Ambient particle inhalation and the cardiovascular system: potential mechanisms.

By Ken Donaldson, Vicki Stone, A. Seaton, W. Macnee. Environmental Health Perspectives, 2001

698 citations recorded by the source corpus.

Well-documented air pollution episodes throughout recent history have led to deaths among individuals with cardiovascular and respiratory disease. Although the components of air pollution that cause the adverse health effects in these individuals are unknown, a small proportion by mass but a large proportion by number of the ambient air particles are ultrafine, i.e., less than 100 nm in diameter. This ultrafine component of particulate matter with a mass median aerodynamic diameter less than 10 microm (PM(10) may mediate some of the adverse health effects reported in epidemiologic studies and for which there is toxicologic evidence to support this contention. The exact mechanism by which ultrafine particles have adverse effects is unknown, but these particles have recently been shown to enhance calcium influx on contact with macrophages. Oxidative stress is also to be anticipated at the huge particle surface; this can be augmented by oxidants generated by recruited inflammatory leukocytes. Atheromatous plaques form in the coronary arteries and are major causes of morbidity and death associated epidemiologically with particulate air pollution. In populations exposed to air pollution episodes, blood viscosity, fibrinogen, and C-reactive protein (CRP) were higher. More recently, increases in heart rate in response to rising air pollution have been described and are most marked in individuals who have high blood viscosity. In our study of elderly individuals, there were significant rises in CRP, an index of inflammation. In this present review, we consider the likely interactions between the ultrafine particles the acute phase response and cardiovascular disease.

Subfields: Health, Toxicology and Mutagenesis, Immunology

View Paper: https://www.semanticscholar.org/paper/78628348268d7964793b6600ca5385351b000316

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Citations in the corpus

Airborne Particulate Matter and Human Health: Toxicological Assessment and Importance of Size and Composition of Particles for Oxidative Damage and Carcinogenic Mechanisms (2008, background): “There are now several studies on potential mechanisms by which longterm exposure to particulate air pollution affects the cardiovascular system (55).”
Rapid DNA methylation changes after exposure to traffic particles. (2009, background): “Previous in vitro experiments have shown that repetitive element hypomethylation and transcription occur in response to biological processes, such as cellular stress and inflammation (4), which are also induced by particulate pollution in exposed subjects (8, 26, 27).”
Atmospheric Movement of Microorganisms in Clouds of Desert Dust and Implications for Human Health (2007, background): “adverse health effects via oxidative stress (47, 52, 263).”
Particle surface characteristics may play an important role in phytotoxicity of alumina nanoparticles. (2005, background): “…with various adverse human health effects including premature mortality, exacerbation of asthma and other respiratory-tract diseases, decreased lung function (Dockery and Pope, 1994; Schwartz et al., 1996; Pope, 1999, 2000), and cardiovascular diseases (Dockery, 2001; Donaldson et al., 2001).”
Potential Role of Ultrafine Particles in Associations between Airborne Particle Mass and Cardiovascular Health (2005, background): “Several excellent reviews of experimental data and methods can be found elsewhere (Donaldson et al. 2001; Utell et al. 2002).”
Acute toxicity and biodistribution of different sized titanium dioxide particles in mice after oral administration. (2007, background): “Additionally, some papers reported that particles could induce cardiovascular disease and impact autonomic nervous system after inhaling much aerosol particles (Donaldson et al., 2001; Neas, 2000; Peters et al., 2006).”
Nanoparticle‐induced platelet aggregation and vascular thrombosis (2005, background): “The other factor is that transition metals on the surface of particles can cause increased generation of reactive oxygen species (ROS) through the Fenton reaction (Donaldson et al., 2001), leading to platelet activation.”