Table 3
Examples of the use of OMICS technologies in occupational and environmental studies that investigate health effects in human populations exposed to benzene or arsenic
| OMICS field | Exposure | Topic | References |
| Genotyping | Benzene | Interaction between SNPs and benzene-induced toxicity | 71–73 77–80 |
| Genotyping | Arsenic | Interaction between SNPs and arsenic-induced skin lesions | 81 82 |
| Genotyping | Arsenic | Interaction between SNPs and arsenic metabolism | 83 84 |
| Genotyping | Arsenic | Interaction between SNPs and exposure to arsenic in relation to non-melanoma skin cancer | 85 |
| CNV | Arsenic | Interaction between DNA CNV and exposure to arsenic in relation to transitional cell carcinoma | 86 |
| CNV | Arsenic | Interaction between DNA CNV and exposure to arsenic in relation to bladder tumours | 87 |
| Epigenomics | Benzene | Relation between gene-specific hypermethylation and exposure to benzene | 88 |
| Epigenomics | Arsenic | Relation between epigenetic silencing of tumour suppressor genes and exposure to both tobacco and arsenic | 89 |
| Epigenomics | Arsenic | Relation between genomic methylation and exposure to arsenic | 90 91 |
| Transcriptomics | Benzene | Relation between gene expression and exposure to benzene | 92 |
| Transcriptomics | Arsenic | Interaction between exposure to arsenic and arsenical skin lesions in relation to genome-wide gene expression | 74 |
| Transcriptomics | Arsenic | Relation between gene expression and exposure to arsenic | 93 94 |
| Proteomics | Benzene | Impact of exposure to benzene on the composition of the proteome | 95 96 |
| Proteomics | Arsenic | Impact of exposure to arsenic on the composition of the proteome | 97 98 |
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CNV, copy number variation; SNP, single nucleotide polymorphism.
