Air Pollution's Harmful Impact On Our Immune System

Air pollution is a serious and common public health concern associated with growing morbidity and mortality worldwide. Inhaled particulates from environmental pollutants accumulate in macrophages in lung-associated lymph nodes over years, compromising immune surveillance via direct effects on immune cell function and lymphoid architecture. These findings reveal the importance of improved air quality to preserve immune health against current and emerging pathogens.

A well-functioning immune system is vital for a healthy body. Inadequate and excessive immune responses underlie diverse pathologies such as serious infections, metastatic malignancies, and auto-immune conditions. Therefore, understanding the effects of ambient pollutants on the immune system is vital to understanding how pollution causes disease, and how that pathology could be abrogated.

Air pollution can stimulate pro-inflammatory immune responses across multiple classes of immune cells. It can enhance T helper lymphocyte type 2 (Th2) and T helper lymphocyte type 17 (Th17) adaptive immune responses, as seen in allergy and asthma, and dysregulate anti-viral immune responses.

The primary site of exposure to air pollution is the respiratory tract following inhalation. The respiratory tract, from nasal passages down through the airways to alveolar gas exchange units in the lungs, represents the prime interface between the immune system and the airborne environment. Inhaled particulates and gases interact with epithelial cells lining the airways and professional immune cells within the airways. These cells sense and can be 'stimulated' by air pollution as pollution constituents trigger cellular signalling pathways. Stimulated cells act as part of multicellular immune responses, and perturbation of these can cause disease.

Air pollution is associated with decreased function of a gene that appears to increase the severity of asthma in children. Exposure to dirty air is linked to changes in a gene that, in turn, is connected to more severe asthma symptoms. Researchers have found that air pollution exposure suppressed the immune system’s regulatory T cells (Treg), and that the decreased level of Treg function was linked to greater severity of asthma symptoms and lower lung capacity. Treg cells are responsible for putting the brakes on the immune system so that it doesn’t react to non-pathogenic substances in the body that are associated with allergy and asthma. When Treg function is low, the cells fail to block the inflammatory responses that are the hallmark of asthma symptoms.

The diminished power of the immune system in older adults is usually blamed on the aging process. But a new study by Columbia immunologists shows that decades of particulate air pollution also take a toll. The study found that inhaled particles from environmental pollutants accumulate over decades inside immune cells in lymph nodes associated with the lung, eventually weakening the cells’ ability to fight respiratory infections.

In summary, air pollution can lower your immune system.

Air pollution can cause the accumulation of inhaled particulates in lung-associated lymph nodes, compromising immune surveillance

The accumulation of inhaled particulates in the lymph nodes is associated with a reduction in immune function. The particulates accumulate in macrophages, a type of immune cell that is responsible for engulfing and destroying harmful substances. The macrophages containing particulates are less capable of ingesting other particles and producing cytokines, which are chemical signals that activate other parts of the immune system.

The accumulation of particulates in the lymph nodes is thought to be due to the composition of the particulates, which can include microbial molecules such as lipopolysaccharide and fungal spores, as well as organic compounds and heavy metals. These components can trigger cellular signalling pathways, such as the Toll-Like Receptor 4 (TLR4) pathway, and induce oxidative stress, leading to inflammation and reduced immune function.

The effects of air pollution on the immune system are particularly relevant in the context of respiratory infections, such as COVID-19 and influenza, as older individuals are more vulnerable to these infections. The accumulation of particulates in the lymph nodes may contribute to the increased susceptibility to respiratory infections in older individuals.

Overall, the available evidence suggests that air pollution can compromise immune surveillance by causing the accumulation of inhaled particulates in lung-associated lymph nodes, leading to a reduction in the function of immune cells.

Air pollution can lead to a reduction in the activation of macrophages and their ability to produce cytokines

Research has shown that exposure to air pollution can have a detrimental impact on the function of macrophages. In one study, it was observed that macrophages containing particles of air pollution were less effective at generating inflammatory signals known as cytokines and ingesting other particles. This impairment in macrophage function can have significant implications for the body's immune response and its ability to defend against pathogens.

Furthermore, air pollution has been found to accumulate in macrophages in lung-associated lymph nodes over time. This accumulation can compromise immune surveillance and directly affect immune cell function and lymphoid architecture. The impact of air pollution on macrophages and cytokine production is particularly relevant in the context of respiratory infections, where a well-functioning immune system is essential for defence against pathogens.

The effects of air pollution on macrophages and cytokine production are not limited to the respiratory system. Air pollution has also been associated with skin inflammation and the development of conditions such as allergic contact dermatitis, atopic dermatitis, and skin cancer. Additionally, air pollution can impact the central nervous system, potentially contributing to cognitive deficits, psychiatric disorders, and neurodegenerative diseases.

Overall, the available evidence suggests that air pollution can lead to a reduction in the activation of macrophages and their ability to produce cytokines, with potential implications for both the innate and adaptive immune systems. Further research is needed to fully understand the mechanisms underlying these effects and to develop strategies to mitigate the impact of air pollution on immune function.

Air pollution can have a detrimental effect on the immune system, particularly the immune organs associated with the respiratory tract

The respiratory tract is the primary site of exposure to air pollution, which consists of gaseous components and particulate matter (PM). The respiratory tract, from nasal passages down through the airways to alveolar gas exchange units in the lungs, represents the prime interface between the immune system and the airborne environment. Inhaled particulates and gases interact with epithelial cells lining the airways and professional immune cells within the airways. These cells sense and can be 'stimulated' by air pollution as pollution constituents trigger cellular signalling pathways. Stimulated cells act as part of multicellular immune responses, and perturbation of these can cause disease.

The immune system itself consists of multiple types of immune cell that act together to generate (or fail to generate) immune responses. Common themes that emerge are the capacity of air pollutants to stimulate pro-inflammatory immune responses across multiple classes of immune cell. Air pollution can enhance T helper lymphocyte type 2 (Th2) and T helper lymphocyte type 17 (Th17) adaptive immune responses, as seen in allergy and asthma, and dysregulate anti-viral immune responses.

The primary site of exposure to air pollution is the respiratory tract following inhalation. The respiratory tract, from nasal passages down through the airways to alveolar gas exchange units in the lungs, represents the prime interface between the immune system and the airborne environment. Inhaled particulates from environmental pollutants accumulate in macrophages in lung-associated lymph nodes over years, compromising immune surveillance via direct effects on immune cell function and lymphoid architecture.

The intake and the uptake represent the two major processes by which a chemical can cross the body from outside. Intake is typically associated with inhalation, eating, or drinking, whereas uptake occurs by dermal contact, through skin absorption. Air pollutants, such as SO2, NOx, CO, PM, and heavy metals, affect the respiratory system and a positive association between air pollution and lung cancer risk and mortality has been demonstrated in several epidemiological studies, particularly in individuals with existing lung disease.

The second process by which a chemical can cross the human body is the uptake that involves skin absorption. Skin is a dynamic barrier of the human body able to maintain the internal homeostasis through neuropeptides, cytokines, hormones, and other effector molecules of the endocrine, immune, and nervous systems. In industrialized countries, hypersensitivity reactions are, by far, the most frequently reported immune-derived effects of chemicals in humans. Major air agents which affect the skin are solar ultraviolet radiation (UV), PAHs, volatile organic compounds, NO2, PM, cigarette smoke, O3, heavy metals, and As. Air contaminants can bind the stratum corneum, may permeate the epidermal barrier, and may enter the systemic circulation. In their passage through the epidermis, they can be metabolized, giving rise to reactive metabolites. The structural and functional integrity of the epidermis may be directly damaged or impaired through indirect phenomena, including inflammation.

Air pollution can also influence skin integrity and may have a significant adverse impact on the immune and nervous system. Exposure to air pollution starts in utero before birth, potentially causing delayed chronic diseases arising later in life. There are, indeed, time windows during the life of individuals who are more susceptible to air pollution exposure, which may result in more severe outcomes.

The effects of air pollution on the immune system are particularly evident in the elderly. Elderly people are especially vulnerable to respiratory infections, a fact brought into stark relief by the COVID pandemic. The death rate from COVID is 80 times greater in people over age 75 than in younger adults, and the elderly are also more vulnerable to influenza and other infections of the lung. The diminished power of the immune system in older adults is usually blamed on the aging process. However, a new study by Columbia immunologists shows that decades of particulate air pollution also take a toll.

The study found that inhaled particles from environmental pollutants accumulate over decades inside immune cells in lymph nodes associated with the lung, eventually weakening the cells’ ability to fight respiratory infections. The macrophages containing particulates were significantly impaired: they were much less capable of ingesting other particles and producing cytokines—chemical "help" signals—that activate other parts of the immune system. Macrophages in those same lymph nodes that did not contain particulates were unimpaired.

In sum, air pollution plays mainly a pro-inflammatory role that could include direct oxidative effects of O3 or induction of ROS. Some variability of these effects was shown among the different exhausts and particles investigated, suggesting that distinct physiochemical properties could arise from different materials generated and collected in specific conditions.

Air pollution can increase the susceptibility of elderly individuals to respiratory infections and other lung diseases

The accumulation of inhaled particulates in the lungs has been shown to increase with age, with a notable increase after the age of 40. This accumulation of particulates in the lungs has been shown to impair the immune system's ability to fight respiratory infections.

The elderly are especially vulnerable to respiratory infections, as seen during the COVID pandemic, where the death rate from COVID was 80 times greater in people over 75 than in younger adults. This increased susceptibility to respiratory infections and other lung diseases, such as chronic obstructive pulmonary disease and cancer, has been attributed to senescent changes in immune cells, which result in systemic inflammation and functional impairments in adaptive immunity.

The effects of air pollution are cumulative and can account for the worse outcomes of respiratory infections in elderly individuals compared to younger populations. The study of the effects of air pollution on the immune system is vital to understanding how pollution causes disease and how that pathology could be abrogated.

Air pollution can cause a reduction in the phagocytic capacity of macrophages

Alveolar macrophages are one of the predominant cell types that process and remove inhaled PM by secreting pro-inflammatory mediators from the lung. Exposure to air pollutants can reduce macrophage phagocytosis, as well as increase macrophage apoptosis.

The ability of macrophage phagocytosis is reduced by exposure to air pollutants. This is due to the direct generation of oxidants (reactive oxygen species) and a reduction in endogenous antioxidants, which leads to increased oxidative stress. This stimulation of oxidative stress by PM contributes to both its organic and metal components. Oxidative stress after PM exposure initiates cellular responses, including the activation of the mitogen-activated protein (MAP) kinase cascade and NF-κB signaling to enhance the production of inflammatory cytokines, which causes further cell injury or apoptosis.

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