Blood Pressure Changes and Chemical Constituents of Particulate Air Pollution: Results from the Healthy Volunteer Natural Relocation (HVNR) Study

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Abstract

Background: Elevated blood pressure (BP) has been associated with particulate matter (PM) air pollution, but associations with PM chemical constituents are still uncertain.

Objectives: We investigated associations of BP with various chemical constituents of fine PM (PM _2.5) during 460 repeated visits among a panel of 39 university students.

Methods: Resting BP was measured using standardized methods before and after the university students relocated from a suburban campus to an urban campus with different air pollution contents in Beijing, China. Air pollution data were obtained from central monitors close to student residences. We used mixed-effects models to estimate associations of various PM _2.5 constituents with systolic BP (SBP), diastolic BP (DBP), and pulse pressure.

Results: An interquartile range increase of 51.2 μg/m ³ in PM _2.5 was associated with a 1.08-mmHg (95% CI: 0.17, 1.99) increase in SBP and a 0.96-mmHg (95% CI: 0.31, 1.61) increase in DBP on the following day. A subset of PM _2.5 constituents, including carbonaceous fractions (organic carbon and elemental carbon), ions (chloride and fluoride), and metals/metalloid elements (nickel, zinc, magnesium, lead, and arsenic), were found to have robust positive associations with different BP variables, though robust negative associations of manganese, chromium, and molybdenum with SBP or DBP also were observed.

Conclusions: Our results support relationships between specific PM _2.5 constituents and BP. These findings have potential implications for the development of pollution abatement strategies that maximize public health benefits.

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Most cited references 35

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Lead Exposure and Cardiovascular Disease—A Systematic Review

Ana Navas-Acien, Eliseo Guallar, Ellen Silbergeld … (2006)

Objective This systematic review evaluates the evidence on the association between lead exposure and cardiovascular end points in human populations. Methods We reviewed all observational studies from database searches and citations regarding lead and cardiovascular end points. Results A positive association of lead exposure with blood pressure has been identified in numerous studies in different settings, including prospective studies and in relatively homogeneous socioeconomic status groups. Several studies have identified a dose–response relationship. Although the magnitude of this association is modest, it may be underestimated by measurement error. The hypertensive effects of lead have been confirmed in experimental models. Beyond hypertension, studies in general populations have identified a positive association of lead exposure with clinical cardiovascular outcomes (cardiovascular, coronary heart disease, and stroke mortality; and peripheral arterial disease), but the number of studies is small. In some studies these associations were observed at blood lead levels < 5 μg/dL. Conclusions We conclude that the evidence is sufficient to infer a causal relationship of lead exposure with hypertension. We conclude that the evidence is suggestive but not sufficient to infer a causal relationship of lead exposure with clinical cardiovascular outcomes. There is also suggestive but insufficient evidence to infer a causal relationship of lead exposure with heart rate variability. Public Health Implications These findings have immediate public health implications. Current occupational safety standards for blood lead must be lowered and a criterion for screening elevated lead exposure needs to be established in adults. Risk assessment and economic analyses of lead exposure impact must include the cardiovascular effects of lead. Finally, regulatory and public health interventions must be developed and implemented to further prevent and reduce lead exposure.

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Insights into the mechanisms and mediators of the effects of air pollution exposure on blood pressure and vascular function in healthy humans.

Robert D Brook, Bruce Urch, J. Dvonch … (2009)

Fine particulate matter air pollution plus ozone impairs vascular function and raises diastolic blood pressure. We aimed to determine the mechanism and air pollutant responsible. The effects of pollution on heart rate variability, blood pressure, biomarkers, and brachial flow-mediated dilatation were determined in 2 randomized, double-blind, crossover studies. In Ann Arbor, 50 subjects were exposed to fine particles (150 microg/m(3)) plus ozone (120 parts per billion) for 2 hours on 3 occasions with pretreatments of an endothelin antagonist (Bosentan, 250 mg), antioxidant (Vitamin C, 2 g), or placebo. In Toronto, 31 subjects were exposed to 4 different conditions (particles plus ozone, particles, ozone, and filtered air). In Toronto, diastolic blood pressure significantly increased (2.9 and 3.6 mm Hg) only during particle-containing exposures in association with particulate matter concentration and reductions in heart rate variability. Flow-mediated dilatation significantly decreased (2.0% and 2.9%) only 24 hours after particle-containing exposures in association with particulate matter concentration and increases in blood tumor necrosis factor alpha. In Ann Arbor, diastolic blood pressure significantly similarly increased during all of the exposures (2.5 to 4.0 mm Hg), a response not mitigated by pretreatments. Flow-mediated dilatation remained unaltered. Particulate matter, not ozone, was responsible for increasing diastolic blood pressure during air pollution inhalation, most plausibly by instigating acute autonomic imbalance. Only particles from urban Toronto additionally impaired endothelial function, likely via slower proinflammatory pathways. Our findings demonstrate credible mechanisms whereby fine particulate matter could trigger acute cardiovascular events and that aspects of exposure location may be an important determinant of the health consequences.

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Ambient air pollution, climate change, and population health in China.

Haidong Kan, Renjie Chen, Shilu Tong (2012)

As the largest developing country, China has been changing rapidly over the last three decades and its economic expansion is largely driven by the use of fossil fuels, which leads to a dramatic increase in emissions of both ambient air pollutants and greenhouse gases (GHGs). China is now facing the worst air pollution problem in the world, and is also the largest emitter of carbon dioxide. A number of epidemiological studies on air pollution and population health have been conducted in China, using time-series, case-crossover, cross-sectional, cohort, panel or intervention designs. The increased health risks observed among Chinese population are somewhat lower in magnitude, per amount of pollution, than the risks found in developed countries. However, the importance of these increased health risks is greater than that in North America or Europe, because the levels of air pollution in China are very high in general and Chinese population accounts for more than one fourth of the world's totals. Meanwhile, evidence is mounting that climate change has already affected human health directly and indirectly in China, including mortality from extreme weather events; changes in air and water quality; and changes in the ecology of infectious diseases. If China acts to reduce the combustion of fossil fuels and the resultant air pollution, it will reap not only the health benefits associated with improvement of air quality but also the reduced GHG emissions. Consideration of the health impact of air pollution and climate change can help the Chinese government move forward towards sustainable development with appropriate urgency. Copyright © 2011 Elsevier Ltd. All rights reserved.

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Author and article information

Journal

Journal ID (nlm-ta): Environ Health Perspect

Journal ID (iso-abbrev): Environ. Health Perspect

Journal ID (publisher-id): EHP

Title: Environmental Health Perspectives

Publisher: National Institute of Environmental Health Sciences

ISSN (Print): 0091-6765

ISSN (Electronic): 1552-9924

Publication date (Electronic): 19 October 2012

Publication date (Print): January 2013

Volume: 121

Issue: 1

Pages: 66-72

Affiliations

[1 ]Department of Occupational and Environmental Health Sciences, Peking University School of Public Health, Beijing, China

[2 ]Department of Cardiology, Peking University People’s Hospital, Beijing, China

[3 ]Department of Public Health, Hyogo College of Medicine, Hyogo, Japan

Author notes

Address correspondence to X. Guo, Department of Occupational and Environmental Health Sciences, Peking University School of Public Health, No. 38 Xueyuan Rd., Beijing 100191 China. Telephone: 86-10-82801176. Fax: 86-10-62375580. E-mail: guoxb@ 123456bjmu.edu.cn

Article

Publisher ID: ehp.1104812

DOI: 10.1289/ehp.1104812

PMC ID: 3546346

PubMed ID: 23086577

SO-VID: 548e940e-a6c8-4944-b1ac-088d26375e22

License:

This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, properly cited.

History

Date received : 02 December 2011

Date accepted : 19 October 2012

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