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 Table of Contents  
REVIEW ARTICLE
Year : 2016  |  Volume : 1  |  Issue : 3  |  Page : 85-89

Pathophysiological effects of particulate matter air pollution on the central nervous system


1 Department of Neurological Surgery, Wayne State University School of Medicine, Detroit, MI, USA
2 Department of Neurological Surgery, Wayne State University School of Medicine, Detroit, MI, USA; Center for Environment and Disease, Beijing Luhe Hospital, Capital Medical University, Beijing, China

Date of Submission05-Sep-2016
Date of Acceptance13-Sep-2016
Date of Web Publication12-Oct-2016

Correspondence Address:
Yuchuan Ding
Department of Neurological Surgery, Wayne State University School of Medicine, Room 48, 550 E Canfield, Detroit, MI, USA

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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/2468-5690.191932

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  Abstract 

Particulate matter (PM) air pollution is a leading public health concern across most of the populated world. Elevated PM levels cause both acute increases in cardiovascular mortality and the development of long-term neurological pathology. Upon inhalation, PM reaches the brain through entry into pulmonary capillaries and directly through the olfactory mucosa. Population-based and animal studies reveal decreases in brain size and increases in inflammatory markers following long-term exposure to elevated PM concentrations. In vitro, cell culture studies indicate that components of PM air pollution are neurotoxic. In addition to direct effects on the central nervous system (CNS), PM induces aberrant local and systemic inflammatory responses that can induce and exacerbate cerebral injury. Hypertension and decreased cerebral blood flow velocity are observed within days of increased PM exposure and may contribute to short-term rises in mortality rate. Substantial epidemiological evidence links PM concentration with both short-term and long-term risk of stroke. It has been suggested that the increased stroke risk is due to potentiation of cerebrovascular inflammation, endothelial cell dysfunction, reactive oxygen species production, and atherosclerosis. This review examines the pathophysiological mechanisms by which PM damages the CNS and the cerebrovasculature.

Keywords: Central nervous system, particulate matter air pollution, pathophysiological effects


How to cite this article:
Wright JC, Ding Y. Pathophysiological effects of particulate matter air pollution on the central nervous system. Environ Dis 2016;1:85-9

How to cite this URL:
Wright JC, Ding Y. Pathophysiological effects of particulate matter air pollution on the central nervous system. Environ Dis [serial online] 2016 [cited 2020 Apr 4];1:85-9. Available from: http://www.environmentmed.org/text.asp?2016/1/3/85/191932


  Introduction Top


A recent analysis concluded that over 87% of the world's population lives in areas exceeding the World Health Organization's (WHO) safe annual average fine particulate matter (PM) pollution (PM 2.5 ). [1] The 2010 global burden of disease study reported PM air pollution as the sixth leading cause of global premature mortality, responsible for approximately 3.2 million deaths in 2010. [2] Clear connections have been elucidated between elevated PM levels and cardiovascular disease, chronic obstructive pulmonary disease, asthma, cerebrovascular disease, diabetes mellitus, neurological damage, and preterm birth. [3],[4],[5],[6],[7] Growing evidence suggests that PM air pollution contributes to the development, morbidity, and mortality associated with many diseases of the central nervous system (CNS). [8] PM air pollution is a heterogeneous mix of metals, dust, various organic compounds, and microorganisms suspended within aerosolized droplets. PM particles range in size from < 0.1 to >10 µm in diameter. The smaller particles compose the largest fraction of PM by number, but they make up the smallest fraction of PM mass. In contrast, there are fewer large particles, but they contain the bulk of PM mass. [9] PM is classified as coarse PM (PM 10 ), PM 2.5 , and ultrafine PM (PM 0.1 ). Particles between 2.5 and 10 µm in diameter are referred to as the coarse fraction (PM c ), and particles between 0.1 and 2.5 µm in diameter make up the fine fraction (PM f ). [9] After inhalation, the coarse fraction cannot travel beyond the bronchi, but the fine fraction descends the bronchial tree to the alveoli. The ultrafine fraction and a portion of the fine fraction traverse the pulmonary endothelium and enter the bloodstream. [10]


  Particulate Matter Direct Neurotoxicity Top


Many compounds within PM of various sizes are toxic to the developing and adult brain. The direct exposure of cultured neurons to PM pollution results in decreased growth at low concentrations and cell death at higher concentrations. Both PM 2.5 and PM 0.1 are neurotoxic using cell culture models. [11] Direct exposure of the brain parenchyma to PM can occur through two different mechanisms. Some PM 0.1 particles are capable of entering the bloodstream and crossing the blood-brain barrier. [12] A small number of larger particles can translocate across the lung epithelium and capillary endothelium after phagocytosis by a macrophage. These particles may subsequently be deposited within secondary organs or enter the blood circulation. [13] A secondary route of entry into the CNS is through the olfactory mucosa. Up to 20% of the PM trapped within the olfactory mucosa travels through the cribriform plate alongside the olfactory neurons to enter the entorhinal cortex. [14]


  Particulate Matter, Brain Pathophysiology, and Stroke Top


Long-term exposure to high PM concentrations can decrease total brain volume and increase the concentration of inflammatory markers. [15] The direct mechanisms responsible for these changes are unknown, but several studies have examined these changes in animal models and human populations. [16] One study utilized a mouse model to examine inflammatory and morphological changes after 3- and 9-month exposure to elevated PM concentrations. At 9 months of exposure, an Alzheimer's disease-like inflammation profile was observed. They found elevated levels of beta-amyloid 1-40 protein levels, beta-site amyloid precursor protein cleaving enzyme, cyclooxygenase 1 and 2, and various cytokines. [16] Further investigation is needed to discover whether this plays a role in human responses to PM.

A Framingham Offspring Study examined the brain of individuals free of dementia who were at least 65 years old and assessed changes between those living in higher pollution and lower pollution areas. Individuals exposed to higher PM levels displayed a smaller total cerebral brain volume and a higher incidence of covert brain infarcts. [15] The authors hypothesize these effects are the result of PM-mediated acceleration of brain atrophy and small vessel disease. More studies should be conducted on these morphological changes, especially in areas where ambient PM levels are much higher than those experienced by the individuals in this study.

Acute vascular changes

Within minutes of exposure to high PM levels, a physiological cascade toward hypertension is initiated. [17] These events trigger increases in systolic blood pressure (SBP) and diastolic blood pressure (DBP) within days of the insult. A meta-analysis of 22 studies analyzing hypertension during PM exposure found that each 10 µg/m 3 increase in PM 2.5 raised SBP by an average of 1.393 mmHg and DBP by an average of 0.895 mmHg. [18] Changes in blood pressure are also mediated by larger PM from the coarse fraction, which indicates that the response is not dependent on PM entering the blood stream. [19] Although a definitive mechanism for this increase in blood pressure has not been established, several possible mechanisms have been hypothesized. One theory is that the response is triggered by an innate immune response to microbial components of the PM. [20] Another explanation is that the pulmonary inflammatory response stimulates the release of endothelin-1 causing pulmonary vasoconstriction. This would stimulate the vagal afferent nerves and cause a change in the systemic autonomic balance. The resulting vasomotor dysfunction could contribute to vasoconstriction-induced hypertension. [17] The increased blood pressure caused by PM exposure increases the risk of ischemic stroke. [21] A study using transcranial Doppler ultrasound determined that these blood pressure changes alter cerebral blood flow. Following exposure to fine PM, individuals displayed lower cerebral blood flow velocities and increased cardiovascular resistance. [22]

Particulate matter and stroke

Stroke is the second most prevalent cause of death and the leading cause of permanent disability globally. [23] In 2012, ischemic and hemorrhagic strokes resulted in combined 6.7 million deaths. [23] Epidemiological studies have revealed many risk factors for the incidence of stroke. One of the most preventable risk factors for ischemic stroke is PM air pollution. Recent modeling estimates that reducing PM emissions to the WHO interim guideline would decrease global mortality by 750,000 deaths/year. [2] Numerous population studies and meta-analyses have revealed a significant link between levels of PM 2.5 and the frequency of stroke. This review provides a summary of the recent insights into mechanisms by which PM 2.5 air pollution initiates and exacerbates ischemic stroke.

The link between PM concentration and stroke risk was first established through various epidemiological studies. Short-term risk for stroke was assessed by comparing recorded PM pollution levels with incidence of hospital admission for stroke [Table 1]. The connection between PM and stroke was supported in many studies although several others were inconclusive. Increasing the sample size by utilizing meta-analysis confirmed the significant increases in stroke risk, stroke morbidity, and stroke mortality after both acute and chronic PM exposure. [30],[31],[32]
Table 1: Hospital admission studies for acute stroke incidence following particulate matter elevation

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The role of long-term exposure to PM air pollution in stroke mortality and morbidity has been analyzed through many population-based studies. [33],[34],[35],[36] A recent meta-analysis of twenty long-term exposure studies consisted of over 10 million people. [32] The result was a strong association between prolonged PM exposure and stroke in all regions. Geographic heterogeneity of stroke risk was observed. This may be due to the variable organic and inorganic components of PM pollution in different parts of the world.

PM stimulates the pathology of ischemic stroke by initiating a systemic inflammatory response, generating oxidative damage, and contributing to the progression of cerebral atherosclerosis. The mechanisms responsible for the pathophysiological process in stroke have been explored as below as follows.

Particulate matter and inflammation

PM initiates a cascade in the lungs that leads to the buildup of reactive oxygen species (ROS) and the development of systemic inflammation. Upon inhalation of PM, the immune response begins within the respiratory macrophages. These macrophages are found within the bronchioles and alveoli, and they detect PM through the surface proteins such as toll-like receptor 4 (TLR4) and scavenger protein A. [37] In addition, PM oxidizes the surfactant molecules coating the alveoli. These oxidized surfactant molecules bind to TLR4 and amplify the activation of respiratory macrophages. [38] Activated macrophages begin secreting interleukin-6 (IL-6), IL-1, tumor necrosis factor alpha, and other pro-inflammatory cytokines. [39]

The macrophage cytokine release facilitates the activation of additional inflammatory processes. One consequence of this aberrant inflammation is the loss of endothelial integrity. Increased production of IL-6 induces the synthesis of hypoxia-inducible factor 1α (HIF-1α) within vascular endothelial cells (VEC). [39] IL-6 signaling also enables HIF-1α to enter the VEC nucleus and act as a regulatory transcription factor. Within the nucleus, HIF-1α acts to decrease cell proliferation and increase the permeability of the vascular endothelium. [39] A recent study revealed that these changes in endothelial integrity are also mediated by damage to the intercellular tight junctions. [40] They found in vitro and in vivo evidence that ROS-mediated activation of the calpain protease can result in cleavage of zona-occludens-1, a tight junction protein. [40]

Another consequence of this inflammatory response is the production of ROS. After macrophage activation, IL-1 triggers neutrophils to produce superoxide anion, a potent oxidative radical. [41] Increases in ROS, both from the PM and secondary neutrophil activation, amplifies the production of redox-associated transcription factors in the bronchial epithelium and capillary endothelium. This ROS activation induces the expression of intercellular adhesion molecule-1 in bronchial epithelial cells and increases the expression of vascular cell adhesion molecule-1 in capillary endothelial cells. These changes facilitate the rapid transport of additional leukocytes and lymphocytes into the airways. [42] This intensifies both the local inflammation and systemic inflammation.

Particulate matter and atherosclerosis

PM air pollution promotes the development of atherosclerosis throughout the cardiovascular system, but this review focuses on cerebrovascular atherosclerosis. [43] Macrophage activation, and the subsequent cytokine release, stimulates systemic superoxide production by neutrophils. These superoxide radicals rapidly increase the concentration of ROS in the bloodstream. Many blood-borne molecules are subsequently oxidized, but the oxidation of low-density lipoproteins (LDLs) contributes to atherosclerotic pathogenesis. Oxidized LDLs have a high affinity for subendothelial macrophages. These macrophages phagocytize large quantities of LDLs and become foam cells, which contribute to the size and instability of subendothelial plaques. [38] This mechanism likely contributes to the increased risk of stroke and myocardial infarction, which is observed in populations in high PM areas. [44]


  Conclusion Top


PM pollution catalyzes systemic inflammatory reactions and oxidative stress, which contribute to the pathophysiology of several neurological and cerebrovascular disease states. Further studies are needed to uncover the mechanisms behind many of the neurological manifestations of PM exposure and the scale of subclinical brain changes due to PM. Decreasing PM concentrations in urban centers around the world would increase the quality of life and life expectancy, in part, by protecting the CNS from inflammatory stressors and atherosclerosis.

Financial support and sponsorship

This work was partially supported by the Wayne State University Neurosurgery Fund, the American Heart Association Grant-in-Aid (14GRNT20460246), and the Merit Review Award (I01RX-001964-01) from the US Department of Veterans Affairs Rehabilitation R & D Service.

Conflicts of interest

There are no conflicts of interest.

 
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