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

Inhal Toxicol. 2014 May;26(6):319-26. doi: 10.3109/08958378.2014.889257. Epub 2014 Mar 24.

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/m(3), 200 µg/m(3), and 300 µg/m(3) 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/m(3) concentration causing minimal cardiovascular effects, while exposure to 300 µg/m(3) 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.

Publication types

  • Research Support, U.S. Gov't, Non-P.H.S.

MeSH terms

  • Aged
  • Blood Pressure
  • Brachial Artery / physiology
  • Dose-Response Relationship, Drug
  • Female
  • Genotype
  • Glutathione Transferase / genetics
  • Glutathione Transferase / physiology*
  • Healthy Volunteers
  • Heart Rate
  • Hemodynamics / drug effects*
  • Humans
  • Male
  • Middle Aged
  • Vasoconstriction
  • Vehicle Emissions / toxicity*

Substances

  • Vehicle Emissions
  • Glutathione Transferase
  • glutathione S-transferase M1