The effect of complex traffic-related mixtures on blood pressure: interaction between particles and gases in a trial of vehicle filtration
Year: 2019
Type: conference-abstract
Abstract: OPS 57: Black carbon exposure and health effects, Room 110, Floor 1, August 26, 2019, 10:30 AM - 12:00 PM Introduction: We have previously found that in-vehicle particle filtration lowers blood pressure relative to no filtration in healthy subjects during a scripted commute. Since traffic-related air pollution is a mixture of particles and gases, we now assessed the interaction between particle count and gas exposure on blood pressure in the commute study. Methods: 16 young healthy participants took three 2-hr drives in heavy Seattle traffic, in a crossover design, double-blinded, randomized to order, and several weeks apart. On two “unfiltered” days, on-road air was entrained into the vehicle cabin through sham filters. On one “filtered” day, the vehicle was equipped with particle and carbon filters. Blood pressure was measured during exposure using a finger pulse-waveform device. In-vehicle particulate matter (particle count, black carbon) and gases (oxides of nitrogen, CO2, and ozone) were measured continuously during the drive. Results: Filtration substantially reduced particle exposure (85% lower particle count—PNC—on filtered days), but not measured gases. Discretized average first-hour PNC (cutoff: 10000 particles/cm3) was significantly associated with 1-hr diastolic blood pressure: 7.0 mmHg higher (95%CI: 1.6, 12.5) for high vs low exposure, essentially mirroring previous filtration effects. PNC effect on diastolic blood pressure was stronger when NO2 was lower (<20 ppb): 15 mmHg (CI 7.1, 25.1) for high vs low PNC compared to 1.5 mmHg when NO2 was higher (CI -5.4, 8.2) (interaction p=0.017). Results were similar for systolic blood pressure. Conclusion: In summary, urban traffic pollutant inhalation causes an acute increase in blood pressure that can be reduced with effective air filtration, and may be modified by exposure to gaseous co-pollutants represented by NO2.
Source: Environmental Epidemiology
Institution: University of Washington
Language: English
Subfield: Health, Toxicology and Mutagenesis
Field: Environmental Science
Domain: Physical Sciences
Open Access status: gold
Estimated APC paid: $1,200
OpenAlex ID: W2981516384
