Residential exposures associated with adiposity and proinflammatory markers in obese adults with metabolic syndrome: a cross-sectional study
Abstract
Abstract Although current research supports associations between residential environment and inflammation and/or adiposity, evidence remains limited and partly contradictory for combined exposures, especially in vulnerable populations. To address this issue, this cross-sectional study, taking place in 2023 and 2024, investigated the associations between residential factors and adiposity and proinflammatory markers in 90 obese adults with metabolic syndrome from Bulgaria. All underwent clinical, anthropometric, and laboratory examinations, and completed a questionnaire. We measured their serum proinflammatory cytokines [interleukin-6 (IL-6), tumour necrosis factor alpha (TNF-α)], C-reactive protein (CRP), and adipokines (visfatin, leptin, adiponectin). Adiposity-related markers included body mass index (BMI), waist-to-hip ratio (WHR), body fat, and visceral fat percentage. Residential air pollution (NO2, PM2.5, PM10), road traffic noise (Lden), domestic burning of solid fuel, total greenness, tree cover, and time spent in nature were linked to these data. There was suggestive evidence that every 10 μg/m3 increase in NO2 levels was associated with higher concentrations of TNF-α (36.27 %; 95 % CI: −5.66 %, 96.83 %), IL-6 (41.63 %; 95 % CI: 8.16 %, 85.46 %), CRP (37.80 %; 95 % CI: 5.89 %, 79.32 %), leptin (25.61 %; 95 % CI: −8.73 %, 72.88 %), and lower adiponectin-leptin ratio (−33.83 %; 95 % CI: −56.59 %, 0.85 %). Additionally, NO2 was associated with higher BMI (6.37 %; 95 % CI: −0.82 %, 14.08 %) and visceral fat (7.52 %; 95 % CI: 1.30 %, 14.12 %). For every 2 h/week spent in nature, TNF-α concentration was lower (−20.49 %; 95 % CI: −37.56 %, 1.23 %), and adiponectin was higher (10.30 %; 95 % CI: 1.36 %, 20.03 %). Other observed associations were largely null, inconsistent, or occasionally showed an unexpected protective direction. These findings can serve as a general roadmap, and only larger longitudinal studies may provide a better insight into the environmental determinants of metabolic inflammation, which could in turn support the development of alternative preventive strategies.