Exploration of the rapid effects of personal fine particulate matter exposure on arterial hemodynamics and vascular function during the same day

Abstract

Background: Levels of fine particulate matter [≤ 2.5 μm in aerodynamic diameter (PM(2.5))] are associated with alterations in arterial hemodynamics and vascular function. However, the characteristics of the same-day exposure-response relationships remain unclear.

Objectives: We aimed to explore the effects of personal PM(2.5) exposures within the preceding 24 hr on blood pressure (BP), heart rate (HR), brachial artery diameter (BAD), endothelial function [flow-mediated dilatation (FMD)], and nitroglycerin-mediated dilatation (NMD).

Methods: Fifty-one nonsmoking subjects had up to 5 consecutive days of 24-hr personal PM(2.5) monitoring and daily cardiovascular (CV) measurements during summer and/or winter periods. The associations between integrated hour-long total personal PM(2.5) exposure (TPE) levels (continuous nephelometry among compliant subjects with low secondhand tobacco smoke exposures; n = 30) with the CV outcomes were assessed over a 24-hr period by linear mixed models.

Results: We observed the strongest associations (and smallest estimation errors) between HR and TPE recorded 1-10 hr before CV measurements. The associations were not pronounced for the other time lags (11-24 hr). The associations between TPE and FMD or BAD did not show as clear a temporal pattern. However, we found some suggestion of a negative association with FMD and a positive association with BAD related to TPE just before measurement (0-2 hr).

Conclusions: Brief elevations in ambient TPE levels encountered during routine daily activity were associated with small increases in HR and trends toward conduit arterial vasodilatation and endothelial dysfunction within a few hours of exposure. These responses could reflect acute PM(2.5)-induced autonomic imbalance and may factor in the associated rapid increase in CV risk among susceptible individuals.

Figure 1

Associations of hourly TPE levels with CV outcomes according to the lag period of exposure: personal PM_2.5 and HR (A), BAD (B), and FMD (C). The x-axis is the period of time (hour lag) before the measurement of the CV outcome; hour 0 = period from 0–60 min before the CV measurement. Points indicate the multivariate-adjusted CV outcome association (β-coefficient per 10-μg/m³ increase in TPE ± 95% confidence intervals) for each hourly time point from the linear mixed model 1. Colored data points indicate statistically significant time points.