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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.

Many factors play a role in the risk of dementia, including the environment. Widespread and significant worldwide exposure to noise, the severity of related health consequences, and the limited tools available to the public to protect themselves strongly support the WHO's argument that 'noise pollution is not only an environmental nuisance but also a threat to public health'. Exposures to noise from industrial activities, airport noise, or occupational noise are very important. One of the limitations of such studies is the lack of information about lifestyle habits that can play a key role in a person's risk of dementia. This review suggests that people with more exposure to ambient noise are at higher risk of Alzheimer’s Disease (AD) and dementia than other people and we examined how chronic noise exposure causes neuropathology such as AD and how it relates to ApoE4 activation. Further studies are essential to expanding global knowledge about the harmful health effects and costs of health care due to noise pollution.

Parkinson’s Disease (PD) is a neurodegenerative disorder characterized by motor deficits caused by the loss of dopaminergic neurons in the Substantia Nigra (SN) and Ventral Tegmental Area (VTA). However, clinical data revealed that not only the dopaminergic system is affected in PD. Pharmacological models support the concept that modification of noradrenergic transmission can influence the PD-like phenotype induced by neurotoxins. 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 stress can be a useful strategy to eliminate the obvious symptoms of neurodegeneration. Overall, in the current mini-review, we examined the neuroprotective role of noradrenaline in the model of oxidative stress and neuroinflammation.