Key result
An interquartile-range increase in PM10 was associated with a 0.93 mmHg increase in systolic blood pressure, and the associations of air pollution with blood pressure and heart rate variability were significantly modified by oxidative stress genetic risk scores.
Why the study?
Does genetic predisposition to oxidative stress modify the effect of air pollution exposure on blood pressure and heart rate variability in elderly urban residents?
Observational (n=547)
No
Does genetic predisposition to oxidative stress modify the effect of air pollution exposure on blood pressure and heart rate variability in elderly urban residents?
Mean Difference: 0.93 (95% CI 0.23–1.63)
Genetic polymorphisms in oxidative stress pathways significantly modify the impact of air pollution on blood pressure and heart rate variability in elderly individuals.
PM10 exposure was associated with higher SBP modified by oxidative stress GRS; leaves open gene-environment interactions for future trials.
BACKGROUND: Oxidative stress has been suggested as a major cause of elevated blood pressure (BP) and reduced heart rate variability (HRV) due to air pollution. We hypothesized that the associations of air pollution exposure with BP and HRV are modified by oxidative stress gene polymorphisms. METHODS: Between 2008 and 2010, we conducted up to 5 surveys of 547 elderly participants, measured their BP and HRV, and genotyped 47 single nucleotide polymorphisms (SNPs) in 18 oxidative stress genes. Linear mixed models were constructed to evaluate the associations of particulate matter ≤10 μm, nitrogen dioxide, and sulfur dioxide with BP and HRV, as well as the modifications of these associations by the genotyped SNPs. RESULTS: Single-SNP analyses revealed interactions between air pollution and 15 SNPs (for BP) and 33 SNPs (for HRV) (all, P for interaction < 0.05). When we generated genetic risk scores for BP and HRV, using the SNPs with interactions in the single-SNP models, we found that associations of air pollution exposure with BP and HRV were modified by the genetic risk scores (P for interaction < 0.05). CONCLUSIONS: These results strongly suggest that the associations of air pollution with BP and HRV are mediated by oxidative stress pathways.
No takes yet. Share an insight, caveat, or question.
Kim et al. (2016) conducted an observational in Air pollution exposure effects on blood pressure and heart rate variability (n=547). Air pollution exposure (PM10, NO2, SO2) vs. Lower levels of air pollution exposure was evaluated on Change in systolic blood pressure per interquartile-range increase in PM10 (β = 0.93, 95% CI 0.23-1.63). An interquartile-range increase in PM10 was associated with a 0.93 mmHg increase in systolic blood pressure, and the associations of air pollution with blood pressure and heart rate variability were significantly modified by oxidative stress genetic risk scores.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: