycyclic aromatic hydrocarbons (PAHs) metabolism have been shown to modify the levels of PAH-DNA adducts in target tissues. In order to study the role of metabolic gene polymorphisms on DNA-adduct formation in sperm, we determined the GSTM1 genotype in a group of men in whom PAH-DNA adducts in sperm had been previously measured by immunofluorescence. The mean level of adducts in sperm was significantly higher in subjects carrying the homozygous deletion variant of GSTM1 than in subjects with a functional GSTM1 (mean fluorescence staining intensity: 1.62+/-0.62 versus 1.33+/-0.55; p=0.02). With respect to environmental factors, subjects who reported occupational exposure to PAHs and who carried the GSTM1 deletion had a significant increase in PAH-DNA adducts in sperm in comparison with subjects who were not exposed and had a functional GSTM1 (mean staining intensity: 1.83+/-0.67 versus 1.30+/-0.53; p=0.05), although among GSTM1-null subjects there was no significant difference with or without occupational exposure. This study presents for the first time the effect of a common polymorphism in a gene that metabolizes PAHs on DNA-adduct levels in sperm.     

The genotoxic risk of underground coal miners from Turkey

A cytogenetic monitoring study was carried out on a group of workers from a bituminous coal mine in Zonguldak province of Turkey, to investigate the genotoxic risk of occupational exposure to coal mine dust. Cytogenetic analysis, namely sister chromatid exchanges (SCEs), chromosomal aberrations (CAs) and micronucleus (MN) tests were performed on a strictly selected group of 39 workers and compared to 34 controls matched for gender, age, and habit. Smoking and age were considered as modulating factors. Both SCE and CA frequencies in coal miners appeared significantly higher than in controls. Similarly, there was a significant increase in the frequency of total micronuclei in exposed group as compared to control group. The effect of smoking on the level of SCE and MN was significant in the control group. A positive correlation between the age and the level of SCE was also found in controls. The frequencies of both SCE and CA were significantly enhanced with the years of exposure. The results of this study demonstrated that occupational exposure to coal mine dust leads to a significant induction of cytogenetic damage in peripheral lymphocytes of workers engaged in underground coal mining.     

The genotoxic risk of underground coal miners from Turkey

A cytogenetic monitoring study was carried out on a group of workers from a bituminous coal mine in Zonguldak province of Turkey, to investigate the genotoxic risk of occupational exposure to coal mine dust. Cytogenetic analysis, namely sister chromatid exchanges (SCEs), chromosomal aberrations (CAs) and micronucleus (MN) tests were performed on a strictly selected group of 39 workers and compared to 34 controls matched for gender, age, and habit. Smoking and age were considered as modulating factors. Both SCE and CA frequencies in coal miners appeared significantly higher than in controls. Similarly, there was a significant increase in the frequency of total micronuclei in exposed group as compared to control group. The effect of smoking on the level of SCE and MN was significant in the control group. A positive correlation between the age and the level of SCE was also found in controls. The frequencies of both SCE and CA were significantly enhanced with the years of exposure. The results of this study demonstrated that occupational exposure to coal mine dust leads to a significant induction of cytogenetic damage in peripheral lymphocytes of workers engaged in underground coal mining.     

Synergistic Impaired Effect between Smoking and Manganese Dust Exposure on Pulmonary Ventilation Function in Guangxi Manganese-Exposed Workers Healthy Cohort (GXMEWHC)

PurposeThe aims of this study were to investigate the effects of manganese (Mn) dust exposure on lung functions and evaluate the potential synergistic effect between smoking and Mn dust exposure among refinery workers.MethodsA retrospective study including 1658 workers in a ferromanganese refinery was conducted, with subjects who were from the Guangxi manganese-exposed workers healthy cohort (GXMEWHC). Based on the Mn manganese cumulative exposure index (Mn-CEI), all subjects were divided into the low exposure group (n = 682) and the high exposure group (n = 976). A pulmonary function test was performed using an electronic spirometer, including the values and percentages of FVC, FEV₁, FEV₁/FVC, MMEF, PEFR, MVV, respectively.ResultsNo significant effect of Mn dust exposure on the pulmonary function was found in the female workers (all p>0.05). However, there was an obvious decrease in the male workers in the high exposure group compared with those in the low exposure group (FVC -60 ml, FEV₁ -120 ml, MMEF -260 ml/s, MVV -5.06 L, all p<0.05). In the high exposure group, the reduction in FVC% predicted, MMEF and MMEF% predicted was 1.0%, 210 mL/s, and 4.9%, respectively. In particular, among the exposed subjects smokers had a statistically significant decrease in lung function compared with non-smokers and the reduction in FVC% predicted, MMEF and MMEF% predicted was 1.0%, 210 mL/s, and 4.9%, respectively (p<0.05). Partial correlation analysis showed that there was also negative correlation between Mn-CEI and decreased changes in MMEF (r = -0.159, p = 0.018) and also MMEF% predicted (r = -0.163, p = 0.015).ConclusionsMn dust can impair the pulmonary ventilation function of male workers but not females, and individual smoking habits and manganese exposure had a synergistic effect on the lung function decrease.     

Cytogenetic analysis of buccal cells from shoe-workers and pathology and anatomy laboratory workers exposed to n-hexane, toluene, methyl ethyl ketone and formaldehyde.

People employed in the shoe manufacture and repair industry are at an increased risk for cancer, the strongest evidence being for nasal cancer and leukaemia. A possible causal role for formaldehyde is likely for cancer of the buccal cavity and nasopharynx. Exfoliated buccal cells are good source of tissue for monitoring human exposure to inhaled and ingested occupational and environmental genotoxicants. To assess the cytogenetic damage related to occupational exposure to airborne chemicals during shoe-making and the processes in pathology and anatomy laboratories, the micronuclei (MN) count per 3000 cells was measured in buccal smears from shoe-workers (group I, n = 22) exposed to mainly n-hexane, toluene and methyl ethyl ketone (MEK) and from anatomy and pathology staff (group II, n = 28) exposed to formaldehyde (FA). Eighteen male university staff were used as controls. The mean time-weighted average (TWA) concentrations of n-hexane, toluene and MEK in 10 small shoe workshops were 58.07 p.p.m., 26.62 p.p.m. and 11.39 p.p.m., respectively. The measured air concentrations of FA in the breathing zone of the anatomy and pathology laboratory workers were between 2 and 4 p.p.m. Levels of 2,5-hexadione (2,5-HD) and hippuric acid (HA), metabolic markers of n-hexane and toluene exposure, respectively, were significantly higher in the urine of workers in group I than in control subjects (p < 0.001 and p < 0.01, respectively). The mean (+/- SD) MN (0/00) [corrected] frequencies in buccal mucosa cells from workers in group I, group II and controls were 0.62 +/- 0.45%, 0.71 +/- 0.56% and 0.33 +/- 0.30%, respectively (p < 0.05 and p < 0.05 compared with controls for group I and group II, respectively). The effects of smoking, age and duration of exposure on the frequency of micronucleated buccal cells from workers in all three groups studied were also evaluated. Overall, the results suggest that occupational exposure to organic solvents, mainly n-hexane, toluene, MEK and FA, may cause cytogenetic damage in buccal cells and that use of exfoliated buccal cells seems to be appropriate to measure exposure to organic solvents.     

Lymphocyte DNA damage is associated with increased aortic intima-media thickness

OBJECTIVES: To investigate whether there is an association between lymphocyte DNA damage and aortic intima-media thickness (IMT). METHODS: We studied 70 patients (mean age: 41.6+/-10 years) who underwent transesophageal echocardiography for various indications. Four different grades were determined according to intima-media thickness (IMT) of thoracic aorta measured by transesophageal echocardiography. DNA damage was assessed by alkaline single cell electrophoresis (comet) assay in peripheral lymphocytes. Plasma level of total antioxidant status (TAS) was determined by using automated measurement method. High sensitive C-reactive protein and other biochemical markers were studied in all subjects. RESULTS: The major increase in lymphocyte DNA damage was observed in patients with grade 4 IMT when compared with other groups (p<0.001, for all). Lymphocyte DNA damage of patients with grade 1 IMT was also lower than patients with grade 2 IMT (p=0.013) and patients with grade 3 IMT (p<0.001). Lymphocyte DNA damage of patients with grade 2 IMT was found at low level compared with patients with grade 3 IMT (p=0.012) as well. In multiple linear regression analysis, IMT was independently correlated with lymphocyte DNA damage (beta=0.515, p<0.001), TAS level (beta=-420, p<0.001), total cholesterol (beta=0.407, p<0.001) and LDL cholesterol level (beta=287, p=0.020). CONCLUSION: Lymphocyte DNA damage may be an independent predictor for the grade of thoracic IMT, and may play a role in pathogenesis of thoracic atherosclerosis besides TAS and cholesterol levels.     

Cytogenetic analysis of nasal mucosa cells and lymphocytes from high-level long-term formaldehyde exposed workers and low-level short-term exposed waiters

The evidence for genotoxic potential of formaldehyde (FA) in humans is insufficient and conflicting. We previously reported a higher frequency of micronuclei in nasal and oral exfoliative cells from students exposed to formaldehyde vapor for short-term. To further evaluate the genetic effects of long-term occupational exposure to FA and short-term exposure to FA of indoor sources, the frequencies of micronuclei (MN) in nasal mucosa cells, sister chromatid exchanges (SCEs) of peripheral lymphocytes, and the lymphocyte subsets were evaluated in 18 non-smoking workers (mean exposure duration was 8.6 years) in an FA factory and 16 non-smoking waiters exposed to FA for 12 weeks in a ballroom. A non-smoking student group without occupational exposure (n=23) to FA was used as control. The 8h time-weighted average (TWA) concentrations of formaldehyde was 0.985+/-0.286 mg/m3 with the ceiling exposure concentration of 1.694 mg/m3 in the workshop, and 0.107+/-0.067 mg/m3 in the ballroom (5 h TWA). Higher frequencies of micronuclei per thousand cells in nasal mucosa cells of workers versus control (2.70+/-1.50 versus 1.25+/-0.65, p<0.05) and higher frequency of SCEs in peripheral lymphocytes of workers group (8.24+/-0.89 versus 6.38+/-0.41, p<0.05) were observed. Increased frequency of micronuclei in nasal mucosa cells or SCE in peripheral lymphocytes was not found among waiters group. The results suggest that the genotoxic potential of high level FA exposure may have occupational risks in long-term exposure groups.