Reased by exposure to nTiO2. Conclusion: Repeated exposure to nanosized TiOReased by exposure to nTiO2.

Reased by exposure to nTiO2. Conclusion: Repeated exposure to nanosized TiO
Reased by exposure to nTiO2. Conclusion: Repeated exposure to nanosized TiO2 particles was associated with modest plaque progression in ApoE-/- mice. There were no associations between the pulmonary TiO2 exposure and inflammation or vasodilatory dysfunction.Introduction The investigation of toxicological effects of nanoparticles is increasingly important due to their growing occupational use and presence as compounds in consumer products. The use of nanometer-size particles in paints can reduce the order Pan-RAS-IN-1 production costs by the addition of lower (mass) concentrations or add novel properties to the final product. TiO2 pigments are widely used by paint and plastic industries for whiteness and opacity. One of the major advantages of TiO 2 is its resistance to* Correspondence: [email protected] 1 Department of Public Health, University of Copenhagen, 1014 Copenhagen K, Denmark Full list of author information is available at the end of the articlediscoloration by UV light. TiO2 particles are considered to have low toxicity to humans and animals [1]. However, it has been shown that decreasing particle size is associated with increased pro-inflammatory properties [2]. An important possible health risk of particle exposure is cardiovascular effects. It has been shown that exposure to combustion-based particles in ambient air is associated with progression of atherosclerosis, myocardial infarction and cardiovascular mortality in humans and the nanosized fraction is considered an important culprit [3-5]. The mechanisms of these effects are considered to involve oxidative stress and inflammation, vasomotor dysfunction, neuronal signalling and possible translocation of particles from the airways to the?2011 Mikkelsen et al; licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.Mikkelsen et al. Particle and Fibre Toxicology 2011, 8:32 http://www.particleandfibretoxicology.com/content/8/1/Page 2 ofcirculation [3]. Pulmonary exposure to carbon-based particles can accelerate plaques progression in animal models [6,7]. However, PubMed ID:https://www.ncbi.nlm.nih.gov/pubmed/27872238 associations between exposure to TiO2 particles and progression of atherosclerosis have not been assessed, whereas pulmonary exposure has been associated with vasomotor dysfunction [8]. Endothelial cells have an important barrier function and produce factors that regulate vascular tone, cellular adhesion, smooth muscle cell proliferation, vessel wall inflammation, and thromboresistance [9,10]. In the functional endothelium, acetylcholine binds to muscarinic receptors on the luminal surface leading to nitric oxide (NO) production by the calcium dependent, constitutive isoform of NO synthase (eNOS) [9]. Impaired endothelium-dependent vasodilation is a central feature of endothelial dysfunction and is associated with increased risk of developing cardiovascular diseases [11]. Endothelial dysfunction is associated with increased levels of proinflammatory factors, such as adhesion molecules and chemoattractants [12], which can lead to atherosclerosis [9,11,13]. This is attributed to increased intravascular generation of reactive oxygen species (ROS) such as superoxide anion radicals, leading to reduced bioavailability of NO [12]. Superoxide dismutase (SOD) converts superoxide anion radicals to hydroge.