O-57: Air pollution-driven inflammation and vascular dysfunction as determinants of neurocognitive risk in youth with type 1 diabetes in Delhi
R Rajput, S Lavania, P Kumar, N MahawarAbstract
Introduction
Youth with type 1 diabetes (T1D) often exhibit chronic low-grade inflammation and early endothelial dysfunction, rendering them uniquely susceptible to environmental insults. In highly polluted urban settings like Delhi, these mechanisms may critically amplify the risk of neurocognitive deficits and cerebral microvascular damage.
Objectives
This study aimed to investigate the association between long-term exposure to major air pollutants and neurocognitive impairment in youth with T1D, with an emphasis on inflammation-mediated vascular and metabolic pathways.
Methods
A prospective cohort of 8,564 adolescents (aged 10–18 years) with established T1D residing in Delhi was analyzed. Long-term exposure to fine particulate matter (PM2.5), nitrogen dioxide (NO2), and ozone (O3) was estimated via district-level monitoring networks. Standardized neuropsychological batteries evaluated cognitive function. Cox proportional hazards and Poisson regression models assessed associations between pollutant exposure, systemic inflammatory markers, early microvascular complications, and neurocognitive decline, adjusting for HbA1c and socioeconomic factors.
Results
Higher long-term exposure to PM2.5 was significantly associated with increased incidences of neurocognitive deficits, specifically impaired executive function and reduced processing speed. These cognitive declines strongly correlated with elevated systemic inflammatory markers and early indices of microvascular endothelial dysfunction. Ozone exposure demonstrated a modest association with neurocognitive decline, supporting a contributory role of oxidative vascular stress in exacerbating diabetes-related neural vulnerability.
Conclusions
In youth with T1D, chronic air pollution exposure appears to amplify neurocognitive risk primarily through inflammation-driven vascular and metabolic dysregulation, rather than direct neurotoxicity alone. These findings highlight a critical pathway linking environmental pollution to early brain health complications in young populations.