The interplay between the potential toxicity of inhaled volatile organic compounds and polycyclic aromatic hydrocarbons with detoxifying glutathione S-transferase and cytochrome peroxidase genes

Document Type : Original Article

Authors

1 Environmental and Occupational Medicine Department, National Research Centre, Egypt

2 Professor of Environmental Health and clinical pathology. Environmental and Occupational Medicine Department- Division of Environmental Research- National Research Centre, Giza, Egypt

3 Professor of environmental health, Environmental and Occupational medicine department, NRC

4 Environmental and Occupational medicine department, National Research Centre, Egypt

5 Department of Clinical and Chemical Pathology, National Research Centre, Egypt

6 Air pollution department National Research Centre, Egypt

7 National Research Centre, Clinical and Chemical Pathology Dept., Medical Research and Clinical Studies Institute, Centre of Excellence, Cairo, Egypt

Abstract

Background: Volatile organic compounds (VOCs) and polycyclic aromatic hydrocarbons (PAHs) stemming from research labs represent potential threats to public health. Aim: This study aimed to identify the profile of organic air pollutants (VOCs and PAH) in research laboratories and the diversity of genetic polymorphism of detoxification enzymes (GSTP1, GSTM1, GSTT1, and CYP2E1) as well as serum immunoglobulins (IgE and IgA) among research workers. Subjects and methods: a descriptive cross-sectional study that included 75 workers from agriculture research labs (ARL) and chemistry research labs (CRL). The main study parameters comprised VOCs and PAHs in the air, serum immunoglobulins (IgE and IgA), and genomic DNA for glutathione-S-transferase (GST) and cytochrome peroxidase (CYP) genes. Results: The concentrations of personal exposure of VOCs could be estimated from the prediction equation as 0.9*concentrations of VOCs at work environment in the same lab. The cumulative gas chromatography-8 working hours- total VOCs concentrations were higher in CRL by about 13.5-32.4% than values in ARL due to different lab activities. Elevated but similar concentrations of benzene and toluene exceeding Egyptian threshold limit value were met in ARL and CRL. PAHs concentrations were within 7-11 ng/m3. Those with null GSTT1, GSTM1 and GSTP1 AA genotypes have a double decrement in the activity of the detoxifying enzyme. The odds ratio of 0.2 times (protective) indicates that elevated IgA is 5 times less likely in present (GSTM1 &/or GSTT1) genotypes compared to the null subgroup, showing that GST genes were protective from elevated IgA. Conclusions: workers carrying null GSTT1 & GSTM1 genotypes are at higher risk making them prone to oxidative stress-associated diseases and VOCs and PAHs induced carcinogenesis.

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