Background and Aims: Autoantibodies against apolipoprotein A-1 (AAA1) represent an independent cardiovascular risk factor in the general population. Genetic and viral infections have been linked to AAA1 occurrence. We studied the contribution of environmental pollution to AAA1 response and established their relationship with life expectancy (LE) in the general population.
Methods: A cross-sectional study was conducted involving 1,867 individuals from the “Bus Santé” cohort in Geneva, Switzerland, characterized for serum AAA1 levels. Exploratory and confirmatory geospatial clustering analyses between AAA1 levels, air pollution (NO2, PM2.5, PM10), proximity to polluted sites, and LE were performed. Environmental data were obtained from the official authorities, and LE data from regional health records. Associations were adjusted for cardiovascular risk factors using the SCORE2 algorithm.
Results: Significant AAA1 hotspots were identified, concentrated in urban areas with heavy traffic and associated with higher levels of air pollutants (e.g., median NO2 levels of 26.90 μg/m3 in hotspots vs. 23.70 μg/m3 in non-hotspots, p<0.001) and greater density of polluted sites (median weighted pollution score of 66.75 vs. 52.07, p=0.008). AAA1 hotspot areas had a median reduction of LE of 4 years compared to non hotstpot areas. (p<0.001), even after adjusting for SCORE2, income, nationality, NO2 levels, and proximity to polluted sites.
Conclusions: AAA1 hotspots are closely associated with environmental pollutants and independently associated with reduced LE in a population-based study in Geneva, suggesting that AAA1 response could be induced by environmental pollution. The possible heavy metals (HM) contribution to AAA1 response needs to be addressed.
