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

Lung cancer Food and Dietary Plans (4)

 4. Food and Dietary Plans in the Prevention/

Control of Lung Cancer

Common phenomena in lung cancer patients are both malnutrition and cancer cachexia [52].

 The prevalence of malnutrition in lung cancer patients ranges from 34.5 to 69%, with the highest incidence in more severe patients and in those undergoing chemotherapies, immunotherapy and/or radiotherapy [53].

 On the other hand, inactivity represents a major risk for loss of functional pulmonary capacities in lung cancer patients [3]. 

Nutritional counselling, planning of meals and use of supplements are essential approaches to counteract malnutrition and sarcopenia in lung cancer. In fact, a nutritional and life-style counselling approach is recommended to control chemotherapy response,

 sarcopenia, prognosis and survival of the lung cancer patients. 

Tanaka et al. (2018) demonstrated that an early nutritional intervention with a dietary counselling in lung cancer patients receiving chemotherapy efficiently counteracts weight loss and sarcopenia [54].

 However, many patients do not achieve recommended dietary intake even after nutritional counselling [55].

 The main nutritional approaches to prevent and

 treat cancer sarcopenia are: an adequate energy intake; an adequate supply of protein for maintenance or gain of muscle; use of supplements.

An adequate protein intake can reduce the incidence and severity of sarcopenia in cancer patients [56].

 It has been demonstrated that a dietary program with energy and protein rich meals and snacks can improve muscle strength and performance status of lung cancer patients [57,58].

The use of supplements in the diet for cancer patients experiencing muscle loss is becoming a very popular approach.

 Several products might be useful in contrasting sarcopenia during cancer (Branched-chain amino acids, carnitine, fish oil,

 Eicosapentaenoic acid (EPA), vitamins and mineral, [59]. Specifically, in lung cancer

, supplementation of diet with EPA and PUFA improves the maintenance of weight and muscle mass in advanced NSCLC patients undergoing chemotherapy as well as physical and cognitive functioning [60,61,62].

Increasing attention has been focused on the possible use of oral ghrelin receptor (G-protein coupled receptor, GHSR-1a) agonists such as anamorelin and HM01 with the aim of exploiting the ghrelin’s orexigenic capacity [63].

 Anamorelin, a ghrelin receptor agonist, has been demonstrated to be able to significantly increase lean body mass [64]. 

Two completed clinical trials (ROMANA1 and 2, NCT01387269 and NCT01387282, respectively), performed on lung patients with inoperable stage III or IV non-small-cell lung cancer and cachexia, demonstrated that anamorelin induces an increase in lean body mass, without modification in the handgrip [65]. A third trial from the same authors, ROMANA3 (NCT01395914) has been completed confirming the improvements in body weight and anorexia-cachexia

 symptoms observed in the original trials, and demonstrating a well toleration to anamorelin administration [66]. 

There are currently two ongoing clinical trials (NCT03743064 and 03743051) investigating the use of anamorelin to treat non-small cell lung cancer-associated weight loss

. Both trials report changes in weight although a definitive result has not been reached. On the contrary, in vitro and vivo data are available about HM01 effects on cachexia but no clinical trials are available yet [67,68].

Regarding the molecular mechanisms underlying anamorelin effects, Garcia and colleagues found the it significantly increases GH, IGF-1 and IGFBP-3 levels with consequent body weight gain [69,70].

 A very recent study compared the two ghrelin receptor agonists anamorelin (non-BBB penetrant) and HM01 (BBB penetrant), demonstrating that HM01

 enhances hypothalamic neuronal activation and increases cumulative food intake compared to ghrelin and anamorelin [71]. The authors also demonstrated that HM01 and anamorelin exert potent effects on calcium mobilization, however anamorelin is potentially more susceptible to treatment-induced tolerance than HM01 due to recruitment of β-arrestin and GHSR-1a internalization [71]

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

Lung cancer Impact of Food Nutrtion Microbiota

 Abstract

Lung cancer still represents the leading cause of cancer-related death, globally. Likewise, 

malnutrition and inactivity represent a major risk for loss of functional pulmonary capacities influencing overall lung cancer severity.

 Therefore, the adhesion to an appropriate

 health lifestyle is crucial in the management of lung cancer patients despite the subtype of cancer. 

This review aims to summarize the available knowledge about dietary approaches as well as physical activity as the major factors that decrease the risk towards lung cancer,

 and improve the response to therapies. 

We discuss the most significant dietary schemes positively associated to body composition and prognosis of lung cancer and the main molecular processes regulated by specific diet schemes, functional foods and physical activity, i.e., inflammation and oxidative stress. 

Finally, we report evidence demonstrating that dysbiosis of lung and/or gut microbiome, as well as their interconnection (the gut–lung axis), are strictly related to dietary patterns and regular physical activity playing a

 key role in lung cancer formation and progression, opening to the avenue of modulating the microbiome as coadjuvant therapy. Altogether, the evidence reported in this review highlights the necessity to consider non-pharmacological interventions (nutrition and physical activity) as effective adjunctive strategies in the management of lung cancer.

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

Lung cancer Genetic and Racial Disparities

 2.3. Genetic and Racial

 Disparities and Lung Cancer Susceptibility

Lung cancer risk is influenced significantly by

 different racial and ethnic disparities.

 Individuals with African ancestry (AA) have

 higher mortality rates and incidence of lung cancer development at an earlier age compared to individuals with European ancestry (EA) due to disparities in preventive screening monitoring and treatment disparities [39,40].

 In addition, there is a significant disparity in the metabolic pathways and how the body processes nicotine between AA and EA groups, as AA has lower levels of cotinine glucuronidation [41]. 

Non-Hispanic AA males show the highest rates of mortality and lung cancer incidence compared to all race-ethnicities [42,43]. 

Similarly, Primm et al. showed persistent disparities in NSCLC incidence between AA and EA men [44]. 

Interestingly, despite disparities in diagnosis and treatment, AA and Asian NSCLC patients demonstrate better outcomes for the same-stage cancer compared to EA patients [45].

 The cause for disparities is genetic ancestry, as AA populations with LUSC have more genomic instability and aggressive molecular traits, while AA patients with LUAD have a higher frequency of PTPRT and JAK2 gene mutations [46,47].

 Additionally, the Asian population demonstrates a higher frequency of STK11, TP53, and EGFR gene mutation [48],

 but they have longer survival rates and higher chemotherapy responses in comparison to EA patients [49]. 

Ok Another study linked TP53, KRAS, and KEAP1 gene mutations with worse overall survival, whereas EGFR gene mutations are associated with a higher chance of survival [50].

Recent studies found that EA patients have higher mortality rates compared to Hispanics and Asians, and they have a higher susceptibility to lung cancer due to higher frequencies in smoking-related loci [51,52].

 Many studies have revealed racial disparities in the genetic mutation profile of lung cancer patients. Compared to Japanese patients, EA-LUSC patients present a higher frequency of mutations in TP53, PIK3CA, KEAP1, and NFE2L2 genes [53]. 

On the contrary, EA-LUAD patients exhibit a significantly lower occurrence of EGFR mutation but an increased frequency of mutation in the PIK3CA, KEAP1, KRAS, TP53, BRAF, NF1, STK11, RBM10, and MET genes.

 Weiner and Winn reported a higher prevalence

 of EGFR gene mutation in the East Asian population and more predominant KRAS and STK11 gene alterations in EA and AA populations [54]. 

Generally, the disparities in survival rates between EA and AA populations are noticeable in patients who are young and have localized tumors [55].

 The disparities also exist in histological subtype, stage, and tumor grade. Asian or Pacific Islander (API) exhibit a higher frequency of adenocarcinoma (ADC) compared to AA, EA, and American Indian/Alaska Native (AIAN) patients [56].

Ref

International Journal of Molecular Sciences logo

Int J Mol Sci. 2025 Apr 17;26(8):3818. doi: 10.3390/ijms26083818

The Current Roadmap of Lung Cancer Biology, Genomics and Racial Disparity

Enas S Alsatari 1,2, Kelly R Smith 1,2, Sapthala P Loku Galappaththi 1,2, Elba A Turbat-Herrera 1,2, Santanu Dasgupta 1,2,3,*

Editor: Robert Arthur Kratzke