Pulmonary exposure of rats to ultrafine titanium dioxide enhances cardiac protein phosphorylation and substance P synthesis in nodose ganglia

Kan, Hong; Wu, Zhong-Xin; Young, Shih Houng; Chen, Teh Hsun; Cumpston, Jared L.; Chen, Fei; Kashon, Michael L.; Castranova, Vincent

doi:10.3109/17435390.2011.611915

Cited by 26 publications

(30 citation statements)

References 48 publications

(59 reference statements)

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“…Secondly, translocation or direct interaction may initiate redox chemistry within the vasculature, as these ENM may be manufactured from or coated with a variety of highly reactive materials capable of producing reactive species or reducing antioxidant competence within a physiological environment [16,51,52]. Lastly, the neural route may stimulate sensory neurons leading to altered afferent and efferent signaling patterns ultimately effecting the maintenance of smooth muscle tone [53,54]. These pathways are not isolated or independent of each other and they may operate in conjunction with the other routes.…”

Section: Resultsmentioning

confidence: 99%

Impairment of Coronary Arteriolar Endothelium-Dependent Dilation after Multi-Walled Carbon Nanotube Inhalation: A Time-Course Study

Stapleton

Minarchick

Cumpston

et al. 2012

IJMS

Self Cite

102

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Engineered nanomaterials have been developed for widespread applications due to many highly unique and desirable characteristics. The purpose of this study was to assess pulmonary inflammation and subepicardial arteriolar reactivity in response to multi-walled carbon nanotube (MWCNT) inhalation and evaluate the time course of vascular alterations. Rats were exposed to MWCNT aerosols producing pulmonary deposition. Pulmonary inflammation via bronchoalveolar lavage and MWCNT translocation from the lungs to systemic organs was evident 24 h post-inhalation. Coronary arterioles were evaluated 24–168 h post-exposure to determine microvascular response to changes in transmural pressure, endothelium-dependent and -independent reactivity. Myogenic responsiveness, vascular smooth muscle reactivity to nitric oxide, and α-adrenergic responses all remained intact. However, a severe impact on endothelium-dependent dilation was observed within 24 h after MWCNT inhalation, a condition which improved, but did not fully return to control after 168 h. In conclusion, results indicate that MWCNT inhalation not only leads to pulmonary inflammation and cytotoxicity at low lung burdens, but also a low level of particle translocation to systemic organs. MWCNT inhalation also leads to impairments of endothelium-dependent dilation in the coronary microcirculation within 24 h, a condition which does not fully dissipate within 168 h. The innovations within the field of nanotechnology, while exciting and novel, can only reach their full potential if toxicity is first properly assessed.

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Section: Resultsmentioning

confidence: 99%

Impairment of Coronary Arteriolar Endothelium-Dependent Dilation after Multi-Walled Carbon Nanotube Inhalation: A Time-Course Study

Stapleton

Minarchick

Cumpston

et al. 2012

IJMS

Self Cite

102

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“…29 Similar microvascular dysfunction has been reported after inhalation of nano-titanium dioxide and has been associated with stimulation of sensory neurons from the lung and enhanced sympathetic input at the systemic arterioles. 30,31 Aspiration of MWCNTs has also been reported to increase baroreflex activity in rats. 32,33 In addition, Erdely et al 34 reported transient elevation of blood inflammatory mediators after aspiration of MWCNTs, which may mediate this systemic microvascular response.…”

Section: Cardiovascular Responsesmentioning

confidence: 99%

Occupational Nanosafety Considerations for Carbon Nanotubes and Carbon Nanofibers

2012

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CONSPECTUSCarbon nanotubes (CNTs) are carbon atoms arranged in a crystalline graphene lattice with a tubular morphology. CNTs exhibit high tensile strength, possess unique electrical properties, are durable, and can be functionalized. These properties allow applications as structural materials, in electronics, as heating elements, in batteries, in the production of stain-resistant fabric, for bone grafting and dental implants, and for targeted drug delivery. Carbon nanofibers (CNFs) are strong, flexible fibers that are currently used to produce composite materials.Agitation can lead to aerosolized CNTs and CNFs, and peak airborne particulate concentrations are associated with workplace activities such as weighing, transferring, mixing, blending, or sonication. Most airborne CNTs or CNFs found in workplaces are loose agglomerates of micrometer diameter. However, due to their low density, they linger in workplace air for a considerable time, and a large fraction of these structures are respirable.In rat and mouse models, pulmonary exposure to single-walled carbon nanotubes (SWCNTs), multi-walled carbon nanotubes (MWCNTs), or CNFs causes the following pulmonary reactions: acute pulmonary inflammation and injury, rapid and persistent formation of granulomatous lesions at deposition sites of large CNT agglomerates, and rapid and progressive alveolar interstitial fibrosis at deposition sites of more dispersed CNT or CNF structures.Pulmonary exposure to SWCNTs can induce oxidant stress in aortic tissue and increases plaque formation in an atherosclerotic mouse model. Pulmonary exposure to MWCNTs depresses the ability of coronary arterioles to respond to dilators. These cardiovascular effects may result from neurogenic signals from sensory irritant receptors in the lung. Pulmonary exposure to MWCNTs also upregulates mRNA for inflammatory mediators in selected brain regions, and pulmonary exposure to SWCNTs upregulates the baroreceptor reflex. In addition, pulmonary exposure to MWCNTs may induce levels of inflammatory mediators in the blood, which may affect the cardiovascular system.

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“…Cardiac inflammation has been shown to occur following exposure to TiO 2 UFP without quantifiable increases in circulating pro-inflammatory cytokines raising further questions on the role of circulating mediators versus direct translocation (Kan et al 2011). It is plausible that low levels of constant circulating inflammatory cytokines over an extended amount of time could be sufficient for the development of chronic cardiovascular diseases.…”

Section: Pulmonary-derived Mediator Release and Systemic Effectsmentioning

confidence: 99%

Manufactured and airborne nanoparticle cardiopulmonary interactions: a review of mechanisms and the possible contribution of mast cells

Shannahan

Kodavanti

Brown

2012

Inhalation Toxicology

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Human inhalation exposures to manufactured nanoparticles (NP) and airborne ultrafine particles (UFP) continues to increase in both occupational and environmental settings. UFP exposures have been associated with increased cardiovascular mortality and morbidity, while ongoing research supports adverse systemic and cardiovascular health effects after NP exposures. Adverse cardiovascular health effects include alterations in heart rate variability, hypertension, thrombosis, arrhythmias, increased myocardial infarction, and atherosclerosis. Exactly how UFP and NP cause these negative cardiovascular effects is poorly understood, however a variety of mediators and mechanisms have been proposed. UFP and NP, as well as their soluble components, are known to systemically translocate from the lung. Translocated particles could mediate cardiovascular toxicity through direct interactions with the vasculature, blood, and heart. Recent study suggests that sensory nerve stimulation within the lung may also contribute to UFP- and NP-induced acute cardiovascular alterations. Activation of sensory nerves, such as C-fibers, within the lung may result in altered cardiac rhythm and function. Lastly, release of pulmonary-derived mediators into systemic circulation has been proposed to facilitate cardiovascular effects. In general, these proposed pulmonary-derived mediators include pro-inflammatory cytokines, oxidatively-modified macromolecules, vasoactive proteins, and prothrombotic factors. These pulmonary-derived mediators have been postulated to contribute to the subsequent prothrombotic, atherogenic, and inflammatory effects after exposure. This review will evaluate the potential contribution of individual mediators and mechanisms in facilitating cardiopulmonary toxicity following inhalation of UFP and NP. Lastly we will appraise the literature and propose a hypothesis regarding the possible role of mast cells in contributing to these systemic effects.

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Pulmonary exposure of rats to ultrafine titanium dioxide enhances cardiac protein phosphorylation and substance P synthesis in nodose ganglia

Cited by 26 publications

References 48 publications

Impairment of Coronary Arteriolar Endothelium-Dependent Dilation after Multi-Walled Carbon Nanotube Inhalation: A Time-Course Study

Impairment of Coronary Arteriolar Endothelium-Dependent Dilation after Multi-Walled Carbon Nanotube Inhalation: A Time-Course Study

Occupational Nanosafety Considerations for Carbon Nanotubes and Carbon Nanofibers

Manufactured and airborne nanoparticle cardiopulmonary interactions: a review of mechanisms and the possible contribution of mast cells

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