Effect of Air Pollution and Neurological Dsease

 

Ref

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).

Effects of Air Pollution and Endocrine Disease

 

Ref

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,*

Endocrine Disease

The known effects of cigarette smoke on reproductive and thyroid hormones provide indications of the risks associated with PM exposure.

 Cigarette smoke is a risk factor in Graves hypothyroidism and is associated with elevated plasma cortisol, aldosterone, adrenal androgens and impacts female fertility by increasing steroid hormone binding globulin and decreasing circulating free estrogens (83–86). 

Several PM species have been identified as endocrine disrupting chemicals (87).

 In humans PM exposure is linked to insulin resistance, elevated circulating adipokines, hypothyroidism and (mixed) estrogenic effects (88). 

Thyroid hormones triiodothyronine (T3) and thyroxine (T4) regulate metabolic rate, cardiovascular tone and promote growth rate during fetal development and early life (89).

 In humans, PM exposure is associated with decreased plasma T4 both in pregnant women and new-borns, as well as congenital hypothyroidism and reduced infant birth weight (90). 

Black carbon, ammonia, organic matter and nitrate PM species appear to have the strongest links to thyroid dysfunction (91–94). 

Effective insulin signaling is required for glucose homeostasis, and insulin resistance is closely associated with obesity and is a risk factor for the onset of type-2 diabetes (95).

 PM exposure is associated with insulin resistance and non-alcoholic fatty liver disease, driven by oxidative stress and dyslipidaemia (96, 97).

 Together these studies highlight the link between air pollution and metabolic diseases including diabetes. Of >106 chemicals to which gas and oil extraction workers are exposed, 21 have been shown to exert estrogenic, androgenic and/or steroidogenic effects (98).

 Some chemicals identified as impacting endocrine function include benzene, toluene, ethylbenzene xylene, mercury, polychlorinated dibenzodioxins (PBDDs) and several polycyclic aromatic hydrocarbons (PAH) (88, 98, 99).

 Atmospheric sources of PAHs are vehicle emissions and biomass and coal combustion. Low molecular weight PAHs are in gas phase whereas high molecular weight PAHs are bound to the surface of PM (100). PAHs are classed as endocrine disrupting compounds and have been found to both increase and decrease estrogen receptor mRNA expression and function (REF). Estrogenic dysfunction has been shown to be both direct at estrogen receptors and indirect via aryl hydrocarbon receptor (AhR) signaling (101, 102). 

PBDDs also exert endocrine effects via AhRs, and preclinical experiments have shown AhR-mediated effects of dioxin exposure to include weight loss, reproductive and developmental toxicity, tumorigenesis and immune system dysfunction (103). 

PM contains many metal elements, some of which interfere with estrogenic signaling by mimicking endogenous estrogens (104). Metalloestrogens include aluminum, selenium, antimony, arsenic (arsenite; NaAsO2), barium, cadmium, chromium, cobalt, copper, lead, mercury, nickel, tin and vanadium (vanadate; V2O5) (16, 104).

Obesity and Diabetes

In humans, the association between PM2.5 exposure and obesity is dependent on age, gender and socioeconomic demographic (105, 106).

 A growing body of evidence indicates that PM2.5 exposure is a risk factor for reduced skeletal muscle mass, obesity, diabetes and hypertension (107–109). 

Long-term PM exposure is associated with a high risk for type 2 diabetes, and road traffic-specific PM is correlated with an elevated risk (110). 

Increased incidence of type-2 diabetes remains when adjusted for age, body mass index (BMI), and socioeconomic status (111, 112). 

PM exposure is associated with higher levels of circulating complement factor 3 (C3c), and women with elevated plasma C3c are more susceptible to diabetes than those with low C3c (112). PM2.5 exposure is associated with a faster decline in insulin sensitivity during childhood and higher BMI by age 18 (113–115). 

The associated between PM exposure and hypertension is greater in overweight and obese children (116). In animal studies, exposure of rats to PM increased chocolate consumption whereas in chow-fed wild-type mice, 10-week PM2.5 exposure increased visceral fat mass, insulin resistance and adipose tissue inflammation (117, 118). In mice, short-term PM exposure increased food intake, fat mass and UCP-1 expression in brown adipose tissue (119). PM exposure also induced hypothalamic inflammation indicated by increased microglia density, increased toll-like receptor-4 and elevated inhibitory nuclear factor-kappa-B-kinase-epsilon expression (119). After 12 weeks of PM exposure, mice exhibited increased food intake and elevated fat mass and had lower energy expenditure. Mice had elevated levels of plasma leptin and insulin and increased Homeostatic Model Assessment for Insulin Resistance (HOMA-IR) indicators of insulin resistance (119). This same study also revealed that PM exposure decreased hypothalamic satiety markers, including reduced levels of phosphorylated STAT 3, and diminished proopiomelanocortin expression (119).

PM exposure to mice was found to induce hepatic oxidative stress, inflammation, negatively affect glucose tolerance and induce insulin resistance (96, 120). Interestingly PM exposure has been found to increase hepatic triacylglycerols, free fatty acids and cholesterol levels in female but not in male mice (96). In addition to insulin resistance, PM exposure has been shown to exert toxic effects directly on the pancreas (121). In a streptozotocin-induced mouse model of type-1 diabetes, PM from diesel exhaust fumes exacerbated pancreatic cell vacuolation and islet cell apoptosis, increased pancreatic amylase activity, increased expression of oxidative stress markers 8-isoprostane and superoxide dismutase and reduced levels of the antioxidant glutathione peroxidase (121). In a rat model of gestational diabetes PM exposure induced maternal pancreatic inflammation indicated by diminished pancreatic glucose transporter-2 expression (122).

Air Pollution Particulate matter and Renal Dsease

Ref

. 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

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).

Figure 1.

Open in a new tab

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

Renal Disease

Human kidneys filter ~180 L of blood each day and are therefore vulnerable to PM exposure (21, 72). 

In people, PM2.5 exposure has been linked to an accelerated decline in glomerular filtration rate,

 diminished glomerular function during pregnancy, increased risks of chronic kidney disease, end stage renal disease, renal failure and chronic kidney disease mortality (72–74).

 Human studies have also revealed that PM2.5 exposure to positively correlate with risk of albuminuria; a marker of glomerular disfunction (72).

 A comparison of renal biomarkers in welders and office workers revealed that 

welders - exposed to much higher levels of PM2.5 that office worker controls –

 had elevated plasma markers of renal tubule damage; urinary kidney injury molecule-1 and neutrophil gelatinase-associated lipocalin (75). 

Another study investigating the potential for tubule damage in humans revealed a 10 μg/m³ increase in PM2.5 exposure to be associated with increased nephritis hospital admissions (76).

 PM2.5 exposure is associated with an elevated risk of adverse post kidney transplant outcomes, including acute rejection, graft failure and death (73, 74). 

A study specifically investigating the impact of PM on post-transplant outcomes found a 10 μg/m³ increase of PM2.5 to correlate with a 1.31-fold increase in the odds 

of transplant failure, a 1.59-fold increase in 

odds of delayed graft function and a 1.15-fold increase in all-cause mortality within 1 year of surgery (77). 

A similar study revealed an increase of 1 μg/m³ in PM10 exposure to be associated with increased risk of biopsy proven rejection, graft failure and mortality (78).

 Intratracheal exposure of PM2.5 to immunodeficient mice revealed no obvious renal histopathology. However, PM exposure was associated with elevated serum markers of renal damage including kidney injury molecule-1, cystatin C and uric acid. Moreover, 14-day PM exposure progressively increased renal concentrations of malondialdehyde, hydrogen peroxide, glutathione peroxidase, nuclear factor kappa-β, tumor necrosis factor-α, transcription factor protein-65, NADPH oxidase 4 and heme oxygenase-1 (79). 

In rats, sub-chronic exposure of PM2.5 resulted in elevated plasma β-2-microglobulin and cystatin-C; serum markers of early-stage kidney damage (80–82). 

PM exposure has also been found to induce histopathological lung damage, increase median blood pressure, increase urine volume and water consumption (80–82).

Exposure of rats to diesel emission PM significantly reduced renal blood flow in controls and to a greater extent in rats with adenine-induced chronic kidney disease (81). 

Similar work in a mouse model of adenine-induced CKD revealed that PM exposure elevated renal tumor necrosis factor-α, lipid peroxidation, reactive oxygen species, collagen deposition, necrotic cell counts, dilated tubules cast formation and collapsing glomeruli (49).

 

वायू प्रदूषणाचे शारीरिक परिणाम:

संदर्भ

फ्रंटियर्स इन पब्लिक हेल्थ. २०२२ जुलै १४;१०:८८२५६९. doi: 10.3389/fpubh.2022.882569

वायू प्रदूषणाचे शारीरिक परिणाम:

कणरूप पदार्थ,

शरीरक्रियाविज्ञान आणि रोग

जॅक टी प्रायर १,२, लॅकलान ओ काउली १, स्टेफनी ई सिमंड्स १,*

सारांश

दहापैकी नऊ लोक अशा हवेत श्वास घेतात जी जागतिक आरोग्य संघटनेच्या प्रदूषण मर्यादेची पूर्तता करत नाही.

वायू प्रदूषकांमध्ये वायू आणि कणरूप पदार्थांचा समावेश होतो आणि ते एकत्रितपणे दरवर्षी सुमारे ८ दशलक्ष मृत्यूंसाठी जबाबदार आहेत.

कणरूप पदार्थ हे वायू प्रदूषणाचे सर्वात धोकादायक स्वरूप आहे,

जे दाहक आणि ऑक्सिडेटिव्ह ऊतींचे नुकसान करतात.

प्रभावी रोग प्रतिबंध आणि उपचारांसाठी कणरूप पदार्थांच्या शारीरिक परिणामांची सखोल माहिती असणे आवश्यक आहे.

हा आढावा कणरूप पदार्थांच्या शारीरिक प्रणालींवरील परिणामांचा सारांश देईल आणि शक्य असेल तेथे संबंधित महामारीविज्ञान आणि विषविज्ञान अभ्यासांचा संदर्भ देईल. उपलब्ध माहितीच्या विस्तृत पैलूंवर चर्चा करून,

आम्हाला आशा आहे की हा आढावा विस्तृत वाचकांना आकर्षित करेल आणि मानवी आरोग्यावर कणरूप पदार्थांच्या परिणामांबद्दल काही अंतर्दृष्टी प्रदान करेल.

कणरूप पदार्थ

कणरूप पदार्थ (PM) हे हवेत निलंबित असलेले घन संयुगे आहेत जे श्वास घेण्याइतके लहान असतात (आकृती १).

PM चे वर्गीकरण कणांच्या व्यासानुसार (μm मध्ये मोजले जाते) केले जाते; PM0.1, PM2.5 आणि PM10, तर

वातावरणातील सांद्रता सहसा μg/m3 मध्ये मोजली जाते.

काही PM नैसर्गिक उत्पत्तीचे असतात (वणवे, धूळ, समुद्राची फवारणी, एरोसोल इत्यादी), परंतु मानवनिर्मित PM (डिझेल, कोळसा आणि बायोमास ज्वलन आणि धातू शुद्धीकरण कारखान्यांमधून होणारे उत्सर्जन इत्यादी) आरोग्यासाठी सर्वात धोकादायक असतात (१३).

मानवनिर्मित PM ची वातावरणातील उच्च सांद्रता आणि विषारी व ऑक्सिडेटिव्ह रासायनिक वैशिष्ट्ये त्यांना असमान प्रमाणात धोकादायक बनवतात (१३).

PM च्या मूलद्रव्यीय आणि जटिल रासायनिक प्रजाती विविध प्रकारच्या असतात, ज्यांच्या पृष्ठभागाचा आकार, रसायनशास्त्र आणि प्रभार उत्सर्जन स्रोत आणि पर्यावरणीय परिस्थितीनुसार प्रभावित होतो. PM चे रसायनशास्त्र हवेतील इतर PM सोबतच्या प्रतिक्रियांमुळे बदलू शकते आणि ओझोनच्या ऑक्सिडेटिव्ह परिणामांमुळे व कमी वातावरणीय pH मुळे प्रभावित होऊ शकते (१४, १५).  आकृती १

PM10, PM2.5, आणि PM0.1 च्या सापेक्ष आकारांचे प्रमाणबद्ध चित्रण. संदर्भासाठी, प्रतिनिधी मॅक्रोफेज आणि मायटोकॉन्ड्रिया प्रमाणानुसार समाविष्ट केले आहेत.

संदर्भ

आकृती १

Figure 1.

.

Figure 1.

कृपया लक्षात घ्या की पुनरावलोकन लवकरच सुरू केले जाईल.

Air Pollution and Disease Mechanisms

 Ref

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 SimParticulate Matter

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 (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).

Figure 1.

Figure 1Particulate 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).

Figure 1.

Open in a new tab

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

Open in a new tab

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

Disease Mechanisms

According to the World Health Organization, air pollution and climate change are the collective No. 1 threat to human health (25).

 Air pollution contributes to 9% of all global human deaths, and of these, 58% are from ischemic heart disease and cerebrovascular disease, 18% are from chronic obstructive pulmonary disease and acute lower respiratory tract infections, 6% are from lung cancer. Causes of death in the remaining 18% are mixed and many (12).

 Not all PM equally toxic, with the pathophysiological mechanisms varying between PM species (26).

 PM are mutagenic, can cause oxidative damage, activate inflammatory signal cascades and induce cell death (27–30).

 Toxicological research has investigated the differential oxidative and inflammatory effects of PM species (including black carbon, ammonia, nitrate and sulfate) and PM of varying origin (13).

 A common anthropogenic source of PM is incomplete combustion of diesel, gasoline, coal, and biomass (13).

 Trace metal content significantly contributes to the oxidative potential of PM (13, 26).

 The oxidative effects of PM can damage mitochondria, endoplasmic reticulum and DNA, can be carcinogenic and activate cell death signaling pathways (26).

 Inside cells, iron-based PM can overwhelm superoxide dismutase and glutathione peroxidase activity, inducing ferroptosis (29).

 PM2.5 can activate cytokine-dependent autophagy pathways, signaling through toll-like receptors, the Janus kinase-signal transducer and activator of transcription (JAK-STAT) pathway, and via cyclooxygenase 2-mitochondrial and prostaglandin E synthase. Here, increased tissue levels of C-reactive protein, tumor necrosis factor-α, interleukins 1, 6 and 8 (31–34). Inflammatory, oxidative, and toxic mechanisms are the primary effectors of PM-induced cell damage. Tissue-specific pathophysiology is an important determining factor in health outcomes, is discussed below and outlined in Figure 4.

Respiratory Disease

The lungs are the primary site of PM-induced pathophysiology and best characterized in terms of the effects of PM exposure. Each 10 μg/m3 increase in ambient PM10 has been linked to a 0.58% increase in respiratory mortality, whist the same increase of PM2.5 has been associated with a 2.07% increase in respiratory disease hospitalization (35, 36). 

Research has shown human exposure to PM to be associated with multiple respiratory diseases including chronic obstructive pulmonary disease, asthma, interstitial lung damage and lung cancers (37–39). 

For patients with idiopathic pulmonary fibrosis, PM exposure has been shown to correlate with reduced lung forced vital capacity (39).

Ex vivo analysis of mouse lungs exposed to PM2.5 for three months exhibited significantly elevated levels of PM2.5, carbon monoxide, nitrogen oxides, interleukin-4, tumor necrosis factor-α and transforming growth factor-β1 when compared to controls (40). 

Of these circulating factors, interleukin-4 is known to promote B lymphocyte production of immunoglobulin E; a driver of allergic diseases including asthma and chronic obstructive pulmonary disease (41). 

PM2.5 exposure has been shown to induce pulmonary fibrosis both in vivo and in vitro experiments (42).

 PM2.5 increased tissue concentrations of transforming growth factor-β1; a fibroblast chemokine that can decrease protease secretion and increase extracellular expression of collagen and fibronectin (43).

 In a mouse model of idiopathic pulmonary fibrosis, ex vivo histological analysis revealed that exposure to black carbon PM2.5 aggravated lung inflammation and exacerbated histopathological changes to lung tissue including increased inflammatory cell infiltration and epithelial cell hyperplasia (44). 

This study also found that exposure to black carbon PM2.5 exacerbated already elevated interleukin-6 mRNA and reduced interferon-γ mRNA expression (44).

 Together, these preclinical studies not only highlight the potential danger of PM to health but also suggest that PM can increase the severity of existing health conditions like idiopathic pulmonary fibrosis. Increased counts of neutrophils, lymphocytes, eosinophils, M1 and M2 macrophages have been found in PM-exposed lung tissue (40).

 Whilst M1 macrophages can induce oxidative damage to lung epithelia, chronic elevation of M2 macrophages can cause pulmonary fibrosis and lung cancer (45–47).

 Mechanisms by which PM may induce fibrosis include increased intracellular edema, microvilli density, lamellar bodies and the density of macrophages containing endocytosed PM (40). 

In mice, PM2.5 exposure reduced mitochondrial density, increased NADPH oxidase 2 expression, significantly reduced total lung capacity, inspiratory capacity, and lung compliance (48). 

This same study found that PM2.5 exposure increased lung epithelia expression of N-Cadherin and reduced that of E-Cadherin; markers of epithelial-mesenchymal transition, a process common to cancer metastasis (48).

Cardiovascular Disease

Air pollution is associated with elevated cardiovascular disease risk and cardiovascular disease-related mortality (49).

 PM2.5 exposure is linked to higher risk of heart attack, heart failure, ischemic heart disease, stroke, atherosclerosis, arrhythmia, hypertension, preeclampsia and neonatal hypertension (50–52). 

Air pollution exacerbates cardiovascular mortality risk for people with pre-existing cardiopulmonary disease (49). 

In adults, exposure to PM exposure has been linked to elevated systolic blood pressure and elevated pulse pressure, 

whilst in children, it has been found to associate with increased mean pulmonary arterial pressure and increased plasma endothelin-1 concentration (53, 54).

 Endothelin-1 is an endogenous atherogenic vasoconstrictor and may contribute to PM induced atherosclerotic plaque accumulation (55).

 The Multi Ethnic Study of Atherosclerosis (MESA) found short-term PM2.5 exposure to associate with to decreased flow-mediated vasodilation and vasoconstriction, indicating that particulates may impair endothelial function (56).

 Analysis of the same MESA cohort revealed a correlation between exposure to black carbon PM and pulmonary vascular remodeling (57).

 Here, changes in vascular volume – indicative of elevated blood pressure – were comparable to the effect of >15 pack years of cigarette smoking (57).

 PM exposure has been found to exacerbate high-risk atherosclerotic plaque progression, plaque destabilization and coronary calcification (58). 

PM exposure has also been linked to atrial fibrillation and reduced heart rate variability, with the later exacerbated by pre-existing diabetes (59).

 Preclinical models have demonstrated that PM can induce hypertension in healthy animals, secondary disease in animal models of heart failure and hypertension, and induce symptoms of cardiovascular dysfunction via central and renal cardiovascular regulation disruption (60–63).

 Exposure of rats to black carbon PM for 4 weeks dose and time dependently increased blood pressure (60). Four-day PM2.5 exposure to spontaneously hypertensive rats significantly increased heart rate and blood pressure and reduced heart rate variability (61). 

In a mouse model of chronic left ventricular heart failure, PM2.5 exposure significantly exacerbated lung oxidative stress, lung fibrosis, inflammation, vascular remodeling, and right ventricle hypertrophy (62, 63).

 Hypertensive, angiotensin II-infused apoe−/− mice, exposed to PM2.5 for 4 weeks had a significantly increased incidence of abdominal aortic aneurysm compared to controls (64).

 Here, aortic aneurysm was associated with significant vascular elastin degradation, increased maximal abdominal aortic diameter and elevated expression of senescence proteins P16 and P21 (64).

 Increased vascular P21 is implicated in the development of atherosclerosis, causes of which include inflammation, hemodynamic damage and aberrant lipid metabolism (65, 66). 

Multiple models have shown PM2.5 exposure to stimulate endothelial release of inflammatory cytokines and adhesion molecules, promote macrophage infiltration, vascular smooth muscle cell dysfunction and plaque formation (67).

 Hypertensive, apolipoprotein-deficient mice exposed to PM2.5 for 3 months exhibited increased atherosclerotic lesion area, hepcidin and iron plaque depositions, increased plasma iron, ferritin, total cholesterol, low density cholesterol, vascular endothelial derived growth factor, monocyte chemoattractant protein-1 and pro-atherosclerotic cytokines interleukin 6 and tumor necrosis factor-α (64). 

Both blood pressure and heart rate are partially regulated by the central nervous system, with sympathetic output from the hypothalamus significantly impacting cardiovascular tone (68).

 Is In wild-type mice, long-term PM2.5 exposure has been found to increase basal blood pressure; an effect that was reversed with central alpha-2 adrenergic receptor antagonism. Concurrent inflammation of the hypothalamic arcuate nucleus was observed in hypertensive PM2.5-exposed mice (69).

Increased noradrenergic signaling in the hypothalamic periventricular nucleus is known to increase sympathetic output and cardiovascular tone (70). 

Exposure of lean Brown Norway rats to PM for 1 day increased noradrenaline concentrations in the paraventricular nucleus and corticotropin releasing hormone concentration in

 the median eminence (71). 

The Physiological Effects of Air Pollution:

 

Ref

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

Please note review will be continued shortly

फायबर-समृद्ध आहाराचा आणि फुफ्फुसांच्या कर्करोगावरील परिणाम

 ५.४. तंतुमय पदार्थांनी समृद्ध आहार

फळे, भाज्या आणि वनस्पतीजन्य पदार्थांमधील काही घटक, जसे की फायबर, हे महत्त्वाच्या गोंधळात टाकणाऱ्या चलांसाठी समायोजन केल्यानंतरही, सिस्टेमिक दाह, लठ्ठपणा आणि मेटाबॉलिक सिंड्रोम कमी करण्याशी संबंधित आहेत [९१].

याव्यतिरिक्त, जास्त फायबरचे सेवन अनेक प्रकारच्या कर्करोगापासून संरक्षण करते असे पूर्वीपासून मानले जात आहे [९२].

या विविध आरोग्य फायद्यांमागील यंत्रणा फायबरमुळे प्रेरित होणाऱ्या आतड्यातील सूक्ष्मजीव आणि चयापचय मार्गांच्या नियमनाशी जोडलेल्या असल्याचे दिसते [९३].

युनायटेड स्टेट्स, युरोप आणि आशियामध्ये केलेल्या अभ्यासांमधील १,४४५,८५० प्रौढांमध्ये, धूम्रपानाची स्थिती, सिगारेटची संख्या आणि फुफ्फुसाच्या कर्करोगाच्या इतर जोखीम घटकांसाठी समायोजन केल्यानंतर, फायबरचे सेवन आणि फुफ्फुसाच्या कर्करोगाचा धोका यांच्यात व्यस्त संबंध आढळला [९४].

त्याचप्रमाणे, मिलर आणि इतरांनी EPIC अभ्यासात समाविष्ट असलेल्या आणि १० युरोपीय देशांमधून भरती केलेल्या ४७८,०२१ व्यक्तींच्या डेटाचा अभ्यास केला, ज्यांनी आहारासंबंधी प्रश्नावली पूर्ण केली होती [९५].

वय, धूम्रपान, उंची, वजन आणि लिंग यासाठी समायोजन केल्यानंतर, फुफ्फुसाच्या कर्करोगाच्या रुग्णांमध्ये फळांचे सेवन आणि फुफ्फुसाच्या कर्करोगाचा धोका यांच्यात एक महत्त्वपूर्ण व्यस्त संबंध आढळला. हा संबंध अभ्यासाच्या सुरुवातीला धूम्रपान करणाऱ्यांमध्ये सर्वात मजबूत होता [९५].

फुफ्फुसाच्या कर्करोगाच्या उपप्रकारांचा विचार करता, बुचनर आणि इतरांनी, २०१० मध्ये, फायबरच्या सेवनामध्ये आणि फुफ्फुसाच्या कर्करोगाच्या धोक्यात व्यस्त संबंध पाहिला, परंतु फुफ्फुसाच्या कर्करोगाच्या विशिष्ट हिस्टोलॉजिकल उपप्रकारांवर कोणताही स्पष्ट परिणाम दिसला नाही [९६].

दुसरीकडे, फायबरच्या वेगवेगळ्या स्रोतांचा विचार करता, ब्रॅडबरी आणि इतरांनी, २०१४ मध्ये नोंदवले की फुफ्फुसाच्या कर्करोगाचा धोका फळांच्या सेवनाशी व्यस्तपणे संबंधित होता, परंतु भाज्यांच्या सेवनाशी संबंधित नव्हता [९७];

तथापि, फळांच्या सेवनाशी असलेला हा संबंध केवळ धूम्रपान करणाऱ्यांपुरता मर्यादित आहे. या डेटानुसार, बुचनर आणि इतरांनी फुफ्फुसाच्या कर्करोगाच्या १८३० नवीन प्रकरणांच्या पाठपुराव्यादरम्यान फळे आणि भाज्यांच्या परिणामांचे विश्लेषण केले; फळे आणि भाज्यांच्या सेवनात दररोज १०० ग्रॅम वाढ केल्याने फुफ्फुसाच्या कर्करोगाचा धोका कमी होतो [९६].

याव्यतिरिक्त, फायबरचे वेगवेगळे स्रोत सकारात्मक परिणाम बदलत नाहीत, जसे की बाल्ड्रिक आणि इतरांनी दाखवून दिले आहे, ज्यांना शेंगांमधून जास्त फायबर असलेल्या आहाराचे सेवन करणाऱ्या माजी/धूम्रपान करणाऱ्यांमध्ये दाहक-विरोधी यंत्रणेद्वारे फायदेशीर परिणाम आढळले [९८]. एकूण फायबरच्या सेवनामध्ये आणि सीओपीडी (COPD) चा धोका कमी होण्यामध्ये एक संबंध आढळून आला आहे, जो सामान्य फुफ्फुसांच्या आरोग्यावर फायदेशीर परिणाम दर्शवतो [99,100].

संदर्भ

Int J Environ Res Public Health. 2021 Mar 1;18(5):2399. doi: 10.3390/ijerph18052399

अन्न, पोषण, शारीरिक क्रियाकलाप आणि मायक्रोबायोटा: फुफ्फुसांच्या कर्करोगावर कोणता परिणाम?

Ersilia Nigro 1,2, Fabio Perrotta 3, Filippo Scialò 2,4, Vito D’Agnano 3, Marta Mallardo 1,2, Andrea Bianco 2,4,*, Aurora Daniele 1,2,*

संपादक: Dagrun Engeset

Ref

Int J Environ Res Public Health. 2021 Mar 1;18(5):2399. doi: 10.3390/ijerph18052399

Food, Nutrition, Physical Activity and Microbiota: Which Impact on Lung Cancer?

Ersilia Nigro 1,2, Fabio Perrotta 3, Filippo Scialò 2,4, Vito D’Agnano 3, Marta Mallardo 1,2, Andrea Bianco 2,4,*, Aurora Daniele 1,2,*

Editor: Dagrun Engeset