Effect of Air Pollution and Neurological Dsease

 

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Front Public Health. 2022 Jul 14;10:882569. doi: 10.3389/fpubh.2022.882569

The Physiological Effects of Air Pollution: 

Particulate Matter,

 Physiology and Disease

Jack T Pryor 1,2, Lachlan O Cowley 1, Stephanie E Simonds 1,*

Abstract

Nine out of 10 people breathe air that does not meet World Health Organization pollution limits. 

Air pollutants include gasses and particulate matter and collectively are responsible for ~8 million annual deaths.

 Particulate matter is the most dangerous form of air pollution, 

causing inflammatory and oxidative tissue damage. 

A deeper understanding of the physiological effects of particulate matter is needed for effective disease prevention and treatment.

 This review will summarize the impact of particulate matter on physiological systems, and where possible will refer to apposite epidemiological and toxicological studies. By discussing a broad cross-section of available data, 

we hope this review appeals to a wide readership and provides some insight on the impacts of particulate matter on human health.

Particulate Matter

Particulate matter (PM) are solid compounds suspended in air that are sufficiently small to be inhaled (Figure 1)

. PM is categorized by particle diameter (measured in μm); PM0.1, PM2.5 and PM10 whilst 

ambient concentration is usually quantified as μg/m3.

 Some PM are of natural origin (bushfires, dust, sea spray, aerosols, etc.) but anthropogenic PM (diesel, coal and biomass combustion and emissions from metal refineries etc.) are the most dangerous to health (13).

 High atmospheric concentrations of human-made PM, and toxic and oxidative chemical characteristics render them disproportionately hazardous (13).

 Elemental and complex chemical species of PM are diverse, with surface shape, chemistry and charge impacted by emission source and environmental conditions. PM chemistry can change through reactions with other airborne PM and be affected by the oxidative effects of ozone and low ambient pH (14, 15).

Fig 1

To scale illustration of the relative sizes of PM10, PM2.5, and PM0.1. Representative macrophage and mitochondria are included to scale for

Reference

Fig1

Neurological Disease

Increased ambient PM concentration positively correlates with the incidence of Alzheimer's disease, Parkinson's disease, Multiple Sclerosis, dementia and autism spectrum disorder (Figure 2) (127)

. Long-term PM2.5 exposure significantly increased age adjusted risk of mortality and hospital admission for Alzheimer's disease, Parkinson's disease and non-Alzheimer's disease dementia (128). 

This study found the strongest correlation to exist between PM2.5 and Alzheimer's disease (128). One longitudinal study found that people living within 50 meters of a main road had a 12% greater chance of dementia diagnosis (129).

 PM2.5 exposure is linked to faster decline in new learning and immediate recall, as well as MRI-detected gray matter atrophy in brain areas vulnerable to Alzheimer's disease pathology (130).

 PM2.5 exposure has been linked to Alzheimer's specific cognitive impairments (CERAD score but not ABC score) however post-mortem analysis of neuropathology in the brains of Alzheimer's disease patients failed to reveal any link between PM2.5 exposure 10 years before death, and disease progression indicated by Braak stage (131)

. The impact of specific PM (including black carbon, organic matter, nitrate, sulfate, sea salt and soil) exposure on the rate of initial Parkinson's disease hospitalization in New York State was investigated. This study revealed that with each standard deviation increase in either nitrate or organic matter PM, the risk of hospitalizations increased 1.06-fold (132).

PM 0.1 can cross the blood brain barrier and cause inflammatory and oxidative tissue damage as well as microglial activation (133). 

Glutamatergic excitotoxicity is a common reported endpoint for acute PM induced pathophysiology in the central nervous system. PM has been found in neurons, glia, endothelium, choroid plexus ependymal cells, cerebrospinal fluid, nasal epithelium, and olfactory epithelium of individuals subjected to PM exposure (134).

 PM2.5 has been found to reduce nervous system expression of the tight junction proteins, zonula occludens 1 and 2 (135). 

This study found a compromised blood brain barrier permeable to macrophage infiltration, and nervous system tissue subject to glutamatergic excitotoxicity, triggered by macrophage-derived glutamate (135).

 In mice, PM2.5 has been shown to reach the olfactory bulb and induce microglial activation and glutamatergic excitotoxicity that could be blocked with the antioxidant N-acetylcysteine (136).

Alzheimer's disease is characterized by cortical and hippocampal amyloid-β plaque and tau tangle deposition. Amyloid-β plaque formation and gliosis underlie at least some of the cognitive deficits associated with 

AD progression (137).

 In a transgenic mouse model of Alzheimer's disease, exposure to diesel emission PM2.5 exacerbated amyloid-β plaque deposition, and increased astrocytosis and microgliosis. Additionally, elevated inflammatory cytokines including tumor necrosis factor, nuclear factor-α, interleukins 1β and 6, interferon-γ and macrophage inflammatory protein-3α were identified in the cortices of double transgenic mice (138).

 In a similar study, 13-week exposure to diesel exhaust PM also accelerated cortical amyloid-β plaque deposition, an effect associated with significant impairments to motor coordination (139). Parkinson's disease is caused by loss of dopaminergic neurons in the substantia nigra of the basal ganglia. Neuron loss results in diminished cortical input and associated behavioral and cognitive deficits. In a rotenone-induced mouse model of Parkinson's disease, PM2.5 exposure induced mitochondrial dysfunction, oxidative stress and apoptosis in the substantia nigra. In the same study, PM exposure also exacerbated motor and somatosensory deficits (140). 

Multiple Sclerosis (MS) is a progressive, demyelinating and neurodegenerative disease of the CNS. Short-term PM exposure is associated with increased MS hospital admissions and relapse (127). In a mouse model of lipophosphatidylcholine-induced demyelination, PM exposure impairs myelin repair and sustains astroglia and microglia dependent neuroinflammation. PM2.5 exposure to rats impaired spatial learning and memory, inquiring ability and sensory function, these changes were related to ultrastructural changes to mitochondria and myelin (141).

 Mice exposed to PM2.5 for 10 months developed structural hippocampal alterations including diminished apical spine density and dendritic branching of hippocampal neurons and behavioral studies revealed reduced spatial learning and memory impairments (142).