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Pollution Air Your Relationship System Immune Stress, and Between The



  • Pollution Air Your Relationship System Immune Stress, and Between The
  • Journal of Toxicology
  • 3 days ago The Relationship Between Stress, Air Pollution and Your Immune System | Online. When we hear about stress we assume it is linked only to life. Similarly, immune responses elicited by exposure to air pollutants are mediated by The strongest evidence of a link between pollutants and respiratory tract studies limits our ability to determine whether this was due to the pollutants acting on Dysfunction of the innate immune system and TLR signaling has been. Oct 30, Then, the scope of our review is narrowed to the research related to the impact of Prolonged activation of the immune system resulting in chronic . Association between air pollution and autoimmunity has also been found.

    Pollution Air Your Relationship System Immune Stress, and Between The

    In addition, circulating cytokines that are released by inflamed peripheral organs or endothelial cells could stimulate peripheral innate immune cells, activate peripheral neuronal afferents, or enter the brain by diffusion and active transport thereby worsening the condition synergistically [ 27 , 28 ]. This system could also be exploited in combination with exposure to other environmental toxins and air pollutants.

    Circumventricular organs are specialized brain structures located around the third and fourth ventricle. They are highly vascularised and lack a BBB; therefore, they allow for a direct uptake of chemicals circulating in the blood stream by neuronal cells [ 31 ].

    The very small UFPs on the other hand easily penetrate cell membranes because of their large surface-to-volume ratio, which also enables them to traverse the classical barriers in the lung and the brain.

    Their ability to cross cell membranes easily explains why PM can be found inside neurons or erythrocytes [ 1 , 32 ]. It has also been proposed that the close contact between endothelial cells and erythrocytes could represent a route for the exchange of PM between activated endothelial cells and UFP-loaded erythrocytes [ 1 , 33 , 34 ].

    Another important and more direct route for UFPs to enter the nervous system is through the olfactory mucosa, which is a neuronal epithelium that is in direct contact with the environmental air [ 35 — 37 ]. Thus, fine and UFPs may reach the brain through olfactory receptor neurons or the trigeminal nerve.

    Olfactory receptor neurons are bipolar sensory neurons that mediate the sense of smell by conveying sensory information from the nose to the CNS. The olfactory epithelium is covered by a layer of sustentacular cells, but olfactory sensory neurons extend their dendrites into the mucous layer covering the olfactory epithelium where they directly interact with odorants inhaled with the air.

    Nasally inhaled pollutants that reach the olfactory mucosa could enter the cilia of olfactory receptor neurons by pinocytosis, simple diffusion, or receptor-mediated endocytosis. Once incorporated into sensory neurons, they could be transported by slow axonal transport along the axons to the olfactory bulb [ 38 ].

    From there, pollutants could be transported further into the CNS along mitral cell axons that project from the olfactory bulb to multiple brain regions, including the olfactory cortex, the anterior olfactory nucleus, the piriform cortex, the amygdale, and the hypothalamus.

    Accordingly, UFPs have been observed in human olfactory bulb periglomerular neurons and trigeminal ganglia capillaries [ 10 ]. Similarly, a decreasing gradient of metal vanadium and nickel deposition and accompanying tissue damage from the nose to the brain has been reported in the canine nervous system, confirming the importance of the nasal route for the entry of air pollutants into the CNS [ 39 ]. Controlled exposures of rats to UFPs and metals also demonstrated their accumulation in the olfactory bulb [ 40 — 42 ].

    Taken together, these findings suggest that NPs can be taken up directly by the olfactory mucosa and enter the CNS or the cerebrospinal fluid by bypassing the circulatory system [ 12 ]. Uptake through the nose might even be enhanced by additional pollutant-induced systemic inflammation by deteriorating the olfactory mucosal barrier, which would result in increased neuropathology. Additional direct neuronal entry routes for NPs have been described that involve the retrograde and anterograde transport in axons and dendrites such as the transport of inhaled NPs to the CNS via sensory nerve fibers that innervate the airway epithelia [ 12 ].

    Ground-level ozone exposure activates the CNS through the vagal nerves without the involvement of the thoracic spinal nerves [ 43 ]. Even though the translocation rate of NPs from their site of entry to secondary organs might be rather low, continuous or chronic exposure to NPs may result in their accumulations in the brain as a secondary target organ in significant amounts [ 12 ].

    Thus, it is also important to obtain data on the retention characteristics of NPs in both primary and secondary target organs, including associated elimination and clearance pathways [ 12 ]. It is conceivable, however, that CSF circulation provides an excretory pathway for NPs that enter via neuronal uptake. Usually, the CSF serves as a fluid cushion for the brain, but also distributes substances to all brain regions and acts as an elimination route for metabolic waste products [ 45 ].

    NPs could be eliminated from the CSF through the same mechanisms: The exact details of NP clearance from the brain, however, await future investigation [ 12 ].

    Results about the direct effects of air pollutants and airborne particles on neuronal cells have been reported from experimental studies in vitro , using cell culture systems and in vivo , using inhalation and instillation paradigms in rodents as well as from epidemiological and controlled clinical studies in humans.

    A variety of in vitro studies assessed the potential toxic effects of air pollutants Table 1 , by measuring changes in cell viability, alterations of apoptosis, the dysfunction of mitochondria, the production of reactive oxygen species ROS , or the production of pro-inflammatory cytokines as sensitive identifiers [ 1 ]. Varying degrees of proinflammatory- and oxidative stress-related cellular responses and decreased cell viability were reported upon stimulation with laboratory-generated or filter-collected ambient air particles in different cell culture systems [ 42 ].

    Of particular interest are studies utilizing neuronal and microglial cell lines or primary cultures of those cells that were exposed to concentrated ambient air particles CAPs , diesel exhaust particles DEPs , toxic gases, such as ozone, bacterial endotoxins, such as LPS, or toxic elements, such as manganese. All investigated neuronal, glial or cerebral endothelial cell types were shown to be targets of the toxic effects of air pollutants [ 46 — 48 ].

    However, the underlying mechanisms could be rather complex, and some insight into the interaction of different cell types was derived from coculture systems. For instance, it was shown that the neurotoxic effects of DEPs on dopaminergic neurons could be either direct or indirect via the release of inflammatory mediators and ROS from activated microglial cells [ 46 , 49 ].

    Interestingly, pretreatment of neuron-glia cocultures with LPS increased the vulnerability of the cells to the toxic effects of DEP, while DEPs alone were not harmful [ 49 ]. An important aspect of in vitro toxicity studies is the establishment of dose-response relationships. Transcriptomic and proteomic profiling of cultured cells upon exposure to CAPs may provide insights into alterations of gene and protein expression.

    One such study demonstrated the upregulation of inflammatory and innate immunity pathway components in mouse immortalized BV2 cells when exposed to CAPs [ 50 ]. Likewise, the expression profiles of microRNAs, which emerged as crucial mediators of posttranscriptional gene regulation, might change during exposure to air pollutants [ 51 ]. Indeed, hexahydro-1,3,5-trinitro-1,3,5-triazine RDX , a common environmental contaminant and explosive nitroamine that is widely used in military ammunition, has been shown to change brain microRNA expression in exposed mice [ 52 ].

    The rapidly growing number of engineered nanoparticles ENPs and nanomaterials NMs might also contribute to air pollution as new nanotechnologies are constantly developed, and NMs are used increasingly in daily life through the advent of new products.

    In addition, ENPs are extensively tested for their usefulness in medical diagnostic and therapeutic applications. Although no human ailments have been directly attributed to NMs so far, preliminary experimental studies indicate that NMs could initiate adverse biological responses and that NPs could have toxicological properties [ 53 ].

    For instance, titanium dioxide, aluminum oxide, and nanosized silica particles were shown to decrease cell viability and to increase apoptosis in neuronal and endothelial cell cultures [ 54 — 58 ]. These substances also increased the amount of ROS, which resulted in concomitant activation of microglia [ 54 — 59 ]. An important point in in vitro nanoneurotoxicity studies is therefore the necessity to accurately characterize particle size, as particles of different size might exert different effects or similar effects to different degrees.

    In addition, a controlled investigation of the physicochemical properties of the NPs over time and their interactions with culture media should also be considered [ 60 , 61 ]. Although NPs in environmental air samples might be much more heterogeneous, epidemiological and toxicological studies with airborne ultrafine particles can be viewed as the basis for the expanding field of nanotoxicology [ 42 ]. In vitro studies bear several distinct advantages for studying neurotoxic effects of air pollutants because the technology is cheap, the cultured cells grow rapidly, and the assays provide reproducible results.

    However, many times immortalized cell lines are used, which might not correctly reflect the more complex responses of native CNS cells or of neurons in their natural complex environment. Unfortunately, long-term and large-scale cultures of primary CNS cells are still challenging and thus might not be useful for high-throughput screening of toxicological effects.

    The emerging field of induced pluripotent stem cells, which can be easily derived from somatic cells such as dermal fibroblasts and keratinocytes, may provide a solution to this problem and induced pluripotent stem cells could soon emerge as a novel experimental paradigm for human neurotoxicity studies [ 62 , 63 ]. Despite their advantages, in vitro studies have also important limitations, some of which are methodological. The interpretation and cross-comparison of results from different research groups might be hampered because of the use of particles with different chemical compositions or different culture cells.

    The duration of exposure and concentrations might differ across laboratories. More importantly, however, responses of cultured cells might not faithfully reflect the responses of the entire body system or target organ.

    In general, ultraphysiological doses of air pollutants are used in cell cultures studies and the long-term study of the effect of chronic exposure to low doses of potentially toxic material is not feasible. Organotypic cell cultures and tissue explant cultures might be more useful in this regard since the integrity of tissue of interest is fully or partially preserved. Because systemic effects and biodistribution of air pollutants cannot be investigated in in vitro assays, in vivo studies provide additional and important information on the adverse effects of air pollutants.

    The confirmation of in vitro results through realistic in vivo studies is mandatory to validate hypotheses generated from in vitro studies [ 12 ]. In vivo studies are invaluable tools for the examination of bio-distribution, the biokinetic properties, and the pathophysiological effects of air pollution on the whole body system.

    They also provide an opportunity to study neurobehavioral effects of air pollution in intact living animals. Novel noninvasive imaging techniques can be used to visualize neuroinflammation, microglia activation, brain redox-status, and BBB integrity in live animals [ 64 , 65 ]. Importantly, in vivo studies allow the use of experimental conditions, routes of administration, and exposure regimes that are not available in cell culture systems.

    For instance, they enable a comparison of the effects of acute, subchronic, and chronic exposure of the whole animal. Likewise, pollutants can be administered through different natural and artificial routes such as inhalation, nasal and intratracheal instillation, or intraperitoneal injection Table 2. Like cell culture studies, whole animal studies are amenable to investigate alterations in gene and protein expression, and activation of signaling pathways upon exposure to air pollutants.

    Finally, prevention strategies and therapeutic approaches can be tested in a preclinical setting. To investigate the effect of certain gene products on the susceptibility to damage by air pollutants, genetically modified animals can be used. In a more recent study, these findings were confirmed, providing evidence that air pollution can produce neuropathological damage in individuals that are susceptible to oxidative stress [ 68 ].

    Six hours after instillation, the mice were intraperitoneally injected with the bacteria cell wall component lipoteichoic acid LTA and the authors could show that LTAtreatment potentiates CB-induced neurological effects. In a recent study by Zanchi et al. ROFA instillation alone induced an increase in lipid peroxidation levels in the striatum and the cerebellum, whereas NAC treatment had preventive effects.

    Ozone is by far the most important air pollutant in terms of its concentration, its persistence, and its ubiquitous occurrence. A list of preclinical studies that investigated the neurotoxic effects of ozone inhalation using different experimental paradigms is given in Table 2. The data suggest that chronic ozone inhalation produces oxidative stress and loss of dopaminergic neurons in the substantia nigra and that the effects can be reduced by treatment with 17[beta]-estradiol [ 71 , 76 ].

    Neural mechanisms underlying adaptive responses to acute ozone exposure were also studied in adult rats that were subjected to 0. In this paradigm, acute ozone exposure had an effect primarily on glial cells in the CNS [ 79 ]. The protein expression levels of vascular endothelial growth factor VEGF were upregulated in central respiratory areas, such as the nucleus tractus solitarius NTS and the ventrolateral medulla VLM. Persistent VEGF upregulation following ozone exposure may contribute to brain repair and consecutive functional adaptations.

    Rats that inhaled 0. It also promoted neuronal activation in other, stress-responsive regions of the CNS as could be demonstrated by up-regulated levels of the immediate early-gene product c-Fos [ 43 ].

    As exemplified above, in vivo studies offer a unique possibility to test the potential of neuroprotective agents such as hormones and antioxidants against air pollutants [ 71 , 73 , 76 , 78 ]. Selective inhibitors of the cyclooxygenase-2 COX-2 enzyme have been tested in young healthy dogs which were residents of highly air polluted urban regions.

    Interestingly, treatment with dark chocolate has also been found to be neuroprotective against long-term air pollution in mice [ 44 ]. Despite the clear advantages of in vivo studies that were summarized here studying pathophysiological mechanisms or neurobehavioral responses and testing preclinical preventive and treatment strategies , a long list of confounding parameters experimentally may obscure the results. Methodological details such as sex, age, strain, dose, and the particular assay that was used to measure the outcome should be considered carefully when comparing results across different studies.

    In particular body size, age, gender, species, and strain are known to have dosimetric effects in air pollution research [ 81 ]. Although there is growing epidemiologic evidence that associations between air pollution and respiratory health differ between females and males, comparative studies or studies on female rodents in general are limited [ 72 , 82 ].

    Likewise, only a single study evaluated the influence of age on air pollution-induced CNS injury [ 78 ]. In this study, ozone inhalation resulted in high-lipid peroxidation in the frontal cortex of old rats, which is in contrast to findings in young rats, where oxidative stress injury occurred in the hippocampus. Region specific inflammation and alterations in gene expression were also seen after DEPs exposure, suggesting a selective vulnerability of specific neuronal subpopulations similarly to the selective loss of specific neurons that is typical for certain neurodegenerative diseases [ 69 , 83 ].

    Although strain difference is an important variable in a variety of lung injury studies, it is a widely neglected parameter in air pollution-induced CNS injury research [ 84 , 85 ]. Variations in the geographic location of sample collection, and seasonal climate variations during the collection of ambient air samples are neglected oftenly as well.

    However, these parameters have a crucial impact on the results and should be clearly described in all studies. Use of filtered ambient air samples may, on one hand, simulate real-world exposure conditions, on the other hand, the samples also contain unidentified or unmeasurable components.

    Thus, the inherent heterogeneities of in vivo experimental paradigms show a need for standardization of test parameters that enables a more reliable comparison between studies from different laboratories. The lack of such a standardized system also hampers the translation of data from preclinical studies to humans. In particular, the anatomy of the respiratory tract and the nasal cavity, the breathing pattern nasal breathing is obligatory for rodents , and brain anatomy differ greatly across species and impede generalization of the results.

    The use of nonhuman primates would provide results more relevant to humans, but poses great ethical concerns. While cardiorespiratory effects of air pollution have been extensively investigated [ 3 ], only preliminary findings are available on the effects of airborne pollutants on the CNS. Stroke is one of the most prevalent CNS disorders which can be caused by air pollution. A relationship between air pollution and stroke was first reported after the Great London fog [ 8 ], but similar results were obtained from different geographic regions that include Canada, Japan, Italy, Sweden, USA, UK, France, Taiwan, and Korea [ 86 — 95 ].

    However, a one-to-one comparison of these studies is difficult because each study measured different pollutants, investigated populations with different genetic background, or people exposed to different environmental conditions, in addition to evaluating different stroke-related parameters. Despite the experimental differences, a large number of studies demonstrated a positive correlation between stroke mortality rates, hospital admission, and outdoor pollution [ 87 — 90 , 92 — 95 ], although contradictory results were reported as well [ 91 , 96 ].

    Interestingly, a Canadian study showed that only a specific subgroup of patients, those suffering from diabetes mellitus, was at high risk for ischemic stroke [ 91 ]. Age and gender may also differentially affect the risk of air pollution-related ischemic stroke. Elderly people and women appear to be more sensitive to the effect of air pollutants [ 87 ]. It also appears that the air pollution-related ischemic stroke risk is higher than the risk for hemorrhagic stroke [ 8 , 86 ].

    Hemorrhagic and ischemic strokes have distinct pathogenesis and also differ in terms of other risk factors. Mechanistically, the correlation between air pollution and stroke might be due to the observation that fine PM and UFPs exert procoagulant effects in vivo [ 97 , 98 ]. Yet, the stroke risk increases with both, short-term and long-term exposure to outdoor air pollution [ 90 , 99 ], although the effects of long-term exposure on stroke risk are less prominent [ 99 ].

    In addition to these epidemiological findings, a limited number of in vivo studies also support a close correlation between air pollution and stroke.

    For instance, SO 2 inhalation caused cerebral changes similar to the alterations resulting from middle cerebral artery occlusion MCAO and aggravated histological changes in ischemic brain regions [ ].

    Air pollution will continue to become a major health problem, especially in developing countries and rapidly growing economies.

    Unfortunately, booming economic development increases air pollution and related disease including stroke.

    Thus, there is a great demand to organize population-based and prospective studies to evaluate and to develop preventive measures against the unfavorable effect of air pollution on severe cerebrovascular diseases, such as ischemic stroke.

    Concomitant with a general increase in life expectancies worldwide, the incidence and prevalence of common neurodegenerative diseases grow as well, thereby increasing the financial and social burden on individuals and society. AD is the most common cause of dementia in aged people, affecting 27 million people globally. Most AD and PD cases are sporadic, and age is the leading risk factor.

    The etiologies of the diseases, however, are multifactorial, and the risk factors include environmental factors and genetic predisposition. Environmental exposures to metals, air pollution, and pesticides as well as nutritional factors are common risk factors for neurodegenerative diseases [ ].

    Although different neurodegenerative diseases have distinct pathologies and clinical presentations, they often share common mechanisms such as protein aggregation, oxidative stress injury, neuroinflammation, microglial activation, apoptosis, and mitochondrial dysfunction, which ultimately result in the loss of specific neurons [ , ].

    Accumulating evidence suggest that exposure to air pollution can trigger these common denominators of neurodegenerative diseases and lead to neuropathology. The first histopathological evidence for a link between air pollution and neuropathology came from studies that were carried out on animal populations that are naturally exposed to polluted urban environments in Mexico City [ 1 ].

    Breakdown of nasal and olfactory barriers, alterations in the BBB, and degeneration of cortical neurons were observed even in animals that were younger than 1 year of age. With growing age, and therefore extended exposure, the dogs exhibited reactive astrogliosis, white matter glial cell apoptosis, ApoE immunoreactivity in vascular cells, and nonneuritic plaques and NFTs.

    These findings suggest an accelerated AD-like neuropathology in chronically exposed animals. Feral dogs naturally exposed to urban air pollution also showed DNA damage in olfactory and hippocampal genomic DNA [ 39 ]. Animals from polluted areas exhibited deposits of diffuse amyloid plaques a decade earlier than control animals from less-polluted regions [ 39 , ].

    Although most animals do not develop the full human pathology of AD, aged dogs are known to suffer from cognitive dysfunctions that resemble key aspects of AD [ ]. However, dense core neuritic plaques and NFTs could not be observed consistently in the dogs. Because of the numerous atmospheric contaminants found in the highly polluted air of Mexico City, postmortem studies on resident feral dogs could only link the neuropathology to the complex mixture of ozone, PM, LPS, and unmeasurable air pollutants [ 14 ].

    However, the oil-combustion PM-associated metals nickel and vanadium, as well as UFPs were detected in the dogs brains, indicating that brain uptake of metals and UFPs may occur in natural exposure settings [ 11 , 39 ].

    Similar findings were recently observed in postmortem examinations of human samples and in laboratory animals [ 1 , 14 ]. Based on evaluation of the clinical medical records and information from relatives and coworkers by 2 physicians, each subject was considered cognitively and neurologically fit when alive [ 9 ].

    The neuropathology, however, could be observed in subjects as early as in the second decade, suggesting that neuropathologies induced by chronic exposure to high levels of air pollution share similarities with the pathology of AD [ ].

    Dopaminergic neurons were found to be selectively vulnerable to DEPs both in vitro and in vivo [ 46 , 49 ]. However, a recent epidemiological study from Canada did not support a direct link between the markers of traffic-generated air pollution and PD, although an association between ambient manganese pollution and the risk of physician-diagnosed PD was reported [ ].

    A further interesting similarity between air pollution-induced neuropathologies and neurodegenerative disorders is the early involvement of the olfactory bulb [ ]. Yet, olfactory dysfunction is also among the first clinical signs of AD and PD [ ]. In sporadic PD, olfactory impairment precedes motor symptoms by years and is independent of the loss of dopaminergic neurons.

    In AD, however, olfactory dysfunction and disease progression correlate [ ]. Recent epidemiological studies combined with psychological tests support an association between chronic exposure to traffic-related air pollution and decreased cognitive function in both genders [ , ]. Altogether, these findings warrant further and more extensive epidemiological, forensic, and toxicological studies that aim to understand the association between chronic exposure and the risk of neurodegenerative diseases development.

    Such efforts may lead to the development of preventative strategies for these devastating diseases in certain risk groups. Normal brain development is a complicated process that involves controlled cell proliferation, neuronal migration from their place of birth to their final location, and the establishment of specific connections between neurons and target tissues [ ].

    All of these processes are tightly controlled, but are also influenced by environmental conditions. Evidence is accumulating that indicates that psychosocial stress, especially chronic stress, worsens the effects of air pollution 2. Possibly that is because in the fight or flight mode, the body cannot deal effectively with the microparticles in the blood. There are types of pollutions that are created by natural causes such as volcanoes and wildfires. They cause a lot of air pollution such as ashes and volcanic ash.

    Then human beings create most of the air pollution that is causing problems in both cities and rural areas. They do this through emissions from factories, farm chemicals, construction materials, car emissions, coal burning, wood burning, kerosene lighting, aeroplane fumes, aerosols, and second-hand cigarette smoke. Air pollution is particularly high in large cities. Sometimes the pollution appears as a cloud that makes the air murky. This is known as smog.

    In the developed world this is no longer a problem except a few cases such as Los Angeles, California in the US. The problem of smog is more common in the large cities in poor and developing countries such as Beijing, China, Cairo in Egypt and New Delhi in India.

    Children tend to be very active, more active than adults through play and sports. So they breathe more rapidly and take in more pollutants than adults do. Also, they tend to breathe through their mouths, bypassing the air filters in the nose, and allowing more pollutants to enter the body. Not forgetting that children spend more time outdoors in summer when smog levels are highest, again breathing in more pollutant than adults. It is possible for children exposed to high levels of air pollutants to suffer from permanent damage and long term problems like coughing, wheezing, chest congestion, allergies, asthma, shortness of breath, painful breathing and bronchitis.

    It is obvious that air pollution, stress and the immune system are closely linked. In order to protect our immune system, especially that of growing children, we must take steps to reduce air pollution in our environment. For example, we can install air purifiers in our homes to reduce the load of particulates that we inhale. We can invoke the health and safety laws of our countries and states and request air purifiers at work as well.

    I am assuming that in every company there is a health and safety officer who can take up the request and speak to management about it, reminding them that a healthy workforce is a productive workforce. Another thing that we can do is to reduce how much vehicle emissions we breathe in. For example, when we speak to the drive-through bank teller or fast food clerk, we can switch off the engine to prevent car fumes from getting into the car. Also, we can take time out to exercise away from busy roads and busy intersections in order to stay fit and to reduce stress levels.

    By reducing stress levels we reduce our susceptibility to the effects of air pollution. Also, by staying fit we improve our immune systems and our ability to withstand the effects of air pollution. In winter the cold air tends to keep polluted air close to the ground instead of allowing it to move away, so air pollution tends to increase in winter.

    If the pollution level is high outside, then stay indoors as much as possible to avoid breathing in pollutants. Of course, indoors you must have air filters installed. Whenever air pollution levels are low, and whether it is hot or cold outside, open windows to let out accumulating carbon dioxide which will make you feel lerthagic. If you can, even take a walk whenever air pollution is low in your area and during weekends take a hike in the hills far from polluted areas. Circulation, Vol 7.

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    Silica phagocytosis causes apoptosis and necrosis by different temporal and molecular pathways in alveolar macrophages. Silica accelerated systemic autoimmune disease in lupus-prone New Zealand mixed mice.

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    Airway antioxidant and inflammatory responses to diesel exhaust exposure in healthy humans. Inhalation of diesel exhaust enhances allergen-related eosinophil recruitment and airway hyperresponsiveness in mice. Mechanisms of particulate matter toxicity. In vitro effect of cadmium on the function of human lymphocytes and neutrophils. Ambient particulate pollutants in the ultrafine range promote early atherosclerosis and systemic oxidative stress. Experimental exposure to wood-smoke particles in healthy humans: Effects on markers of inflammation, coagulation, and lipid peroxidation.

    Particulate matter air pollution stimulates monocyte release from the bone marrow. Interaction of alveolar macrophages and airway epithelial cells following exposure to particulate matter produces mediators that stimulate the bone marrow. J Expo Anal Environ Epidemiol.

    Flow cytometric characterisation of antigen presenting dendritic cells after in vitro exposure to diesel exhaust particles. Becker S, Soukup J. J Toxicol Environ Health, A. Diesel exhaust particle-exposed human bronchial epithelial cells induce dendritic cell maturation and polarization via thymic stromal lymphopoietin.

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    Journal of Toxicology

    Stress, especially chronic stress, can weaken the body's immune system. Past studies have identified a link between exposure to ambient air pollution and. Nov 15, Entry of Air Pollutants into the Central Nervous System creating local oxidative stress or by causing proinflammatory effects similar to those seen in lung tissue. responses directly by activating the brain's innate immune system. .. A relationship between air pollution and stroke was first reported after the. A small number of studies have found an association between air pollution between the pollutants and the developing intestine and immune system. . stress and increased permeability to solutes In this way, the pollutants . EW conceived of the review, participated in its design, and helped to draft the manuscript.




    Stress, especially chronic stress, can weaken the body's immune system. Past studies have identified a link between exposure to ambient air pollution and.


    Nov 15, Entry of Air Pollutants into the Central Nervous System creating local oxidative stress or by causing proinflammatory effects similar to those seen in lung tissue. responses directly by activating the brain's innate immune system. .. A relationship between air pollution and stroke was first reported after the.


    A small number of studies have found an association between air pollution between the pollutants and the developing intestine and immune system. . stress and increased permeability to solutes In this way, the pollutants . EW conceived of the review, participated in its design, and helped to draft the manuscript.


    Mar 21, homeostasis of the body and its immune system. . Air Quality Index and their relationship with oxidative stress biomarkers in epithelial cells.


    Aug 15, Particle Pollution and Your Patients' Health Mobilization of the pulmonary immune system and other defense mechanisms is The study shows an association between improvements in air quality in southern California and temperature, allergens, viral infection, stress, and inhalation of air pollutants.


    Jun 25, The innate immune system is one of the first lines of defense against or oxidative stress pathways may contribute to the diverse range of the One pathway implicated in the response to inhaled air pollutants is for the association between air pollution and TLR activation has yet to be clearly identified.

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