Allergy and asthma season is back. Since 1984, the Asthma and Allergy Foundation has recognized May as “National Asthma and Allergy Awareness Month.” Over 65 million individuals in the U.S. have allergies and asthma. Unfortunately, there is no cure for allergies or asthma; however, these conditions can be managed with the appropriate treatment and prevention.

Asthma is a chronic illness that causes swelling and inflammation of the airways. This, in turn, causes the airways to narrow, which makes breathing harder. According to the CDC, about 1 in 13 individuals in the U.S. have asthma (approximately 25 million people). Asthma affects all ages but usually starts in childhood. Asthma symptoms include wheezing, coughing, shortness of breath, and chest tightness. These symptoms can be triggered by various things such as allergens (e.g., pollen, dust, pet dander), cold air, exercise, infections, and tobacco smoke. If these symptoms become worse than usual, it is called an asthma attack. Asthma attacks can be life-threatening. In 2018, asthma led to more than 170,000 hospital stays and 1.6 million emergency department visits. Approximately 11 people in the U.S. die from asthma daily.

Your healthcare provider can diagnose asthma by medical history, physical exam, and lung function tests to see how well your lungs work. Treatment of asthma includes managing your symptoms and preventing asthma attacks. Short-term medications are used for quick symptom relief. These medications open up swollen airways quickly. Usually, this is an inhaler that is carried at all times. Long-term medications are used daily to keep asthma under control. These medications work to reduce inflammation and narrowing of the airways. Prevention includes knowing and avoiding triggers, avoiding smoke exposure, staying up to date on vaccinations, taking medications as prescribed, and recognizing signs that your asthma is getting worse.

Allergies are another chronic illness—more than 50 million individuals in the U.S. experience some variation of allergies each year. An allergy is when your immune system reacts to a foreign substance. This substance is something you eat, inject, inhale or touch. Symptoms of an allergic reaction include hives, rashes, itchy eyes, sneezing, and scratchy throat. Anaphylaxis, a severe allergy attack, can cause shortness of breath, low blood pressure, asthma attacks, and possible death. Most people with allergies have more than one type. Some examples of allergens include pollen, dust, pet dander, and certain foods or medications. Your healthcare provider can diagnose allergies by medical history, physical exam, and allergen tests (e.g., skin, patch, or blood). These tests alone can’t diagnose allergies but can be used as a guide for diagnosis.

Treatment of allergies includes avoiding allergens, taking medications, and/or immunotherapy. One common medication is antihistamines (e.g., Zyrtec, Claritin, Benadryl). These medications block histamine, which is responsible for the allergic response. Another common medication is nasal corticosteroids (e.g., Flonase) which reduce the swelling that causes a stuffy, runny nose. In more severe reactions, oral corticosteroids and/or epinephrine may be needed. Immunotherapy can be an option for some allergies. The most common types include allergy shots and sublingual immunotherapy (SLIT). Both options introduce the allergen in small doses over time to eventually make the person less sensitive to that allergen.

If you have asthma, allergies, or both, please talk to your healthcare provider about the available treatment options to have the best management strategy. Get treated early this May so you can take full advantage of the beautiful outdoors.

Dr. Abraham is a resident physician who sees patients of all ages and provides obstetrical services at Lone Star Family Health Center, a non-profit 501©3 Federally Qualified Health Center operating facilities in Conroe, Spring, Willis, Grangerland, and Huntsville, and serving as home to a fully integrated Family Medicine Residency Program to increase the number of Family Medicine physicians for Texas and our community.

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I was cooking dinner for my kids when a radio report stopped me, mid-stir: “Why gas stoves are bad for the climate–and you.” My ears perked up as the broadcaster specified that pollutants from gas stoves are especially harmful to kids. I looked down at the blue flames licking up the sides of the simmering pasta pot. Um, oops? 

As a parent, my capacity for things-you-really-should-worry-about feels entirely maxed out. Is it really so bad? I wondered. And why am I only hearing about this now? 

But it turns out multiple studies have found that gas stoves emit indoor air pollutants including methane gas, which is bad for the environment, and nitrogen oxide particles, which are bad for our lungs. In fact, these particles can decrease lung function and trigger or exacerbate asthma in kids, with symptoms such as wheezing, chest tightness and shortness of breath. Some gas stoves can leak methane continuously—even when the burners aren’t in use. 

Anne Hicks, a paediatric lung doctor in Edmonton and the clinical lead at the Children’s Environmental Health Clinic at the University of Alberta, says that studies examining gas stoves and indoor air quality have actually been around since the 1990s.

It’s become the topic du jour though, partly because of a new study out of Stanford University in January 2022, which sparked media attention when researchers found that gas stoves emitted alarming levels of methane gas, which is a greenhouse gas that’s bad for the environment.

While all of this was news to me, it’s not surprising to an expert like Hicks, who studies environmental exposures and respiratory outcomes in children. “There’s a lot of fuel-burning sources of air pollution inside our homes, and all of them have an impact on children,” says Hicks, who’s also an assistant professor in paediatric respiratory medicine.

The good news? “It’s not as if families need to go out and remove their gas stoves today.” But understanding gas appliances and their potential effects can help you make the best decisions for your family. Here is what you should know.

How do gas stoves work?  

The natural gas that powers a household appliance like a gas range is mostly methane (with a few other hydrocarbons in the mix). That burning blue flame releases carbon monoxide, sulfur dioxide, traces of formaldehyde, nitrogen oxides and microscopic particles, or aerosols, of soot. 

One often-cited study on emissions from gas stoves was published in 2018 by Tara Kahan, an associate professor at the University of Saskatchewan and an environmental analytical chemist who studies indoor air quality. 

“We were looking at nitrogen oxides specifically—similar to what makes up smog,” says Kahan. That’s because nitrogen oxide can exacerbate asthma and even, with long-term exposure, cause asthma. 

“These markers of bad air quality went up when people were cooking, and they lingered even when the stove was turned off,” says Kahan. “Most of us had gas stoves at the time, so we were upset when we saw the results.”

How bad is my gas stove for my kids?

Kahan, who has a six-year-old daughter, says more studies are needed to determine the exact health impacts for families. “Are there immediate detrimental effects? Probably not,” she says.  “But is it bad over years and years of use? Maybe. We don’t know. It’s a newer area of study.”

Hicks agrees it’s a tricky question to answer, because there’s no way to tell whether a person’s lung damage or inflammation is from gas stoves or something else, and because respiratory problems like asthma are what’s called “epigenetic—this means it’s both nature and nurture.” 

Family history of asthma, and then the different exposures and triggers in your lifetime, all have an effect, she explains. Do you live in a high-traffic city with lots of outdoor air pollution? Are wildfires common in your area? Does anyone smoke inside the home? Do you have a wood-burning stove as well as a gas range? All of these things can contribute to our susceptibility to lung diseases. 

But even though we don’t know exactly how gas stoves might affect each individual, because lung damage is cumulative over time, looking at all the sources of air pollution in, and near, your home is wise, experts agree. 

Should you get rid of your gas stove immediately? 

No, says Hicks. But the health—and environmental—effects of gas appliances are definitely worth considering the next time you’re shopping to replace appliances. 

This is especially the case if you have a family history of allergies or asthma, including things like hay fever, food allergies, or even eczema—as your kids are more likely to be susceptible to asthma in the first place, so it’s a good idea to be more mindful of indoor air quality in general.

“Wood-burning fireplaces, smoking or vaping tobacco or cannabis products, or simply having an attached garage instead of a detached one—all of these things also contribute to indoor air pollution,” she says. 

One silver lining of the COVID pandemic, and even the wildfires in Western Canada, she says, is that parents are generally more mindful of indoor and outdoor air quality these days. 

Another consideration is the age of your kids, as babies and toddlers are also more susceptible to environmental exposures, says Hicks. Their airways are smaller, and for kids with asthma, getting a run-of-the-mill cold triggers the airway to swell and narrow. Your windpipe is the size of your little finger, and in kids, it may only be 3 or 3.5 mm wide, she explains—that’s smaller than the width of a drinking straw. A virus can also cause extra mucus, which can block your breathing, and that’s why some kids get sicker. Plus, many babies and toddlers are just building up their immunity to common viruses. 

But it’s never too late, she says, to improve indoor air quality for the whole family, no matter how old your kids are. Parents in the home can benefit from cleaner air, too. 

Alternatives to gas stoves

If you are planning to replace your gas stove, you’ll be looking at either an electric stove or an induction stove. Electric stoves have coil burners (usually covered with a glass or ceramic cooktop) and are the less expensive of the two options. An induction cooktop uses copper coils which create a magnetic current with the pot or pan and heats the cookware directly. This provides quick, even heating, but induction cooktops require specific cookware, which is a potential added expense. 

According the data from the Stanford study, it’s not helpful to simply replace an old gas stove with a new one. It compared newer models of gas stoves (about three years old) with older gas models (more like 30 years old) and did not find a compelling difference between the two. It also didn’t matter whether you bought a fancier, more expensive gas stove or an inexpensive one.

How else can I mitigate the effects of gas stoves?

If you have a gas stove that’s sticking around, there are still ways to reduce the potential negative effects. Both Kahan and Hicks say we should always turn the hood fan on when we’re cooking on a gas range, which helps ventilate your kitchen and reduces both the aerosols produced when cooking and the nitrogen oxide. 

Kahan also suggests opening the windows in your kitchen, which will help increase the ventilation. Using a high-quality air purifier with a HEPA filter in the kitchen will help reduce the aerosols as they are released by the stove, she says, but it won’t address the nitrogen oxides. You could also keep air purifiers in the kids’ bedrooms and/or main play space and living areas for general air quality purposes. 

To reduce the amount you are using your gas stove, you can use an electric kettle instead of a kettle that goes on a stove burner, cook more microwaveable recipes, or opt for a countertop induction burner (which you plug in). Popular countertop appliances such as the Instant Pot or  air fryer are also good alternatives. 

“Our house came with a gas stove, and I’m not going to go and rip it out immediately,” says Hicks. “But I’m keeping the hood fan on, and I’m using the Crockpot instead of cooking soup on the stove all afternoon, which also decreases our family’s carbon footprint.”

Kahan also says that cooking on the back burners of a gas stove is better than using the front burners, because those gasses are better captured by the stove’s hood fan. 

You could also confirm that your range’s hood fan does in fact ventilate directly outside, says Kahan, and isn’t just pumping the same air back inside. “If it’s what’s called a ‘recirculating hood,’ those don’t tend to do much good.”

Do I also need to worry about my gas hot water heater, gas furnace, or a gas fireplace?

These also are likely to leak a bit, but since they all have a vent or chimney that leads to the outside, and they’re usually in the basement (where most families don’t spend as much time as the kitchen), the indoor air pollution generated isn’t as bad for your family’s health—just the environment. But the Stanford researchers do plan on studying this further in the future. 

This may feel overwhelming, but it’s all about moderation and mitigation, says Hicks. “Life is a bit hazardous. It’s about finding the things you CAN fix, and making life as safe as you can.” 

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The latest move provides customers with an affordable, lightweight solution that they can pair with their existing treatments. AirPhysio only needs to be used a few times each day to see an improvement in breathing and lung strength.

For more information, please visit:

The new store expansion features the most up-to-date AirPhysio product, which has received mainstream attention across a wide range of outlets in Australia. Now it’s available to US-based customers wanting to improve their breathing and lifestyle.

Customers will find that AirPhysio uses oscillating positive expiratory pressure (OPEP) to loosen the bond of mucus on the airway walls. This is achieved through natural vibration, and repeated use of the device makes it easier to expel or swallow the mucus that builds up with lung conditions.

The latest data shows that around 25 million Americans are living with asthma. Symptoms include wheezing, shortness of breath, and coughing. Many people also suffer from tightness in the chest, which can cause trouble sleeping if left untreated.

Those seeking a natural and easy way to manage these symptoms are encouraged to try the AirPhysio for themselves. Frequent use results in a strengthening of the lungs, allowing customers to breathe more comfortably throughout the day.

Life Wellness Healthcare is run by a team of caring and compassionate specialists who understand the impact that asthma and COPD can have on families. It’s for this reason that they secure high-quality products at an affordable price.

Along with the above-mentioned AirPhysio device for asthma, the store stocks a varied range of other solutions for those with lung disease or respiratory trouble. A specially designed AirPhysio filter can be added to any order, which compliments the device and improves lung health.

A recent customer said of their purchase: “Having only used this product for a couple of weeks, I can already feel a difference. I am very satisfied with this product, as I can breathe better and that makes me feel better overall.”

Those wishing to find out more can visit:

Contact Info:
Name: Matthew
Email: Send Email
Organization: Life Wellness Healthcare
Address: PO BOX 6662, Tweed Heads, NSW 2486, Australia
Phone: +61-7-3608-5683

Release ID: 89075077

If you detect any issues, problems, or errors in this press release content, kindly contact [email protected] to notify us. We will respond and rectify the situation in the next 8 hours.

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Chronic obstructive pulmonary disease (COPD) has an increasing rate of incidence in recent years and causes three million deaths annually, which brings about a heavy economic burden.1 Currently, there are no effective target drugs applied to clinical practice so it is urgent to mine promising drug targets. Airway inflammation is an important feature and contributes to the pathogenesis and progression of COPD.2 Ferroptosis refers to the programmed cell death induced by lipid peroxidation via iron-dependent pathway with unique morphological and biological features.3 Usually under environmental stresses or intra/inter-cellular signaling, many metabolic products such as reactive oxygen species (ROS) and phospholipid containing polyunsaturated fatty acid chain(s) (PUFA-PL) can trigger phospholipid peroxidation.4 Previous study proved that ferroptosis was involved in the pathogenesis of COPD.5 Stimulated by cigarette smoke, bronchial epithelium produced reactive oxygen species, which induced lipid peroxidation, membrane damage and even ferroptosis.6–8 Glutathione peroxidase 4 (GPX4) – a vital antioxidant regulator – is also impaired during ferroptosis.9 Cigarette smoke extract altered ferroptosis-related genes expression in bronchoalveolar epithelial cells. Hypermethylation of the nuclear factor erythroid 2-related factor 2 (Nrf2) promoter could inhibit Nrf2/GPX4 axis, thus affecting ferroptosis in COPD.10 Otherwise, many studies suggest that various immune cells play vital roles in chronic airway diseases such as COPD. Innate immune cells, which were enhanced in small airways, modulated airway inflammation and remodeling.11 Previous study reported that CD8+ T cells enhanced ferroptosis-specific lipid peroxidation in tumor cells.12 The proliferation of B cells and antibody production was influenced by iron ion regulating the expression of Cyclin E1.13 Macrophages recognized oxidized phospholipids on the cell surface to clear ferroptosis cells via toll-like receptor 2 (TLR2).14 However, the interaction between ferroptosis and immune cells infiltration in COPD pathogenesis remains unclear.

The aim of this research is to identify ferroptosis-related hub genes and their association with immune cells infiltration in COPD lung tissues compared with normal ones. Additionally, we intend to construct interactive networks of hub genes with miRNAs, transcription factors and signal molecules and evaluate the diagnostic values of hub genes.

Materials and Methods

Data Acquisition

The mRNA expression microarray data of GSE38974,15 including 23 patients with COPD and 9 normal controls, were extracted from the Gene Expression Omnibus (GEO) datasets.16 The platform was GPL4133 Agilent-014850 Whole Human Genome Microarray 4x44K G4112F (Feature Number version). Lung tissues from 9 smokers with no evidence of obstructive lung disease and 23 smokers with COPD were examined for mRNA expression. All the clinical information including age, gender, sample source, smoking history, GOLD stage and FVC group was publicly accessible in GEO database (

The 259 ferroptosis-related genes (FRGs) were downloaded from the FerrDb database.17

Identification of Differentially Expressed FRGs

The GEO2R is a web tool internally stalled in GEO database specialized for analyzing differentially expressed genes between experimental group and control group. The GEO2R analysis between COPD group and control group was performed on the GEO datasets and the result of differential expression analysis was downloaded for further analysis. The cut‐off criteria for differential gene expression were the absolute value of log fold change (FC) >1 and P value <0.05. The gene list of differential expression analysis and FRGs were intersected to obtain the differentially expressed FRGs. The expressions of differentially expressed FRGs were plotted using the R package Complex Heatmap.18 The expression differences of differentially expressed FRGs between COPD group and normal group in GSE38974 were compared using Kruskal–Wallis test and Dunn’s test. The correlation analysis of differentially expressed FRGs was performed using Spearman’s correlation.

Gene Ontology (GO) Terms and Kyoto Encyclopedia of Genes and Genomes (KEGG) Pathways Analyses

The GO and KEGG enrichment analyses were conducted using the R package clusterProfiler.19 The screening criteria for significant terms were adjusted P values less than 0.05 and q values less than 0.2. Combined with logFC values, the enrichment analyses were performed by calculating the Z-scores using the R package GOplot.20

STRING Database and Cytoscape Software

The STRING database is an online tool for analyzing protein–protein interaction. The PPI analysis was carried out using the STRING database.21 Cytoscape is a computer software that graphically displays, analyzes and edits the network, which contains multiple plugins. The results were processed and visualized in Cytoscape software (version 3.9.0). The key module was screened by the Molecular Complex Detection (MCODE) plugin. The differentially expressed FRGs were ranked by degrees and the top five genes were considered to be hub genes by cytoHubba plugin.

The Comparative Toxicomics Database

The Comparative Toxicomics Database (CTD) provides integrated information on complex interactions among chemical exposures, genes, proteins and diseases.22 In this study, we used it to estimate the inference scores of hub genes in several respiratory tract diseases.

miRNet, NetworkAnalyst and Encyclopedia of RNA Interactomes (ENCORI)

There are multiple online tools to analyze the interaction between non-coding RNAs and genes and predict target molecules. The miRNet is a useful online tool centering around miRNAs and their interacting molecules.23 The NetworkAnalyst is an integrated and powerful database for gene expression analysis and construction of interacting networks.24 In this article, they were utilized to explore and visualize the networks between hub genes and miRNAs, transcription factors and signal molecules. The ENCORI focuses on predicting RNA interaction.25 Here, it was used to predict the upstream molecules lncRNAs targeting screened miRNAs. The screening criterion was set as strict stringency (the number of Ago CLIP-seq experiments is no less than five) and the top three lncRNAs were selected.

The Receiver Operating Characteristic (ROC) Curves of Hub Genes

The logistic regression model of hub genes was constructed using glm function in R software, and the ROC curves were plotted using R package pROC. The ROC curve of each hub gene can help us determine whether its expression has diagnostic value to some extent. The true positive rate (TPR) or sensitivity refers to the number of true positive samples detected divided by the number of all true positive samples. The false-positive rate (FPR) refers to the number of false-positive samples detected divided by the number of all true negative samples. Specificity refers to the number of true negative samples detected divided by the number of all true negative samples. The abscissa represents 1 – specificity and the ordinate represents sensitivity. The area under the curve (AUC) is used to determine the prediction accuracy. The AUC is usually between 0.5 and 1.0. The ROC curve has low/moderate/high accuracy when the AUC is 0.5~0.7/0.7~0.9/more than 0.9, respectively. The Youden’s index (sensitivity plus specificity minus one) is used to assess the authenticity of the model. As it gets closer to 1.0, the model is much more authentic.


CIBERSORT is an R/web tool for deconvolution of expression matrices of human immune cell subtypes based on the principle of linear support vector regression.26 By the way of the CIBERSORT algorithm, we analyzed the proportions of 22 types of immune cells infiltration in patients with COPD and normal controls. The infiltration differences in patients with COPD and normal controls were compared using Kruskal–Wallis test and Dunn’s test. The Spearman correlation analysis was carried out to show the correlation within differentially infiltrated immune cells and the association between hub genes and differentially infiltrated immune cells.

Statistical Methods

All the statistical calculations were conducted in R software (version 3.6.3). The corresponding R packages were described as above. The statistical significance was marked as follows: ns, p≥0.05; *p< 0.05; **p < 0.01; ***p < 0.001. A p.adjust was the corrected p value obtained by the p value correction method; a q-value was an adjusted p-value, taking into account the false discovery rate (FDR). As the p value/p.adjust/q-value is less than 0.0001, scientific notation (exponent, E) is used. For instance, 0.0000267 is written as 2.67E-05.


Identification of Differentially Expressed FRGs

The design of this research was shown in the flow chart (Figure 1). Principal component analysis (PCA) was conducted to show that there was a good degree of clustering between the two groups (Figure 2A). After intersection, 102 genes were obtained (Figure 2B). Under the condition of absolute values of logFC > 1 and P values <0.05, 15 differentially expressed FRGs were discovered including 11 upregulated genes and 4 downregulated genes (Table 1). The 15 differentially expressed FRGs between COPD and normal groups were presented in volcano plot and heatmap (Figure 2C and D). The volcano plot showed the distribution of gene expression between COPD and normal groups. Genes with an adjusted P-value <0.05 and absolute fold-change value > 1 were considered as differentially expressed genes. Each point represented one gene. Red dots indicated significantly upregulated genes and blue dots indicated significantly downregulated genes. The top three upregulated genes included IL6, ATM and TNFAIP3 and the top two downregulated genes included IL33 and TGFBR1. Furthermore, the expression differences of 15 differentially expressed FRGs between the COPD and normal groups in GSE38974 were shown in box plots (Figure 3A). As shown in Figure 3A, 15 ferroptosis-related genes were all significantly differentially expressed between COPD group and normal samples, which was consistent with Figure 2C and D. To explore the expression correlation of these ferroptosis-related genes, correlation analysis was performed. The Spearman correlation analyses of 15 differentially expressed FRGs were shown in heatmap (Figure 3B). As shown in Figure 3B, the expressions of most up-regulating genes were significantly positively correlated with each other, so were the down-regulating genes. Similarly, the expressions of the most up-regulated genes had a significantly negative correlation with those of the four down-regulated genes.

Table 1 The Differentially Expressed FRGs in COPD Group Compared with Normal Group

Figure 1 Flow chart.

Figure 2 Identification of differentially expressed ferroptosis-related genes (FRGs). (A) The principal component analysis (PCA) plot of samples in GSE38974. (B) Venn diagram of GEO2R result and FRGs. (C) Volcano plot of differential genes between COPD and normal groups. The top five genes were labelled (upregulated-IL6, ATM and TNFAIP3, downregulated-IL33 and TNFBR1). (D) Heatmap of 15 differentially expressed FRGs.

Figure 3 Expression and correlation of differentially expressed FRGs. (A) Box plot of 15 differentially expressed FRGs in COPD group compared with normal group. The significance markers are shown as: *, P<0.05; **, P<0.01; ***, P<0.001. (B) Heatmap of correlation of 15 differentially expressed FRGs.

The GO and KEGG Enrichment Analyses of Differentially Expressed FRGs

To analyze the potential biological functions of these differentially expressed ferroptosis-related genes, we carried out GO and KEGG enrichment analyses by way of R software. In total, 739 biological processes (BPs), 11 cellular components (CCs), 21 molecular functions (MFs) and 26 KEGG pathways were enriched. The GO term results exhibited that differentially expressed FRGs were mainly involved in regulation of smooth muscle cell proliferation, membrane microdomain, membrane raft, caveola, cytokine receptor binding, cytokine activity, and transforming growth factor beta receptor binding. The KEGG analysis indicated that differentially expressed FRGs participated in cell senescence pathway, FoxO signaling pathway and HIF1 signaling pathway (Figure 4A and B, Table 2). After combining with expression levels (logFC), the Z-scores showed that all the significant terms could be positively regulated by differentially expressed FRGs (Z-scores >0) (Figure 4C and D). These findings implied that 15 differentially expressed FRGs may participate in inflammatory responses and airway remodeling in COPD pathogenesis.

Table 2 The Most Significant Terms of GO and KEGG Enrichment Analyses

Figure 4 GO and KEGG enrichment analyses of differentially expressed FRGs. (A) Lollipop plot of significant terms. (B) Circular network of significant terms and genes. Blue nodes represent terms, red nodes represent genes, and connecting lines represent the relationship between terms and genes. (C) Bubble plot of significant terms combined with logFC. A Z-score greater than zero indicates positive regulation, a Z-score less than zero indicates negative regulation, and absolute value of Z-score represents the probability of regulation. (D) Donut plot of significant terms combined with logFC. Each column of the inner circle corresponds to one term, the height of column represents adjusted P value, and the filled color represents Z-score of each term.

Construction of Protein–Protein Interaction (PPI) Network and Identification of Key Module and Hub Genes

To determine the interactive relationship among differentially expressed FRGs, the protein–protein interaction analysis was conducted. The interaction of 15 candidate genes was analyzed in STRING database, and the results were visualized in Cytoscape software. The results showed that these differentially expressed FRGs interacted with each other (Figure 5A) and displayed the interaction number of each gene (Figure 5B, Supplementary Table 1). In total, there existed 15 nodes and 134 edges. The MCODE plugin analysis showed that there existed one key module containing 11 nodes and 50 edges including GDF15, IL6, ATF3, PTGS2, TGFBR1, HIF1A, CDKN1A, ATM, HMOX1, TNFAIP3 and MYB (Figure 5C). The cytoHubba plugin analysis identified five hub genes, including HIF1A, IL6, PTGS2, CDKN1A and ATM (Figure 5D). The Venn diagram indicated the overlap of predicted hub genes (Figure 5E). The detailed information of five hub genes can be seen in Supplementary Table 2.

Figure 5 PPI network, key module and hub genes of differentially expressed FRGs. (A) The PPI among 15 differentially expressed FRGs. (B) The interaction number of each differentially expressed FRG. (C) Key module of the PPI network screened by MCODE plugin. (D) Hub genes screened by cytoHubba plugin. (E) The overlap of predicted hub genes.

Evaluation of Correlation Between Hub Genes and Respiratory Tract Diseases

In order to estimate the theoretical association between predicted hub genes and chemical/environmental exposures, the five hub genes were analyzed in the Comparative Toxicomics Database and four respiratory tract diseases were chosen including COPD, chronic bronchitis, pulmonary emphysema and non-small cell lung cancer (NSCLC). The average inference scores of five hub genes in COPD (46.85) were higher than those in chronic bronchitis (35.72) and pulmonary emphysema (17.17) but lower than those in NSCLC (55.56) (Figure 6). The findings implied that five predicted hub genes might participate in multiple pathophysiological processes in respiratory diseases.

Figure 6 The correlations between hub genes and respiratory tract diseases in comparative toxicomics database.

Construction of the Networks Between Hub Genes with miRNAs, Transcription Factors and Signal Molecules

The hub genes could probably play a role by acting as transcription factors and vital signal molecules or interacting with intracellular non-coding RNAs. In order to predict upstream or downstream molecules of five hub genes and speculate on the mechanism of action of each hub gene, interactive network analysis was conducted. The five hub genes were uploaded to the miRNet online database to analyze the interaction with miRNAs and transcription factors in human lung tissues. In total, 44 miRNAs were predicted and two miRNAs, hsa-let-7b-5p and hsa-miR-1-3p, both targeting five hub genes, were selected for further exploration (Figure 7A, Supplementary Table 3). The transcription factor-hub gene regulatory network consisted of 217 interactions between 164 transcription factors and five hub genes. Five transcription factors including EGR1, NFKB1, RELA, SP1 and STAT3, which had the highest connectivity with hub genes, were selected (Figure 7B, Supplementary Table 3). The ENCORI database was used to screen upstream lncRNAs of the two miRNAs. Six lncRNAs were predicted: NUTM2A-AS19, XIST and NEAT1 (targeting hsa-let-7b-5p); RMRP, MALAT1 and AL162431.2 (targeting hsa-miR-1-3p) (Figure 7C, Supplementary Table 3). Next, five hub genes were uploaded into the NetworkAnalyst database to analyze the interaction with signal molecules. TP53 was prominent due to interacting with three hub genes in a network of signal molecules (Figure 7D, Supplementary Table 3).

Figure 7 The interaction network of hub genes in miRNet and network Analyst. (A) The network of hub genes with miRNAs. (B) The network of hub genes with transcription factors. The fuchsia nodes represent hub genes and the green nodes represent transcription factors. The five transcription factors that connect with at least four hub genes are labelled. (C) The network of hub genes with signal molecules. The signal molecules that connect with at least two hub genes are labelled. (D) The predicted lncRNA-miRNA-hub gene regulatory network. Yellow diamonds represent lncRNAs, green ellipses represent miRNAs, and blue rectangles represent hub genes.

The ROC Curves of Hub Genes

To determine the diagnostic value in discriminating COPD patients from normal controls, the ROC curves of each hub gene were plotted using R software. The logistic regression model of hub genes was constructed based on glm function. The formula was “-88.166 + 3.0089*HIF1A + −2.8988*IL6 + 2.8957*PTGS2 + 3.2435*CDKN1A + 7.3934*ATM”. As shown in Figure 8, the expression levels of HIF1A (AUC: 0.923, CI: 0.804-1.00) and ATM (AUC: 0.976, CI: 0.926-1.000) had high predictive accuracy (Figure 8A and E). The expression levels of IL6 (AUC: 0.826, CI: 0.608-1.000) and CDKN1A (AUC: 0.860, CI: 0.653-1.000) had moderate predictive accuracy (Figure 8B and D). The expression level of PTGS2 had low predictive accuracy (AUC: 0.681, CI: 0.471-0.892) (Figure 8C). The AUC of combination of five hub genes was 0.981 (CI: 0.940-1.000) (Figure 8F). When the cut-off threshold was 1.398, the sensitivity, specificity and Youden index were 0.957, 1.000 and 0.957, respectively. These results indicated that this model had high accuracy and authenticity to distinguish COPD group from normal group.

Figure 8 The receiver operating characteristic (ROC) curves of hub genes. (A) ROC curve of HIF1A. (B) ROC curve of IL6. (C) ROC curve of PTGS2. (D) ROC curve of CDKN1A. (E) ROC curve of ATM. (F) ROC curve of five genes combination.

The Immune Cells Infiltration Characteristics in Patients with COPD and Normal Controls

The infiltrating status of various immune cells in lung tissues had obvious differences (Figure 9A). Monocytes and macrophages accounted for the majority of all infiltrating cells, especially in COPD lung tissues. The infiltration differences in both groups are shown in Figure 9B. Seven types of immune cells, including CD8 T cells, activated NK cells, monocytes, M0 macrophages, M2 macrophages, resting dendritic cells and resting mast cells, had differential infiltration in patients with COPD compared with normal controls. The adjusted P-values of seven kinds of immune cells were 0.002, 0.001, 0.025, <0.001, 0.002, 0.008 and 0.020, respectively. Monocytes and M0 macrophages were upregulated in COPD lung tissues, while CD8 T cells, activated NK cells, M2 macrophages, resting dendritic cells and resting mast cells were downregulated. Figure 10A reveals the correlations between differentially infiltrated immune cells. Monocytes had positive correlations with CD8 T cells, M2 macrophages and resting dendritic cells (r=−0.39, −0.67 and −0.46, respectively). M0 macrophages had inverse correlations with CD8 T cells and activated NK cells (r=−0.38 and −0.58, respectively). However, CD8 T cells had positive correlations with M2 macrophages, resting dendritic cells and resting mast cells (r = 0.54, 0.40 and 0.56, respectively). Resting mast cells were positively associated with M2 macrophages and resting dendritic cells (r = 0.36 and 0.61, respectively). The correlations between the expression of hub genes and differentially infiltrated immune cells are displayed in Figure 10B. Positive associations were observed between monocytes and IL6, monocytes and PTGS2, monocytes and CDKN1A (r = 0.53, 0.42 and 0.62, respectively). M0 macrophages were also positively associated with HIF1A and ATM (r = 0.50 and 0.52, respectively). However, CD8 T cells were strongly negatively associated with HIF1A, IL6, PTGS2 and CDKN1A (r=−0.68, −0.83, −0.72 and −0.79, respectively). The remaining several types of immune cells also had weakly to moderately negative correlations with the expression of most of the hub genes as displayed in the heatmap.

Figure 9 Immune infiltration of COPD lung tissues compared with normal tissues. (A) Stack bar chart of proportions of the immune cells infiltration. (B) Box plot of proportions of the immune cells infiltration. The significance markers are shown as: ns, P>0.05; *, P<0.05; **, P<0.01; ***, P<0.001.

Figure 10 Differentially infiltrated immune cells and hub genes. (A) Heatmap of correlations of differentially infiltrated immune cells. (B) Heatmap of correlations of hub genes with differentially infiltrated immune cells. The significance markers are shown as: *, P<0.05; **, P<0.01.


Accumulating evidence indicates that ferroptosis participates in the pathogenesis of COPD. Previous review summarized that ferroptosis can affect inflammation through immunogenicity and ferroptosis inhibitors may benefit certain diseases through their anti-inflammatory effects.2 However, more research is required to better our understanding of ferroptosis in pathogenesis of COPD. In our study, we obtained 15 differentially expressed FRGs in patients with COPD compared with normal controls through bioinformatics analysis. Several hub genes were reported in the previous study. For instance, HIF1A, as a switch gene, was upregulated in COPD cases using network-based analysis implemented by SWIM software.27 CDKN1A played important functions in the development and progression of COPD.28 In our study, the enrichment analyses of 15 differentially expressed FRGs were conducted to explore their potential functions. The results indicated that they were associated with airway inflammatory response and remodeling. For example, cell senescence occurs in many pathological processes in COPD, which is consistent with previous reports. Cell senescence impedes iron-mediated cell death pathways by impairing ferritinophagy, a lysosomal process that promotes ferritin degradation.29

Next, we constructed a PPI network of 15 differentially expressed FRGs and first identified five ferroptosis-related hub genes, including HIF1A, IL6, PTGS2, CDKN1A and ATM. To further explore the correlation between hub genes and diseases, we analyzed the inference scores for four respiratory tract diseases in CTD and found that five hub genes were closely correlated with COPD and other respiratory tract diseases. These findings reminded us that it was vital to clarify the mechanism of action of these genes in COPD pathogenesis.

Bioinformatics methods provide us with a convenient way to predict crosstalk networks and screen potential biomarkers in COPD. A large number of miRNAs and lncRNAs were reported to be involved in COPD initiation and development. MALAT1/miR-146a/COX2 (namely PTGS2) axis affected the lung function of patients with COPD.30 Some non-coding RNA targets including miR-195, miR-181c and TUG1 are viable for alleviating COPD in vivo.31 However, to our knowledge, previous articles reporting the correlation between non-coding RNAs and ferroptosis mainly focused on multiple cancers. The present study constructed the networks of hub genes with miRNAs and transcription factors in miRNet database and identified two key miRNAs, namely, hsa-let-7b-5p and hsa-miR-1-3p. The hsa-let-7b-5p participated in endothelial mitochondrial dynamics and acted as a biomarker for diagnosing Parkinsonian Syndromes.32,33 The hsa-miR-1-3p inhibited lung adenocarcinoma cell tumorigenesis and improved gefitinib resistance in EGFR mutant lung cancer cell.34,35 Additionally, the upstream lncRNAs of two miRNAs were predicted using ENCORI database and we found six lncRNAs with the most experimental evidence. Among them, NUTM2A-AS19 and AL162431.2 are newly reported in this study. XIST and MALAT1 played an important role in mitochondrial dysfunction, cell senescence and epigenetic alterations in COPD pathogenesis under the condition of tobacco smoke exposure.36 NEAT1 promoted activation of inflammasomes in macrophages.37 RMRP promoted the progression of NSCLC via competing with miR-1-3p.38 Thus, we speculate that the following axes may regulate ferroptosis in COPD pathogenesis including NUTM2A-AS19 or XIST or NEAT1/hsa-let-7b-5p/hub gene axes and RMRP or MALAT1 or AL162431.2/hsa-miR-1-3p/hub gene axes. Moreover, the identification of five important transcription factors including EGR1, NFKB1, RELA, SP1 and STAT3 would be the groundwork for molecular mechanisms of ferroptosis in COPD pathogenesis. EGR1 was indispensable for MUC5AC expression induced by cigarette smoke in human bronchial epithelial cells.39 Genetic knockdown of RELA (NFKB subunit) diminished IL6 production in HBE cells.40 SP1 was crucial for anti-inflammatory molecule IL10 secretion in the phototherapy effect in HBE cells.41 STAT3 was a vital molecule in regulating the expression of inflammatory cytokines in COPD murine model.42 Notably, the signal molecule network revealed that TP53 connected with IL6, CDKN1A and ATM, suggesting that TP53 may be a potential driver of COPD towards lung cancer. This indicated that ferroptosis may also participate in COPD-related carcinogenesis.

Previous studies concentrated on the construction of a ferroptosis-related gene model for prognosis in cancer. For example, researchers screened ten ferroptosis-related genes, which served as potential prognostic biomarkers.43 To testify the diagnostic values of hub genes, we conducted ROC analyses and discovered that each of them varied in predictive accuracy, while combination of five genes could serve as a fine model to distinguish patients with COPD from normal controls (AUC: 0.981, CI: 0.940-1.000).

Although immune infiltration in malignancies keeps attracting the attention of researchers, very few reports explored the immune infiltration in COPD. The spatially confined eosinophil-rich type 2 microenvironments were identified in COPD.44 The proportion of T cells decreased in the lungs of current smokers and patients with COPD, whereas the proportion of macrophages increased.45 In our study, we uncovered the immune infiltration status in patients with COPD compared with normal controls. Monocytes were the majority of immune cells in both groups and increased prominently in COPD group. Monocytes, as an essential part of innate immune system, influence human diseases both by direct effects and by differentiating into macrophages.46 The cytokine response of monocytes to bacteria was compromised in smoking-induced COPD and thus impaired immune response.47 Macrophages are plastic in response to various tissue microenvironment and external stimuli. We found that the proportion of M0 macrophages increased markedly, which could serve as reserves ready for polarization stimuli. M1 macrophages primarily take part in pro-inflammatory responses, however, they were not observed to increase remarkably in this study. M2 macrophages, which primarily participate in anti-inflammatory responses, decreased dramatically in COPD group, suggesting that their functions may be undermined in COPD pathogenesis. CD8 T cells were observed to decrease drastically, which was inconsistent with previous researches. The number of IFN-γ-producing CD8+ and CD4+ lymphocytes increased in the lungs of patients with COPD.48 The frequencies of CD8+ T cell subsets increased observably in patients with COPD compared with normal controls and non-smokers.49 It may be partial due to the difference between statistics-based bioinformatics methods and flow cytometry assays. Activated NK cells decreased in COPD lung tissues. However, evidence from other studies revealed that the proportions of NK cells increased in BAL fluid of patients with COPD.50 Another two researches claimed that the number of NK cells in the lung parenchyma of patients with COPD was at the same level as that in the peripheral blood, and bronchoalveolar lavage fluid in healthy smokers.51,52 It seems that NK cells in lung tissues may have different effects compared with those from blood and BALF. Moreover, we found resting dendritic cells and resting mast cells, which were the minority of infiltrating immune cells, decreased in patients with COPD. Dendritic cells present antigens and activate naive T and B cells.53,54 Mast cells can interact with multiple immune cells and structural cells and thereby facilitate inflammatory responses, airway remodeling and angiogenesis.55,56 The functions of them might be antagonized by monocytes and M0 macrophages in some degree in COPD lung tissues. The proportions of monocytes and M0 macrophages were positively associated with most of hub genes, whereas CD8 T cells, activated NK cells, M2 macrophages, resting dendritic cells and resting mast cells were negatively associated most of the hub genes. It can be inferred that the functions of monocyte and M0 macrophages may be promoted by these hub genes. The other types of infiltrating cells, for instance, CD8 T cells, were likely to be inhibited by these hub genes. HIF1A was validated to drive ferroptosis in clear cell carcinomas and ATM was essential for promoting ferroptosis.57,58 IL6 and PTGS2 were confirmed as the downstream markers of ferroptosis.59,60 CDKN1A was required to suppress ferroptosis.61 We speculate that these high-expressed hub genes in COPD group may get involved in the regulation of ferroptosis in structural cells of pulmonary parenchyma and thus affect the infiltrating immune cells residing in pulmonary interstitium or recruited from peripheral blood, which could lead to differentially histopathological changes in the lungs of patients with COPD. Taken together, the immune cells infiltration contributes to the pathogenesis of COPD in a sophisticated manner and more research is in urgent need to elucidate the situation.

Our study had obvious limitations. The number of cases included in our study was relatively small. Due to the lack of detailed clinical information, correlations between hub genes and clinical characteristics cannot be explored. Another apparent deficiency is that we did not perform basic experiments to validate the expression of hub genes and their correlation with immune cells. For now, our study can provide a theoretical basis for further explorations of ferroptosis-related phenotypes in COPD research.


We identified five ferroptosis-related hub genes (HIF1A, IL6, PTGS2, CDKN1A and ATM) in COPD, a combination of which had diagnostic value. Two miRNAs, five transcription factors and one signal molecule were predicted to target these hub genes, and the lncRNA-miRNA-hub gene regulatory network was constructed. Ferroptosis-related hub genes were significantly associated with immune infiltration in the lung tissues of patients with COPD.


AUC, area under the curve; BP, biological process; CC, cellular component; CI, confidence interval; COPD, chronic obstructive pulmonary disease; CTD, Comparative Toxicomics Database; ENCORI, Encyclopedia of RNA Interactomes; FC, fold change; FRG, ferroptosis-related gene; FVC, forced vital capacity; GEO, Gene Expression Omnibus; GO, Gene Ontology; GOLD, Global Initiative for Chronic Obstructive Lung Disease; GPX4, glutathione peroxidase 4; KEGG, Kyoto Encyclopedia of Genes and Genomes; MCODE, Molecular Complex Detection; MF, molecular function; Nrf2, nuclear factor erythroid 2-related factor 2; NSCLC, non-small cell lung cancer; PCA, principal component analysis; PPI, protein–protein interaction; PUFA-PL, phospholipid containing polyunsaturated fatty acid chain(s); ROC, receiver operating characteristic; ROS, reactive oxygen species; TLR2, toll-like receptor 2.

Ethics Statement

This study was reviewed by Medical Ethics Committee of Qilu Hospital of Shandong University and exempted from ethical approval due to the usage of human data from the open and public Gene Expression Omnibus database.


This study was supported by the National Natural Science Foundation of China (grant No. 81800039) and the Jinan Clinical Research Center for Prevention and Control Project of Major Respiratory Diseases (grant No. 201912011).


The authors report no conflicts of interest in this work.


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A pulmonary embolism (PE) occurs when blood flow to an artery that supplies blood to the lungs has become blocked, typically due to a blood clot. Complications can develop from either the clot or the treatment for the PE.

PE may begin with a blood clot, or thrombus, that forms in another part of the body, such as the leg. The blood clot can travel to the lung through the circulatory system and lodge in an artery.

Symptoms may include breathlessness, chest pain, cough, fainting, rapid breathing, or an irregular heartbeat.

PE can permanently damage the lungs or result in blood oxygen levels so low that other organs become damaged.

If the clot is small, there may be no complications. However, if the clot is large, it can lead to issues with the lungs or heart or an increased risk of sudden death.

This article discusses the complications that can occur as a result of a PE.

Complications of a pulmonary embolism.Share on Pinterest
Photography courtesy of James Heilman, MD/Wikimedia & gilaxia/Getty Images

PE is a type of venous thromboembolism (VTE). A 2015 article notes that the likelihood of recurrence after a person first develops VTE is 5–7% each year.


After a PE diagnosis, a healthcare professional will prescribe anticoagulants, or blood-thinning medications. This helps prevent future blood clots.

However, anticoagulants can lead to side effects, such as excessive bleeding. People should contact a healthcare professional to discuss the best course of treatment for them.

Approximately 5% of individuals with PE develop chronic thromboembolic pulmonary hypertension (CTEPH), or high blood pressure in the arteries of the lungs, as a result.

Scarring of the blood vessels in the lung narrows their passageways, resulting in labored breathing.

If a person develops persistent or progressive shortness of breath between the first 3 months to 2 years after receiving a PE diagnosis, a doctor may investigate further.

The doctor may order:


People may need to undergo a surgical procedure health experts call pulmonary thromboendarterectomy. This is a complex procedure to remove blood clots from the pulmonary arteries.

A person with CTEPH may need to take anticoagulant medication for the rest of their life.

Pulmonary infarction (PI) occurs when a blood clot blocks the peripheral arteries, preventing some of the lung tissue from receiving enough blood and oxygen. The lung tissue then dies.

According to research from 2021, 30% of people with PE show signs of PI.

Individuals may experience:


There is no specific treatment for PI. Healthcare professionals will focus on treating the PE using anticoagulants and supportive care.

PE is one of the most common causes of pleural effusion, which affects 20–55% of people with PE.

Pleural effusion is when there is a buildup of fluid between the tissues that line the lungs and the chest, called the pleura.

Symptoms can include:

  • sharp chest pain
  • shortness of breath
  • cough


Alongside treating the PE, a healthcare professional may perform surgery to drain the fluid. They may also prescribe diuretics.

For 10–15% of individuals with PE, the heart is unable to pump enough oxygen and blood to the brain and other organs in the body. This can cause a drop in blood pressure and slow down a person’s pulse.

A person may experience:

Cardiogenic shock is a life threatening emergency, as it can result in brain injury or organ failure.


The National Heart, Lung, and Blood Institute notes that treatment focuses on protecting the organs from damage and getting the blood flowing properly.

People may require a heart transplant.

A PE can lead to a cardiac arrest, which increases the risk of death by 95%. Healthcare professionals would classify this as a massive PE.

A cardiac arrest is when the heart suddenly stops beating.


Healthcare professionals may administer a drug called tissue plasminogen activator. This will help break up the blood clots.

A person may also require surgery called venoarterial extracorporeal membrane oxygenation, which is a type of cardiopulmonary bypass surgery.

According to a 2019 article, a PE is the third most common cause of death related to the heart. Approximately 45% of those with acute PE will experience right ventricular failure.

The authors note that the right ventricle is designed to deal with a low resistance afterload. Afterload refers to the pressure that the heart works against in order to eject blood from the chambers and into the arteries.

An increase in the afterload can negatively affect the right ventricle’s ability to function, resulting in right heart failure.

Symptoms can include:


A doctor will first assess the severity of the condition.

Treatment may involve:

Treatment for blood clots involves anticoagulants. If the blood becomes too thin, and a cut or abrasion occurs, an individual can bleed too much.

Symptoms can include:


The American College of Cardiology notes that if the bleeding events are minor, a healthcare professional may recommend missing a few doses of the blood-thinning medication.

In more severe cases, however, they may suggest reversal agents, such as andexanet alfa.

Without treatment, 30% of individuals with PE will die. If a person is able to get treatment, this number reduces to 8%.

If a person experiences any symptoms of a PE, they should seek immediate medical attention.

People may have an increased risk of developing a PE if they have been in any of the following situations:

  • They have recently had a surgery, especially joint replacement surgery.
  • They have experienced physical trauma, such as a broken leg.
  • They have taken hormone-based medicine, including oral birth control.
  • They have been pregnant or given birth.
  • They have had cancer or heart or lung disease.
  • They have not moved for a long period, for instance, due to bed rest or a long trip.

Other factors that increase risk include:

  • being over 40 years of age
  • having a family history of blood clots
  • having obesity

To prevent complications from PE, early diagnosis is essential. If any symptoms of PE arise, a person should seek medical attention immediately.

These symptoms include:

Some complications develop due to underlying heart or lung conditions. To prevent PE complications, a person can try the following:

PE can be a serious condition if the blood clot is large or if there are many blood clots.

If any symptoms of PE develop, a person should seek medical attention right away. If a PE has already occurred, and any new symptoms, such as shortness of breath, develop, people should contact a doctor immediately.

If an individual takes blood thinners, and they experience excessive bleeding, a healthcare professional may need to adjust their treatment.

PE is a serious condition that occurs due to a blood clot traveling to an artery in the lung. It may first form in the leg, abdomen, or pelvis and travel to the lung via the circulatory system.

PE may lead to complications. These may include excessive bleeding from treatment with blood thinners, recurring blood clots, pulmonary hypertension, or cardiogenic shock.

Some factors increase the risk of a PE, such as bed rest, long travel, recent trauma, pregnancy or giving birth, and taking hormone-based medication.

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Airway Management Devices Market Outlook 2031

  • The global airway management devices market was valued at US$ 1.1 Bn in 2021
  • The global market is projected to expand at a CAGR of 7.7% from 2022 to 2031
  • The global airway management devices market is anticipated to reach US$ 2.3 Bn by the end of 2031

Analysts’ Viewpoint on Airway Management Devices Market Scenario

The global airway management devices market is majorly driven by rise in prevalence of chronic respiratory diseases across the globe. Strategic acquisition & collaborative agreements between key players and small players in emerging markets such as India, increasing geriatric population, rising incidences of preterm births, and corresponding efforts to improve survival rates are contributing to the market growth. However, companies in the global airway management market should focus on developing cost-efficient devices for the patients. Moreover, as patient admissions to emergency care departments and ICUs increased due to the COVID-19 pandemic, healthcare centers have become cautious and are procuring respiratory devices to address demand during pandemic-like situations in the future.

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Overview of Airway Management Devices Market

According to the latest report published by Transparency Market Research, the global airway management devices market is projected to expand at a considerable growth rate from 2022 to 2031, due to rising prevalence of chronic respiratory diseases such as asthma and COPD globally.

Patients with severe respiratory infections or low oxygen saturation often require positive air pressure devices such as ventilators. Airway management equipment include airway management tubes (endotracheal tube), laryngoscope handle and blade, positive airway pressure devices, and various sized oropharyngeal airways. These devices are mainly used in operating rooms during surgeries. In addition, for better patient outcomes, leading players operating in the global airway management devices market are focusing on developing technologically advanced respiratory devices.

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Rise in Prevalence of Respiratory Diseases Globally to Fuel Airway Management Devices Market Growth

Increase in incidences of chronic respiratory diseases such as asthma, and chronic obstructive lung disease (COPD) is driving the demand for airway management devices. Chronic obstructive pulmonary diseases, bronchitis, and emphysema, lung cancer, neoplasms of the respiratory tract, etc., significantly affect airways and lung structures. The incidence of respiratory diseases is increasing due to environmental and lifestyle-related factors such as air pollution, smoking habits, sedentary lifestyles, and stress. Rise in the number of patients suffering from such diseases, and rapid introduction & availability of portable, cost-contained, and easy-to-use airway equipment for the treatment of such conditions drive demand for airway management devices. Airway stenting and airway clearance system are unique therapy systems that use airway management devices.

Request for Analysis of COVID19 Impact on Airway Management Devices

According to the World Health Organization (WHO), in 2019, over 65 million people suffered from chronic obstructive pulmonary disease (COPD), and 3 million succumbed to it, making it the third-leading cause of death globally. Over 80% of these deaths occurred in low- and middle-income countries (LMIC). Over 262 million people suffer from asthma, the most common chronic pediatric disease that affects 14% of all children globally every year. In 2020, around 10 million people developed tuberculosis (TB) and 1.4 million lost their lives, making it the most common lethal infectious disease. Lung cancer accounts for 1.6 million deaths each year and is the most lethal form of cancer. Globally, 4 million people die prematurely from chronic respiratory disease. At least 2 billion people are exposed to indoor toxic smoke, 1 billion inhale outdoor pollutants in the air, and 1 billion are exposed to tobacco smoke.

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Increase in Adoption of Technologically Advanced Infraglottic Devices

In terms of product type, the global airway management devices has been classified into supraglottic device, infraglottic device, resuscitators, and laryngoscope. Infraglottic devices are expected to account for a dominant share of the global market in the upcoming years. Tracheostomy tubes and endotracheal Tubes (ETTS) are some of the popular infraglottic devices used by patients. Technological advancements in these devices and their increasing application during emergencies are major factors fueling the demand for infraglottic airway devices, particularly in developed regions such as Europe and North America.

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By Express News Service

BENGALURU: Those who had contracted the Omicron variant of Covid-19 may develop Long Covid less frequently than those who had other variants, authors of a new study out of Japan concluded. However, anecdotal findings of doctors in Karnataka are mixed. While some patients did report Long Covid symptoms, doctors say a majority had symptoms like hair loss, depression, brain fog, anxiety etc, but did not have many respiratory related symptoms as in post-Delta infection. 

Dr Satyanarayana Mysore, HoD and Consultant, Pulmonology, Lung Transplant Physician, Manipal Hospital, says, “The established fact and our observation is that people who developed Omicron did have different sets of Long Covid symptoms which range from cough, feverishness and day time sleepiness. We did not find Omicron give rise to less Long Covid by definition.” 

The study, published in journal preprint server medRxiv, reviewed and approved by the ethics committee of the Center Hospital of the National Center for Global Health and Medicine, said it represents first time epidemiological data on Long Covid in Omicron patients. But more research is needed to see if findings are applicable to Omicron patients as a whole, and to determine the long-term impact of the variant “on health-related quality of life and social productivity”, the paper stated.

Dr Sunil Kumar K, Lead and Sr Consultant, Interventional Pulmonology, Aster CMI Hospital, said during the second wave, patients suffered post-viral bronchitis and complained of dry cough and throat discomfort post recovery. He explains, “Post-Covid symptoms can manifest, no matter which variant it is. However, the incidence of post-Covid symptoms caused by Omicron does not seem to cause a high or persistent rise in inflammatory markers in the body during infection.

Depending on the severity of the virus, Long Covid symptoms are likely to increase. As Omicron was less severe, we are seeing fewer people with post-Covid symptoms.” According to doctors, some Long Covid symptoms included fatigue, difficulty in breathing, cough, hair loss, depression, brain fog, difficulty in concentrating and memory issues. Dr Mahesh Gowda, Director, Spandana Hospitals, said, “Post Omicron, there have been patients with symptoms of prolonged depression, anxiety and brain fog. However, some of these symptoms were part of Delta infections too.” 

Meanwhile, agreeing that there are not as many long covid cases as earlier Dr Shalini Joshi, Senior Consultant, Internal Medicine, Fortis Hospitals says, "We saw many cases of Omicron since January but we have seen very few patients coming in for long covid symptoms."

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CUMBERLAND, Md., May 23, 2022 (GLOBE NEWSWIRE) -- RS BioTherapeutics, whose mission is to harness its strong and thorough understanding of the endocannabinoid system to research, develop and commercialize interventions to address chronic and acute pulmonary (lung) inflammation-based diseases, is pleased to announce that is has entered into a license agreement with Synthonics, Inc. for the exclusive, worldwide right to use Synthonics’ metal coordinated cannabinoid in nebulized form for the treatment of pulmonary inflammatory disorders. RS BioTherapeutics is developing its lead compound, RSBT-001, as both an alternative and a complement to corticosteroids for the treatment of chronic obstructive pulmonary disease (COPD).

COPD is a chronic inflammatory lung disease that causes obstructed airflow from the lungs and includes emphysema, chronic bronchitis, asthma and more. According to the American Lung Association, 156,045 people died from COPD in 2018, making it the third highest disease-related cause of death behind heart disease and cancer. It is estimated that more than 250 million people globally may have the condition and more than 65 million people around the world have moderate or severe COPD. Experts predict that this number will continue to rise worldwide over the next 50 years. The CDC estimates that 16 million Americans suffer from COPD. People with COPD are at increased risk of developing heart disease, lung cancer, and a variety of other conditions. If chronic pulmonary inflammation is untreated, it can lead to fibrosis, organ damage, and loss of organ function.

Commenting on the potential benefits of this first investigational compound, RSBT-001, Justin Molignoni, CRNP, Chief Strategy Officer and Co-Founder of RS BioTherapeutics, said, “Alternatives to corticosteroids are needed for people with chronic inflammatory diseases. We believe RSBT-001 has the clinical potential to address exacerbation and prevent progression of both acute and chronic pulmonary inflammation related to respiratory diseases including COPD, SARS-COV-2, Cystic Fibrosis, Asthma, Bronchitis, and Acute Respiratory Distress Syndrome.”

John Tinkham, CEO and Co-Founder of Synthonics, added, “We believe that metal coordination can significantly enhance the effectiveness of cannabinoid-based pharmaceuticals and are delighted to partner with RS BioTherapeutics on this project. We look forward to working closely with RS BioTherapeutics to assist on the development of RSBT-001.”

Various sources estimate the global pulmonary drug delivery systems market was approximately $51 billion in 2021, and it is expected to be worth around $92 billion by 2030, with a compound annual growth rate of 6.6 percent within in next 10 years.

About RS BioTherapeutics Founded by experts in pulmonary diseases and the endocannabinoid system, RS BioTherapeutics is a wholly owned subsidiary of Real Science Holdco LLC. The company’s mission is to harness its strong and thorough understanding of the Endocannabinoid System in the research, development, and commercialization of forward-thinking interventions to address chronic and acute pulmonary inflammation-based diseases.   More information on RS Biotherapeutics can be found at

About SynthonicsSynthonics, Inc. is a privately-held specialty pharmaceutical company focused on the discovery and development of patentable drugs that incorporate its proprietary metal coordination chemistry. It binds metals to known pharmaceutical agents to create new products that are better absorbed and thus have greater therapeutic benefits than their predecessors. More information on Synthonics can be found at

Media Contact: David Gutierrez, Dresner Corporate Services, (312) 780-7204, [email protected]


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Source: RS BioTherapeutics

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Global Chronic Obstructive Pulmonary Disease (COPD) Drug Market Overview:

The large scale Chronic Obstructive Pulmonary Disease (COPD) Drug Market report consists of most-detailed market segmentation, thorough analysis of major market players, trends in consumer and supply chain dynamics, and insights about new geographical markets. All the data and statistics covered in this business report lead to an actionable ideas, improved decision-making and better mapping business strategies. This report analyses the Healthcare industry from top to bottom by considering myriad of aspects. Businesses can rely upon this top-notch market report to accomplish an utter success. Global Chronic Obstructive Pulmonary Disease (COPD) Drug Market report offers better solution for refining the business strategies to thrive in this competitive market place.

The data and information regarding Healthcare industry are taken from reliable sources such as websites, annual reports of the companies, and journals etc. and were checked and validated by the market experts. Chronic Obstructive Pulmonary Disease (COPD) Drug Market report helps in planning by providing precise and state-of-the-art information about the consumer’s demands, preferences, attitudes and their changing tastes about the specific product. This report has been prepared by considering various steps for collecting, recording and analysing market data. An influential Chronic Obstructive Pulmonary Disease (COPD) Drug report employs various basic steps of market analysis that include survey, focus groups, personal interviews, observations, and field trials.

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The Global Chronic Obstructive Pulmonary Disease (COPD) Drug Market is expected to witness market growth at a rate of 5.05% in the forecast period of 2022 to 2029.

According to market research study, Chronic Obstructive Pulmonary Disease (COPD) refers to a common, preventable, incurable, and treatable disease which displays persistent respiratory symptoms and airflow limitation. Chronic inflammation in the airways leading to alveolar abnormalities could be caused by long-term exposure to noxious particles or gases such as cigarette smoke and environmental pollution.

Some of most important key factors driving the growth of the Global Chronic Obstructive Pulmonary Disease (COPD) Drug Market are increase in the prevalence of respiratory diseases globally, rise in the prevalence of chronic obstructive pulmonary disease (COPD) among population across the globe, increase in demand for home care therapeutic and treatments for the chronic respiratory disease due to the comfort and ease and rise in demand for the drugs to treat breathing difficulty, cough, mucus production and wheezing.

The Global Chronic Obstructive Pulmonary Disease (COPD) Drug Market is segmented on the basis of Drug Type, Product Type, Type, Diagnosis, Treatment and End-User.

Based on the Drug Type, the chronic obstructive pulmonary disease (COPD) drug market is segmented into phosphodiestrase-4 inhibitors, long-acting bronchodilators, short-acting bronchodilators, methylxanthines and corticosteroids.

Based on the Product Type, the chronic obstructive pulmonary disease (COPD) drug market is segmented into inhalers and nebulizers.

Based on the Type, the chronic obstructive pulmonary disease (COPD) drug market is segmented into chronic bronchitis and emphysema.

Based on the Diagnosis, the chronic obstructive pulmonary disease (COPD) drug market is segmented into pirometry, diagnostic tests and others.

Based on the Treatment, the chronic obstructive pulmonary disease (COPD) drug market is segmented into oxygen therapy, lung transplant, drug therapy, vaccination, surgery and others.

Based on the End-User, the chronic obstructive pulmonary disease (COPD) drug market is segmented into hospitals and clinics, home care settings and others.

In terms of the geographic analysis, North America dominates the chronic obstructive pulmonary disease (COPD) drug market due to the increasing patient population suffering from COPD and the presence of major market players within the region. APAC is expected to witness the fastest growth during the forecast period of 2022 to 2029 because of the high patient population suffering from COPD and the rising prevalence of respiratory disease.

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Top Leading Key in Players Global Chronic Obstructive Pulmonary Disease (COPD) Drug Market: AstraZeneca, GlaxoSmithKline plc, Novartis AG, Boehringer Ingelheim International GmbH, Teva Pharmaceutical Industries Ltd, Aché Laboratórios Farmacêuticos S.A., bioMARCK, Aquinox Pharmaceuticals, Astellas Pharma Inc., Abbott., F. Hoffmann-La Roche Ltd, Adamis Pharmaceuticals Corporation, Sunovion Pharmaceuticals Inc., Mylan N.V., Orion Corporation, Grifols, S.A., Theravance Biopharma, Circassia, ResMed and others. New product launches and continuous technological innovations are the key strategies adopted by the major players.

Region segment: Chronic Obstructive Pulmonary Disease (COPD) Drug Market report is segmented into several key regions, with sales, revenue, market share (%) and growth Rate (%) of Chronic Obstructive Pulmonary Disease (COPD) Drug in these regions, from 2013 to 2025 (forecast), covering: North America, Europe, Asia Pacific, Middle East & Africa and South America

This study answers to the below key questions:

1 What will the market size be in 2029?

2 What are the key factors driving the Global Chronic Obstructive Pulmonary Disease (COPD) Drug Market?

3 What are the challenges to market growth?

4 Who are the key players in the Chronic Obstructive Pulmonary Disease (COPD) Drug Market?

5 What are the market opportunities and threats faced by the key players?

For More Insights Get FREE Detailed TOC of “Global Chronic Obstructive Pulmonary Disease (COPD) Drug Market Report 2022” @ .

Major Highlights of TOC: Global Chronic Obstructive Pulmonary Disease (COPD) Drug Market

1 Global Chronic Obstructive Pulmonary Disease (COPD) Drug Market Overview

2 Global Chronic Obstructive Pulmonary Disease (COPD) Drug Market Competitions by Manufacturers

3 Global Chronic Obstructive Pulmonary Disease (COPD) Drug Capacity, Production, Revenue (Value) by Region (2022-2029

4 Global Chronic Obstructive Pulmonary Disease (COPD) Drug Supply (Production), Consumption, Export, Import by Region (2022-2029)

5 Global Chronic Obstructive Pulmonary Disease (COPD) Drug Production, Revenue (Value), Price Trend by Type

6 Global Chronic Obstructive Pulmonary Disease (COPD) Drug Market Analysis by Application

7 Global Chronic Obstructive Pulmonary Disease (COPD) Drug Manufacturers Profiles/Analysis

8 Chronic Obstructive Pulmonary Disease (COPD) Drug Manufacturing Cost Analysis

9 Industrial Chain, Sourcing Strategy and Downstream Buyers

10 Marketing Strategy Analysis, Distributors/Traders

11 Market Effect Factors Analysis

12 Global Chronic Obstructive Pulmonary Disease (COPD) Drug Market Forecast (2022-2029)

13 Research Findings and Conclusion

14 Appendix

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The infection rate of SARS-CoV-2, the virus that causes COVID-19, is 24 times higher in laboratory cultured respiratory cells from humans with chronic obstructive pulmonary disease (COPD) than in those from healthy people, a study shows.

This increased susceptibility to infection, which makes severe outcomes more likely, was associated with higher enzyme levels that the virus uses to penetrate cells, as well as higher pro-inflammatory molecular levels and lower levels of antiviral proteins.

“Together, these results have enabled us to understand the mechanisms behind increased COVID-19 susceptibility in COPD patients,” said Phil Hansbro, PhD, the study’s senior author in a Press release. Hansbro is Professor of Microbiology at the University of Newcastle and Director of the Centenary UTS Center for Inflammation, both in Australia,

“We believe in the new [therapies] Targeting relevant enzymes and pro-inflammatory responses in SARS-CoV-2 infection could have excellent therapeutic potential to reduce the severity of COVID-19 in patients with COPD, ”added Hansbro.

The study, “Increased SARS-CoV-2 infection, protease and inflammatory responses in COPD primary bronchial epithelial cells defined by single cell RNA sequencing“was published in American Journal of Respiratory and Critical Care Medicine.

Mainly associated with prolonged exposure to irritants such as cigarette smoke, COPD is characterized by excessive airway inflammation, pulmonary tissue remodeling and the progressive destruction of the alveoli – the small lung air sacs responsible for gas exchange.

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Rising evidence shows COPD patients are more susceptible to severe COVID-19, but the underlying mechanisms of this susceptibility remain largely unclear.

One potential factor is the increased production of ACE2 – the cell surface receptor that SARS-CoV-2 binds to enter cells – in airway cells after exposure to cigarette smoke. Also, COPD patients’ lungs have higher than normal levels of proteases, a family of enzymes that include those used by SARS-CoV-2 to penetrate cells.

To learn more about what contributes to COPD patients’ increased susceptibility to SARS-CoV-2 infection, Hansbro’s research team, together with colleagues in Australia, analyzed the viral load and gene activity profiles of laboratory-grown airway cells – called primary bronchial epithelial cells (pBECs) – from four adults. with COPD and three healthy adults using a high-resolution technique called single-cell RNA sequencing.

Patients included two women and two men (age range, 67-85 years), while healthy controls included two women and one man (age range, 55-75 years). No participant had a history of respiratory infection within the past month or a lung cancer diagnosis.

The results showed that seven days after cells were exposed to SARS-CoV-2, “there was a 24-fold increase in the amount of virus in the COPD patient’s airway cells compared to the cells taken from healthy individuals,” Matt Johansen, PhD, the study’s first author from Centenary UTS Center for Inflammation, said.

Gene activity profiles between infected and present cells in both groups were generally similar, highlighting that “there are commonly used pathways in SARS-CoV-2 [infection]which are independent of pre-existing disease status, ”the researchers wrote.

Compared with controls, airway cells from COPD patients showed significantly increased levels of transmembrane protease serine 2 (TMPRSS2), cathepsin B (CTSB) and cathepsin L (CTSL), three proteases known to promote the entry of SARS-CoV-2 into cells.

In turn, the levels of more serpins – proteins known to suppress the activity of proteases – were significantly reduced in COPD cells compared to healthy controls, regardless of infection.

These results “highlight a protease imbalance in COPD-pBECs that may be crucial for increased SARS-CoV-2 infectivity and serious disease,” the researchers wrote.

“Simply put, milder and increased cell infection makes it far more likely that people with COPD will have more serious disease outcomes,” Johansen said.

The team also found that the levels of pro-inflammatory molecules associated with COPD’s sudden disease aggravating episodes and severe COVID-19 were significantly increased in both infected and uninfected respiratory cells from people with COPD.

“COPD is an inflammatory disease in which patients have increased inflammation… compared to healthy people,” and “it is highly likely that SARS-CoV-2 exacerbates this existing high level of inflammation, leading to even worse outcomes,” Johansen said.

Key antiviral responses involving proteins called interferons were also largely blunt-ended in respiratory cells from COPD patients compared to those from controls, which may be “a key driver for increased susceptibility to elevated inflammatory and viral responses. [infection]”, wrote the research team.

ACE2 was found to be significantly increased by infection in both COPD and control cells, but there were no significant differences between the groups, suggesting that ACE2 may not be a contributing factor to increased infection susceptibility in COPD.

In addition, therapeutic interventions that suppress either TMPRSS2, CTSB, inflammation, or all three at the same time significantly reduced SARS-CoV-2 load and pro-inflammatory molecules in especially COPD patient cells.

This is the “first study to show biological evidence that COPD pBECs are significantly more tolerant of SARSCoV-2 infection compared to healthy pBECs,” the researchers wrote.

The results also highlighted that this increased susceptibility is due to protease imbalances, major inflammatory responses, and reduced interferon responses, potentially describing “biological mechanisms responsible for exacerbations and severe COVID-19 in COPD,” the research team wrote.

Several studies are needed to analyze the relevance of these candidates, as well as the therapeutic potential of targeting protease imbalance, excessive inflammation, or deficient interferon response in COPD patients with COVID-19.

Hansbro said these findings are critical as hundreds of millions of people are affected by COPD globally and COVID-19 is likely to exist in the coming years.

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COVID-19 has been frustrating for exercise rats. Even before scientists knew much about this particular virus, it was pretty clear that it was an easy way to get respiratory diseases by breathing heavily in a confined space with lots of other people around, and gyms were among the first companies to closed early in the pandemic. These suspicions have since been confirmed by science: aerosols – small droplets that disperse through the air as we breathe – have been identified as a significant source of COVID-19 infection, especially when people breathe faster and deeper. During the entire pandemic, training at spin classes, fitness clubs and sports games has been identified as the source of dozens of new cases.

Now a new experiment has given us a more accurate sense of how many aerosols a single person can spit out during an intense workout – and the results are not pretty. According to research conducted by researchers in Germany published in PNAS on May 23132 times as many aerosols per minute during high-intensity training than when at rest, researchers warn, increases the risk of a person infected with COVID-19 triggering a superspreader event. At rest, people emitted an average of 580 particles per minute, but during maximal training – where researchers gradually increased the intensity until the subjects were exhausted – people emitted an average of 76,200 particles per minute.

The authors of the study acknowledge that their work has limitations. First of all, the sample size was only 16 people. In addition, none of the subjects were infected with COVID-19; in the paper, the researchers note that there was no way to make it safe, due to ethical concerns about health risks for the participants.

Nevertheless, there were some valuable results to get out of the work. “[As an exercise physiologist], and we knew before that when you train, more air comes out of a person, ”says Henning Wackerhage, co-author and professor of training biology at the Technische Universität München. “But we did not know it before, and what I honestly did not expect is that even when we train hard: there are more particles per liter of air.”

The unusual experimental design allowed the researchers to get a more accurate sense of the released particles. While training on a stationary bike, each of the 16 subjects breathed clean air through a silicone face mask and then exhaled in a plastic bag. This allowed researchers to eliminate sources of pollution and get more reliable results, says Christian Kähler, professor at the Institute of Fluid Mechanics and Aerodynamics at the Universität der Bundeswehr München, who co-authored the study.

Some of the participants also emitted much more aerosols during high-intensity training than others; especially fitters with more experience in endurance training emitted 85% more aerosols than people without such training. Dr. Michael Klompas, a hospital epidemiologist and infectious disease physician at Brigham and Women’s Hospital who did not participate in the study, explains that this may be a function of the way individuals’ bodies become more efficient at moving large amounts of air. “They get their muscles to do a tremendous amount of work, and they have to support that by giving their muscles huge amounts of oxygen and helping to remove waste products,” he says.

If this gives you a break from your current workout program, keep in mind that not all gyms are the same – and the right policies and setup can help keep you safe. For example, the amount of space per. person crucial; large spaces, especially those with high ceilings, give the air more space, says Thomas Allison, director of Cardiopulmonary Exercise Testing Laboratories at the Mayo Clinic. Other things to look for in a gym, Klompas says, are a vaccination requirement, a facility that has professionally measured airflow and put air filters in place, and ideally a test requirement. In Klompas’ opinion, masks are potentially useful, but they are probably not reliable during training – looser masks will not do much during vigorous training, and it is impractical to expect people to wear N95s while exerting themselves.

The researchers note that factors besides fitness status can also affect how many aerosols people emit. Wackerhage says they are also investigating how factors such as body mass index, age and lung condition play a role.

Ultimately, says Klompas, whether you go to a gym or not, your risk tolerance and weighting of the costs and benefits of going to the gym for you personally depends. But, he says, do not pretend that exercising indoors and around other people does not pose a risk. “If you’re not willing to get COVID, then do not go,” Klompas says. “At a time like this, when there is a lot of COVID around, it’s a high-risk proposal.”

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An aerobic walking workout is one of the best walking techniques that’ll help increase your overall fitness. It is a type of walk which is brisk and long enough to enhance your heart rate and keep it there for a few minutes, preferably for half an hour to 50 minutes. The major elements of aerobic walking include walking very fast, sweating, and breathing very hard.

The aerobic walk should not be extended for more than 45 minutes to an hour and should include a quick warm-up session, a few stretching exercises, and a cooldown.

How to get started?

Here’s a step-by-step instruction on how you can start aerobic walking.

  • Start by walking at an easy pace for at least 10 minutes.
  • Stop for a few minutes and do some stretching exercises for five minutes to build your flexibility and improve your mobility.
  • Then, continue to walk at a pace that elevates your heart rate up to 70% of your maximum heart rate. This is the pace where you can speak in short sentences and breathe hard. Walk for about 50 minutes at this pace.
  • Cool down with 10 minutes of walking at an easy pace.
  • End the session with five minutes of easy stretching and flexibility workouts.

The primary benefits of aerobic walking:

Aerobic walking helps improve your overall aerobic fitness so that you can exercise more intensely and for an extended duration of time. It also develops your lung power and enhances the size as well as the number of blood vessels in your muscles. At aerobic walk intensity, a total of 50% of your calories that are burned are fats, proteins, and carbohydrates. The aerobic phase of your walking, however, should be no more than 50 minutes so as to prevent the buildup of lactic acid in your body.

If you want to walk longer than an hour, it is recommended to slow your pace at the ending phase of your walk.

Where can you do the aerobic walking workout and what all do you need?

You can do an aerobic walk on an indoor walking track, outside, or inside on a treadmill. You simply need to find a course where you can walk easily without any interruptions. You’ll also need flexible and comfortable running shoes for a fast walking pace and to bring your heart rate up. When it comes to clothes, on the other hand, make sure you wear light clothes that are comfortable and give you full freedom of movement and also absorb sweat. Since you’ll be sweating and getting tired a lot, don’t forget to carry a water bottle to keep your body hydrated. Drink water every 20 to 25 minutes to hydrate yourself.

When can you perform an aerobic walking workout?

You can do an aerobic walk workout every alternate day, and on the days in between, you can incorporate a weight training or strength training exercise instead. Combining workouts will give your body the proper time to replenish its strength and to avail the advantages of the workout.

How can you increase your aerobic walking pace and heart rate?

  • If you are walking on a treadmill, you may increase the incline and raise your heart rate so that you can achieve that benefit at a slower speed.
  • If you are walking outdoors, find a walking route that has stairs, hills and other terrains that can elevate your heart rate. Additionally, you may add fitness walking poles to raise your heart rate.

If you are a fit person, there is a chance that you may not be able to get your heart rate up to 70 to 80% of maximum heart rate by simply walking. In this case, you may want to add running intervals in between your walks to keep your heart rate high.

There are several reasons why increasing your aerobic walking pace can be beneficial to your health. Before just throwing yourself into an aerobic walk workout, figure out your fitness goals and determine your walking speed. Also, make sure you wear the right kind of shoes and clothes to keep the session comfortable.

Take time to correct your walking posture, give attention to your arm movement, and make sure there is no pain or injury in your body. Checking all this is a good investment of time as it will help keep your entire aerobic walking session safe and effective.

Edited by Jodi Whisenhunt

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A new combination of asthma drugs not only works better for treating asthma attacks, but also lowers patients’ chances of future attacks, according to a big study by researchers at Rutgers and Italy’s University of Ferrara.

“This represents a paradigm shift in the treatment of asthma,” Rutgers professor of medicine Reynold Panettieri Jr. said in a statement. “We see this combination treatment, which is the first of its kind, as becoming part of standard therapy.”

Hard to breathe: Asthma is a chronic breathing disorder caused by the airways of the lung being swollen or inflamed. These passageways are then more susceptible to triggers, like cold weather, dust, or pet dander.

When you breathe in a trigger, the passageways inflame even more, and the muscles which surround them can become tighter — leading to a frightening, and potentially life-threatening, asthma attack.

The disease burden is high; the WHO estimates that 262 million people were afflicted with asthma in 2019, with 455,000 dying prematurely from it.

The drug combination lowered both the short and long term the risk of asthma attacks.

The usual: The standard “maintenance” treatment of asthma involves using inhalants with two different asthma drugs, the researchers said. One is a long-acting drug which binds to proteins on the muscles called beta receptors, causing the muscles to relax; the other is a corticosteroid, which inhibits inflammation.

During an asthma attack, patients use what are called “rescue” medications like albuterol, which rapidly bind to the beta proteins, and they may even be prescribed oral steroids. 

Oral steroids, while effective, can cause myriad side effects, including fluid retention, weight gain, high blood pressure, and psychological effects like mood swings, memory irregularities, and confusion.

For this reason, the researchers are looking for ways to reduce oral steroid dependency.

Combining asthma drugs: In their study, published in the New England Journal of Medicine, they tested whether a combination of albuterol and the corticosteroid budesonide could lower the number of asthma attacks when taken together. Budesonide decreases the severity and regularity of asthma attacks when taken daily, but it doesn’t work as a rescue medication by itself.

The team enrolled 3,312 asthma patients from the US, Europe, and South America into a randomized controlled trial to test both the safety and effectiveness of the inhaled combination of the asthma drugs.

“This represents a paradigm shift in the treatment of asthma. We see this combination treatment, which is the first of its kind, as becoming part of standard therapy.”

Reynold Panettieri Jr

Since many of the patients were already on maintenance therapies, they randomly received one of three rescue medication combinations: albuterol and a high dose of budesonide; albuterol and a low dose of budesonide; and a control group of albuterol alone. 

The high-dose combination reduced the chances of another asthma attack by 24% in the short term, and 27% in the long term. The combo actually allowed for 33% reduction in the use of corticosteroids because it delivers them so effectively.

“With this new inhaler that delivers more inhaled steroids every time patients take the rescue therapy, they’re getting more at a time when they’re having a flare-up and when they need it,” Panettieri said. 

We’d love to hear from you! If you have a comment about this article or if you have a tip for a future Freethink story, please email us at [email protected]

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Elkin and Philip report no relevant financial disclosures. Please see the study for all other authors’ relevant financial disclosures.

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An online breathing and well-being program improved health-related quality of life and persistent breathlessness in individuals with ongoing symptoms following COVID-19, researchers reported in The Lancet Respiratory Medicine.

“We urgently need evidence-based treatments and interventions for people with long COVID, which currently affects approximately 1 in 50 people in the U.K.,” Keir E. J. Philip, MRCP, clinical research fellow at the National Heart and Lung Institute and the NIHR Imperial Biomedical Research Centre at Imperial College London, and colleagues said in a related press release. “Our study suggests that arts-in-health interventions can be effective tools for carefully selected participants, especially when successfully integrated with clinical services.”

woman of computer

Source: Adobe Stock.

Philip and colleagues conducted a parallel-group, single-blind, randomized controlled trial that enrolled 150 adults referred from one of 51 U.K.-based long COVID clinics. All patients were recovering from COVID-19 with continuous breathlessness, with or without anxiety, for at least 4 weeks after symptom onset. Patients had internet access with the appropriate devices and were randomly assigned to participate in the English National Opera (ENO) Breathe program (n = 74; mean age, 49 years; 78% women) or usual care (n = 76; mean age, 50 years; 83% women).

The ENO Breathe program group participated in a 6-week online breathing and well-being program that focused on breathing retraining using singing techniques.

The primary outcome was change in health-related quality of life assessed by mental health composite and physical health composite scores. Secondary outcomes included COPD assessment test score, visual analogue scales for breathlessness and dyspnea-12, Generalized Anxiety Disorder 7-item scale and SF-6D scores. The trial was conducted from April to May 2021.

Those in the ENO Breathe program group experienced improvement in mental health composite scores (P = .047) but not physical health composite scores (P = .54) compared with usual care, according to the results. The intervention was also associated with better visual analogue scale scores for breathlessness (P = .0026).

The researchers reported no significant differences between the two groups in other secondary outcomes.

The health improvements observed in this study were further analyzed via focus groups and questionnaires. Analyses showed that individuals who participated in the ENO Breathe program reported experiencing more improvements in their symptoms, felt the program complemented other care they were receiving, and that using singing techniques and music suited their needs. Additional analyses focused on participants who completed all sessions highlighted improvements in a wider range of respiratory symptoms, anxiety and greater quality of life improvements. For example, 40% of those in the ENO Breathe group had a five-point improvement in the mental component of quality of life compared with 17% in the usual care group, according to the press release.

One participant in the ENO Breathe program group reported feeling dizzy using a computer for extended periods. No other adverse events were reported.

“As we continue to recover from the impact of the pandemic, it’s vital we find ways to support people with long COVID who are experiencing debilitating symptoms long after recovering from their initial COVID-19 infection,” Sarah Elkin, MD, consultant lead for the ENO Breathe program and respiratory consultant at the National Heart and Lung Institute at Imperial College Healthcare NHS Trust, London, said in the release. “It is extremely important to build an evidence base for programs such as ENO Breathe, so we can continue to understand how best to support people with long COVID and make improvements that can lead to better outcomes.”


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Somniphobia means you're scared to sleep, and it can be caused by a host of different things.

Image Credit:
Tero Vesalainen/iStock/GettyImages

When you were little, you might've been afraid to drift off to dreamland, worried about a monster under your bed. As adults, most of us outgrow this nighttime fear.

But for people with somniphobia, falling sleep still triggers terror. Sometimes referred to as "sleep dread," somniphobia is a specific type of anxiety or fear related to sleep that typically increases as bedtime approaches, says sleep expert Wendy Troxel, PhD, a senior behavioral and social scientist at the RAND Corporation and author of ​Sharing the Covers: Every Couple's Guide to Better Sleep​​.

Fear of sleep isn't just an inconvenience — it can also affect your mental and physical health. So, if you're wondering ​why am I scared to sleep?​ (and your anxiety is getting in the way of your day-to-day functioning)​,​ read on to learn about the signs of somniphobia and effective ways to cope with this condition.

Somniphobia is just that: a phobia.

A phobia is defined as an extreme, irrational fear of something that presents little or no actual danger, according to the National Institute of Mental Health (NIMH).

Approximately 12.5 percent of American adults wrestle with a specific phobia during their lifetimes, per the NIMH.

In the case of somniphobia, sleep — something our bodies need to function properly — is the thing that brings up severe anxiety.

Like other types of phobias, somniphobia can be very stressful and lead to serious consequences, most notably sleep deprivation, Troxel says.

Indeed, chronic sleep loss is linked to an increased risk of heart disease, kidney disease, high blood pressure, diabetes, stroke, obesity, depression and other cognitive issues, according to the National Heart, Lung, and Blood Institute.

Signs of somniphobia resemble the common symptoms of anxiety or panic, Troxel says. The main difference is timing: Somniphobia symptoms specifically occur close to bedtime, while trying to fall asleep or in the middle of the night, she explains.

  • Feeling
    stressed, overwhelmed, nervous, agitated, restless and fearful
  • Upset
  • Rapid heart
    rate and/or breathing
  • Muscle
  • Shakiness or
  • Sweating
  • Nocturnal
    panic (a sudden and intense burst of extreme fear or anxiety that occurs during
    sleep, causing one to wake up in a startled, often terrified state)

Experts don't really know what causes somniphobia (or other phobias, for that matter), Troxel says.

But one thing is for certain: You're more likely to experience somniphobia if you have anxiety or a sleep disorder, or if you have a family history of phobias or other mental health disorders, Troxel says.

For instance, sometimes somniphobia appears to arise in response to a difficulty with sleep. "Most often we see this in individuals who have a sleep disorder, such as insomnia or obstructive sleep apnea, who over time, after not sleeping well, develop anxiety around their ability to sleep soundly at night," Troxel says.

"Somniphobia also commonly occurs among individuals with other mental health disorders, including post-traumatic stress disorder (PTSD)," Troxel says. People dealing with this distressing disorder may develop somniphobia (or even avoid sleep altogether) to prevent nightmares, a cardinal symptom of PTSD, she explains.

Many people with somniphobia will also actively avoid sleep by using excessive alcohol or caffeine, Troxel says.

"Unfortunately, these avoidance strategies only make the situation worse as one becomes more sleep-deprived," Troxel adds.

3 Ways to Manage Somniphobia

If you're battling fear at bedtime and it's affecting your quality of life, try these strategies to help you cope with the condition and hit the hay for good health.

"Treatment [for somniphobia] really depends on the underlying cause of the symptoms," Troxel says. "Therefore, the first step is to talk with a sleep or mental health professional to determine if another sleep disorder or mental health disorder is driving the symptoms."

The good news: Effective treatments exist, no matter the reason for your fear of sleep.

For example, cognitive behavioral therapy (CBT) can be very useful for those with insomnia-induced somniphobia. CBT "involves a set of behavioral 'prescriptions' to regularize sleep habits and work through unhelpful thoughts or fears about sleep," Troxel says.

"And for those who have nightmares, imagery rehearsal therapy (IRT) is a behavioral treatment proven to be effective in reducing nightmare frequency and intensity," Troxel says.

IRT entails "practicing" (via imagery) a more pleasant dream experience during the daytime to help shift your mindset and "break the habit" of having disturbing dreams at night, she explains.

2. Try Relaxation Techniques

"Finding ways to unwind and reduce anxiety at night, such as mediation, yoga or deep breathing exercises, can also be helpful," Troxel says.

Specifically, meditation is an amazing method to mellow out before bed. Case in point: An April 2015 study in ​​JAMA Internal Medicine​​ found that practicing mindfulness meditation reduced insomnia, fatigue, depression, anxiety and stress among adults with chronic sleep problems.

New to meditation? Sleep apps — which offer everything from guided sleep meditations to soothing nature sounds and calming music — are a great place to start for sound slumber.

3. Practice Good Sleep Hygiene

Healthy sleep behaviors like setting consistent bedtimes and wake times, and limiting bright screen use before bed are also critical for catching quality zzzs, Troxel says.

Similarly, steer clear of alcohol or caffeine at night, which can disrupt and sabotage your shut-eye, she adds.

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FeNO (pronounced “fee-no”) stands for fractional exhaled nitric oxide. While this gas is found in the atmosphere, the body also produces nitric oxide when inflammation is present in the airways.

FeNO testing isn’t new — it’s been used in the diagnosis and management of asthma since the 1990s. The first commercial device was manufactured about 20 years ago. Today, devices that measure FeNO include NIOX VERO, Fenom Pro, and the NObreath FeNO Monitor.

Here’s more about what these tests measure, how they’re performed, and their accuracy.

FeNO tests measure the amount of fractional exhaled nitric oxide present in the airways. If you have a high amount of this gas in your breath when you exhale, it may mean that you have inflammation. This is common for people with asthma, allergies, or eczema.

A doctor can use this information to help them diagnose certain types of asthma, but it’s important to note that a FeNO test by itself cannot diagnose asthma. Instead, the National Heart, Lung, and Blood Institute (NHLBI) says a FeNO test helps to confirm an asthma diagnosis. The test can also help rule out similar conditions and predict how well your body may respond to the use of corticosteroids as asthma treatments.

How does the FeNO test help those with asthma?

If you already know you have asthma, FeNO tests can help your doctor track if your current treatment plan is working. For example, the test can show whether your medications need to be increased or decreased in order to better control your inflammation, according to the Asthma and Allergy Foundation of America (AAFA). It may also help indicate how regularly you have been taking your prescribed treatments.

FeNO tests may even help your doctor pinpoint what type of asthma you have, like allergic asthma or eosinophilic asthma. They can also give valuable information about your inflammation markers over time.

As with any medical test, there are certain pros and cons to FeNO testing. If you have concerns, consider discussing these points with your doctor before undergoing testing.

The biggest possible advantage is fewer asthma exacerbations. A 2016 study showed that people who had FeNO testing were less likely to have asthma attacks than people who did not have testing. Overall, the FeNO group had 41 percent fewer asthma attacks over the course of a year than the control group.

Other advantages of the FeNO test are that it:

  • takes only a few minutes
  • is noninvasive
  • has low or no side effects
  • requires very little preparation
  • provides results right away

Some disadvantages of the FeNO test are that it:

  • needs to be performed in a doctor’s office
  • does not diagnose all types of asthma
  • cannot be used for kids under 5 years old
  • may cause short-term lightheadedness
  • can be expensive without insurance

Preparation for the test is simple. For best results, according to Asthma+ Lung UK, make sure to avoid the following in the hour before your test:

  • eating foods that are rich in nitrates, like leafy greens
  • consuming any alcohol or caffeine
  • using your steroid or rescue inhaler

A FeNO test involves breathing slowly into a tube to measure your levels. The AAFA says it’s quick and painless and provides results immediately.

  1. Place clips onto your nose.
  2. Empty your lungs by breathing out completely.
  3. Place the device’s mouthpiece into your mouth and inhale slowly to fill your lungs.
  4. Exhale again slowly until your device beeps. Then repeat the slow inhale and exhale pattern as indicated by your device or doctor’s instructions.

You may feel momentarily lightheaded after breathing in slowly and deeply, but the test is safe. Tell your doctor if you don’t feel well. Sitting down and allowing your breathing to return to usual can help that feeling pass.

The cost of a FeNO test is usually somewhere between $2,000 and $3,000 without insurance, according to a 2019 study.

If you have insurance, the test may or may not be covered by your carrier. Aetna, for instance, has designated FeNO testing as medically necessary for its subscribers and covers it in part or in full, depending on your healthcare plan. Call your insurance carrier to find out if FeNO testing is covered under your plan as well as to find out your associated copay or deductible.

FeNO NIOX test manufacturer Circassia explains that people with Medicare and Medicare Advantage plans may also find that the costs are covered or reimbursed. This may happen if the test is deemed medically necessary by your healthcare professional.

Nitric oxide is measured in parts per billion (ppb). The American Thoracic Society defines the ranges as follows:

Once they record a baseline value, your doctor can use this information to track your condition. Your follow-up readings may also help indicate how well your treatment is working. For example, a significant decrease in your reading may be a good indication that your course of treatment is working well.

FeNO tests do have limitations. The American Thoracic Society explains that airway inflammation isn’t always directly associated with increased FeNO levels. If a person has been recently treated with inhaled steroids, they may receive a false negative or testing.

In a 2017 review, other researchers explain that FeNO can be a useful tool for supporting an asthma diagnosis. They specify that it’s more useful with “ruling in” asthma than it is with “ruling out” the condition.

Remember that other factors, like diet, can affect FeNO results as well. For the best accuracy, Asthma+ Lung UK recommends avoiding foods and beverages in the hour before your test that are rich in nitrates, like beetroot and green leafy vegetables, as well as alcohol and caffeine.

FeNO stands for fractional exhaled nitric oxide. The FeNO test is a common test to help measure the inflammation of your lungs, diagnose asthma, and monitor how well your current asthma treatments are working.

Ask your doctor about FeNO testing if you are having unexplained breathing issues or other symptoms that point to asthma. If you have health insurance, your provider may cover the cost of the test. But it’s a good idea to call ahead to make sure you have coverage.

FeNO isn’t the only type of breathing test, so keep in mind that your doctor may order other tests to get a fuller understanding of your respiratory health and asthma symptoms.

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During a ministry trip to Honduras in 2017, I stayed at a small ranch in the hills above the capital, Tegucigalpa. I was looking forward to exploring the local trails during my pre-breakfast runs. When one of the men at the ranch heard of my plans, he sternly warned me to stick to the gravel and paved roads and to always look down on the roads while I ran. I asked him why. He told me that several weeks ago while walking on a dirt trail, he stepped on a log that had fallen across the trail. The “log” turned out to be a giant constrictor snake. Fortunately for him, the snake had just consumed a large animal and didn’t bother to retaliate or to seek an easy meal.

Constrictor Characteristics
Zoologists have long recognized that constrictors are amazingly designed animals. Thanks to a set of experiments performed by a team of six zoologists led by John Capano, the designs have shown to be even more astounding.1

Constrictors are nonvenomous, large, heavily-muscled snakes. The smallest constrictors are the boas, with adult body lengths ranging from 1.0 to 4.3 meters (3–14 feet). Pythons have adult body lengths ranging from 0.6 to 9.2 meters (2–30 feet). The largest constrictors are the anaconda, which attain adult body lengths from 6.1 to 9.4 meters (20 to 31 feet) and body weights of up to 250 kilograms (555 pounds).

Constrictors swallow their prey whole. Their upper and lower jaws can disconnect to permit the passage of large-diameter animals, which allows them to swallow prey as large as their body weight. Likewise, their ribs can spread apart to allow such animals to proceed into the constrictor’s stomach. Remarkably, such spreading apart of the ribs has little impact on the constrictor’s breathing.

Constrictors kill their prey by ambushing it and wrapping a few coils around it. They do not crush their prey to death. They simply apply enough pressure (constriction) to induce cardiac arrest.

Simultaneous Squeezing and Breathing
Campano’s team observed that for larger prey it can take many minutes for the constrictor to induce a severe enough cardiac arrest to result in the prey’s death. They wondered how the constrictor’s efforts to kill its prey impact its respiration (breathing). To determine the impact of constricting on breathing, Campano’s team performed experiments on captive boa constrictors.

Campano and his colleagues applied a blood-pressure cuff to constrict different portions of a boa constrictor’s body. They observed that when the cuff immobilized a region of the boa where they saw breathing movement, the boa shifted its breathing to other parts of its body. The boa was able to perform such shifting in its breathing over nearly the whole length of its body.

The ability of constrictor snakes to shift their breathing this way explains how they are able to capture and kill sufficient prey for their survival. It doesn’t matter which part of their bodies they use to form constricting coils around their prey. Whichever part a constrictor uses, it can use the remainder of its body to breathe. Therefore, a constrictor can remain hidden and coiled up in an ambush position where it can seize unsuspecting prey and quickly wrap a few tight coils around the animal. The constrictor need not apply a specific part of its body to wrap around its prey. Consequently, the success rate in capturing and killing prey is high enough to allow constrictors to survive throughout a broad range of habitats.

Amazing Designs
This breathing capability of constrictors is possible not only because of their uniquely designed skeletons and muscles but also because of their uniquely designed lungs. The combination and complexity of these designs testify of the intelligence, knowledge, and power of the constrictors’ Creator. These creatures also provide yet another illustration of the message of God’s greatness in Psalm 104, a hymn of creation. Psalm 104 describes how God has packed Earth with the greatest possible biomass and biodiversity. My favorite verse in Psalm 104 is verse 24:

How many are your works, Lord! In wisdom you made them all; the earth is full of your creatures.


  1. John G. Capano et al., “Modular Lung Ventilation in Boa Constrictor,” Journal of Experimental Biology 225, no. 6 (March 2022): id. jeb243119, doi:10.1242/jeb.243119.

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Most people at this point have a COVID story, whether it’s an experience having it, knowing someone who’s had it, or knowing someone who’s sadly passed away from it, we’ve all been impacted in some way.

In honor of mental health awareness month, I’d like to share my experience with having COVID, the connection it had to past health stressors in childhood, and the deeper healing experience I was able to achieve.

My symptoms with COVID began very mild, eventually evolving into a dry cough and upper respiratory irritation, but thankfully nothing ever needing medical attention or a hospital. I took my vitamins and supplements, followed the CDC’s recommended guidelines for isolation, and waited the appropriate time until it was safe to be around loved ones again. But as the days went by, I started to notice chest tension, tightness, and lung irritation when engaging in daily activities.

After a couple days, even as the symptoms began to fade and the COVID virus was no longer detectible in my system, I began to notice myself feeling irritable and anxious. I noticed parts of me getting worried that the anxiety symptoms I had once experienced overwhelming in my life were coming back and would eventually take over. “Oh no!” I thought, I didn’t want to experience this overwhelm of anxiety again, and pretty soon, the worry and resistance to the anxiety began to increase my irritability with those around me and decrease my ability to stay present in the moment.

Natalie Deering is a mental health therapist and owner of ND Wellness Psychological Services in Northern Kentucky. Visit her website at

One evening, I attended a virtual consultation group with six other IFS (internal family systems) therapists where I shared about the parts of me feeling anxious and irritable regarding the COVID symptoms that had impacted my breathing. As I shared with the group, it came to my attention that I felt my anxious and irritable parts were being triggered by past experiences I had had when younger. I remembered that at a young age I had been exposed to tuberculosis and eventually had many instances with pneumonia, bronchitis, and asthma symptoms. As I came to the realization about the connection between my childhood experiences and the current lung issues I was experiencing, I knew I needed to meet with my own IFS therapist to address this insight, and luckily I had a session already scheduled the following week.

As I waited for my IFS session to begin, I engaged in some embodiment work by rolling my feet, back, and chest with a therapy ball until it was time for my virtual appointment. As I used the therapy ball on my body and tension began to release, I suddenly heard the statement, “I can’t breathe!” The statement was loud and clear in my mind and I knew immediately this was connected to the part of me that was being triggered by my experience with chest tightness and upper respiratory issues.

During my therapy session, I was grateful that I was able to connect to the much younger part of me that was carrying the burden of fear and anxiety related to past health stressors regarding my lungs and breathing. I was able to witness my younger part’s experience, provide her with what she needed at the time but didn’t get, and then invite her to come to the present with me to release the burdens out of her body. Once her burdens of fear and anxiety were released, she was able to invite in the qualities of calm, confidence, and courage.

After my session, I felt lighter and freer, my lungs felt clear and open, and the younger part of me felt safe and calm. By inviting this younger part to release the burdens of fear and anxiety, I was able to finally believe with full confidence that my lungs were healthy and strong. The younger part of me was no longer stuck in the past activating my anxiety telling me I was in danger. She was able to see that there was no longer any reason for the anxiety and irritability to hold on, she was safe, I was safe, and therefore I could finally accept that I was healthy and my body had healed.

I hope that by sharing my experience with COVID and how it activated my past health trauma you can see how IFS can possibly help you with accessing calm and resiliency to stressors, both past and present. If you’re interested in knowing more about the healing and unburdening process of IFS, please check out the IFS Institute at for more information and to find an IFS therapist in your area.

Our breath is a beautiful and amazing tool. There are many ways to invite balance and regulation with various types of breathing exercises. Here are some breathing techniques you can invite into your daily practice to help connect to your inner strength and resilience:

1. Spine Filled with Light: Sit comfortably. Eyes open or closed. Bring awareness to your breath. Bring attention to your spine. Feel its internal support extending from the steady base of your pelvis up through the crown of your head. Allow each breath to invite a little more space between vertebrae, gently elongating your spine. Image your spine is transforming from a solid structure into a warm, brilliant ray of light. Focus on this image of light infusing all of your being, allowing yourself to become brighter and more radiant as you sit for 5-10 minutes of meditation.

2. Alternate Nostril Breathing: Sit comfortably. Eyes open or closed. Place your right thumb gently on your right nostril and your right ring finger gently on your left nostril. Gently close your right nostril with your thumb and breath in through your left nostril. Gently close your left nostril with your left ring finger and breath out through your right nostril. Inhale through your right nostril with the left nostril still gently closed. Gently close your right nostril and exhale through your left nostril before breathing in again through the left nostril. Repeat for 2-5 minutes.

3. Mantra Breathing: Sit comfortable. Eyes open or closed. Say internally to yourself “I am” on the inhale, and then on the exhale say a word that resonates with what you need energetically. For example, “I am… Calm.”

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Kolkata: Children were the worst sufferers of air pollution because of their higher breathing rate, narrower windpipe, still-developing lungs and immune system, said Ray at a recent symposium by the SwitchON Foundation, a Kolkata-based climate advocacy group.
“Air pollution triggers asthma exacerbation in children,” said Arup Haldar, a senior pulmonologist, adding, “As India has the most polluted megacities in the world, we also have the highest number of COPD (chronic obstructive pulmonary disease) and second-highest number of asthma deaths.” Every one in 4 OPD patients across hospitals have respiratory distress and one in every three deaths is due to respiratory diseases, the study claims.
“The fine and ultra-fine particulate matter may directly traverse blood vessels and affect the heart and become a systemic inflammation,” Ray added. “It can cause diabetes and dementia and even hamper neurological development in children. The recent State of Global Air (SOGA) report linked air pollution to even as a cause of neonatal mortality (in terms of causing preterm births and low birth-weight babies).”
Rajiv Khurana, joining the event from The Lung Care Foundation, said: “Before we ask children of today about what their future plans would be, it is our primary responsibility to secure their future by providing them clean air and a healthy environment.... It is time to fight for them and also fight along with them to secure their right to healthy clean air. Every micro action can collectively create a macro impact.”

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Hiccups are annoying and uncomfortable, everyone has experienced them, although sometimes they last for a short period, on other occasions, they last longer.

According to Medical News Today, hiccups which are medically termed as ‘singultus’, often come after eating or drinking too much or too quickly. The stomach, which is directly below the diaphragm, becomes bloated. This irritates the diaphragm and causes it to contract, as it does when we breathe in.


Dr Edem Danyo, a health practitioner, says that hiccups occur when there is a contraction of the diaphragm involuntary. The diaphragm is a muscle that helps you breathe. It sits under your lungs and splits your chest cavity from your abdomen.


He says that what triggers hiccups is eating heavy meals or eating quickly, taking carbonated drinks, excessive alcohol intake, being exposed to quick changes in temperature, and excitement and emotional stress.  


Not all these triggers result in hiccups that will last less than 48 hours. But when they last more than 48 hours, they may be a result of tumours in the neck, gastric reflux, meningitis, stroke, anaesthesia, and drugs such as steroids. If they exceed 48 hours, see the doctor, Dr Danyo says.

Medical experts emphasise that there are two types of hiccups. The ones that stay on for more than two days are referred to as persistent hiccups, whilst the ones that linger for more than a month are known as intractable hiccups. These are known to be part of a larger, underlying medical problem and might not go away until that issue is corrected. Some of these larger, underlying conditions include; cancer and tumours, stroke, disorders of the stomach or oesophagus, pleuritis (inflammation of the lining of the lung), uraemia (abnormally high levels of waste products in the blood), pneumonia, bowel diseases, among others. 

Home remedies  

“Practice measured breathing, breathe in from zero to five and breathe out while counting, from zero to five. You can do this as much as necessary, the effect of this is that it distracts the breathing cycle,” Dr Danyo says.

He says to breathe into a paper bag, place the paper bag on your nose and mouth, and breathe, in and out. This increases the level of carbon dioxide in the blood.

“Increased carbon dioxide levels in the lungs may relax the diaphragm, stopping the spasms and, thus, the hiccups,” he says.

Dr Danyo says that another technique that can be effective is the use of the Valsalva manoeuvre, which is a breathing method that may slow your heart when it’s beating too fast. With this method, you exhale while you pinch your nose, keep your mouth closed, and be as if you’re having a bowel movement. You can do this for 10 to 15 seconds.

Dr Danyo explains that you can also drink cold or ice water, when you do it slowly, it fuels the vagus nerve (responsible for the regulation of internal organ functions, such as digestion, heart rate, and respiratory rate). Cold water stops the irritation produced in the diaphragm and it resumes its normal movement.

He also advises sucking on ice cubes, keeping about one ice cube in your mouth, and sucking it slowly until it melts. This stimulates the vagus nerve as well.

You can also distract yourself with something engaging, either playing puzzles, video games, or doing anything to divert yourself from thinking about the hiccups as a remedy,” he says.


Dr Danyo says that prevention is based on lifestyle changes, eating smaller amounts of food per serving, avoiding spicy foods, and avoiding excessive alcohol intake and carbonated drinks.

According to Healthline, there’s no proven method for preventing hiccups. However, if you experience hiccups frequently, you can try to reduce your exposure to known triggers. Hiccups have a wide range of possible triggers, from drinking soda and eating certain foods to medication use and underlying conditions. A number of possible treatments are also available.

In rare instances, hiccups can last longer than 48 hours. If your hiccups last longer than 48 hours, don’t respond to treatment, or you aren’t sure what’s causing them, see a doctor for a diagnosis.

Also, see a doctor or seek emergency help if you’re having numbness and coordination issues alongside your persistent hiccups. These may be symptoms of a stroke, Healthline suggests.

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