CYTOGENETIC STUDY ON WORKMEN OCCUPATIONALLY EXPOSED TO PESTICIDES
Omari YI*
*Corresponding Author: Yousif I. Omari, D.Sc., LFIBA, Department of Biological Sciences, Faculty of Science, University of Jordan, Amman, Jordan; +962-6-5355000, Ext. 22210; Fax: +962-6-5355000E-mail: yomari@ju.edu.jo
page: 51

DISCUSSION

Extensive studies have been carried out to investigate the genotoxic effects of organophosphorus pesticides [1]. The in vitro and in vivo cytogenetic assay is important for monitoring the genotoxicity of these pesticides [3,16,18,26]. In the present study, a cytogenetic investigation was carried out on field workers who were exposed to pesticides and given to the habit of smoking (Table 1). For comparison, studies were also carried out on smokers and non smokers who were not exposed to pesticides (Table 2). The breaks induced were mainly of the chromatid type, indicating damage at the G2 phase of the cell cycle (Table 1). Similar effects had been recorded earlier on other mammalian system [27,28].

Statistical analysis revealed that there was a significant increase in chromosomal aberration rate in smokers exposed to pesticides compared to smokers who were not exposed (Table 3). This does not agree with the reported results [29].

As Tables 2 and 3 indicate, the control smokers showed a significant increase in chromosomal aberration rate when compared to non smokers controls. This provides further evidence for the intrinsic mutagenic activity of smoking and agrees with observations reported [30-34].

This study demonstrated a high statistically significant increase in the chromosomal aberrations in the lymphocytes of the exposed smoker and non smoker workers compared with the controls (Table 3). These findings agree with the observations made by several authors [3,16,18-20]. However, two aspects in the induction of these chromosomal aberrations must be considered. One is that the chromosomal aberration increase could be attributed to the fact that workers were exposed to the pesticides for long periods each year and the level of exposure was enough to produce chromosomal aberrations. The second aspect is that the higher chromosomal aberration frequency might be due to the combined activity of the pesticides. Taking into account that those workers use a large spectrum of pesticides and most of them are not protected by safety measures and, possibly, this kind of exposure is responsible for the observed chromosomal aberration increase. Moreover, this finding is consistent with the observations reported by other authors [18,35-39]. Since the significant increase in chromosomal aberration in the present study could be due to the fact that the workers were exposed to two pesticides, a further study should include a cytogenetic evaluation of individual pesticide.




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