Concentrated Ambient Ultrafine Particle Exposure Induces Cardiac Changes in Young Healthy Volunteers

Samet, James M.; Rappold, Ana G.; Graff, Donald W.; Cascio, Wayne E.; Berntsen, Jon; Huang, Y.-C. T.; Herbst, M; Bassett, Maryann; Montilla, Tracey; Hazucha, Milan J.; Bromberg, Philip A.; Devlin, Robert B.

doi:10.1164/rccm.200807-1043oc

Cited by 151 publications

(119 citation statements)

References 62 publications

Supporting

Mentioning

102

Contrasting

Unclassified

Order By: Relevance

“…At 24 hours post-inhalation, endothelium-dependent vasodilatation (induced by acetylcholine and bradykinin) remained impaired, while endothelium-independent vasodilatation (using sodium nitroprusside and verapamil) and t-PA release were unaffected, in the presence of mild sytemic inflammation ). These and other (Bonzini et al 2010, Chuang et al 2007, Ghio et al 2003, Samet et al 2009) studies did not demonstrate an assocation between PM exposure and baseline levels (not bradykinin-induced) of t-PA. While studies, based on controlled exposure to diluted diesel exhaust , Carlsten et al 2007 or concentrated ambient particles (Ghio et al 2003), did not observe increases in the levels of plasminogen activator inhibitor-1 (PAI-1), some epidemiological or animal studies, focussing on urban PM, did: a study in 76 young healthy students demonstrated elevated PAI-1 concentrations in association with the mean PM 2.5 or PM 10 concentration at their university's campus over 1 to 3 days (Chuang et al 2007).…”

Section: Endothelial Function and Fibrinolysismentioning

confidence: 41%

Air Pollution and Cardiovascular Disease

Emmerechts¹,

Jacobs²,

Hoylaerts³

2011

The Impact of Air Pollution on Health, Economy, Environment and Agricultural Sources

View full text Add to dashboard Cite

Section: Endothelial Function and Fibrinolysismentioning

confidence: 41%

Air Pollution and Cardiovascular Disease

Emmerechts¹,

Jacobs²,

Hoylaerts³

2011

The Impact of Air Pollution on Health, Economy, Environment and Agricultural Sources

View full text Add to dashboard Cite

“…We have previously reported that activation of fibrinolysis pathways and increased levels of D-dimer (a fibrin breakdown product) are associated with exposure to PM air pollution in humans. 28 We also show that ozone can mirror the established effects of PM and cause changes in HRV and cardiac repolarization. We observed a decrease in the HF component of HRV immediately after ozone exposure, which is consistent with findings in multiple PM studies (PM Integrated Science Assessment).…”

Section: Discussionmentioning

confidence: 53%

Controlled Exposure of Healthy Young Volunteers to Ozone Causes Cardiovascular Effects

et al. 2012

Self Cite

View full text Add to dashboard Cite

Background— Recent epidemiology studies have reported associations between short-term ozone exposure and mortality. Such studies have previously reported associations between airborne particulate matter pollution and mortality, and support for a causal relationship has come from controlled-exposure studies that describe pathophysiological mechanisms by which particulate matter could induce acute mortality. In contrast, for ozone, almost no controlled-human-exposure studies have tested whether ozone exposure can modulate the cardiovascular system. Methods and Results— Twenty-three young healthy individuals were exposed in a randomized crossover fashion to clean air and to 0.3-ppm ozone for 2 hours while intermittently exercising. Blood was obtained immediately before exposure, immediately afterward, and the next morning. Continuous Holter monitoring began immediately before exposure and continued for 24 hours. Lung function was performed immediately before and immediately after exposure, and bronchoalveolar lavage was performed 24 hours after exposure. Immediately after ozone exposure, we observed a 98.9% increase in interleukin-8, a 21.4% decrease in plasminogen activator inhibitor-1, a 51.3% decrease in the high-frequency component of heart rate variability, and a 1.2% increase in QT duration. Changes in interleukin-1B and plasminogen activator inhibitor-1 were apparent 24 hours after exposure. In agreement with previous studies, we also observed ozone-induced drops in lung function and an increase in pulmonary inflammation. Conclusions— This controlled-human-exposure study shows that ozone can cause an increase in vascular markers of inflammation and changes in markers of fibrinolysis and markers that affect autonomic control of heart rate and repolarization. We believe that these findings provide biological plausibility for the epidemiology studies that associate ozone exposure with mortality. Clinical Trial Registration— URL: http://www.clinicaltrials.gov . Unique identifier: NCT01492517.

show abstract

“…Chalk PM 2.5 could also stimulate alveolar macrophages to produce reactive oxygen species and cause oxidative stress and cytotoxicity (Zhang et al, 2015a, b). Although the adverse health effects of ultrafine particles remains uncertain, various experimental studies have indicated that human exposure to nanoparticles is related to cardiovascular diseases (Lucking et al, 2008;Langrish et al, 2009;Samet et al, 2009). According to Figs.…”

Section: Particle Size Distribution Of Chalk Dustmentioning

confidence: 99%

Effects of Chalk Use on Dust Exposure and Classroom Air Quality

Lin

Lee

Huang

2015

Aerosol Air Qual. Res.

View full text Add to dashboard Cite

This study explores human exposure to harmful dust when antidust chalk is used for teaching, as well as dust particle size distribution and how chalk dust affects indoor air quality. In this study, a classroom with 5 ventilation modes was selected. A dust size analyzer and a scanning mobility particle sizer were employed to measure the mass concentration and particle size distribution of chalk dust based on the frequency of chalk use during classes. The results indicate that antidust chalk can generate considerable quantities of dust particles and substantially increase the mass concentration of dust in the proximity of the chalkboard. Approximately 15% of observed chalk dust particles were respirable and high concentrations of chalk dust deteriorated the indoor air quality. Moreover, chalk dust was the primary source of indoor coarse particles. Mechanical ventilation resuspended the settled chalk dust particles, thereby increasing the mass concentration of airborne dust. Using antidust chalk generates coarse, fine, and ultrafine particles, particularly when cleaning the chalkboard. The best ventilation mode to reduce dust accumulated in the chalk teaching classroom was to open doors and turn on ceiling fans. Wearing face masks and increasing distance between seats and blackboard can also prevent teachers and students from chalk dust hazard. The results of this study should serve as a reference for improving indoor air quality and protecting teachers and students from harmful dust particles in classrooms.

show abstract

Concentrated Ambient Ultrafine Particle Exposure Induces Cardiac Changes in Young Healthy Volunteers

Abstract: These findings show mild inflammatory and prothrombic responses and are suggestive of alterations in cardiac repolarization induced by UFCAP inhalation.

Cited by 151 publications

References 62 publications

Air Pollution and Cardiovascular Disease

Air Pollution and Cardiovascular Disease

Controlled Exposure of Healthy Young Volunteers to Ozone Causes Cardiovascular Effects

Effects of Chalk Use on Dust Exposure and Classroom Air Quality

Contact Info

Product

Resources

About