The Impact of Long-term Exposure to Air Pollution on Proteomic and Metabolomic Profiles in UK Biobank
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This is an abstract on long-term air pollution exposure and 'omic measures in the UK Biobank for submission to the 2024 ISEE Annual Meeting
Background
Air pollution is associated with numerous adverse health outcomes. However, there remains a need to understand the biological mechanisms, particularly proteomic and metabolomic changes associated with air pollution exposure. This study investigates associations between long-term air pollution exposures and proteomic and metabolomic profiles in the UK Biobank.
Method
Long-term exposures to air pollutants (PM2.5, PM2.5 absorbance, and NO2) were estimated using a land use regression model designed for the European Study of Cohorts for Air Pollution Effects. Air pollution exposure for UK Biobank participants was determined based on the geocoded residential address at baseline. Proteomic profiling was performed on blood plasma samples of study participants, capturing 2,923 unique proteins. Metabolomic profiling was performed on the baseline plasma samples using NMR spectroscopy. In this analysis, 44,013 and 224,298 samples were available for proteomic analysis and metabolomic analysis, respectively. Linear regression models were applied to test the associations of long-term air pollution exposure with blood proteomic and metabolomic profiles, adjusting for age, sex, ethnic background, study center, Townsend deprivation index, estimated glomerular filtration rate, platelet count, red blood cell count, white blood cell count, and C-reactive protein. Benjamini-Hochberg false discovery rate (FDR) corrected p-values are presented.
Results
We observed 362, 1198, and 379 significant associations for PM2.5, PM2.5 absorbance, and NO2 respectively. The strongest associations were observed for PM2.5 and included lactate (β= -0.04; P= 7.1x10-70), glucose (β= 0.02; P= 1.1x10-23), and HDL concentration (β= -0.02; P = 3.5x10-23). Proteomic pathway analyses (via Reactome) highlighted neutrophil degranulation as it was the only pathway enriched for all three pollutants.
Conclusions
These analyses highlight the role of long-term air pollution exposure in metabolic changes and neutrophil degranulation. Further exploration of the results may reveal novel unique and shared pathways among pollutants which link exposure and health outcomes. This abstract does not reflect USEPA policy.