Xenobiotic pulmonary exposure and systemic cardiovascular response via neurological links

Abstract

The cardiovascular response to xenobiotic particle exposure has been increasingly studied over the last two decades, producing an extraordinary scope and depth of research findings. With the flourishing of nanotechnology, the term "xenobiotic particles" has expanded to encompass not only air pollution particulate matter (PM) but also anthropogenic particles, such as engineered nanomaterials (ENMs). Historically, the majority of research in these fields has focused on pulmonary exposure and the adverse physiological effects associated with a host inflammatory response or direct particle-tissue interactions. Because these hypotheses can neither account entirely for the deleterious cardiovascular effects of xenobiotic particle exposure nor their time course, the case for substantial neurological involvement is apparent. Indeed, considerable evidence suggests that not only is neural involvement a significant contributor but also a reality that needs to be investigated more thoroughly when assessing xenobiotic particle toxicities. Therefore, the scope of this review is several-fold. First, we provide a brief overview of the major anatomical components of the central and peripheral nervous systems, giving consideration to the potential biologic targets affected by inhaled particles. Second, the autonomic arcs and mechanisms that may be involved are reviewed. Third, the cardiovascular outcomes following neurological responses are discussed. Lastly, unique problems, future risks, and hurdles associated with xenobiotic particle exposure are discussed. A better understanding of these neural issues may facilitate research that in conjunction with existing research, will ultimately prevent the untoward cardiovascular outcomes associated with PM exposures and/or identify safe ENMs for the advancement of human health.

Whole-body inhalation of nano-sized carbon black: a surrogate model of military burn pit exposure

“…Adverse health effects include eye and throat irritation, inflammation, pulmonary disease, and reduced or impaired cognitive function. Multiple organs and systems are known to be targeted by toxic airborne exposures, including blood, lungs, cardiovascular, and central nervous systems [34][35][36][37]. One of the most intensely tested concepts concerning health effects of exposure to airborne toxins is that the onset of inflammatory responses mediates the causal path from pulmonary exposure to development of pulmonary, cardiovascular, metabolic, malignant, and neurodegenerative diseases [29,38,39].…”

Impact of pulmonary exposure to gold core silver nanoparticles of different size and capping agents on cardiovascular injury

“…To date, there is little consensus regarding the safety of engineered nanomaterials, the mechanisms by which they may induce a toxic response, or how these mechanisms may be influenced by particle size or modifications such as addition of capping agents. There is current literature evidence that pulmonary exposure to PM and ENMs can alter to progression of or to cardiovascular disease (CVD) and dysfunction through multiple pathways, including inflammation [ 15 , 33 , 36 ], autonomic dysfunction [ 25 , 37 , 38 ], oxidative stress [ 39 – 41 ] or mitochondrial dysfunction [ 42 , 43 ]. We evaluated the impact of a pulmonary exposure to 2 different sized silver nanoparticles (AgNP) with different capping agents on pulmonary BAL cells and protein, serum cytokine (as a surrogate for systemic inflammation), protein oxidation in lung and heart, vascular function, and myocardial ischemia reperfusion (I/R) injury.…”

Exacerbation of Thrombotic Responses to Silver Nanoparticles in Hypertensive Mouse Model

“…Although the number of evidence about the toxic effects and mechanisms induced by AgNPs on heart is limited, there are much fewer investigations on the impeding effects of these nanoparticles on populations with cardiovascular pathologies such as hypertension. In this regard, previous studies have demonstrated that pulmonary exposure to engineered nanomaterials is capable of aggravating cardiovascular dysfunction via mechanisms including systemic inflammation, coronary artery dysfunction, metabolic derangement, autonomic dysregulation, and oxidative stress [15][16][17][18]. Oxidative stress contributed by increased reactive oxygen species level generates an imbalance between reactive oxygen species generation and antioxidant defence mechanism such as catalase and superoxide dismutase [19].…”