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Controlled Clinical Trial
. 2009 Jul;117(7):1089-94.
doi: 10.1289/ehp0900558. Epub 2009 Mar 23.

Exposure to concentrated coarse air pollution particles causes mild cardiopulmonary effects in healthy young adults

Affiliations
Controlled Clinical Trial

Exposure to concentrated coarse air pollution particles causes mild cardiopulmonary effects in healthy young adults

Donald W Graff et al. Environ Health Perspect. 2009 Jul.

Abstract

Background: There is ample epidemiologic and toxicologic evidence that exposure to fine particulate matter (PM) air pollution [aerodynamic diameter < or = 2.5 microm (PM(2.5))], which derives primarily from combustion processes, can result in increased mortality and morbidity. There is less certainty as to the contribution of coarse PM (PM(2.5-10)), which derives from crustal materials and from mechanical processes, to mortality and morbidity.

Objective: To determine whether coarse PM causes cardiopulmonary effects, we exposed 14 healthy young volunteers to coarse concentrated ambient particles (CAPs) and filtered air. Coarse PM concentration averaged 89.0 microg/m(3) (range, 23.7-159.6 microg/m(3)). Volunteers were exposed to coarse CAPs and filtered air for 2 hr while they underwent intermittent exercise in a single-blind, crossover study. We measured pulmonary, cardiac, and hematologic end points before exposure, immediately after exposure, and again 20 hr after exposure.

Results: Compared with filtered air exposure, coarse CAP exposure produced a small increase in polymorphonuclear neutrophils in the bronchoalveolar lavage fluid 20 hr postexposure, indicating mild pulmonary inflammation. We observed no changes in pulmonary function. Blood tissue plasminogen activator, which is involved in fibrinolysis, was decreased 20 hr after exposure. The standard deviation of normal-to-normal intervals (SDNN), a measure of overall heart rate variability, also decreased 20 hr after exposure to CAPs.

Conclusions: Coarse CAP exposure produces a mild physiologic response in healthy young volunteers approximately 20 hr postexposure. These changes are similar in scope and magnitude to changes we and others have previously reported for volunteers exposed to fine CAPs, suggesting that both size fractions are comparable at inducing cardiopulmonary changes in acute exposure settings.

Keywords: cardiovascular effects; coarse PM human study.

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Figures

Figure 1
Figure 1
Correlation between coarse PM concentration in the exposure chamber and date of PM exposure. The solid line represents the linear regression line. The correlation of determination (r2) is 0.55 (p = 0.0025).
Figure 2
Figure 2
Changes in the percentage of each cell type in the BL and BAL fluids. Most participants had zero basophils and eosinophils in either fraction (data not shown).
Figure 3
Figure 3
Changes in inflammatory mediators in the BL and BAL fluids. A1AT, α1-antitrypsin.
Figure 4
Figure 4
Changes in measures of pulmonary function: immediately after exposure (Post) and approximately 20 hr after exposure (Follow-up).
Figure 5
Figure 5
Changes in mediators of coagulation: immediately after exposure (Post) and approximately 20 hr after exposure (Follow-up). PAI-1, plasminogen activator inhibitor-1.
Figure 6
Figure 6
Changes in resting HRV measurements: immediately after exposure (Post) and approximately 20 hr after exposure (Follow-up).

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