Journal of the American Society of Hypertension
Review ArticleParticulate matter, air pollution, and blood pressure
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
References (79)
- et al.
Effects of particulate air pollution on systolic blood pressure: a population based approach
Environ Res
(2006) - et al.
PM-induced cardiac oxidative stress and dysfunction are mediated by autonomic stimulation
Biochimica Biophysica Acta
(2005) - et al.
Reactive oxygen species and hypertension. An update
Am J Hypertens
(2004) Oxidant mechanisms in response to ambient air particles
Mol Aspects Med
(2004)- et al.
Air pollution exposure and self-reported cardiovascular disease
Environ Research
(2009) - et al.
Identification of oxidative stress and toll-like receptor 4 signaling as a key pathway of acute lung injury
Cell
(2008) - et al.
TLR-2 is involved in airway epithelial cell response to air pollution particles
Toxicol Appl Pharmacol
(2005) - et al.
Evaluation of the direct systemic and cardiopulmonary effects of diesel particles in spontaneously hypertensive rats
Toxicology
(2009) - et al.
Air pollution and cardiovascular disease: a statement for healthcare professionals from the expert panel on population and prevention science of the American Heart Association
Circulation
(2004) - et al.
Health effects of fine particulate air pollution: lines that connect
J Air Waste Manage Assoc
(2006)
Cardiovascular effects of air pollution
Clin Sci
Why physicians who treat hypertension should know more about air pollution
J Clin Hypertens
Day-to-day particulate exposures and health changes in Los Angeles area residents with severe lung disease
J Air Waste Manag Assoc
Effects of air pollution on blood pressure: a population-based approach
Am J Public Health
Effects of particulate air pollution on blood pressure and heart rate in subjects with CV disease: a multicenter approach
Environ Health Perspect
Ambient pollution and blood pressure in cardiac rehabilitation patients
Circulation
Effects of air pollution on blood pressure and heart rate variability: a panel study of vehicular traffic controllers in the city of São Paulo, Brazil
Euro Heart J
Associations between submicrometer particles exposures and blood pressure and heart rate in patients with lung function impairments
J Occup Environ Med
Associations between recent exposure to ambient fine particulate matter and blood pressure in the Multi-Ethnic Study of Atherosclerosis (MESA)
Environ Health Perspect
Chimney stove intervention to reduce long-term wood smoke exposure lowers blood pressure among Guatemalan women
Environ Health Perspect
Seasonal variation of effect of air pollution on blood pressure
J Epidemiol Community Health
Influence of personal exposure to particulate air pollution on cardiovascular physiology and biomarkers of inflammation and oxidative stress in subjects with diabetes
J Occup Environ Med
Associations between environmental exposure and blood pressure among participants in the Oslo Health Study (HUBRO)
European J Epidemiol
Acute effects of ambient particulate matter on blood pressure: differential effects across urban communities
Hypertension
Adverse cardiovascular responses to alterations in daily levels of personal and ambient fine particulate matter air pollution
Circulation
Exposure of chronic obstructive pulmonary disease patients to particles: respiratory and cardiovascular health effects
J Expos Anal Environ Epidemiol
Acute blood pressure responses in healthy adults during controlled air pollution exposures
Environ Health Perspect
Diesel exhaust inhalation causes vascular dysfunction and impaired endogenous fibrinolysis
Circulation
Controlled exposures of healthy and asthmatic volunteers to concentrated ambient fine particles in Los Angeles
Inhalant Toxicol
Acute changes in vascular function among welders exposed to metal-rich particulate matter
Epidemiology
Insights into the mechanisms and mediators of the effects of air pollution exposure on blood pressure and vascular function in healthy humans
Hypertension
Particulate air pollution and vascular reactivity: the bus stop study
Int Arch Occup Environ Health
Indoor particles affect vascular function in the aged: an air filtration-based intervention study
Am J Respir Crit Care Med
Ischemic and thrombotic effects of dilute diesel-exhaust inhalation in men with coronary heart disease
N Engl J Med
Exposure to concentrated ambient particles does not affect vascular function in patients with coronary heart disease
Environ Health Perspect
Effect of inhaled carbon ultra-fine particles on reactive hyperemia in healthy human subjects
Environ Health Perspect
Effects of instilled combustion-derived particles in spontaneously hypertensive rats. Part I: cardiovascular responses
Inhalant Toxicol
Effects of concentrated ambient fine particles on heart rate and blood pressure in pulmonary hypertensive rats
Environ Health Perspect
Effects of concentrated ambient particles on heart rate, blood pressure, and cardiac contractility in spontaneously hypertensive rats
Inhalant Toxicol
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Conflict of interest: none.