Short-Term Blood Pressure Responses to Ambient Fine Particulate Matter Exposures at the Extremes of Global Air Pollution Concentrations

Abstract BACKGROUND Fine particulate matter (PM2.5) air pollution is a leading cause of global cardiovascular mortality. A key mechanism may be PM2.5-induced blood pressure (BP) elevations. Whether consistent prohypertensive responses persist across the breadth of worldwide pollution concentrations...

Full description

Saved in:
Bibliographic Details
Published inAmerican journal of hypertension Vol. 31; no. 5; pp. 590 - 599
Main Authors Huang, Wei, Wang, Lu, Li, Jianping, Liu, Mochuan, Xu, Hongbing, Liu, Shengcong, Chen, Jie, Zhang, Yi, Morishita, Masako, Bard, Robert L, Harkema, Jack R, Rajagopalan, Sanjay, Brook, Robert D
Format Journal Article
LanguageEnglish
Published US Oxford University Press 13.04.2018
Subjects
Online AccessGet full text

Cover

Loading…
More Information
Summary:Abstract BACKGROUND Fine particulate matter (PM2.5) air pollution is a leading cause of global cardiovascular mortality. A key mechanism may be PM2.5-induced blood pressure (BP) elevations. Whether consistent prohypertensive responses persist across the breadth of worldwide pollution concentrations has never been investigated. METHODS We evaluated the hemodynamic impact of short-term exposures to ambient PM2.5 in harmonized studies of healthy normotensive adults (4 BP measurements per participant) living in both a highly polluted (Beijing) and clean (Michigan) location. RESULTS Prior 7-day outdoor-ambient and 24-hour personal-level PM2.5 concentration averages were much higher in Beijing (86.7 ± 52.1 and 52.4 ± 79.2 µg/m3) compared to Michigan (9.1 ± 1.8 and 12.2 ± 17.0 µg/m3). In Beijing (n = 73), increased outdoor-ambient exposures (per 10 µg/m3) during the prior 1–7 days were associated with significant elevations in diastolic BP (0.15–0.17 mm Hg). In overweight adults (body mass index ≥25 kg/m2), significant increases in both systolic (0.34–0.44 mm Hg) and diastolic (0.22–0.66 mm Hg) BP levels were observed. Prior 24-hour personal-level exposures also significantly increased BP (0.41/0.61 mm Hg) in overweight participants. Conversely, low PM2.5 concentrations in Michigan (n = 50), on average within Air Quality Guidelines, were not associated with BP elevations. CONCLUSIONS Our findings demonstrate that short-term exposures to ambient PM2.5 in a highly polluted environment can promote elevations in BP even among healthy adults. The fact that no adverse hemodynamic responses were observed in a clean location supports the key public health importance of international efforts to improve air quality as part of the global battle against hypertension.
Bibliography:ObjectType-Article-1
SourceType-Scholarly Journals-1
ObjectType-Feature-2
content type line 23
ISSN:0895-7061
1941-7225
DOI:10.1093/ajh/hpx216