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

Impact of Fiber -Enriched Diet and Lung Cancer

 5.4. Fibers-Enriched Diet

Fruit, vegetables and certain components of

 plant foods, such as fiber, are associated with a reduction in systemic inflammation, obesity and metabolic syndrome, even after adjustment for important confounding variables [91].

 In addition, high fiber intake has long been thought to protect against several types of cancer [92]. 

The mechanisms for those various health benefits seem to be linked to the modulation of the gut microbiota and metabolic pathways that fibers can induce [93].

 Fiber intake is inversely associated with lung cancer risk after adjustment for status and pack-years of smoking and other lung cancer risk factors in 1,445,850 adults from studies that were conducted in the United States, Europe, and Asia [94]. 

Similarly, Miller et al. studied data from 478,021 individuals included in the EPIC study, and recruited from 10 European countries and who completed a dietary questionnaire [95]. 

After adjustment for age, smoking, height, weight and gender, there was a significant inverse association between fruit consumption and lung cancer risk in lung cancer patients. The association was strongest among current smokers at baseline [95].

Considering subtypes of lung cancer, Büchner et al., 2010 observed an inverse association between the consumption of fibers and risk of lung cancer without a clear effect on specific histological subtypes of lung cancer [96].

On the other hand, considering different sources of fibers, Bradbury et al., 2014 reported that the risk of cancer of the lung was inversely associated with fruit intake but was not associated with vegetable intake [97]; 

however, this association with fruit intake is restricted to smokers. In accordance with this data, Büchner et al. analyzed the effects of fruits and vegetables during a follow-up of 1830 incident cases of lung cancer; a 100 g/day increase in fruit and vegetables consumption was associated with a reduced lung cancer risk [96]. 

 In addition, different sources of fibers do not alter positive effects, as demonstrated by Baldrick et al. that found beneficial effects in ex/smokers following a diet with high intake of fibers from legumes through anti-inflammatory mechanisms [98].

An association has been also found between total fiber intake and decreased COPD risk suggesting a beneficial impact on general lung health [99,100].

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

Effect of Food and dietary Plans on Lung Cancer

 5. Effects of Food and Dietary Plans on Lung Cancer

As said above, body composition and eventually the presence of sarcopenia are crucial factors determining the risk, response to therapy and therefore the prognosis of lung cancer patients. 

Considering nutritional status as a determining factor of the body composition, in recent years growing attention has been paid to the choice of dietary plans as well as to performing physical activity.

 Dietary schemes as well as specific foods-enriched diet influence the predisposition towards cancer disease and the response to therapies and therefore the prognosis. 

The main molecular processes regulated by specific diet patterns, functional foods and physical activity in relation to cancer are the inflammation and oxidative stress. 

In the next paragraphs, we report the main dietary schemes associated to body composition, response to therapy and prognosis of lung cancer patients: caloric restriction, PUFA-enriched diets, Dietary Approaches to Stop Hypertension (DASH), fibers-enriched diet and diary-enriched diet. Since a considerable variety of bioactive ingredients have been identified in foods, we will also report interesting data for single compounds.

5.1. Caloric Restriction

It is widely believed that calorie restriction can extend the lifespan of model organisms and protect against aging-related diseases, such as lung cancer. 

In breast cancer, Simone et al. demonstrated that caloric restriction can augment the effects of radiation therapy as well as chemotherapy in a mouse model of breast cancer [72]. 

Interestingly, Safdie et al. analyzed patients diagnosed with a variety of malignancies (one with lung cancer) that voluntarily fasted prior to (48–140 h) and/or following (5–56 h) chemotherapy reporting a reduction in fatigue, weakness and gastrointestinal side effects while fasting [73]. 

The molecular mechanism of caloric restriction action is mainly related to the decrease of chemotherapy-induced inflammation and induction of energy stress resulting in increased efficacy of therapy. 

In lung cancer, Caiola et al. suggested, through in vitro studies, that caloric restriction regimens may sensitize NSCLC lesions carrying KRAS mutation and LKB1 loss to cytotoxic chemotherapy through induction of energy stress [74]. 

Resveratrol has been proposed as an active molecule mimicking the effects of caloric restriction which may have beneficial effects against numerous diseases such as type 2 diabetes, cardiovascular diseases, and cancer [75]. 

The positive effects in cancer are related to by the inhibition of oxidative stress, inflammation, aging, and fibrosis [76,77].

 In lung cancer, and more widely, in lung diseases resveratrol represents a promising natural compound to be used in association with other drugs [78].

 Although it is clear that resveratrol has shown excellent anti-cancer properties, most of the studies were performed in vitro or in pre-clinical models. Few clinical trials have been developed on the administration of resveratrol in cancer patients [79,80]. 

In addition, resveratrol in its current form is not ideal as therapy because, even at very high doses, it has modest efficacy and many downstream effects [81].

 The identification of the cellular targets responsible for resveratrol effects would help in the development of target specific therapies based on this drug

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