Table 2.
Findings from selected biomarker studies on the relationship between environmental exposures and health outcomes.
| Description of Epidemiology Study Design & Subjects | Method of exposure assessment | Biological sample and (immune biomarkers employed) | Key findings and evaluation of concordance | |
|---|---|---|---|---|
| Atopy | Longitudinal/Prospective; (n = 3,062), combined birth cohorts (ages 1–8 years) | Questionnaire; indoor environment, pet exposure | Peripheral blood (total and specific IgE and CD14/IL13 genotypes) | Atopy influenced by IL13 in <8 years and CD14 with pet interaction in ages 4 and 8 (Bottema et al. 2008) [37] |
| Longitudinal; birth cohort (n = 172) | Peripheral blood (differential cell counts and IFN-γ, TNF-α, IL-4, IL-5, IL-9, Il-10, IL-13 by ELISA) | Atopy associated with increased Th2; bronchial hyperresponsiveness associated with Th1 (Heaton et al. 2005) [38] | ||
| Cross-sectional; children ages 6–16 (n = 24) vs. reference group | Questionnaire; parental tobacco smoke | Nasopharangeal aspirate (analyzed for IL-13 cytokine levels) | ETS augments secretion of IL-13 (Feleszko et al. 2006) [39] | |
| Asthma | Longitudinal/Prospective; birth cohort (n = 239) | Questionnaire; pesticide and allergen exposures | Peripheral blood (intracellular IFN-γ and IL-4 in T-helper cells) | Th2 cells associated with asthma and wheeze; Th1 associated with breastfeeding and parental occupation in agriculture (Duramad et al. 2006) [40] |
| Asthma | Cross-sectional; children with asthma (n = 33) vs. health controls | Questionnaire | Exhaled breath condensate (IFN-γ, TNF-α, IL-2, IL-4, IL-5, IL-10) | Cytokine levels low but detectable; processing method needs improvement (Robroeks et al. 2006) [22] |
| Case-control retrospective; adults ages 20–79 (n = 3,443) | Questionnaire and blood evaluation: ethanol levels, CDT1, GGT, ASAT, ALAT | Peripheral Blood; (serum IgE) | Positive associations between alcohol consumption and total IgE serum levels in atopic subjects (Friedrich et al. 2008) [41] | |
| Chronic Obstructive Pulmonary Disease (COPD) | Cross-sectional; patients with COPD (n = 35), non-smokers (n = 18), and smokers (n = 20) | Questionnaire; criteria for non-smokers was normal spirometry results | Induced sputum (differential cell counts; CXCL9, CXCL10, CXCL11, and CCL5 by ELISA) | CXCR3 and CCL5 increased in COPD patients compared with non smokers (Costa, et al. 2008) [42] |
| Cross-sectional; patients with COPD (n = 26), smokers (n = 19), healthy non-smokers (n = 5) | Questionnaire; history of smoking | Bronchial Alveolar Lavage (BAL) and peripheral blood (CD3, CD4, CD8, CD45RA, CD25, CD69) | Increased CD8 and CD4+CD25+ in COPD BAL samples (Smyth et al. 2007) [43] | |
| Cross-sectional; COPD (n = 30), divided into two categories: Forced-expiratory volume in 1 second (FEV1) <50% and >50% | Questionnaire; smoking status | Induced sputum (IL-6, IL-8 and TNF-α) | Mean levels of three cytokines elevated in severe vs. moderate COPD (Hacievliyagil et al. 2005) [44] |
1
carbohydrate-deficient transferring (CDT), gamma-glutamyl transferase (GGT), aspartate-amino transferase (ASAT), alanine-amino transferase (ALAT) are biomarkers of recent and long-term exposure to alcohol [45].