SAP kinases, thrombin receptors, and Gn-RH receptors. Inflammatory response genes (angiotensinogen and MHC class Ib). Xenobiotic metabolism-related genes (cytochrome P450 PB1, Y-b3 glutathione-S-transferase, betaine, and homocystein methyltransferase). Mmp12, Cd5l, Loc50101, Loc69183, Spp1, and Slc26a4 were similarly or more markedly upregulated in exposure group. Trem2 expression was elevated in recovery group.

Genes associated with signal transduction, cell growth, differentiation, transcription factor, and protein synthesis. Cathepsin E, dipeptidase, aflatoxin B1 aldehyde reductase, peroximal membrane protein 1, and NAD isocitrate dehydrogenase. Gene of stress-related proteins (2,4-dienoyl-CoA reductase precursor, thioredoxin reductase (TrxR2), glucocorticoid-regulated kinase, heat shock protein 70 (Hsp 70), and pyruvate carboxylase.

The transcriptional changes that occur during repeated exposure provides important information on the inflammation and repair processes following welding-fume-induced lung injury.

Non-human Primate

With exposure: Genes involved in signaling pathways (DGKB, PIAS2, AXIN2), metal ion binding (TRIM2), DNA binding (HIST1, H2BC), metabolism of immunological disease (CHIT1), genetic disorders, cancer, inflammatory diseases, cellular growth, proliferation, and development (CHI3L1, RARRES1, DDHD1 and CTSB). With recovery: Genes involved in tRNA aminoacylation (IGL@, TARS), antigen presentation, or immune response (HLA-DPB1, IGHM, GAGE12F), cell differentiation or development (THOC5, FNDC3A, DOCK7), metabolism (CHIT1, CPT1A), and apoptosis (240890_at, JAK2). Genes involved in cancer, immunological diseases, and inflammatory diseases ranked high, other genes involved in cellular growth, proliferation, and cell cycle were also observed. PPID, CFLAR, CPT1A and INSR.

Genes involved in transport (ABCA13, STEAP2, KCNH2, KCNV1), transcription (236231_at, ZNF738, HEY2), cell adhesion (ACTN2), rRNA processing (ADAT2), and protein binding (SLITRK6). GM2A, GRAP, CYP1B1, PTGFRN ID4, and NRGN.


Genes involved in heat shock protein binding (DNAJC6, NTRK2, DNAJC10), signal transduction (RGS4), proteolysis (DPP10), antigen presentation (HLA-DPA1), cell cycle arrest (GAS2L3), transcription (ZNF483), and development (RICTOR). KLKB1, ATM, RAG1, UBASH3A, IGKC, and PTPN22. CHI3L1, GM2A, RARRES1, CTSK, DDHD1, and CTSB.

It changed ..the genes involved in the G1/S transition of the cell cycle; TR/RXR activation and fibrosis were identified in both the exposure and recovery groups. It changed the genes involved in gene regulation mechanisms by peroxisome proliferation, RAR activation, and oxidative stress response mediated by NRF2 were identified in the recovery group. It provides important information on the inflammation and repair processes from lung injury.


Xenobiotic metabolism-related genes (cytochrome P-450 family 1 sub- family B polypeptide, glutathione S-transferase) Stress-related genes (heat-shock protein 90, paraoxonase) Cathepsin S as a cystein protease working in antigen presentation and autoimmunity. Apoptosis WT1 regulator, interleukin (IL) 3 receptor alpha, cysteine sulfinic acid decarboxylase, and coronin.

Tumor necrosis factor (TNF)-alpha gene, which is known to increase its expression with short-term welding fume exposure in vitro, was essentially unchanged. Genes that decreased the most were synuclein beta, ribonuclease H1, angiotensin receptor, and glycosyltransferase.

Most of these genes were disease- and immunity-related genes functioning for elimination of toxic material and disease reduction.

Table 1: Toxicogenomic classification of significantly changed genes according to function following welding fume exposure.