Review Article
Particulate matter, air pollution, and blood pressure

https://doi.org/10.1016/j.jash.2009.08.005Get rights and content

Abstract

A short-term increase in fine particulate matter air pollution (PM2.5) concentration increases the risk for myocardial infarctions, strokes, and heart failure exacerbations. An important mechanism likely contributing to these associations is an elevation in arterial blood pressure (BP). Exposure to ambient PM2.5 even at present-day concentrations can increase BP within a period of a few days while long-term exposure might also promote the development of chronic hypertension. Controlled human and animal experiments have corroborated the veracity of these findings and elucidated plausible biological mechanisms. PM2.5 deposition within the pulmonary tree is capable of rapidly triggering autonomic nervous system imbalance, thereby increasing BP within minutes of inhalation. In addition, fine particles can instigate a systemic pro-inflammatory response over a more prolonged period of exposure. Higher circulating levels of activated immune cells and inflammatory cytokines could consequently cause vascular endothelial dysfunction leading to an imbalance in vascular homeostatic responses. Indeed, chronic PM2.5 exposure augments pro-vasoconstrictive pathways while blunting vasodilator capacity. Finally, certain particle constituents (e.g., metals, organic compounds, and ultra-fine particles) might also be capable of reaching the systemic circulation upon inhalation and thereafter directly impair vascular function. At the molecular level, the generation of oxidative stress with the consequent up-regulation of redox sensitive pathways appears to be a common and fundamental mechanism involved in the instigation of these pro-hypertensive responses. Due to the ubiquitous, continuous and often involuntary nature of exposure, PM2.5 may be an important and under-appreciated worldwide environmental risk factor for increased arterial BP.

Introduction

Air pollution is a complex mixture of particulate matter (PM), gases, and vapor-phase molecules continuously interacting with each other and the atmosphere.1 PM itself is an amalgam of multiple compounds (e.g., elemental and organic carbon, transition metals, nitrates, and sulfates) ranging in size from several nanometers to >10 μm in diameter. In the modern and urban world, anthropogenic fossil fuel (e.g., coal, oil, and diesel) combustion by industry, power generation, and automobile traffic is the major source. Over the past few decades, many studies conducted worldwide have demonstrated that a higher level of ambient fine PM<2.5 μm in diameter (PM2.5) is associated with an increased risk for acute cardiovascular (CV) events.1 Short-term elevations over a period of a few hours-to-days can trigger myocardial infarctions, strokes, and heart failure exacerbations.1, 2, 3, 4 An increase of PM2.5 mass by 10 μg/m3 over a single day (∼1 standard deviation change within the United States) is associated with an approximate 1.0% elevation in premature CV mortality within a few days.1, 2, 3, 4 Similar exposures over a longer duration, such as occurs due to residing within more polluted locations over a few years, led to an even more marked increase in this risk (e.g., between 10%-76%). In this study, it has been estimated that PM2.5 contributes to approximately 800,000 premature deaths per year and ranks as the 13th leading cause of worldwide mortality.1

Over the past few years, several plausible biological mechanisms have been demonstrated that could help explain the epidemiological observations.1, 2, 3, 4 PM2.5 exposure is able to promote systemic inflammation and oxidative stress, enhance thrombotic and coagulation potential, instigate autonomic nervous system (ANS) imbalance and arrhythmias, and trigger vascular endothelial cell dysfunction.1, 2, 3 Long-term exposure has also proven capable of enhancing the development of systemic atherosclerosis.1, 2, 3 Regarding arterial blood pressure (BP), a growing body of evidence supports that PM2.5 exposure is also capable of altering systemic hemodynamics.4 Epidemiological studies show that even present-day levels of air pollution (considerably lower than concentrations 30 or more years ago)1 can increase BP in certain situations within a period of a few hours-to-days.5, 6, 7, 8, 9, 10, 11, 12, 13, 14, 15, 16, 17, 18, 19 Controlled human20, 21, 22, 23, 24, 25, 26, 27, 28, 29 and animal experiments30, 31, 32, 33, 34, 35, 36 have corroborated the veracity of this relationship and provided insight into the biological mechanisms.37, 38, 39, 40, 41, 42

While some studies have not observed an association, the overall evidence supports that a 10 μg/m3 increase in PM2.5 can raise BP by approximately 1 to 5 mm Hg (Table 1). The nature of the dose-response relationship and whether there is a threshold level below which PM concentrations do not raise BP are not fully elucidated. However, some data suggest that a linear or log-linear dose-response relationship might exist12, 17 whereby greater elevations in fine particle levels (e.g., >100 μg/m3), such that occur during severe pollution episodes or more routinely in developing regions,1, 2 would be associated with even greater increases in BP. Some evidence also supports that certain susceptible individuals (e.g., patients with hypertension12 and those not on BP-lowering medications17) may respond in an exaggerated fashion. However, the clinical significance of this pro-hypertensive response and its relative importance in the etiology of PM2.5-mediated CV events remains uncertain. Whether long-term exposures are a risk factor for a chronic elevation in BP and/or even overt hypertension also requires more investigation. Finally, the temporal nature of the exposure-response relationship and the specific compound or combination of constituents responsible (e.g., organic carbon chemicals and metals) within the air pollution mixture are important issues to further elucidate. Nonetheless, given the omnipresent nature of both air pollution and hypertension throughout the world, even a modest causal relationship would be of tremendous public health importance.

The purpose of this article is to review the effects of air pollution exposure on BP and to evaluate the coherence and consistency of the literature in order to draw conclusions from the evidence when appropriate per the consensus of the authors. MEDLINE and Google internet searches were performed using the parameters of “BP or hypertension” and “air pollution or PM”. All identified studies were included. Additional studies were found within the references of the identified studies. Finally, the results of one published abstract (unpublished manuscript by the authors) were included in this review given the relative importance of the findings to this field. It is possible that data from studies that were not identified or that remain unpublished at the time of the literature search may not be included in this review. There is also the possibility that more positive than negative publications were identified and discussed due to previous publication bias.

Section snippets

Epidemiological Studies

There is mounting evidence supporting that PM2.5 is capable of altering BP, at least under certain circumstances (Table 1). Though gaseous air pollutants (e.g., ozone, NOx, and SOx) may be linked with CV diseases1 and changes in arterial pressure or vascular function,9, 41 very few studies have been performed in this regard. Thus, the focus of this review will be for the most part on the hemodynamic effects of particle exposure. It is important to note at the outset that there have been

Controlled Human Exposure Studies

In order to corroborate the biological plausibility of the epidemiological associations, randomized controlled human exposure experiments have also been performed (Table 2).20, 21, 22, 23, 24, 25, 26, 27, 28, 29 Again, not all studies have been positive and few were designed to focus on BP changes. They may have thus suffered from methodological insufficiencies (e.g., small sample sizes, inaccurate or sub-optimal BP measurement methods, and timing) that limit that power to detect relatively

Animal Exposure Studies

There have been few controlled animal experiments evaluating the effect of PM2.5 exposure on BP (Table 3).30, 31, 32, 33, 34, 35, 36 Similar to the human studies, the responses have been mixed. In general, the more recent or larger studies tended to find significant increases in BP, while earlier experiments or those with fewer animals have been less consistent in their findings. Further variation among results is likely due to differences in the methodologies of exposure (e.g., CAP vs.

Biological Mechanisms

The study results indicate that the mechanisms raising BP within minutes of PM2.5 exposure likely differ from those responsible for the changes occurring hours to days later. There are 3 non-mutually exclusive “broad pathways” potentially involved and which may become more/less important at varying time points related to exposure (Figure). These include: 1) ANS imbalance, 2) the generation/release of endogenous biological mediators (e.g., cytokines) from various sources (most notably lung

On-going Research

More research is required to determine to reasons behind the discrepancies among study findings. However, it is very likely that much of the variation is at least partially explained by differences among the numerous variables involved. These include BP response determinants: patient characteristics (e.g., co-morbidities, initial BP), the variable nature of BP per se, the animal models evaluated, underlying susceptibility (e.g., anti-oxidant defenses, predisposing genotypes), and the integrity

Conclusion

The evidence reviewed in this manuscript supports that both short- and long-term exposures to PM2.5, even at present-day ambient levels, can cause an elevation in arterial BP–at least in susceptible individuals and under certain scenarios. In the context of air pollution-mediated acute CV events, it is probable that the health effects of short-term exposure vary depending upon the susceptibility/vulnerability of the patient. In accord with the epidemiology,1 a young or healthy individual will

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