Table 2.
Studies of the effect of GSTM 1 absence on respiratory system.
| No. | Author | Sample number | Pollutant type | Parameters measured | Result |
|---|---|---|---|---|---|
| 1. | Yang et al. [30] | 1180 | PM2.5 | Low respiratory tract infection (LRTI) | In utero exposure to PM2.5, especially during the third trimester of pregnancy, is associated with a higher frequency of lower respiratory tract problems at one year, especially in the absence of GSTM1 in the mother |
| 2. | Reddy et al. [71] | 129 | PM10, SO2, NO2, and NO | Percent change in intraday variability of forced expiratory volume 1 (FEV) | Higher exposure to SO2 associates with more significant FEV1 intraday variability on those with GSTM1 deletion |
| Children with GSTM1 positive genotype associate with | |||||
| 3. | Romieu et al. [72] | 151 | Ozone | Respiratory symptoms and lung function | Asthmatic children with GSTM1 null genotype showed increase of reported breathing difficulty associated with ozone exposure |
| 4. | Alexis et al. [73] | 35 | Ozone | Lung function and inflammation | GSTM1 did not modify lung function and granulocyte influx after acute ozone exposure, but GSTM1 null genotype person showed a significant increase of airways neutrophils and increase expression of HLA-DR 24 hours after ozone exposure |
| 5. | Framptom et al. [74] | 24 | Ozone | Pulmonary, systemic vascular function, and cardiac function | There were no consistent effects of ozone exposure with all parameters measured. All the results were not dependent on the GSTM1 genotype |
| 6. | Yang et al. [30] | 307 | Indoor PM2.5 and environmental tobacco smoke (ETS) | Susceptibility to RTIs | Deletion of GSTM1 increases the susceptibility of RTIs associated with prenatal exposure of indoor PM2.5 and ETS |
| 7. | Kim et al. [75] | 59 | Ozone | Pulmonary function and subjective symptom | GSTM1 genotype alone did not modify ozone induces an increase in neutrophilic inflammation in the airways and decrease of FEV1 |
| 8. | Ghosh et al. [76] | 793 | Second-hand smoke (SHS), polycyclic aromatic hydrocarbons (PAH), and PM2.5 | Acute bronchitis | GSTM1 genotype did not modify the risk to develop acute bronchitis in preschool children after exposure to SHS, PAH, and PM2.5 |
| 9. | Hersoug et al. [77] | 3471 | The indoor source of PM | Objective markers of respiratory disease | GSTM1 genotype did not modify the change of objective markers of respiratory disease after exposure to the indoor source of PM |
| 10. | Romieu et al. [78] | 158 | Ozone | Forced expiratory flow | Asthmatic children with GSTM1 null genotype were more prone to deleterious effects on airways related to ozone exposure |
| 11. | Curjuric et al. [79] | 4365 | PM10 | Lung function | GSTM1 genotype did not modify the change of lung function after exposure to PM10 |
| 12. | Madden et al. [80] | 15 | Diesel exhaust (DE) and ozone | Lung function | GSTM1 genotype did not modify the changes in lung function associated with DE and ozone exposure |
| 13. | Lan et al. [81] | 244 | Indoor smoky coal emission | Lung cancer | GSTM1 null genotype is associated with a higher risk of lung cancer in smoky coal use. |
| 14. | Dey et al. [82] | 155 | They were non-respirable PM, SO2, NO2, organic silicone, and aliphatic C–F compounds in the air. | Lung function | GSTM1 null genotype modify the changes of lung function in smokers living around coal mines. |
| 15. | Bowatte et al. [83] | 620 | Traffic-related air pollution (TRAP) | Asthma, wheeze, and hay fever | GSTM1 null genotype modifies the risk of asthma and wheeze, but not hay fever related to TRAP exposure during the first year of life |
| 16. | Chen et al. [84] | 210 | Ozone | Lung function | GSTM1 null/NQO1 Pro187 Pro-combination, but not GSTM1 null genotype alone is associated with ozone-related changes in lung function |
| 17. | Bergamaschi et al. [85] | 24 | Ozone | Lung function and blood parameter | Participants with NOQ1 WT and GSTM1 null show lung function and serum CC16 change associated with ozone level |
| 18. | Dillon et al. [86] | 35 | Clinical Center Reference Endotoxin (CCRE) | Airway and systemic inflammation parameter | The participant with GSTM1 null genotype shows a significant increase of circulating white blood cells, polymorphonuclear neutrophils, platelets, and sputum after the challenge with CCRE |
| 19. | Castro-Giner et al. [87] | 2920 | Local traffic-related air pollution (estimated NO2) | Asthma | GSTM1 null genotype did not modify the effect of local traffic-related air pollution exposure with asthma prevalence |
| 20. | Zhang et al. [31] | 17 | Diesel exhaust (DE) and allergen | Lung function | GSTM1 genotype did not modify the change of lung function after exposure to DE or allergen |