Bull S Evidence for Genotoxicity of Pesticides in Pesticide Applicators a Review
Indian J Hum Genet. 2011 Sep-Dec; 17(3): 179–187.
Evaluation of DNA impairment in agricultural workers exposed to pesticides using unmarried jail cell gel electrophoresis (comet) assay
Raminderjeet Kaur
Department of Human Biology, Punjabi University, Patiala-147 002, Punjab, India
Satbir Kaur
Department of Human Biology, Panjabi University, Patiala-147 002, Punjab, Bharat
Mukesh Lata
Department of Human Biological science, Panjabi University, Patiala-147 002, Punjab, Bharat
Abstract
BACKGROUND:
Pesticides are used in agriculture to protect crops, but they pose a potential adventure to farmers and surround. The aim of the present written report is to investigate the relation between the occupational exposure to various pesticides and the presence of Deoxyribonucleic acid damage.
MATERIALS AND METHODS:
Blood samples of 210 exposed workers (after a mean solar day of intense spraying) and 50 control subjects belonging to diverse districts of Punjab (India) were evaluated using Comet assay. Lx workers who showed Dna damage were selected for follow up at 5-half-dozen months afterwards the first sampling during a low or goose egg spraying period.
RESULTS:
Significant differences were establish in DNA damage between freshly exposed workers and controls and freshly exposed and followed up cases. There was significant increase in the comet parameters viz. mean comet tail length and frequency of cells showing migration in exposed workers every bit compared to controls (72.22 ± xx.76 vs. 46.92 ± viii.17, P<0.001; 31.79 vs. v.77, P<0.001). In the 2d samples, followed upward cases showed significant decrease in frequency of damaged cells as compared to freshly exposed workers of commencement sampling (P<0.05). The confounding factors such as variable duration of pesticide exposure, age, smoking, drinking and dietary habits etc which were expected to modulate the damage, were instead establish to have no pregnant effect on DNA fragmentation.
Decision:
The evidence of a genetic gamble related to exposure resulting from the intensive use of pesticides stresses the demand for educational programs for agricultural workers to reduce the apply of chemicals in agriculture.
Keywords: Agricultural workers, comet assay, Deoxyribonucleic acid impairment, genotoxicity, pesticides, Punjab
Introduction
Pesticides are extensively used all over the world to increase food product and control vector-borne diseases and in recent years their use was increased dramatically. Unfortunately, large amounts of these chemicals are released into the environment and many of them impact non-target organisms, being a potential hazard to human health. Fifty-6 pesticides have been classified as carcinogenic to laboratory animals by the IARC.[1] Meta-analyses showed that pesticide-exposed farmers are at adventure for specific tumors, including leukemia,[2–four] non-Hodgkin's lymphoma,[5] soft tissue sarcoma,[6] Parkinson illness,[7] multiple myeloma,[8] stomach and prostate malignancies.[9] Some selected pesticides have been tested individually by in vitro genotoxicity testing methods and considered as potential chemical mutagens.[ten] However, the effective dose in many single tests is mostly very high. As nearly occupational and environmental exposures are exposure to mixtures of pesticides, the genotoxic potential evaluated on single compounds could not be extrapolated to humans. Hence, the genotoxicological cess in human being populations is a useful tool to approximate the genetic risk from an integrated exposure to circuitous mixtures of pesticide. Several cytogenetic assays have been used to evaluate the potential genotoxicity of pesticide exposures in occupationally exposed populations. However, at that place are reports on positive genotoxic effects in populations exposed to pesticides[eleven–13] likewise as negative findings.[14,15]
Alkylating abilities of the pesticide chemicals induce breaks in DNA[16] and thus impact DNA replicating ability and its ability to carry information.[17] Dna damage together with cellular response can institute genomic instability through multiple pathways[18] and tin be considered as an effective strategy for risk assessment. Individuals occupationally exposed to pesticides have great genotoxic risk and assessment of this risk in exposed subjects tin exist used as adequately reliable biomarker of early biological alterations.[nineteen] Biomarkers frequently used to appraise genotoxic effects of pesticides include chromosomal aberration (CA), micronuclei formation (MN), sister chromatid exchanges (SCEs) and comet assay.
From the past few years, single jail cell gel electrophoresis (SCGE) or comet analysis has been used as a sensitive, visual, reliable, rapid and cheap technique for measuring and analyzing DNA unmarried and double-strand breaks, brine-labile sites, DNA cross- linking and delayed repair-site detection in eukaryotic individual cells.[xx,21] The sensitivity also as the specificity of comet assay can be increased by incorporating an extra footstep of digestion with a lesion-specific endonuclease post-obit lysis.[22] The relevance of technique lies in its requirement of small amount of claret sample and its ability to evaluate alphabetize of genetic damage in the non-proliferating cells. Though the technique is extensively used in fundamental DNA-repair studies, toxicology and biomonitoring studies, all the same merely a limited number of biomonitoring studies on the genotoxic effects due to occupational exposure to pesticides in sprayers have been reported.[23–29] These studies have revealed significant increase in DNA damage in exposed workers in comparing to control subjects. A few studies have as well reported negative results.[30] Genetic polymorphism of the metabolic enzyme GSTP1 has been found to be associated with greater risk of DNA damage in pesticide exposed workers.[29] Yet, there is a scarcity of data pertaining to studies conducted on blood samples of individuals during intense spraying activeness alternating with no spraying/very low spraying of pesticide. Moreover, in developing countries like India, nigh of the pesticide applicators are illiterate and untrained and do not use appropriate protective clothing / devices and accept never been monitored for the genotoxic effects of pesticides they are being exposed to.
Earlier data suggests that endogenous and exogenous factors are involved in modulating the effects of pesticides and hence the individuals of different genetic constitution may reply differently to pesticide exposure. The present report is thus designed to evaluate the extent of possible Dna harm amidst freshly exposed workers during intense spraying flavor and follow upward cases during depression exposure period among the pesticide sprayers of Punjab (India) who were occupationally exposed to various pesticides for variable duration of exposure.
Materials and Methods
Written report population
The study was carried out on a group of 210 male farm workers (Vegetables, Orchards, Cotton, Paddy and Wheat Sprayers) belonging to various districts of Punjab and being exposed to various pesticides. This was a longitudinal study in which each farmer was his own control. This approach removed problems generated by the option of unexposed command and their similarity to exposed population for any epidemiological parameter except exposure. Still an attempt was made to compare the exposed and not-exposed group. So the 50 age-matched healthy male individuals were selected as command from general population having no history of occupational exposure to pesticides, whatever serious medical problem and intake of drugs or other therapeutic medicines (at least from the past one yr from the day of sampling). Both, the exposed workers and unexposed subjects were selected from the same region. In Punjab, agronomical work is in the hand of males mainly and participation of females is least. And so females were excluded from the written report. A follow upward study was conducted at 5–6 months later on the get-go sampling, in a depression exposure period. A total of 60 samples were selected from the exposed group who showed any Dna impairment during intense spraying period. Blood samples were nerveless from December, 2003 to January, 2006. Approximately 0.5 ml of blood sample was collected from each subject in an Eppendorf tube containing i drop of the anticoagulant EDTA.Gii solution. A gentle prick was given on the fingertip using a sterilized lancet. Tubes were serially numbered and were brought to the laboratory in an air tight ice container for assay. Samples were transported to the laboratory at or below 8°C and were processed within 1–eight h of collection. Before comet assay, full cell count and jail cell viability were evaluated using the Trypan blue exclusion method. The cell viability was plant to exist about 98% in all samples.
All participants signed a written consent before sampling. Complete information regarding sex, historic period, marital condition, medical history, life style (smoking, drinking, drug intake habits etc.) forth with the occupational history regarding various aspects of pesticides, duration of exposure, working hours/twenty-four hour period, name and grade of pesticides, protective measures used etc. was enquired from the workers and recorded in the questionnaire. In all cases, individuals who smoked more 5 cigarettes per day for at least ane twelvemonth were considered as smokers.
The exposed group workers and control accept an boilerplate age of 32.92 + 11.03 years (17- 45 years) and 26.34 + 7.41 (18- fifty years) respectively. The duration of exposure to pesticides varied from 1 to 25 years in exposed workers with an average of ten.75 + vii.92 years. The exposed grouping handled pesticides throughout the year and the average number of hours that the workers had been directly involved in handling these chemicals were approximately half dozen h. The demographic characteristics of the studied group are described in Tabular array i. Workers worked in open up fields and pesticides were applied in a higher place the head. Very few workers used some kind of protective measures (gloves, shoes, mask etc.) during the training and awarding of pesticides. Carbamates, organophosphates and pyrethroids were the nigh used families of the pesticides. A list of various pesticides used by the farm workers along with their frequency is given in Table two.
Table one
Demographic characteristics of the report group and command
Table two
Pesticides used by the study group along with their WHO classification and frequency of use
Experimental design
The alkaline single jail cell gel electrophoresis analysis was carried out according to the technique given by Singh et al,[xx] with slight modification incorporated later on in the original technique past Ahuja and Saran[31] to access DNA harm. Silver staining method was used to get the results. Slides were prepared in triplicates per subject. Clean and dry out drinking glass slides were coated past putting a small amount of ane% normal melting bespeak agarose (NMPA) (40-42°C) and dried at 37°C for 2-iii h. An aliquot of 25 μl of whole blood was mixed with 0.5% of 75 μl depression melting point agarose (LMPA 37°C). Second layer of 100 μl of this mixture was pipetted onto the precoated slides and covered with coverslips. These slides were immune to solidify at four°C for 30 min. After solidification, coverslips were removed and a third layer of 100 μl of LMPA was pipetted onto the slides and made to spread properly with the help of coverslip. These slides were again kept at 4°C for another 30 min. LMPA and NMPA were prepared in phosphate buffer saline (136 mM NaCl, 2.68 Mm KCl, 8.10Mm Na2HPOiv, 1.47 Mm KHiiPOfour and pH 7.4). After removing coverslips, slides were immersed in freshly prepared cold lysing solution [2.5 M NaCl, 100 mM NatwoEDTA, 10mM tris-HCl, pH x, 1% Trition Ten-100 and 10% DMSO (added just before use)] for two h.
Slides were then placed in alkaline buffer (300 mM NaOH and i mM Na2EDTA, pH xiii) in a horizontal electrophoretic chamber for xx min to let the unwinding of the DNA and expression of alkali-labile sites. Electrophoresis was conducted for 30-35 min at 25 V (0.66 V/cm) and 300 mA current. The current was adjusted to 300 mA by raising or lowering the buffer level in the tank. Electrophoresis procedure and the efficiency of each electrophoresis run were checked using negative controls, consisting of whole homo unmodified blood nerveless in the laboratory. Each electrophoresis run was considered as valid simply if the negative controls yielded the expected results. Slides were dried, placed on a tray and done thrice for ten min each with neutralization buffer (0.iv M tris-HCl, pH 7.v). The whole procedure was carried out in dim light to avoid boosted Dna damage. The gel was dried for ane h at room temperature and fixed for x min in fixing solution (15w/v trichloroacetic acid, 5% zinc sulfate, five% glycerol) and dried at 37°C for 1 h. The staining solution was prepared fresh before use past mixing 34 ml of solution A (0.2% ammonium nitrate, 0.2% silver nitrate, and 0.5% formaldehyde) with 66 ml of solution B (5% sodium carbonate) and poured over the samples very gently. The slides were immersed for 30 min and shook until grey colour appeared. After staining, slides were washed 3 to four times with deionized water, air stale and viewed under a trinocular Zeiss-microscope. All slides were coded to blind assay and were scored by one person, to avert inter-scorer variability. These slides were examined at 100X magnification using 10X objective and 10X eyepiece. A total of 100 cells were scanned per subject. Undamaged cells accept intact nuclei without a tail and appear as a 'halo'and damaged cells take the appearance of comets. The length of DNA migration in the comet tail gives an estimate of the extent of Deoxyribonucleic acid harm and was measured with an ocular micrometer calibrated with the help of a stage micrometer at 100X magnification. Each division on the micrometer scale was equivalent to xv μm Deoxyribonucleic acid migration length. DNA impairment for each cell was quantified every bit follows: Comet tail length (μm) = Maximum total length - head diameter
Hateful tail length in μm was calculated past taking the average of the measurements obtained for all the comets. Frequency of cells showing migration (number of cells with comets/ total cells scored × 100) was also determined in each group. These comets were randomly selected for taking measurements from each individual by avoiding the edges and the damaged parts of the gel and the superimposed comets. The Deoxyribonucleic acid damage was also assessed by visual scoring, but we found measurements of tail length more reliable and therefore considered merely tail lengths and frequency of cells showing Dna damage as a tool to quantify DNA impairment.
Statistical assay
Hateful and standard deviation (mean ±Due south.D) were calculated for each parameter studied. The statistical assay of differences in DNA impairment, as measured past the comet assay, was carried out using t-exam. The selection of t-test was fabricated after finding variables to prevarication in the normal distribution bend. χtwo- test and multifactor analysis of variance (ANOVA) were used to check the significant differences. Correlations between different variables were determined by Spearman rank correlation test. The disquisitional level for rejection of the zip hypothesis was considered to exist a P-value of 5%. All analyses were performed with the SPSS ten.0 version software packages.
Results
Results are expressed equally mean + South.D. A complete history including age, duration of exposure, smoking habits etc. are given in Table ane. Most of the workers used cocktail of 2 or more than pesticides belonging to dissimilar chemical groups. In that location were 58 (27.62%) smokers in the exposed group and no smoker in the control grouping. The average biddi (locally made cigarette) consumption of smokers was almost ten biddies per mean solar day. All control individuals in this written report were selected to be not-smokers in order to eliminate confounding effect of smoking. About twoscore.47% of the workers were alcoholic. Regarding the protective measures, only eight.09% workers used some kind of protection during the preparation and application of pesticides.
Comet assay assay of the 210 exposed workers revealed Deoxyribonucleic acid damage in 35.71% of the cases, while in controls, the damage was detected in only eight% of the cases [Tabular array 3]. These differences were highly significant (P<0.001). But 25% of the followed upwards cases exhibited DNA damage which was significantly lower than fresh cases (P<0.05). In the first samples of intense spraying, there was significant increase in the comet parameters viz. mean comet tail length and frequency of cells showing migration in exposed workers every bit compared to control (72.22 ± twenty.76 vs. 46.92 ± viii.17, P<0.001; 31.79 vs. 5.77, P<0.001). In the second samples, of low or no spray, followed upwards cases showed significant decrease in frequency of damaged cells as compared to first samples of freshly exposed workers (P <0.05) [Table iv]. Negative command for each electrophoresis demonstrated negative results.
Tabular array three
Frequency of DNA impairment in the full sample and control
Tabular array iv
Comet parameters in the freshly exposed cases, followed up cases and controls.
Effects of variables such as historic period, smoking, drinking and dietary habits and duration of exposure and employ of protective measures were evaluated in the exposed group of first samples merely. None of these confounding factors, except dietary habits, revealed a significant influence over the comet parameters or exhibited any association with increased Deoxyribonucleic acid damage. The frequency of cells showing migration was significantly high in the non-vegetarian exposed cases [Tabular array v].
Tabular array v
Comet parameters in 75 freshly exposed cases showing Dna impairment in relation to duration of exposure, age, smoking, drinking and dietary habits
Discussion
Base line genetic damage is influenced by various intrinsic and extrinsic factors, but it is not still articulate how an individual'southward inborn genetic constitution may influence yield of such damage. For this reason, cess of level of Deoxyribonucleic acid impairment in 210 occupationally exposed Punjab farmers along with 50 matched control subjects was done by taking two quantitative exposure parameters i.e. intense pesticide spraying season alternating with periods of reduced or null exposure, to determine the effects of immediate exposure too as accumulated exposure. Results have shown a pregnant increase in the level of DNA damage in the exposed workers every bit compared to controls [Table 1]. Previous studies both in vivo and in vitro are in agreement with the present findings except the comet tail length seems to be comparatively more in the present workers.[27–29,32,33] This may exist due to unwise and indiscriminate utilise of pesticides by these workers. Moreover, in majority of the cases, no protective measure was taken past these workers and cocktail of 2 or more than pesticides were used, belonging to unlike chemical groups and which may probably be causing some antagonestic or synergic event as well. Some investigators had studied Dna damage in the farmers who were recurrently exposed to pesticides,[19,23,24] whereas others had studied DNA impairment in pesticide manufacturing workers who were continuously exposed to pesticides.[25,27,34] There are a few studies in which no pregnant increment in DNA damage in exposed workers in comparing to control was found[30,35] which could exist due to the differences in work conditions like use of varied quality of protective equipment, variable duration of exposure etc.
Genetic susceptibility has been reported to modulate the level of genotoxic risk. Many studies accept shown an association between Dna harm and glutathione-Due south-transferase polymorphisms.[29] Inheritance of unfavorable genes has been shown to crusade reduced detoxification and elimination of environmental mutagen as pesticides. When they are not efficient in detoxification, the metabolic sub-products accrue, contributing to the tumorigenic process.[36,37] Certain pesticides (parathion, carbaryl, chlorpyrifos etc.) are known to inhibit P450 enzyme organisation and results in free radical production, which causes DNA damage.[38,39] In the present work, simply 35.71% sprayers showed DNA damage and the remaining 64.29% sprayers who did not prove any damage might take some intrinsic protective mechanism working against the pesticide exposure or else they might exist having oxidative DNA damage which we could non detect with the standard comet assay as this technique detects but strand breaks and alkali-labile sites. Deoxyribonucleic acid impairment was significantly decreased in the followed up cases in comparison to fresh cases. Similar findings of reduced Dna damage in the followed up cases have as well been revealed past Garaj-Vrhovac and Zeljezic.[19] Cytogenetic studies take besides reported decrease in genetic harm during the period of low exposure.[40–41] The decrease in DNA damage in followed up cases could be attributed to three contained physiological processes: repair of Deoxyribonucleic acid damage, emptying of cells due to death of highly damaged cells, dilution of cells carrying Dna damage past the product of undamaged lymphocytes from the stem prison cell pool.[42–44] Before followed up studies have revealed that comet assay is more efficient in detecting ongoing exposure rather than accumulated exposure.[23,45,46] Non-exposed farmers were not compared with the follow upwards cases as longitudinal study on the same subjects is a powerful mean to observe modification than a comparison between two different populations.
Some other factors like historic period, smoking, drinking and dietary habits were also analyzed while interpreting the results. No relationship between DNA damage and duration of exposure was found [Tabular array 5]. Before cytogenetic studies of pesticide sprayers take shown similar results.[12,41] Even so, a few studies have reported positive relationship.[19,25,29]
No meaning increase in Dna impairment with increase in age was observed in the nowadays sprayers. Similarly no association of DNA harm with age was observed in earlier studies.[23,25,27,28,47] There are evidences that certain vegetables and fruits contain anticlastogenic agents and have antioxidant properties.[48,49] Non-significant increase in non-vegetarian workers was observed and was in agreement with the results of Giovannelli et al[fifty] and Dhawan et al.[51] No significant human relationship has been detected between DNA damage and smoking. These findings are in accordance with the findings of the other workers.[28,48,52] The harm was rather slightly higher (not-significant) in the non-smokers than smokers. Like findings take been reported by some other authors.[23,28,46,53–55] Non-meaning increase in Deoxyribonucleic acid harm was observed in alcoholics. Non-significant differences in DNA damage was reported in the farmers who used protective measures [Table v]. This may be due to large number of workers who did not use any rubber measure out while spraying in this written report. Several studies take reported less DNA damage in workers who used some kind of protective measures.[40,52]
It is concluded that pesticides did cause DNA damage irrespective of duration of exposure. The harm caused past pesticides seems to be repaired as the follow upwards cases which were studied during null or depression menstruation of spraying did reveal significantly lower frequency of Dna damage in comparison to fresh cases. The confounding factors including age, smoking and diet were expected to modulate the genotoxic effect of xenobiotics, but the absenteeism of any positive correlation between these factors and comet parameters advise that the DNA damage was probably caused past pesticides only.
Footnotes
Source of Support: Nix,
Conflict of Interest: None declared.
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Articles from Indian Journal of Human Genetics are provided here courtesy of Wolters Kluwer -- Medknow Publications
Source: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3276987/
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