title: Cardiovascular effects caused by increasing concentrations of diesel exhaust in middle-aged healthy GSTM1 null human volunteers.
abstract: BACKGROUND
  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.
  
  
  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).
  
  
  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.
authors.affiliation: Environmental Public Health Division, National Health and Environmental Effects Research Laboratory, US Environmental Protection Agency, Research Triangle Park , NC , USA .
authors.forename: Haiyan
authors.initials: H
authors.lastname: Tong
authors.forename: Ana G
authors.initials: AG
authors.lastname: Rappold
authors.forename: Melissa
authors.initials: M
authors.lastname: Caughey
authors.forename: Alan L
authors.initials: AL
authors.lastname: Hinderliter
authors.forename: Donald W
authors.initials: DW
authors.lastname: Graff
authors.forename: Jon H
authors.initials: JH
authors.lastname: Berntsen
authors.forename: Wayne E
authors.initials: WE
authors.lastname: Cascio
authors.forename: Robert B
authors.initials: RB
authors.lastname: Devlin
authors.forename: James M
authors.initials: JM
authors.lastname: Samet
mesh_terms: D000368:Aged; D001794:Blood Pressure; D001916:Brachial Artery / Q000502:physiology; D004305:Dose-Response Relationship, Drug; D005260:Female; D005838:Genotype; D005982:Glutathione Transferase / Q000235:genetics / Q000502:physiology*; D064368:Healthy Volunteers; D006339:Heart Rate; D006439:Hemodynamics / Q000187:drug effects*; D006801:Humans; D008297:Male; D008875:Middle Aged; D014661:Vasoconstriction; D001335:Vehicle Emissions / Q000633:toxicity*
chemical_list: D005982:Glutathione Transferase; D001335:Vehicle Emissions