TY - JOUR
T1 - Arterial blood pressure responses to short-term exposure to low and high traffic-related air pollution with and without moderate physical activity
AU - Kubesch, N.
AU - De Nazelle, A.
AU - Guerra, S.
AU - Westerdahl, D.
AU - Martinez, D.
AU - Bouso, L.
AU - Carrasco-Turigas, G.
AU - Hoffmann, B.
AU - Nieuwenhuijsen, M. J.
PY - 2015/5/15
Y1 - 2015/5/15
N2 - Background: Short-term exposure to traffic-related air pollution (TRAP) has been associated with adverse cardiovascular outcomes. Physical activity (PA) in polluted air may increase pollutant uptake and increase these effects. Methods: Crossover real-world exposure study in 28 healthy participants comparing systolic (SBP) and diastolic blood pressure (DBP) responses to four different exposure scenarios: 2 h exposure in high or low-TRAP environment, each at rest and combined with intermittent moderate PA consisting of 15 min intervals alternating rest and cycling on a stationary bicycle. Data was analyzed using mixed effect models for repeated measures. Results: Exposure to high TRAP was associated with higher DBP (1.1 mm/Hg, p0.002) post-exposure, irrespective of exercise status. Ultrafine particles (UFP) increased DBP post-exposure (0.9 mm/Hg, p0.004). Interquartile increases in black carbon (BC), fine particulate matter (PM10 and PMcoarse), UFP, and nitric oxides (NOx) were associated with statistically significantly higher SBP post-exposure (1.2, 1.0, 1.1, and 1.1 mm/Hg, respectively). Intermittent PA compared with rest was associated with lower SBP post-exposure (-2.4 mm/Hg, p<0.001). PA lowered SBP more after exposure to the low-TRAP site (-2.3 mm/Hg) compared with the high-TRAP site (-1.6 mm/Hg). We only found evidence of an interaction between PA and both PM10 and PMcoarse, increasing SBP. Conclusion: Both SBP and DBP increase after exposure to TRAP. Intermittent PA attenuates the TRAP-related increases in SBP, with the exception of PM10 and PMcoarse, which potentiate these increases. We showed that in low-TRAP environments intermittent PA has stronger beneficial effects on SBP than in high-TRAP environments.
AB - Background: Short-term exposure to traffic-related air pollution (TRAP) has been associated with adverse cardiovascular outcomes. Physical activity (PA) in polluted air may increase pollutant uptake and increase these effects. Methods: Crossover real-world exposure study in 28 healthy participants comparing systolic (SBP) and diastolic blood pressure (DBP) responses to four different exposure scenarios: 2 h exposure in high or low-TRAP environment, each at rest and combined with intermittent moderate PA consisting of 15 min intervals alternating rest and cycling on a stationary bicycle. Data was analyzed using mixed effect models for repeated measures. Results: Exposure to high TRAP was associated with higher DBP (1.1 mm/Hg, p0.002) post-exposure, irrespective of exercise status. Ultrafine particles (UFP) increased DBP post-exposure (0.9 mm/Hg, p0.004). Interquartile increases in black carbon (BC), fine particulate matter (PM10 and PMcoarse), UFP, and nitric oxides (NOx) were associated with statistically significantly higher SBP post-exposure (1.2, 1.0, 1.1, and 1.1 mm/Hg, respectively). Intermittent PA compared with rest was associated with lower SBP post-exposure (-2.4 mm/Hg, p<0.001). PA lowered SBP more after exposure to the low-TRAP site (-2.3 mm/Hg) compared with the high-TRAP site (-1.6 mm/Hg). We only found evidence of an interaction between PA and both PM10 and PMcoarse, increasing SBP. Conclusion: Both SBP and DBP increase after exposure to TRAP. Intermittent PA attenuates the TRAP-related increases in SBP, with the exception of PM10 and PMcoarse, which potentiate these increases. We showed that in low-TRAP environments intermittent PA has stronger beneficial effects on SBP than in high-TRAP environments.
KW - Blood pressure
KW - cycling
KW - particulate matter
KW - physical activity
KW - short-term exposure
KW - traffic-related air pollution
UR - https://www.scopus.com/pages/publications/84927611642
UR - https://www.scopus.com/inward/citedby.url?scp=84927611642&partnerID=8YFLogxK
U2 - 10.1177/2047487314555602
DO - 10.1177/2047487314555602
M3 - Article
C2 - 25326542
AN - SCOPUS:84927611642
SN - 2047-4873
VL - 22
SP - 548
EP - 557
JO - European Journal of Preventive Cardiology
JF - European Journal of Preventive Cardiology
IS - 5
ER -