Carbon Disulfide ( CS 2 ) Induced Chromosomal Alterations and Apoptosis in Circulated Blood Lymphocytes of Personnel Working in Viscose Industry

Circulated blood lymphocytes (PBL) of 41 workers occupationally exposed to Carbon disulfide (CS2) exposed from viscose industry were investigated to collect data on the effects and to find a possible relationship between in-vivo CS2 induced apoptosis and genotoxic effects. The subjects were divided into three groups: 41 subjects exposed to CS2 together with various confounding factors, another 41 subjects inhabitant of Viscose industry partially exposed to CS2 in long periods. The results were compared with 41 control subjects without known occupational exposure. Ambient air concentrations of CS2 were measured in different workplaces. Measures of genotoxicity included the determination of the frequencies of chromosomal aberrations (CA), sister-chromatid exchange (SCE), HPRT mutations (variant frequency, VF) and the measurement of UV-induced unscheduled DNA-repair synthesis (UDS). The percentages of premature centromere division (PCD) and of cells with a high frequency of SCE (HF/SCE) were also scored. Apoptosis and cell proliferation were determined by flow cytometry. In both CS2 exposed groups, the apoptotic activity and the CA levels in PBLs were significantly higher than in controls. The CA was mostly breaks of the chromatid type. In the second the group, which was partially exposed to CS2, CA was slightly lower in comparison with group I fully exposed to CS2 and other confounding factors, which may be attributed to a different rate of elimination of damaged lymphocytes as a consequence of CS2 induced apoptotic activity. In conclusion, the results demonstrate that exposure to CS2 induces apoptosis and CA, indicating an excess cancer risk among subjects occupationally exposed to CS2. The results also emphasize the importance of the measurement of occupationally exposed pollutants, such as CS2, in order to avoid genotoxic effects in the workers also the habit of cigarette smoking and alcohol consumption among the viscose workers had a synergistic effect on inducing cancer risk.


Introduction
caused deceleration of intra-cardiac impulse conduction and modified arrhythmia in the coronary occlusion.An extensive literature is available on the toxic effects and genetic and chromosomal damage of CS 2 on circulating blood lymphocytes and human sperm samples [12][13][14].In addition, Bao et al., (1996) reported an increased incidence of chromosomal aberrations in the pronuclei of zygotes in adult female mice exposed to 10/100 mg/m 3 of CS 2 for 3 weeks and mated with unexposed male mice.In-vitro exposure of human sperm to CS 2 concentrations of 10 micromole/liter (μmol/L) resulted in increased occurrences of chromosomal aberrations [15].Furthermore, the mutagenicity and genotoxicity potential of CS 2 has been evaluated in vitro and in-vivo experiments with crucial confounding factors [14,[16][17][18].Previously CS 2 does not exhibit mutagenic activity in bacteria with or without the presence of activation system [19].Additional in vitro tests, including host-mediated assay, unscheduled DNA synthesis in human fibroblasts and primary cultures of human leucocytes, are unconvincing.However, the significance of these tests cannot be properly evaluated because of methodological problems including the lack of proper positive controls [20].
Therefore, insufficient data are currently available to evaluate the mutagenic and genotoxic potential of CS 2 .A quantitative assessment of published data, with workers heavily exposed to CS 2 , provides some evidence to support the hypothesis of an association with numerous diseases, but these meta-analyses are showed significant genetic changes induced by the potential confounding factors like smoking and alcohol.Today, chromosomal alterations in human peripheral lymphocytes (PBL) are recognized as a valuable biomarker of the effect of toxic chemicals, probably the only one which has been standardized and validated [21] method to detect the genetic level damage.SCE frequency in human PBL has been used as the best indicator of chromosome damage [22].To assess early carcinogenic effects of various genotoxic markers involved DNA alterations [23] have been also used for molecular epidemiological studies [24,25].
Cytogenetic studies of occupational exposure population have been reported genetic damage in viscose industry workers [18,26] even though the results were rather contradictory.However, there is still no consistent evidence that exposure of CS 2 causes chromosome damage.The inconsistent genotoxicity data could be due to differences in levels of direct and indirect exposures or in the end-points utilized.Hence, there is a need to evaluate different populations to analyze various genotoxic parameters on CS 2 exposed workers.Early identification of hazards is crucial to reduce the exposure and carcinogenic risk.A literature survey has revealed that no investigation has been conducted in this region of workers with different cytogenetic tools based on the different levels of CS 2 exposure.
The focal aim of present study was to identify genetic alterations of viscose factory workers occupationally exposed to CS 2 , Tamil Nadu, South India by using the relevant cytogenetic tools such as apoptosis induced factors, chromosomal aberrations (CA) and Sister Chromatid exchange (SCE) assay with various confounding factors.To evaluate the possibility of effect due to toxic chemicals at the workplace, confounding factors and other influences associated with work duration must be taken into consideration.

Selection of subjects
Altogether 123 subjects from various viscose industries in Tamilnadu state especially Tiruppur and Erode districts.Subjects were divided into three groups such as I group consists of 41 subjects directly involved and exposed to CS 2 in viscose industry, II group comprising 41 subjects not exposed to CS 2 but they are inhabitants near viscose industries, III group consists of 41 subjects belonging to control groups.In additionally, I group were divided based on their duration of exposure (0-3; 4-6; 7-9; 10-12; 13-15 years) and they were known to be exposed to CS 2 for a minimum of 8 hrs per day.II group subjects were those who had not directly exposed to CS 2 , but they were inhabitants nearby viscose industry for past 2 decades in additionally they were further categorized based on the year of residence (20-30; 31-40; 41-50; 51-60 and 61-70 years).Control subjects were normal and healthy individuals who have not been exposed to any kind of chemicals and radiation hazards, control subjects were matched to the age of exposed groups.All the groups were further categorized based on their age (Group I, <40 years; Group II, >40 years).A face to face questionnaire which recorded standard demographic profile as well as questions relating to lifestyle, consumption habits such as smoking, alcohol intake, medication, recent viral infections, vaccinations, diagnostic tests or previous occupational exposures to chemicals was completed by all donors.It was also ensured that all the subjects have not been taking any medicines nor been exposed to any kind of hazards for at least 12 months before sampling.Individuals (both experimental and controls) who smoked for at least 1 year (more than 15 cigarettes/day) were considered as smokers.Informed consent was obtained from all the subjects.CS 2 concentrations in ambient air were measured at fixed locations in the industries, and the concentrations were in the range of 0.13-1.20 mg corresponding to an 8-h time-weighted average exposure (TWA-8) of 0.9 mg/m 3 , which exceeds the limits of both the short-term exposure (0.6 mg/m 3 ) and TWA-8 (0.6 mg/m 3 ).All subjects complained about acute toxic effects (eye irritation) and the presence of CS 2 was perceivable in each industry.Data concerning the ambient air concentration measurements for these chemicals were not available to us, but ambient air concentrations for each of these chemicals were much below both the 8-h time weighted average exposure (TWA-8) and short-term exposure limits in the selected region.Only active smokers were considered to be smokers.considered as high-frequency SCE cells (HFC/SCE), according to Tates et al., (1991) and Major et al., (1996).

Flow-cytometric analysis of apoptosis and cell proliferation in PBL
For the measurement of the percentage apoptosis and the S-phase, PBL were separated from the blood samples on Histopaque 1,077 gradients and cultured in RPMI-1640 medium supplemented with 20% fetal calf serum and 0.5% phytohemagglutinin-P (PHA) for 50 h without antibiotics in a standard thermostat at 37 o C in a humidified atmosphere containing 5% CO 2 .One hour prior to the termination of the incubations, 5 µg/ml BrdU was added to the cultures.Cells were washed twice with PBS, fixed in 1ml ice-cold 70% ethanol and stored at -20 o C until further processing.DNA denaturation prior to propidium iodide (PI) and fluorescein isothiocyanate (FITC) labeled monoclonal anti-BrdU staining was performed at room temperature with 2MHCl containing 0.2 mg/ml pepsin, according to the method of van Erp et al. (1988).DNA was stained with PI and the incorporated BrdU was detected by use of immunocytochemistry with FITC labeled monoclonal antibody.
Flow-cytometric analysis was performed with a FACS Calibur flow cytometer.Data for at least 10,000 lymphocytes per sample were acquired; CellQuestPro Software was used for the analysis.
Cell proliferation was also characterized by flow-cytometric measurement of the expression of the cell-activation marker CD71 on T-lymphocytes (Biro et al., 2002).Briefly, heparinized whole blood was mixed and incubated at room temperature for 20 min with the appropriate amount of fluorescence-labeled monoclonal antibodies against surface antigens.The following monoclonal antibodies were used: peridinin-chlorophyll-protein complex (PerCP)-labelled anti-CD3 (T-cell marker), FITC-labelled anti-CD71 ( t r a n s f e r r i n r e c e p t o r ) a n d a l l o p h y c o c y a n i n (APC)-labelled anti-CD45.The erythrocytes were removed through lysis by addition of FACS Lysing solution.After washing with phosphate-buffered saline (PBS), samples were analyzed within 4 h after labeling or fixed with 2% paraformaldehyde.Flow-cytometric analysis was performed on a Becton Dickinson FACS Calibur flow cytometer.Standard forward and side scatter gating combined with CD45 was used to set the lymphocyte gate.Data for at least 10,000 leukocytes per samples were acquired; CellQuest Pro Software (Becton Dickinson) was used for analysis.Phenotypes are expressed as a percentage of positive cells of the given lymphocyte subpopulation.

Statistical analysis
Statistical analysis was made using the GraphPad Prism 3.02 software.Differences between the study groups and the control group were tested with Student's t-test, p < 0.05 was considered as statistically significant.A standard linear correlation analysis was used to determine the relationship between apoptosis, CA and PCD.

The determination of HPRT gene mutations and UVinduced DNA synthesis (UDS) in PBL
The determination of HPRT gene mutations, PBLs were separated from the blood samples on Histopaque 1,077 gradients and cultured in RPMI-1640 medium supplemented with 20% fetal calf serum and 0.5% phytohemagglutinin-P (PHA) without antibiotics in a standard thermostat at 37oC in a humidified atmosphere containing 5% CO 2 .The determination of the frequency of gene mutations at the HPRT locus (variant frequency, VF) was performed by autoradiography of the cells cultured in the presence of 3H-thymidine reagent (3H-TdR) and a selective agent (10−4 M 6-thioguanine), applying the modified method of Strauss and Albertini (1979).The lectin labeling index (LI) and the HPRT mutation frequency were determined from the same samples, as previously described [27,28] finally the VF was calculated according to the equation of Strauss and Albertini (2000).
The measurement of UDS was carried out according to Bianchi et al. (1981), as previously described briefly, PBLs have separated on Histopaque 1,077 gradients by density centrifugation.After separation, PBLs were irradiated in open petri-dishes by UV light (24 J/m 2 ) and then incubated for 3 h with 10 o C i/ml3H-TdR in the presence of 2.5 m Mhydroxy urea.The degree of 'de novo' UDS was measured by scintillometry based on 3H-TdR incorporation in separated lymphocytes.UDS was calculated as the difference between radioactivities of the incorporated 3H-TdR in UV-irradiated and control subjects.

Determination of CA and SCE frequencies
Whole blood samples were processed for studies of CA and SCE.The cell culture methods were identical in both protocols: samples of 0.8 ml heparinized blood were cultured in duplicate at 37 o C, in 5% CO 2 atmosphere, in 10 ml RPMI-1640 supplemented with 20% fetal calf serum and 0.5% PHA without antibiotics.For CA and SCE analyses, the cultures were incubated for 50 and 72 hours, respectively.5-Bromo-2µ-deoxyuridine (BrdU) used in SCE analysis to identify the first and subsequent metaphases, was added at a concentration of 5 µg/ml at 22 hours of culture.Culture harvest, slide preparation and, staining were conducted following the standard methods using 5% Giemsa stain for CA (Moorhead et al, 1960), and according to the Fluorescence-plus-Giemsa method of Perry and Wolff (1974) for SCE.CA characterization was carried out in 100 metaphases with 46±1 chromosomes per subject according to Carrano and Natarajan (1988).Mitoses with unmatched (45 or 47) chromosomes were considered as aneuploidy cells.Mitoses containing only achromatic lesions (gaps) and/or aneuploidy were not considered aberrant.Premature centromere division (PCD) was scored according to Mehes and Bajnoczky (1981).Total PCD and mitoses with more than three chromosomes with PCD (PCD/CSG, centromere separation general) were also scored.Cells with a higher number of SCE per cell than the 95 percentile of the control (≥10), were

Results
Main demographic data of the experimental groups and control groups are summarized in Table 1.The age of experimental subjects was in the range of 22-60 years, for the personnel in the first and in the second group, and same years for the control groups respectively.The time of exposure in service as viscose industry workers were 21.8 years (ranging from 7 to 34 years) and 17.7 years (ranging from 4 to 34 years) for the subjects in the three groups, respectively.The number of current smokers was slightly elevated among the exposed donors.The present study describes the lifestyle characteristics such as gender, smoking status, smokers (43.96%) and nonsmokers (48.78%) and a number of subjects based on age factor seen in group I (31.05 ±2.14) and in group II (42 ± 2.47) and control subjects.
The experimental subjects and controls were matched for age and gender and there was no identified difference in gender.Accordingly, gender, 26 males (63.41%) and 15 females (36.58%) were recruited for the present study.Chromosomal aberrations and SCE were depicted in Table 2. Circulated lymphocytes of Group I and II workers in compared with the equal quantity of control subjects.The comparative data for general characters, chromosomal alterations, and SCE/1,000 cells are noted Table 2. in addition CA and SCE frequency based on the CS 2 exposure in air and in urine were also depicted in the same Table .In total CS2 exposure to air, the Group I subjects show 1.42±0.004(mg/m 3 ), which was higher compared to Group II subjects (0.054±0.002 mg/m 3 ) and controls (0.021±0.004 mg/m3).From the mean ± SD values, it was found that the total CA (5.41±2.48)and SCE ( for Group I subjects was found to be higher compared to II group subjects (9.31±2.73)and controls (3.62±1.18).The values obtained in Group I subjects were found to be statistically significant when compared to their respective controls.Tables 3 and 4 depict the mean ± SD values of CA and SCE frequencies of group I and II subjects, respectively.The frequency of total CA found in group I subjects was higher [8.62±2.36(13-15 yrs)] compared to other groups [7.32±0.81(10-12 yrs), 9.46 ± 4.04 (7-9 yrs), 3.70±0.84(4-6 yrs); 1.86±0.62(0-3)] (Table.4).In group I subjects the total SCA was higher in 10-12 years exposure (21.06±3.42)compare other groups of exposed subjects [19.32±3.82(13-15 yrs), 18.06±1.86(7-9 yrs), 16.80±3.39(4-6 yrs) and 13.04±3.46(1-3 yrs)] which were found to be statistically significant when compared to other groups and their respective controls.The second group of subjects the total CA (6.01±2.10)and SCA (18.26±1.86)frequency were higher in 61-70 years residence.The present study showed elevated levels of CA are presented Group I, II and controls Table 4. Furthermore, statistical significance for the frequency of CA expressed in mean ± SD was established using the analysis of variance (ANOVA).Cell cultures were effectively established from the blood samples collected from all the subjects.The overall CA and SCA frequency for CS 2 exposures were significantly different (Tables 2, 3, 4) from that of the controls for both chromatid and chromosome type aberrations (P value is 0.03 by ANOVA).
The results of the flow-cytometric measurements on the percentage of apoptotic cells, cells in S-phase and CD71 expression, together with the mean values of LI, VF, and UDS, are summarized in Table 5.The mean percentage of apoptotic cells was significantly higher in I and II groups (8.57±1.10,5.04±0.48) of investigated subjects in comparison with the mean values of the controls (3.91±0.27).Fascinatingly, the percentage of apoptotic cells was even higher in the group I exposed to CS 2 only, in comparison with the groups II and III exposed to CS 2 , while this was not statistically significant (p = 0.33).
The mean percentage of cells in S-phase, measured by flow cytometry, as well as the mean values of LI, was slightly increased in the samples of both groups of exposed subjects in comparison with the control subjects.There were no significant differences in SCE between the groups of exposed and controls.The mean percentage of HF/SCE showed a non-significant (p = 0.16) increase among subjects in the second group, exposed mainly to CS 2 .The percentages of PCDs were significantly higher in both experimental (Groups I and II) subjects, in comparison with the controls (Group III).

Discussion
The results of the present study revealed cytogenetic alterations and induction of apoptosis among viscose factory workers occupationally exposed to CS 2 .Moreover, the considerable CS 2 concentration was always present in the working environments, and the presence of CS 2 in the air was always observable by olfactory perception.Safety measures and devices were introduced in the last few years in these industries, and the employees have used these protective devices during their work.But none of the workers have worn masks or similar personal safety devices equipped with specific filters for CS 2 .Therefore, to assess the excess risk among these workers in the second group, we should consider the effects of low dose exposure to organic solvents as a confounding factor and as a cause of bias on the effects of CS 2 .On the other hand, the persons in the first group were almost exclusively exposed to CS 2 , as they have situated nearby these industries.
Furthermore, major effluent water mostly contaminated with CS 2 moreover some of the industries in our study area release their effluents either on the open land or in surrounding surface water bodies contaminating the soil, surface water ultimately turned into groundwater.Much of the groundwater is unsuitable for irrigation, and hundreds of wells in the region can no longer be used.Based on these earlier reports, we recruited experimental subjects who were known to live for the past 3 decades in and around our study area and were occupationally exposed to CS 2 by mode of air and water (drinking).
Mutagenesis is involved in the pathogenesis of many neoplasias.Occupational exposure may contribute to Continuous efforts have been made to identify genotoxic agents, to determine conditions of harmful exposure and to monitor populations that are excessively exposed [29].The present study was designed to assess the genetic damage among viscose plant workers who are occupationally exposed to CS 2 .CA and SCE is a valuable method for detection of occupational and environmental exposures to genotoxicants, and it can be used as a tool in risk assessment for hazard characterization [29,30] of various in vitro and in vivo studies [31][32][33].
An epidemiological study showed a strong correlation between CS 2 concentrations from workers in viscose rayon factory and CS 2 factory indoor air concentrations up to 64 mg/m3 (20.5 ppm).Ghittori et al., (1998) used personal passive samplers installed in the breathing zones to measure the airborne CS 2 levels for 4 hours.Most of the indoor air samples revealed CS 2 at levels below the TLV of 31 mg/m 3 .
Previous studies concluded that urinary CS 2 may be a good indicator to estimate the levels of exposure to CS 2 in the workplace.A positive correlation or urinary concentrations and indoor air levels indicated that a mean level of 15.5 μg/ CS2/L (95% CI 13.8-17.1 μg) was excreted following exposure to CS2 at 31 mg/m3 current occupational exposure limit in viscose industry [34].Cox et al., (1998) investigated 2-thiothiazolidine-4-carboxylic acid (TTCA) concentrations as a biomarker of CS 2 exposure.The present study finds out that collected urine samples from workers in suggested that more emphasis should be placed on workplace protection factors rather than just addressing the indoor air CS 2 concentrations.Present findings also suggested that urinary concentrations allow determinations of the workplace protection factor afforded workers using respirators and assist in determining who are not wearing respirators and not adhering to safety precautions in the workplace [35].Moreover, the present finding depicted CS 2 level was more in the first group of subjects compare with second and control subjects.
On the other hand Jian and Hu, (2000) investigated the mechanism of action of CS 2 on the antioxidative stress mechanisms and measured enzymes linked to oxidative stress, including Cuprozinc-superoxide dismutase (CuZnSOD) and malonyl dialdehyde (MDA) levels in the serum of viscose rayon factory workers and in control subjects.The workers were between 20 to 41 years of age and had been exposed to CS 2 from 2 to 14 years, with an average exposure of 8 years this effect showed a dose-response relationship.Serum MDA levels were also increased in CS 2 exposed workers in both a concentration and in an exposure duration-dependent manner.The enzymes (i.e., CuZnSOD and MDA) may serve as biomarkers for inclusion in worker's health surveillance to determine early stages of impairment of the anti-oxidative stress response resulting from CS 2 exposure (Jian and Hu, 2000).
Flow-cytometric measurements detected an induction of apoptosis among both experimental and control groups of occupationally exposed to CS 2 from viscose factory.Our results are in better agreement with the findings of the in vitro experiments by Bao et al., (1996) demonstrating that higher doses of CS 2 induce apoptosis.However, cell proliferation, as determined by flow-cytometric measurements of the S-phase and expression of CD71, and from the measures of LI, was not decreased in our study, although in vitro experiments have shown a decrease in the viability and mitotic activity of cells at CS 2 doses inducing apoptosis.These differences between the findings of the in vitro studies and our results may be attributed, among others, to differences in doses, duration of exposure, and differences in cell types.The slight decrease in apoptosis among the workers with ages above the mean in the second group, exposed mainly to CS 2 , may be a consequence of adaptation to CS 2 exposure.Mean CA frequencies were significantly elevated in both groups of pathology personnel, in comparison with the controls.This increase is indicative of exposure to clastogenic agents among viscose industry workers.As the mean CA frequencies were also significantly elevated in viscose factory workers in the second group, who were partially exposed to CS 2 , the CA-inducing effect found in our study can be attributed to CS 2 as a clastogenic agent.Our findings on the elevated CA frequencies in both groups of workers exposed to a mean ambient air concentration of 0.9mg/m3 CS 2 , are in good agreement with most of the literature dealing with CS 2 induced CA (and/or SCE) among viscose industry workers [7,9,10] Moreover in vitro experiments [15]showed that CS 2 induces CA in PBL among viscose factory workers, increased frequencies of CA in PBL were observed in the study of Le and Fu, 1996 in the same manner elevated CA level was identified in the PBL of the exposed workers in our study.However, in the second group of the exposed persons with ages above the mean, a significantly increased SCE was observed, but this increase could probably be attributed to the effect of smoking, as all the smokers in this group belonged to this subgroup with ages above the mean.In a study by Bao et al., (1996), no increase in the SCE frequencies in lymphocytes from CS 2 exposed viscose factory workers was observed.PCD and PCD/CSG, a disturbance in the process of mitotic division of chromosomes, were significantly increased in both groups, indicating an effect of genotoxic exposure inducing PCDs as suggested by previous studies.
The observation of higher frequencies of CA in the lymphocytes of exposed individuals agrees with the earlier reports Le and Fu 1996 regarding viscose rayon workers.These are considered S-dependent alterations, frequently observed due to human chronic exposure to chemical mutagens.In the present study, CA was observed to increase with age and exposure period in the exposed groups and based on age in the controls, though it was very low in the latter.The results of the present study also indicate a role played by age in the development of CA observed in PBL of controls.
In the present investigation, a notable CA was observed among the healthy controls.It is due to the assay being widely used in studying CA in healthy individuals.There was a significant difference between experimental and control subjects who are occupationally exposed to CS 2 .In past years, CS 2 concentrations in viscose rayon plants averaged about 250 mg/m3; they were subsequently reduced to 50-150 mg/m3 and more recently exposure levels of CS 2 are mostly below 31 mg/m3 [36].
A report on hypospermia, asthenospermia, and teratospermia in young workers exposed to 40-80 mg/m3 of CS 2 confirmed gonadal injury [37].Le and Fu, (1996) showed that the CS 2 induce chromosome aberration in human sperm.Numerous epidemiological reports concluded that the CS 2 is toxicant to viscose industry workers [16,17,38].In this study, experimental subjects with smoking habits showed maximum levels of chromosome and SCE alterations when compared to respective controls, which shows that the CS 2 exposure with cigarette smoking has a synergistic effect on inducing genetic damage.Chromosomal aberrations were shown to be good indicators of future risk of cancer [24].On the other hand, genetic damages are the ultimate causes of cancer because DNA base changes can be mutagenic [25].The present findings highlight the importance of investigating the genotoxicity of CS 2 on viscose plant workers occupationally exposed to this organic solvent when the smoking habit is associated since this information provides an increased degree of identification for the positive response.
The relation between exposure to CS 2 and the induction of apoptosis and changes in CA, PCDs and PCD/CSG needs further investigation, and more data from larger groups of CS 2 exposed individuals from different industries are also needed to analyze the confounding effects of smoking.Similarly, as in the present study, the investigated viscose factory workers were maximum men only, further investigations are needed to collect data from women workers, in order to study the possible effect of gender on CS 2 induced apoptosis and changes in the cytogenetic end-points.
In conclusion, the results of this study demonstrate that occupational exposure to CS 2 can induce apoptosis, CA and SCE on circulating fluids, thus indicating a possible excess cancer risk among exposed subjects.The multiple end-point genotoxicological monitors, developed and run in our laboratory, is able to detect changes in cytogenetic and cell proliferation biomarkers.The results emphasize the importance of personal safeguard at workplaces, with possible occupational exposure.Therefore, the aim of our study was to investigate the genotoxic effects associated with occupational exposure to CS 2 by analyzing apoptosis induction, CS, and SCE in circulated blood lymphocytes of workers associated with viscose industry and subjects living in the region surrounding these industries.However, the magnitude of this risk depends on the extent of exposure.Therefore, studies employing indicators for assessing the exposure and biological effects are strongly recommended.

Table 2 .
Comparative Analysis Of Chromosome Aberrations And SCE Based On The CS2 Level In Workplace Environment And Urine Samples

Table 3 .
Chromosome Aberration Frequency and SCE in Group I Subjects Based on Their Work Duration

Table 4 .
Chromosome Aberration Frequency and SCE in Group II Subjects Based on Their Year of Residence

Table 5 .
Mean Value of Cell Induction (%) Cell Proliferation, HPRT Mutation Frequency and DNA Repair Capacity in Cultured Peripheral Lymphocytes among Viscose Factory Workers Occupationally Exposed to CS2 Flow Chart 1. Graphical Representation of CA Value in Group I and Group II Subjects

Table 6 .
X Axis Value the development of pernicious illnesses, many times through mechanisms that involve genotoxic changes.