Research ArticleAcute increase in blood pressure during inhalation of coarse particulate matter air pollution from an urban location
Introduction
Fine particulate matter (PM) <2.5 μm air pollution is a leading cause of global morbidity and mortality.1, 2 A multitude of studies across scientific disciplines provide consistent and coherent evidence that fine PM is causally related to cardiovascular diseases.2 Particles of this minute size are principally derived from urban-industrial combustion processes (eg, coal-fired power plants, vehicle exhaust).2 Although fine PM has been linked to a wide array of adverse biological responses, mounting evidence supports that both short- and long-term exposures are capable of raising arterial blood pressure (BP).3, 4, 5, 6, 7 The underlying mechanisms are likely related to sympathetic nervous system (SNS) activation and/or vascular endothelial dysfunction.2, 3
On the other hand, the cardiovascular health effects of coarse PM (2.5–10 μm) are less conclusive, despite the fact that it is an important contributor to worldwide air pollution.8, 9, 10, 11, 12 In addition to its larger size range, its sources and components differ from fine PM. Coarse PM is a mixture of particles typically generated from mechanical processes (eg, crushing, grinding, or resuspension of ground material) with sources ranging from agriculture, roadway dust, fugitive emissions, to construction. The constituents substantially vary according to nearby activities and landscapes (eg, deserts, soil, vegetation) and include metals, crustal elements (eg, silicon, calcium, magnesium, iron, potassium), and bioaerosols (eg, pollen, endotoxin).8, 9
We recently demonstrated that 2-hour exposure to coarse PM in a rural setting promotes an acute elevation in BP, most likely due to autonomic nervous system imbalance (ie, parasympathetic withdraw and/or SNS activation) as supported by changes in heart rate variability (HRV).7 Several metals and crustal element particle constituents were associated with the prohypertensive response.13 Because of the fact that the sources and components of coarse PM are known to substantively differ between locations (which might influence the ensuing health responses),8, 9 the aims of this study were to investigate if brief exposure to coarse PM derived from an urban setting (where the ever-growing majority of the global population lives in present-day societies)14 is also capable of raising arterial BP and secondarily to explore the biological mechanisms potentially responsible.
Section snippets
Methods
The study was approved by the Institutional Review Board of the University of Michigan, and all participants signed a written informed consent document during a screening visit. Participants were healthy nonsmoking adults (living in nonsmoking households within 100 miles of the exposure site location) aged 18–50 years without a history of cardiovascular disease or risk factors (screening visit BP <140/90 mm Hg and fasting glucose <126 mg/dL). Screening BP was measured in triplicate in the
Results
Study participants (n = 29; nine women) were young (30.2 ± 8.2 years) with a mean body mass index of 27.5 ± 6.0 kg/m2 and fasting glucose of 86.9 ± 6.9 mg/dL. Total cholesterol (164 ± 31 mg/dL), triglycerides (106 ± 81 mg/dL), high-density lipoprotein cholesterol (55 ± 16 mg/dL), and low-density lipoprotein cholesterol (89 ± 26 mg/dL) values were within normal ranges. Coarse PM concentrations were higher during CAP compared with FA exposures (Table 1). Mean systolic and diastolic BP levels
Discussion
We have shown for the first time that the inhalation of coarse PM from an urban environment can promote a rapid elevation in BP. There was no evidence that autonomic balance or vascular function was substantively altered, and thus, the underlying mechanisms must remain speculative. Nevertheless, the demonstration that brief exposure to urban coarse particles significantly raises BP adds important mechanistic support to the emerging epidemiologic evidence that coarse PM may be capable of
Conclusions
Two-hour exposure to coarse PM air pollution within an urban location induces a small elevation in systolic and diastolic BP. Taken together with our prior studies and the published literature on air pollution,3, 4 there is convincing evidence that both fine and coarse PM pollutants from a variety of sources are capable of raising BP.
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This study was funded by grants from the NIH CTSA grant (UL1RR024986) and from the United States Environmental Protection Agency RD83479701 and R833740.
Conflict of interest: None.