Lung cancer risk in workers occupationally exposed to polycyclic aromatic hydrocarbons with emphasis on the role of DNA repair gene

被引:16
|
作者
Moubarz, Gehan [1 ]
Saad-Hussein, Amal [1 ]
Shahy, Eman M. [1 ]
Mahdy-Abdallah, Heba [1 ]
Mohammed, Atef M. F. [2 ]
Saleh, Inas A. [2 ]
Abo-Zeid, Mona A. M. [3 ,4 ]
Abo-Elfadl, Mahmoud T. [4 ,5 ]
机构
[1] Natl Res Ctr, Environm & Climate Change Res Inst, Environm & Occupat Med Dept, Giza, Egypt
[2] Natl Res Ctr, Environm & Climate Change Res Inst, Air Pollut Res Dept, Giza, Egypt
[3] Natl Res Ctr, Genet Engn & Biotechnol Res Inst, Genet & Cytol Dept, Giza, Egypt
[4] Natl Res Ctr, Ctr Excellence Adv Sci, Canc Biol & Genet Lab, Giza, Egypt
[5] Natl Res Ctr, Genet Engn & Biotechnol Res Inst, Biochem Dept, Giza, Egypt
关键词
Polycyclic aromatic hydrocarbons (PAHs); Alpha 1 antitrypsin (A1AT); APEX1; gene; Tumor biomarkers; APURINIC/APYRIMIDINIC ENDONUCLEASE; CELL-CARCINOMA; ADDUCTS; ALPHA-1-ANTITRYPSIN; PAHS; POLYMORPHISMS; DAMAGE; AIR; ALPHA(1)-ANTITRYPSIN; INFLAMMATION;
D O I
10.1007/s00420-022-01926-9
中图分类号
R1 [预防医学、卫生学];
学科分类号
1004 ; 120402 ;
摘要
Objective Workers in secondary aluminum production plants are occupationally exposed to polycyclic aromatic hydrocarbons (PAHs). We aimed to monitor the concentrations of PAHs in air and in serum of workers at two secondary aluminum production plants. We also investigated the potential risk of lung cancer development among PAHs exposed workers with emphasis on the role of A1AT mutation and APEX1 gene polymorphisms. Methods This study included 177 workers from administrative departments and production lines. Blood samples were obtained for estimation of benzo(a)pyrene diol epoxide albumin adduct (BPDE-Alb adduct), anti-Cyclin-B1 marker (CCNB1) and squamous cell carcinoma antigen (SCCAg). Genes' polymorphism for human apurinic/apyrimidinic endonuclease (APEX1) and alpha-1-anti-trypsin (A1AT) gene mutation were detected. Results There was a significant increase in the level of BPDE-Alb adduct among exposed workers in comparison to non-exposed group. Moreover, 41.67% of exposed workers in El Tebbin had BPDE-Alb adduct level >= 15 ng/ml versus 29.6% of workers in Helwan factory. There was a significant increase in tumor markers (SCCAg and CCNB1) among workers whose BPDE-Alb adduct >= 15 ng/ml. There was a significant increase in the level of BPDE-Alb adducts in exposed workers carrying homozygous APEX1 genotype Glu/Glu. Furthermore, exposed workers with the Glu/Glu genotype had high tumor markers levels. There was a significant increase in levels of BPDE-Alb adducts in workers carrying A1AT mutant allele. Moreover, workers with mutant A1AT genotype had significantly high tumor markers (SCCAg and CCNB1) levels. Conclusion Therefore, we conclude that aluminum workers may be at a potential risk of lung cancer development due to PAHs exposure. Although PAHs concentrations in air were within the permissible limits, yet evidence of DNA damage was present as expressed by high BPDE-albumin adduct level in exposed workers. Also, elevation of tumor markers (SCCAg and CCNB1) in exposed workers points to the importance of periodic biological monitoring of such workers to protect them from cancer risk.
引用
收藏
页码:313 / 329
页数:17
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