Research Article
Acute increase in blood pressure during inhalation of coarse particulate matter air pollution from an urban location

https://doi.org/10.1016/j.jash.2015.11.015Get rights and content

Highlights

  • Particulate matter (PM) air pollution is a leading cause of global mortality.

  • Coarse PM exposure triggered an acute increase in blood pressure in healthy adults.

  • Coarse PM exposure did not acutely impact autonomic balance or vascular function.

  • An elevation in blood pressure may be a mechanism whereby coarse PM promotes cardiovascular events.

Abstract

Particulate matter (PM) air pollution is a leading global risk factor for cardiovascular mortality. Although exposure to fine PM <2.5 μm raises arterial blood pressure (BP), few studies have evaluated the impact of coarse PM which differs in size (2.5–10 μm), sources, and chemistry. Twenty-nine healthy adults (30.4 ± 8.2 years) underwent a randomized double-blind crossover study involving 2-hour exposures to concentrated ambient coarse PM (164.2 ± 80.4 μg/m3) at an urban location (Dearborn, Michigan) versus filtered air. Cardiovascular outcomes were measured during, immediately, and 2 hours after exposures. Both systolic (1.9 mm Hg; 95% confidence interval: 0.96, 2.8; P < .001) and diastolic (1.9 mm Hg; 95% confidence interval: 1.1, 2.7; P < .001) BP levels were higher throughout coarse PM compared with filtered air exposures by mixed-model analyses. Heart rate variability, endothelial function, and arterial compliance were not significantly affected. Brief exposure to coarse PM in an urban environment raises arterial BP. These findings add mechanistic support to the contention that coarse PM may be capable of promoting cardiovascular events.

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.

References (22)

  • B. Brunekreef et al.

    Epidemiological evidence on effects of coarse airborne particles on health

    Eur Respir J

    (2005)
  • Cited by (38)

    • Effects of airway deformation and alveolar pores on particle deposition in the lungs

      2022, Science of the Total Environment
      Citation Excerpt :

      Particulate matter in polluted air that can enter the diatal lungs (i.e., PM2.5) has a serious impact on people's health (Mateos et al., 2018; Stockfelt et al., 2017). Epidemiological studies show that PM2.5 is associated with respiratory diseases (Brook et al., 2014; Byrd et al., 2016; Lee et al., 2015). Anatomical studies show that the distal lung of adults contains about 480 million alveoli, and the equivalent diameter of a single alveolus is about 200 μm (Cordingley, 1972; Ochs et al., 2004).

    • Assessing short-term impacts of PM<inf>2.5</inf> constituents on cardiorespiratory hospitalizations: Multi-city evidence from China

      2022, International Journal of Hygiene and Environmental Health
      Citation Excerpt :

      Besides immediate effects, our study suggested stronger cumulative lag effects at lag 04-day on CVD hospitalizations. It is plausible to some extent since exposure to ambient air pollution can affect blood pressure for days (Byrd et al., 2016; Giorgini et al., 2016). There is no evident lag pattern for cardiorespiratory subcategories.

    View all citing articles on Scopus

    Supplemental Material can be found at www.ashjournal.com.

    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.

    View full text