Atherosclerosis and vasomotor dysfunction in arteries of animals after exposure to combustion-derived particulate matter or nanomaterials

Abstract

Exposure to particulate matter (PM) from traffic vehicles is hazardous to the vascular system, leading to clinical manifestations and mortality due to ischemic heart disease. By analogy, nanomaterials may also be associated with the same outcomes. Here, the effects of exposure to PM from ambient air, diesel exhaust and certain nanomaterials on atherosclerosis and vasomotor function in animals have been assessed. The majority of studies have used pulmonary exposure by inhalation or instillation, although there are some studies on non-pulmonary routes such as the gastrointestinal tract. Airway exposure to air pollution particles and nanomaterials is associated with similar effects on atherosclerosis progression, augmented vasoconstriction and blunted vasorelaxation responses in arteries, whereas exposure to diesel exhaust is associated with lower responses. At present, there is no convincing evidence of dose-dependent effects across studies. Oxidative stress and inflammation have been observed in the arterial wall of PM-exposed animals with vasomotor dysfunction or plaque progression. From the data, it is evident that pulmonary and systemic inflammation does not seem to be necessary for these vascular effects to occur. Furthermore, there is inconsistent evidence with regard to altered plasma lipid profile and systemic inflammation as a key step in vasomotor dysfunction and progression of atherosclerosis in PM-exposed animals. In summary, the results show that certain nanomaterials, including TiO2, carbon black and carbon nanotubes, have similar hazards to the vascular system as combustion-derived PM.

Multi-walled carbon nanotube-physicochemical properties predict the systemic acute phase response following pulmonary exposure in mice

“…However, since SAA1/2 levels did not correlate with neutrophil influx or plasma content of SAA3 in the present study (Fig 4A and 4B), the induction of hepatic APR protein after MWCNT-exposure is likely regulated by other signaling pathways than the pulmonary acute phase response. Similar pulmonary inflammation-independent associations between ENM exposure and changes related to CVD have been reported earlier [24;80–82]. This contrast the proposed important role of pulmonary inflammation in the development of CVD by several studies [83–86].…”

Application of Scanning Electron Microscopy With Energy-Dispersive X-Ray Spectroscopy for Analyzing Ocular Surface Particles on Schirmer Strips

“…There is overwhelming evidence that PM exposure leads to oxidative stress with a downstream cascade of biological responses that have been implicated in both circulatory and pulmonary disease. 23 For example, PM 2.5 exposure has been found to contribute to the development of atherosclerosis 24 , facilitate vasomotor dysfunction and plaque progression 25 , thicken alveolar walls, and increase both serum and lung homogenate 26 due to its pro-oxidant and pro-inflammatory properties. The assessment of PM on the ocular surface will enable researchers to assess biological manifestations of PM exposure on the ocular surface.…”

Differences in inflammation and acute phase response but similar genotoxicity in mice following pulmonary exposure to graphene oxide and reduced graphene oxide

“…air pollution is associated with risk of cardiovascular disease [9], where initiation of systemic acute phase response (APR) and increase in APR proteins in the blood (e.g. C-reactive protein and SAA) have been proposed as a pathogenic mechanisms [10,11].…”