Abstract
Abstract
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.
Funder
National Research Centre
National Research Centre Egypt
Publisher
Springer Science and Business Media LLC
Subject
Public Health, Environmental and Occupational Health
Reference78 articles.
1. Agaçhan B, Küçükhüseyin O, Aksoy Q, Turna A, Yaylim I, Görmüs U, Ergen A, Zeybek U, Dalan B, Isbir T (2009) Apurinic/apyrimidinic endonuclease (APE1) gene polymorphisms and lung cancer risk in relation to tobacco smoking. Anticancer Res 29:2417–2420
2. Alhamdow A, Lindh C, Hagberg J, Graff P, Westberg H, Krais AM (2018) DNA methylation of the cancer-related genes F2RL3 and AHRR is associated with occupational exposure to polycyclic aromatic hydrocarbons. Carcinogenesis 39:869–878
3. Ando K, Hirao S, Kabe Y, Sato I, Yamaguchi Y, Wada T, Handa H (2008) A new APE1/Ref-1-dependentpathway leading to reduction of NF-kappaB and AP-1, andactivation of their DNA-binding activity. Nucleic Acids Res 36:4327–4336
4. Barraza-Villarreal A, Escamilla-Nuñez MC, Schilmann A, Hernandez-Cadena L, Li Z, Romanoff L, Sjödin A, Del Río-Navarro BE, Díaz-Sanchez D, Díaz-Barriga F, Sly P, Romieu I (2014) Lung function, airway inflammation, and polycyclic aromatic hydrocarbons exposure in mexican schoolchildren: a pilot study. J Occup Environ Med 56:415–419
5. Benhamou S, Sarasin A (2000) Variability in nucleotide excision repair and cancer risk: a review. Mutat Res 462:149–158
Cited by
15 articles.
订阅此论文施引文献
订阅此论文施引文献,注册后可以免费订阅5篇论文的施引文献,订阅后可以查看论文全部施引文献