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Inhalation Toxicology
International Forum for Respiratory Research
Volume 26, 2014 - Issue 6
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Research Article

Cardiovascular effects caused by increasing concentrations of diesel exhaust in middle-aged healthy GSTM1 null human volunteers

, , , , , , , & show all
Pages 319-326 | Received 27 Aug 2013, Accepted 27 Jan 2014, Published online: 24 Mar 2014
 

Abstract

Context: Epidemiological studies have shown an association between the incidence of adverse cardiovascular effects and exposure to ambient particulate matter (PM). Diesel exhaust (DE) is a major contributor to ambient PM and gaseous emissions in urban areas.

Objective: This was a pilot study designed to evaluate concentration-dependent effects of short-term exposure to whole DE on the cardiovascular system in order to identify a threshold concentration that can elicit biological responses in healthy human volunteers.

Materials and methods: Six healthy middle-aged participants with glutathione-S-transferase-Mu 1 (GSTM1) null genotype underwent sequential exposures to 100 µg/m3, 200 µg/m3, and 300 µg/m3 whole DE generated in real time using an idling diesel truck engine. Exposures were separated by 14 d and each was 2 h in duration.

Results: We report concentration-dependent effects of exposure to DE, with 100 µg/m3 concentration causing minimal cardiovascular effects, while exposure to 300 µg/m3 DE for 2 h resulted in a borderline significant reduction of baseline brachial artery diameter (3.34 ± 0.27 mm pre- versus 3.23 ± 0.25 mm post-exposure; p = 0.08). Exposure to the highest concentration of DE also resulted in increases of 5 mmHg in diastolic blood pressure as well as a decrease in indices of the frequency domain of heart rate variability (HRV).

Discussion and conclusions: These findings demonstrate that acute exposure to relatively high concentrations of DE produces cardiovascular changes in middle-aged GSTM1 null individuals. This study therefore suggests that arterial vasoconstriction and changes in HRV are responses through which traffic-related air pollution increases the risk of adverse cardiovascular outcomes.

Acknowledgements

The US Environmental Protection Agency Intramural Research Program supported this research. We thank Maryann Bassett, Tracey Montilla, and Michael Schmitt for their excellent medical and technical assistance in the execution of this study.

Declarations of interest

All authors report no declaration of interests.

Disclaimer

The research described in this article has been reviewed by the National Health and Environmental Effects Research Laboratory, US EPA, and approved for publication. The contents of this article should not be construed to represent Agency policy nor does mention of trade names or commercial products constitute endorsement or recommendation for use.

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