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Assessment of the deoxyribonucleic acid damage caused by occupational exposure to chemical compounds in Isfahan Polyacryl Company.

Etebari M, Jafarian-Dehkordi A, Kahookar A, Moradi S - J Res Med Sci (2014)

Bottom Line: Furthermore, the effect of age, smoking, duration of working in the company and working in two parts of the company on the degree of vulnerability to genotoxicity was assessed.DNA damage was significantly higher in smoker groups compared with non-smoker target group and control group, 4.18 versus 3.07 and 1.52 respectively as tail moment, (P < 0.0001).Furthermore, it was higher in person working in two different parts of the company compared to those work in one part and control group, 4.63 versus 3.74 and 1.52 respectively as tail moment, (P < 0.0001).

View Article: PubMed Central - PubMed

Affiliation: Department of Pharmacology, Isfahan Pharmaceutical Sciences Research Center, School of Pharmacy and Pharmaceutical Sciences, Isfahan University of Medical Sciences, Isfahan, Iran.

ABSTRACT

Background: Chemical pollutants found in industrial environments can cause chronic genotoxicity in vulnerable individuals during the long-term exposure. The primary purpose of the present study was to assess the deoxyribonucleic acid (DNA) damage caused by occupational exposure to industrial chemicals and secondary purpose is to investigate the effect of possible risk factors of genotoxicity.

Materials and methods: The blood samples of the workers of Isfahan Polyacryl Company were evaluated in terms of genotoxicity using the comet assay method. The percentage of DNA in the tail and tail moment were measured and DNA damage was evaluated. Furthermore, the effect of age, smoking, duration of working in the company and working in two parts of the company on the degree of vulnerability to genotoxicity was assessed.

Results: The amount of DNA damage in the target group (the production line workers) was significantly higher than the control group (the staffs), 3.87 versus 1.52 as tail moment, (P < 0.0001). DNA damage was significantly higher in smoker groups compared with non-smoker target group and control group, 4.18 versus 3.07 and 1.52 respectively as tail moment, (P < 0.0001). Furthermore, it was higher in person working in two different parts of the company compared to those work in one part and control group, 4.63 versus 3.74 and 1.52 respectively as tail moment, (P < 0.0001).

Conclusion: Occupational exposure to Polyacryl caused DNA damage. Smoking and working in two parts of the company may have a significant role in DNA damage.

No MeSH data available.


Related in: MedlinePlus

(a) Comparison of % deoxyribonucleic acid in tail and (b) tail moment of the smoker and non-smoker workers in all parts of the company. Each graph has been represented as mean ± standard error of mean for 50 workers
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Figure 3: (a) Comparison of % deoxyribonucleic acid in tail and (b) tail moment of the smoker and non-smoker workers in all parts of the company. Each graph has been represented as mean ± standard error of mean for 50 workers

Mentions: Smoking is one of the personal risk factors may predispose the workers to possible genotoxicity. Based on the pre-filled questionnaires, 11.6% of the total studied population used to smoke cigarettes. The percentage of DNA in the tail and tail moment (% DNA in tail × tail length), were calculated for these workers and showed a significant difference in the one-way analysis (ANOVA) results (P < 0.0001). Moreover, the Tukey's multiple comparison post hoc test results showed significant (P < 0.001) increase in the percentage of DNA in the tail for both smoker and non-smoker groups in comparison with the control group while comparison of this parameter in smokers with non-smoker was significant (P < 0.05) [Figure 3a]. The One-way analysis of the tail moment data showed significant (P < 0.0001). Tukey's multiple comparison post hoc tests showed both groups had significant difference with the control group and with each other (respectively P < 0.001 and P < 0.01) [Figure 3b].


Assessment of the deoxyribonucleic acid damage caused by occupational exposure to chemical compounds in Isfahan Polyacryl Company.

Etebari M, Jafarian-Dehkordi A, Kahookar A, Moradi S - J Res Med Sci (2014)

(a) Comparison of % deoxyribonucleic acid in tail and (b) tail moment of the smoker and non-smoker workers in all parts of the company. Each graph has been represented as mean ± standard error of mean for 50 workers
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4155710&req=5

Figure 3: (a) Comparison of % deoxyribonucleic acid in tail and (b) tail moment of the smoker and non-smoker workers in all parts of the company. Each graph has been represented as mean ± standard error of mean for 50 workers
Mentions: Smoking is one of the personal risk factors may predispose the workers to possible genotoxicity. Based on the pre-filled questionnaires, 11.6% of the total studied population used to smoke cigarettes. The percentage of DNA in the tail and tail moment (% DNA in tail × tail length), were calculated for these workers and showed a significant difference in the one-way analysis (ANOVA) results (P < 0.0001). Moreover, the Tukey's multiple comparison post hoc test results showed significant (P < 0.001) increase in the percentage of DNA in the tail for both smoker and non-smoker groups in comparison with the control group while comparison of this parameter in smokers with non-smoker was significant (P < 0.05) [Figure 3a]. The One-way analysis of the tail moment data showed significant (P < 0.0001). Tukey's multiple comparison post hoc tests showed both groups had significant difference with the control group and with each other (respectively P < 0.001 and P < 0.01) [Figure 3b].

Bottom Line: Furthermore, the effect of age, smoking, duration of working in the company and working in two parts of the company on the degree of vulnerability to genotoxicity was assessed.DNA damage was significantly higher in smoker groups compared with non-smoker target group and control group, 4.18 versus 3.07 and 1.52 respectively as tail moment, (P < 0.0001).Furthermore, it was higher in person working in two different parts of the company compared to those work in one part and control group, 4.63 versus 3.74 and 1.52 respectively as tail moment, (P < 0.0001).

View Article: PubMed Central - PubMed

Affiliation: Department of Pharmacology, Isfahan Pharmaceutical Sciences Research Center, School of Pharmacy and Pharmaceutical Sciences, Isfahan University of Medical Sciences, Isfahan, Iran.

ABSTRACT

Background: Chemical pollutants found in industrial environments can cause chronic genotoxicity in vulnerable individuals during the long-term exposure. The primary purpose of the present study was to assess the deoxyribonucleic acid (DNA) damage caused by occupational exposure to industrial chemicals and secondary purpose is to investigate the effect of possible risk factors of genotoxicity.

Materials and methods: The blood samples of the workers of Isfahan Polyacryl Company were evaluated in terms of genotoxicity using the comet assay method. The percentage of DNA in the tail and tail moment were measured and DNA damage was evaluated. Furthermore, the effect of age, smoking, duration of working in the company and working in two parts of the company on the degree of vulnerability to genotoxicity was assessed.

Results: The amount of DNA damage in the target group (the production line workers) was significantly higher than the control group (the staffs), 3.87 versus 1.52 as tail moment, (P < 0.0001). DNA damage was significantly higher in smoker groups compared with non-smoker target group and control group, 4.18 versus 3.07 and 1.52 respectively as tail moment, (P < 0.0001). Furthermore, it was higher in person working in two different parts of the company compared to those work in one part and control group, 4.63 versus 3.74 and 1.52 respectively as tail moment, (P < 0.0001).

Conclusion: Occupational exposure to Polyacryl caused DNA damage. Smoking and working in two parts of the company may have a significant role in DNA damage.

No MeSH data available.


Related in: MedlinePlus