Exposure to Ambient Ultra-Fine Particles and Stroke

It is estimated that more than two-thirds of air pollution-related deaths are due to cardiovascular causes. Significant studies have now indicated that exposure to urban air pollutants is known to be a source of oxidative stress and inflammation that causes cardiovascular disease. Nitrogen oxides, Particulate Matter (PM) such as coarse particle (PM10, PM <10μm), fine particles (PM2.5, PM <2.5μm) and Ultra-Fine Particles (UFPs or PM0.1, PM <0.1μm,), ozone and transition metals are oxidant potent capable of producing Reactive Oxygen Species (ROS). Although several biological mechanisms are involved in cardiovascular disease, oxidative stress is an important observation in many levels of cardiovascular failure due to exposure to air pollutants. This mini-review cites evidence that oxidative stress is a key pathway for various cardiovascular measures of exposure to air pollution.

Section: Exposure To Air Pollutionmentioning

confidence: 99%

Section: Epidemiological Evidence Overview Of Air Pollution and Cardi...mentioning

confidence: 99%

Exposure to Urban Air Pollution Nanoparticles: Oxidative Stress and Cardiovascular Disease

Ehsanifar¹,

Montazeri²,

Rafati³

2022

“…There are several pathways via which can be transmitted infl ammatory signals from environment to brain [5], so in people exposed to urban air pollutants, activation of the peripheral immune system may lead to neuroinfl ammation [9]. Neuroinfl ammatory reactions are triggered by oxidative stress, cytokines, and chemokines and can lead to impaired neurotransmitter and neurotrophin signaling disorders, abnormal protein accumulation, neurodegeneration, and neuronal remodeling [10].…”

Section: Introductionmentioning

confidence: 99%

Neuroprotective Effects of Thiazolidine-4-Carboxylic Acid Derivatives on Memory Impairment and Neurodegeneration

Ehsanifar¹,

Montazeri²

2022

Some studies have shown numerous biological activities of Thiazolidine derivatives, including neuroprotection. The production of inflammatory markers and Reactive Oxygen Species (ROS) plays a major role in nerve damage that leads to memory impairment. Several studies have shown that alcohol consumption impairs memory in adults. However, the underlying mechanism is still unclear. Ethanol treatment also leads to memory impairment in mice. Exposure to ambient pollutants such as air pollutants also can be adversely impacted the Central Nervous System (CNS) by the activation of proinflammatory pathways and reactive oxygen species. Thus, targeting neuroinflammation and oxidative distress can be a useful strategy to eliminate the obvious symptoms of neurodegeneration. In addition, treatment with Thiazolidine-4-Carboxylic Acid derivatives reduces oxidative stress, neuroinflammation, and ethanol-induced memory impairment. In general, Thiazolidine derivatives may be useful in reducing neuroinflammation by acting on different stages of inflammation. In the current mini-review, we examined the neuroprotective potential of these compounds in a model of ethanol-induced neuritis.

“…The WHO reported that exposure to air pollution is responsible for around 7 million deaths per year [1]. Exposure to air pollution has previously has been characterized to contribute to detrimental CNS occurrences such as neuroinfl ammation, neurodegeneration, and stroke [2][3][4]. While a variety of environmental factors are involved in neuronal infl ammation leading to CNS disease, air pollutants may be the most common source of environmental oxidative stress and infl ammation.…”

Section: Introductionmentioning

confidence: 99%

CNS Demyelination Diseases Following Exposure to Urban Air Pollution

Ehsanifar¹

2022

Epidemiology findings show that exposure to urban air pollutants as a source of oxidative stress and neuroinflammation is associated with the Central Nervous System (CNS) demyelinating diseases, such as Multiple Sclerosis (MS). An autoimmune response involving increased inflammation and demyelination in the CNS leads to the pathophysiology of MS, which is more common in adult young females. Particulate Matter (PM), including fine particles (PM <2.5μm, PM 2.5) and very fine particles (PM <0.1μm, PM 0.1), transition metals, and ozone are of potent or oxidant capable of producing Reactive Oxygen Species (ROS). Redox-sensitive pathways can be caused by oxidative stress, leading to various biological processes, including inflammation and other harmful outcomes in the brain. Exposure to Diesel Exhaust Particles (DEPs) mediates significant alterations in myelination across various regions in the brain. There is also an increase in ROS production in the CNS of DEPs exposed mice. Thus, targeting neuroinflammation and oxidative stress can be a useful strategy to eliminate the obvious symptoms of the CNS demyelinating diseases. Overall, in the current mini-review, we examined the exposure to air pollutants nanoparticles associated with the CNS demyelinating diseases, such as MS.