Gene–environment interactions in asthma; exposure to outdoor and indoor air pollutants
| Place, population (ref) | Type of study | Phenotype | Genes, genotype (chromosome) | Exposure | Cases/controls | Main results |
|---|---|---|---|---|---|---|
| Taiwan, children (Lee, 2004)51 | Case–control | Asthma | GSTP1: Val105Ile; Ala114Val (11q13) | District levels of Nox and SO2 | 61/95 | Ile105Ile: Moderate pollution: OR = 4.14 (1.17–16.54) High pollution: OR = 5.52 (1.64–21.25) Ala114Val: 100% of subjects Dose-response relationship |
| Mexico, asthmatic children (David, 2003)26 | Case–parent triad design (case–control) | Asthma | NQO1 Pro187Ser (16q22) GSTM1 null (−) (1p13,3) | Ozone (high exposure in Mexico city) | 218 cases | GTSM1(−)+ NQ01Ser/−: RR = 0.4 (0.2–0.8) |
| Mexico, asthmatic children (Romieu, 2003)83 | Case-case design | Asthma | GSTM1 null (−) (1p13,3) | Ozone (high exposure in Mexico city) and supplementation with antioxidants | 158 cases | GTSM1(−) ozone related decrements in FEF25-75: −2.5% (−5.2 to −0.6. p = 0.01). not found in GSTM(+): −0.6(−2.1 to 0.9) Antioxidant effect stronger in GTSM1(−) ozone |
| South Korea, adults living around citrus farms (Cho, 2000)78 | Case–control | CRM asthma | HLA-DRB1: 07;04 (6p21,3) | Citrus red mite | 91/98 | DRB1*04:OR = 0.36 (0.31–0.42) DRB1*07:OR = 5.01 (3.65–6.87) |
| Spain, asthmatics (Soriano, 1997)79 | Case–control | Asthma Atopy BHR | HLAII-DR: 1 to 10 HLAII-DQ: 2 to 6 (6p21,3) | Soybean dust | 78/67/168 | DRB1*13:OR = 3.22 (1.38–7.50) |
| USA, volunteers (Guilliland, 2004)27 | Crossover | Nasal allergic response IgE levels Histamine levels IL4 levels IFNγ levels | GSTM1: null (−)(1p13,3) GSTP1: Val105Ile (11q13) GSTT1: null (−)(22q11,2) | Ragweed allergen Diesel exhaust particles | 19 non-smoking subjects, with positive skin test to short ragweed and allergic rhinitis | GSTM1(−): increase IgE (p = 0.03) and histamine (p = 0.02) levels after diesel plus allergen exposure GSTP1(Ile105): increase IgE (p = 0.03) and histamine (p = 0.01) levels after diesel plus allergen exposure |
| Germany, general population (ECRHS) (Werner, 2003)57 | Case–control | Asthma | TLR4: D299G;T399I (9q32–q33) | Endotoxin (measurements in house dust) | 55/279 | OR for G299/I399 = 0.67 (0.06–8.06) 2°tertile and 1.33 (0.17–10.58) 3°tertile OR for D299/T399(wt) = 5.66 (1.23–29.04)2°tertile and 4.29 (0.9–20.45)3°tertile |
| South Korea, general population (Kim, 2001)76 | Case–control | Sensitisation to D.P. Rhinitis or asthma symptoms | HLA-DRB1: 1,15,16,3,4,11,12,13,14,7,8,9,10 (6p21,3) | House dust mite (Dermatiphagoides pteronyssinus) | 178/99 | DRB1*07: OR = 4.43 (1.14–17.16) DRB1*04: OR = 0.46 (0.34–0.63) No significant results for the other genotypes |
| UK, children (Simpson, 2006)59 | Cohort | Atopy Allergic sensitisation Wheeze Eczema | CD14:T-159C (5q31) | Home dust endotoxin (HDE) | 442 | No significant results for TT and CT genotypes Allergic sensitisation decreased with endotoxin load among CC carriers. OR = 0.70 (0.55–0.89) p = 0.004 Eczema decreased with endotoxin load among CC carriers. OR = 0.73 (0.56–0.95) p = 0.02 Non-atopic wheeze increased with endotoxin load among CC carriers. OR = 1.42 (1.01–1.99) p = 0.04 |
| Barbados, African descent (Zambelli-Weiner, 2005)58 | Family based case–control | Current asthma Allergic sensitisation Pulmonary function | CD14: C-260T;G-1461T;C-1721T (5q31) | Home dust endotoxin (HDE) | 293/454 | No significant results for G-1461T and C-1721T Low HDE CD14-260 TT vs CC/CT: OR = 0.09 [0.03–0.27] High HDE CD14-260 TT vs CC/CT: OR = 11.66 [1.03–131.7] |
| Taiwan, asthmatic children families (Wang, 2006)77 | Family based | Asthma IgE levels | IL-9: GT short tandem repeats (5q31.1) | House dust (HD) Pets | 460 subjects of 123 families with asthmatic proband | Obtained with transmission disequilibrium test (TDT) Allele 122: OR = 2.20 (p = 0.03) to asthma with specific IgE against house dust OR = 3.30 (p = 0.047) to asthma with exposure to fur of pets |