Chronic obstructive pulmonary disease (COPD) is a prevalent chronic respiratory condition that represents the third leading cause of death worldwide.1,2 According to the Global Initiative for Chronic Obstructive Lung Disease (GOLD) 2023 definition, COPD is a

Heterogeneous lung condition characterized by chronic respiratory symptoms (dyspnea, cough, expectoration, and/or exacerbations) due to abnormalities of the airways (bronchitis, bronchiolitis) and/or alveoli (emphysema) that cause persistent, often progressive, airflow obstruction.2

People with HIV (PWH) are particularly vulnerable to the development and progression of COPD, with both higher rates of COPD and an earlier and more rapid decline in lung function than in the general population, even after accounting for cigarette smoking and other known risk factors, such as intravenous drug use.3–7 The exact mechanisms that underlie HIV-associated COPD are incompletely known, but environmental exposures, heightened immune activation and systemic inflammation, accelerated aging, a predilection for the development of pneumonia, and alterations in the lung microbiome likely play important roles (Figure 1).8–11 The purpose of this review is to describe what is currently understood about the epidemiology and pathobiology of COPD among PWH, to indicate selected areas of active investigation, and to outline screening, diagnostic, prevention, and treatment strategies.

Figure 1 Drivers of COPD in PWH.



As survival among PWH has improved with the use of antiretroviral therapy (ART), COPD has become an increasingly important comorbidity. PWH develop an earlier and more rapid decline in lung function, even after adjustment for traditional risk factors.3,5–7,12–15 A recent retrospective study evaluating comorbidities in PWH based on hospital discharge data found that COPD was the most common comorbidity across the 10-year study period and that COPD prevalence was higher among PWH than among those without HIV (23.5% versus 14.0%).16 Prevalence estimates of COPD among PWH have ranged from 3.4% to over 40% in prior studies; notably, most of these have been conducted in Europe and North America.17,18 Part of this heterogeneity is due to differences in COPD classification methods, such as self-report, International Classification of Diseases (ICD) diagnostic codes, use of CT scans, and spirometry.17,19 For example, a systematic review and meta-analysis by Bigna et al evaluating the global prevalence of COPD among PWH found that the prevalence varied from 5.6% to 10.6% depending on the diagnostic criteria used, with a higher prevalence when using spirometric criteria instead of self-report or ICD diagnostic codes.4


COPD in PWH occurs anywhere PWH reside. However, the risk factors for the development of COPD in PWH vary regionally due to differences in age, rates and duration of tobacco smoking, exposure to biomass fuels, and prevalence of tuberculosis, all of which have been implicated in COPD development.2,20–22 While the majority of studies on COPD in PWH have been conducted in the US and Europe, most PWH live in sub-Saharan Africa, where there is a high prevalence of both tuberculosis (TB) and exposure to biomass fuels, and where patients are typically younger and less likely to smoke tobacco. While earlier studies suggested that ART itself may be a risk factor for worsening lung function,23,24 Kunisaki et al conducted a multinational randomized controlled trial (RCT) in the modern ART era and did not find a difference in lung function based on timing of ART initiation.25

Biologic Sex

Biologic sex may also contribute to differences in COPD trajectories among PWH. In one study of longitudinal lung function changes in PWH, female sex was associated with distinct lung function trajectories, including baseline low diffusing capacity for carbon monoxide (DLco).26 In a study by McNeil et al of virally suppressed adults with HIV and their seronegative counterparts in Uganda, women with HIV demonstrated an accelerated FEV1 decline as compared to women without HIV, a finding that was not seen among men with and without HIV.27 Interestingly, in a large US-based cross-sectional analysis comparing women with and without HIV, women with HIV had a lower DLco than women without HIV, but there were no differences in spirometric outcomes by HIV status.28,29 In another study including the same cohort of women, baseline COPD prevalence was similar among men with and without HIV and women with and without HIV, but COPD incidence was higher among men with HIV when compared to men without HIV.30 In contrast, Abelman et al found in a post-pneumonia Ugandan cohort that women with HIV had over three-fold higher odds of COPD on spirometry compared to men with HIV, a sex-based difference not found in women and men without HIV.31 Further work is currently underway to investigate whether these reported HIV-associated sex-specific differences in COPD rates are driven by immunologic, hormonal, or environmental factors.

Risk Factors for COPD in PWH

There are many risk factors for the development of COPD in PWH including HIV itself,5,32 cigarette smoking and other inhalational exposures, air pollution, opportunistic infections and pneumonia, microbiome alterations,33,34 accelerated aging,35–38 and socioeconomic factors.39 This section focuses on the major drivers, such as smoking, as well as potential risk factors under investigation, such as chronic cytomegalovirus (CMV) coinfection.


Smoking is the key risk factor for COPD in PWH. Smoking is more prevalent among PWH compared to their seronegative counterparts.40–42 However, studies of co-exposure to HIV and tobacco smoke suggest that PWH who smoke may also be more susceptible to smoking-induced lung damage than HIV-uninfected people who smoke. For example, Diaz et al found emphysema to be more prevalent among smokers with HIV as compared to smokers without HIV.43 Further, in a longitudinal multi-center cohort of 13,687 veterans with and without HIV, Crothers et al found that the prevalence and incidence of both COPD and lung cancer were higher among those with HIV compared to those without HIV despite similar levels of smoking.5 Importantly, among PWH on ART, smoking may reduce life expectancy more than HIV itself.44–46 While the pathophysiologic mechanism driving this HIV-associated difference is incompletely known, recent work suggests that, among PWH, tobacco smoke suppresses alveolar macrophage production of T-cell recruiting chemokines. This impairs the migration of cytotoxic T cells from the airway mucosa into the alveolar space, leading to localized airway mucosa inflammation and tissue destruction.47

Air Pollution

Air pollution – the leading environmental cause of death globally48 – is now the greatest threat to human health,49 and COPD is a leading cause of the nearly 7 million annual deaths attributed to air pollution.48,50 Air pollution results from a variety of human-related activities and natural events that include emissions from vehicles, factories, and power plants; traffic-related products; biomass fuel burning (ie, charcoal, firewood, animal dung, crop residues) for cooking and heating; dust storms; forest fires; and volcanic eruptions. The dominant pollution sources vary by region. Traffic- and industry-related sources drive exposure in high-income countries and urban settings, while biomass-related sources drive exposure in low- and middle-income countries and rural settings.51 Air pollution causes acute and chronic lung dysfunction, structural lung abnormalities, submaximal lung growth in childhood and adolescence, and augments lung disease risk in vulnerable populations.52–63 Even small acute increases in fine particulate matter (PM2.5) exposure worsen mortality,64 and there is no “safe” level of exposure.65 Biomass-associated COPD, compared to tobacco-associated COPD, is characterized by more small airways disease and fibrosis, less emphysema, higher DLco, and less airflow obstruction – in effect, a more fibrotic and less emphysematous phenotype.66–69 Exposure to biomass fuel smoke has also been associated with defective bacterial phagocytosis.70 In addition, PM2.5 exposure may also potentiate TB risk,21,71,72 which by itself is a risk factor for COPD and an important consideration in TB-endemic regions.

Similar to the influence of tobacco smoke, PWH may be more susceptible to air pollution-associated lung damage. For example, among PWH living in San Francisco, exposure to higher levels of outdoor air pollution was associated with increased susceptibility to Pneumocystis infection.73–75 Using ambulatory carbon monoxide (CO) sensors to measure personal air pollution exposure among 260 adults with and without HIV in rural Uganda, North et al found that exposure to short-term CO levels that exceed WHO air quality guidelines was associated with self-reported respiratory symptoms among PWH but not among HIV-uninfected comparators.76 Characterizing air pollution exposure among PWH and exploring the potentially outsized influence of air pollution exposure on lung health in this population is an area of ongoing investigation. As global smoking prevalence continues to decline and rapid industrialization and urbanization progresses, air pollution is poised to replace tobacco as the leading cause of chronic lung disease,77–79 and a multifaceted approach that also focuses on this often overlooked risk factor for lung disease among PWH is critical.

Opportunistic Infections and Pneumonia

PWH have historically had higher rates of pneumonia, and while incidence of bacterial pneumonia has decreased with the advent of ART,80,81 it remains common in this population.82–84 In the current era, PWH have similar rates of acute respiratory infections as people without HIV, but PWH experience more severe disease.85 Pneumonia has been associated with higher rates of COPD and lung function abnormalities in PWH.86–89 For example, Drummond et al conducted a US-based multi-center study evaluating spirometry in adults with and without HIV and found that participants with airflow obstruction were more likely to have a history of bacterial pneumonia and Pneumocystis jirovecii (PJP) infection.90 Specifically, PJP, an opportunistic infection that occurs in PWH with CD4 counts <200 cells/mm,3 elevated HIV RNA, and colonization by Pneumocystis have each been associated with higher risk of COPD among PWH.88,91,92 There are numerous contributors to the increased risk of pneumonia in PWH, including alterations in immunity, which lead to persistently elevated markers of immune activation and inflammation, as well as environmental and behavioral risk factors, and a higher prevalence of COPD, which is both a consequence of and a risk factor for pneumonia.9,93–96

Globally, tuberculosis is the leading infectious cause of death among PWH;97 PWH are 19 times more likely to develop TB disease than their seronegative counterparts.98,99 Pulmonary TB has been found to cause permanent scarring, bronchiectasis, pleural fibrosis, damage to small and large airways, as well as lung parenchymal damage, all of which may contribute to permanent lung function impairment.20,100 Whereas during the treatment phase of TB this impairment is typically restrictive, there is increasing evidence of a relationship between prior pulmonary TB infection and the subsequent development of obstruction and COPD.20,87 Rates differ significantly by the population under study, but pulmonary TB has been found to lead to airway obstruction in 18.4–86% of people in the general population.100 HIV is now recognized as a risk factor for post-TB lung disease, although the extent of this relationship is currently under study.87,100–104 There is some evidence to suggest that HIV may be associated with reduced severity of post-TB lung disease, but this is an area that merits further evaluation.100,105,106

Chronic CMV Infection

CMV is an important and omnipresent coinfection in HIV that has been associated with cardiovascular and cerebrovascular disease, other non-AIDS events, and increased mortality.107–112 Given the high rates of CMV antibody seropositivity among PWH, CMV IgG titers are commonly used as markers of CMV activity and have been shown to correlate with adverse outcomes.112,113 However, studies of CMV’s effect on lung function and COPD in PWH are limited. While chronic CMV infection in children with perinatally acquired HIV on ART has been associated with an abnormal FEV1,114 CMV’s association with COPD and other chronic lung diseases in adults with HIV has not been evaluated. Emerging data from the general population, however, suggest that chronic CMV infection is associated with COPD,115 and that higher CMV IgG titers are associated with COPD-related mortality.113 CMV is also associated with abnormal DLco in solid organ transplant recipients, although this has not been studied in PWH.116–118

There are several proposed mechanisms for CMV-mediated systemic immune effects, including persistent immune activation, endothelial dysfunction, and alterations in the gut microbiome.17,119–121 Similar biomarker activation patterns are noted in PWH with CMV and those with COPD. For example, sCD163, sCD14, and IL-6 are increased in both CMV IgG-positive PWH122–124 and PWH with lung function abnormalities, including both abnormal spirometry and abnormal DLco.10,121 These data suggest that there may be a shared mechanistic pathway between chronic CMV infection and chronic lung disease in PWH, but further work is needed to understand and characterize this relationship.

HIV-Specific Influences on COPD Pathogenesis

Several HIV-specific mechanisms may contribute to the increased incidence and accelerated development of COPD in PWH. Chronic HIV infection and the direct effects of HIV-related proteins on lung cells, altered lung and systemic immune responses (both immunosuppressive and pro-inflammatory), altered airway and gut microbial communities, impaired response to pathogens, and toxicity from antiretroviral therapies may all contribute to COPD pathogenesis in this population.23,24,125–132

HIV Infection

As the lung acts as a reservoir for HIV even after viral suppression, chronic HIV infection may directly contribute to COPD pathogenesis in various ways.132–134 Newly replicated viral particles released slowly over time bind to and interact with many cell types within the lung, which can lead to direct injury, oxidative stress, low-level chronic inflammation, and impaired response to pathogens.128,135 Although other cell types in the lung may be infected, alveolar macrophages are the best studied reservoir of HIV in the lung.132 HIV infection impairs macrophage phagocytic activity, thus hindering response to pathogens.127,132 HIV also skews the macrophage phenotype towards a pro-inflammatory and protease-producing phenotype through the release of a host of cytokines, chemokines, oxidants, and proteases, all of which contribute to COPD pathology. Cytokine and chemokine signaling in HIV-infected macrophages trigger a pro-inflammatory response including neutrophil and lymphocyte infiltration. Kaner et al found that alveolar macrophage expression of proteases such as matrix metalloproteinases 9 and 12 (MMP-9, MMP-12) is higher in PWH who smoke with emphysema than their seronegative counterparts.131 In murine models, MMPs degrade the extracellular matrix, directly contributing to emphysematous tissue destruction.136

Altered Adaptive Immune Responses

COPD development is not only mediated by HIV direct effects, but also by the altered cell-mediated adaptive immune responses in PWH, in particular, altered CD4+ T-cell responses. Numerous studies have shown a relationship between low CD4+ T cell counts and COPD or accelerated lung function decline, although conflicting data also exists.23,125,126,137 T cell exhaustion is typically seen in response to chronic antigen stimulation, such as chronic viral infection, and results in decreased functionality. In PWH, CD4+ T cells show signs of exhaustion even in the presence of ART, with an increased expression of programmed cell death protein-1 (PD-1), as well as impaired proliferative capacity.130,138,139 Furthermore, in PWH with COPD, airway mucosal CD4+ T cell numbers are depleted and poorly responsive to pathogens.130 These findings suggest that dysfunctional CD4+ T cell responses may uniquely contribute to COPD pathogenesis in PWH.

Activated and dysfunctional CD8+ T cells also appear to contribute to the disordered adaptive immune response in chronic HIV infection, and thus could contribute to COPD pathogenesis.138,139 PWH show persistent expansion of CD8+ T cells in blood and alveolar compartments, and the decreased CD4+/CD8+ ratio is associated with lung abnormalities even in PWH on ART.140,141 These expanded CD8+ T cell populations also show dysfunction, which is typically indicative of an accelerated aging or “immunosenescent” response. Like CD4+ T cells, CD8+ T cells display exhaustion markers, including PD-1, and a low proliferative capacity.138,139 The expanded population skews towards memory T cell and terminally differentiated CD8+ T cell populations unable to respond to new insults. Despite their impaired function, these exhausted T-cells produce a low-grade inflammatory response at mucosal surfaces, which is considered central to COPD pathology.

Changes to the Airway Epithelium

Alterations to the airway epithelium, the main barrier protecting the lungs from outside insults, such as cigarette smoke, air pollution, and inhaled toxins, can also play a major role in COPD pathogenesis. HIV has both direct and indirect effects on the airway epithelium, contributing to disordered barrier function, decreased mucociliary clearance, and generation of pro-inflammatory mediators. For example, HIV enters epithelial cells and disrupts cell–cell adhesion.129 HIV-associated proteins released from other infected cells disrupt epithelial tight junctions and induce oxidative stress.142 HIV and cigarette smoke synergistically disrupt mucociliary clearance, additively suppressing CFTR expression to decrease mucus hydration in cell culture models and inducing goblet cell metaplasia/hyperplasia to increase mucus production in simian models.143,144 Finally, when HIV binds specifically to basal cells, epithelial progenitor cells release proteases such as MMP-9 and pro-inflammatory mediators that induce migration and proliferation of macrophages and neutrophils.145

Changes in the Lung and Gut Microbiome

Lastly, shifts in both the lung and the gut microbiome can also contribute to chronic inflammatory responses in the lung and, hence, COPD pathogenesis. Data are conflicting on whether lung microbial communities differ in PWH based on 16S sequencing.146–148 However, subtle differences in the microbiome at the species or strain level or at a functional level cannot be discerned via these sequencing methods. It is plausible that at least a subset of PWH experience pathologic microbial alterations in the airways because of a more hospitable environment for pathogen growth. If present in PWH, microbiome perturbations could contribute to chronic airway inflammation. Furthermore, microbial translocation from a compromised gut mucosa, stimulating a chronic systemic inflammatory response, may contribute to lung disease in PWH as has been seen in asthma and pulmonary infections.149

Diagnosis and Clinical Findings of COPD in PWH

Screening and Diagnosis

COPD remains both underdiagnosed and misdiagnosed in people with HIV.150,151 While currently the US Preventative Services Task Force does not recommend screening for COPD in the general population,152 higher COPD prevalence among PWH raises the question whether screening should be done in this subpopulation. Currently, there are no screening and diagnostic criteria specific to PWH. While several studies have evaluated different screening approaches, no conclusive recommendations can be made regarding COPD screening and diagnosis in PWH at this time.150,153–156 For example, a group in Canada offered screening spirometry to all patients in an HIV clinic;156 notably, less than a third of the invited participants agreed to participate, and only 11% had airflow obstruction.

Recruitment and retention throughout the screening-to-diagnosis cascade have been major challenges in all studies. For example, a group in Italy implemented a three-step case-finding program, involving a 5-question screening questionnaire (which included questions about age, smoking history, cough and sputum production, shortness of breath, and exercise limitation), portable spirometry, and diagnostic spirometry.150 They found that 282 participants (19.6%) had a positive screening questionnaire, defined as having a positive answer to at least three questions, but only 33 participants ultimately completed diagnostic spirometry, of whom 22 met criteria for COPD. High participant dropout at each step of the screening process has been similarly reported elsewhere,153–155 even when the authors bypassed the screening spirometry and had a shorter questionnaire.155 Even within these limitations, COPD prevalence based on the screening outcomes has been consistently higher than the known COPD prevalence in each respective clinic,154 further underscoring the underappreciated burden of chronic lung disease in this population. Additional challenges with screening this high-risk population include lack of a high-performing, validated screening questionnaire in PWH and poor correlation between respiratory symptoms and obstruction on pulmonary function tests (PFTs).155 To our knowledge, qualitative studies focused on identifying patient, provider, or systems-level issues contributing to high dropout rates in screening studies among PWH have not been conducted. Having diagnostic spirometry available at the time of a positive screening questionnaire may help reduce high dropout rates.

Any PWH suspected of having COPD should undergo diagnostic testing with, at a minimum, portable spirometry and, in our opinion, full PFTs with pre- and post-bronchodilator spirometry, total lung capacity and lung volumes if spirometry is abnormal, and DLco measurement. Chest radiography demonstrates classic findings (Figure 2) mostly in individuals with advanced disease but is useful in ruling out alternative etiologies that also present with respiratory symptoms similar to those of COPD. Occasionally, additional testing such as chest computed tomography (CT) scans may be warranted to characterize the observed PFT abnormalities, and certain CT findings such as the presence of large bulla (Figure 3) may lead to consideration of additional therapies (eg, bullectomy).

Figure 2 Chest radiograph from person with HIV and COPD demonstrating hyperinflation, flattened diaphragms, and bilateral bullous lung disease (Courtesy of Laurence Huang, MD).

Figure 3 Chest computed tomography from the same person with HIV and COPD demonstrating large, bilateral bullae. This individual eventually underwent bullectomy with dramatic improvement in his respiratory status (Courtesy of Laurence Huang, MD).

Longitudinal Lung Function Trajectories of COPD in PWH

While there is a paucity of data on the natural history of COPD in PWH, lung function declines faster in PWH compared to HIV-negative controls, even when HIV is well-controlled and smoking rates are comparable.6,7,157 Notably, findings from the Pittsburgh HIV Lung Cohort suggested that there may be distinct lung function trajectories among PWH, in which differences in the rate of decline are associated with specific symptoms and distinct profiles of elevated immune activation biomarkers.26 Importantly, this study did not exclusively enroll individuals with COPD. In the general population, COPD studies have shown that lung function decline accelerates as COPD severity increases,158 but whether similar trajectories are seen in PWH is an area currently under study. In a study evaluating factors associated with lung function decline among PWH by Li et al, the authors found that lung function decline occurred more rapidly in older individuals and those with GOLD stage 1 than those with GOLD stage 0 COPD.126 Taken together, these studies suggest that PWH with COPD may demonstrate distinct lung function trajectories when compared to their seronegative counterparts, although additional study is needed in this area.

Lung Function Trajectories in People with Perinatally Acquired HIV

While this review is focused on COPD in adults with HIV, the growing number of individuals with perinatally acquired HIV and their lung function trajectory should also be considered. Children and adolescents with HIV have a higher risk of pulmonary infections, including TB, and even with early ART initiation they remain more vulnerable to small airways dysfunction and risk of obstructive lung disease and other pulmonary abnormalities on spirometry and imaging.159–166 Even children who were exposed to but not infected with HIV remain at risk for abnormal lung function.167 Further, lung function in children seems to be affected by the timing of maternal ART initiation (pre-pregnancy versus during pregnancy).167 In addition, lung development and the ability to reach maximal lung function is impaired by HIV, repeat infections, smoking, pollution, and poverty, which in turn increases the risk for the development of chronic lung disease in adulthood.168,169 As this vulnerable population ages, we are likely to see an increased burden of chronic obstructive disease earlier in life. As most of our understanding of lung function trajectories in PWH with COPD comes from adult PWH from higher income settings, focused efforts for early screening, diagnosis, and management of this condition are needed in areas with high prevalence of adolescents and adults with perinatally acquired HIV.

Diffusing Capacity for Carbon Monoxide

Abnormal diffusing capacity for carbon monoxide is the most prevalent finding on PFTs in PWH, even when spirometry is normal.29,170 DLco impairment is non-specific and can be attributed to emphysema, fibrosis, pulmonary hypertension, or anemia. In PWH, it is also often associated with prior respiratory infections such as PJP, TB, or bacterial pneumonia, and the DLco abnormality may persist long after clinical and radiographic resolution of infection.89,126 Other risk factors for abnormal DLco include HIV infection, CD4 < 200 cells/mm,3 intravenous drug use, and hepatitis C infection.29,101,170–172

DLco abnormalities can predict the development, symptoms, and outcomes of COPD. Among people who smoke, DLco can become abnormal before spirometric criteria for COPD are met; DLco may also be a marker of early emphysema prior to the development of spirometric obstruction, small airways disease, or early vascular abnormalities.173–175 While there are additional and unique risk factors for abnormal DLco in PWH compared to the general population, perhaps suggestive of an HIV-specific lung function abnormality,10,176 it is also plausible that isolated DLco abnormalities may serve as a marker for early COPD in some patients. Among PWH, abnormal DLco, like abnormal FEV1, is an independent predictor of worse respiratory symptoms (such as dyspnea, cough, and mucus production),170 as well as a worse 6-minute walk test.177,178 Finally, abnormal DLco is an independent predictor of mortality in PWH with COPD.179,180

Imaging Findings in PWH with COPD

New techniques for quantitative imaging assessment have allowed in-depth characterization of imaging abnormalities in people with COPD. As current GOLD criteria define COPD based on chronic respiratory symptoms,2 chest imaging findings such as emphysema describe the structural abnormalities that drive this clinical entity. In the general population of people who smoke, studies have found that evidence of small airways disease and air trapping on imaging could predict COPD development and faster spirometry decline.181,182 Importantly, multiple imaging findings such as early interstitial lung abnormalities,183 pulmonary artery to aorta ratio >1,184 pulmonary arterial vascular pruning,185 progression186 and homogeneity of emphysema,187 airway wall thickness,188,189 and air trapping have all been associated with disease severity and adverse outcomes in COPD.181

Studies in PWH have shown a high prevalence of emphysema even in individuals without overt respiratory disease.190 In addition, Leung et al found that people with low DLco and a combination of centrilobular and paraseptal emphysema were more likely to have progression of emphysema,191 and significant emphysema burden was associated with increased mortality.192 Elevated TNFα and IL-1β, soluble CD14, nadir CD4, and low CD4/CD8 ratio are also independently associated with emphysema in PWH,140,193,194 although reports of a direct association of HIV with emphysema are contradictory.194,195 While the exact mechanisms are an area of active investigation, HIV-mediated chronic inflammation and immune dysregulation likely play an important role in emphysema formation.

Symptoms, Exacerbations, and Mortality

Compared to HIV-negative individuals, PWH with COPD have a higher respiratory symptom burden, worse quality of life, and an increased risk for COPD exacerbations.24,196–202 For example, PWH with emphysema have a worse chronic cough, increased mucus production, and decreased 6-minute walk distance compared to HIV-negative controls.198 In PWH who inject drugs, obstructive lung disease has been associated with more severe dyspnea than in their seronegative counterparts.203 In addition, PWH perform worse on six-minute walk testing.178 While COPD is associated with increased frailty in individuals with and without HIV, physical limitation scores are worse among PWH.204,205 Finally, COPD in PWH is not only often comorbid with cardiovascular disease, but also a risk factor for myocardial infarction206 and has been associated with increased mortality.180,192

Management of COPD in PWH

PWH have historically been excluded from large randomized controlled trials of COPD treatments. Therefore, there are very few HIV-specific data on COPD management, and instead general COPD guidelines for both chronic disease management and COPD exacerbations are applied to PWH.207 These management strategies include guideline-driven inhaler therapy, pulmonary rehabilitation, routine vaccinations, surgical or bronchoscopic lung volume reduction in qualifying patients, and management of other medical comorbidities.2 Here, we will focus on a few HIV-specific considerations.

Smoking Cessation

Given the high smoking prevalence among PWH and the excess morbidity and mortality associated with smoking in this population, smoking cessation remains a fundamental aspect of COPD care in PWH. Unfortunately, prescribing rates for smoking cessation therapies have been low for PWH with tobacco use disorder for many reasons, including competing clinical priorities, lack of time, low rates of provider training in smoking cessation interventions, and limited knowledge of nicotine replacement therapies and varenicline.208,209 In addition, PWH face additional challenges on the path to sustained smoking cessation that are due to HIV-related stigma, high rates of comorbid substance use, anxiety and depression, financial instability, lack of insurance, low level of education, and racial biases.210–213 Tailoring smoking cessation therapies to this population is an active area of research.209,214–226 Increased awareness among HIV care providers of the importance of smoking cessation, financial support for smoking cessation initiatives, and intervention studies inclusive of PWH are needed to identify the best ways to support smokers with HIV on their path to quitting.

Choice of Inhalers

Special attention should be paid in the treatment of COPD to PWH who are taking ritonavir or other boosted ART regimens. Ritonavir and cobicistat block the CYP3A4 isozyme and can increase the concentration of most corticosteroids. As a result, use of inhaled corticosteroids (ICS) in patients on these medications has been reported to cause Cushing’s syndrome.227–230 Beclomethasone is the ICS drug with the best side effect profile and can be used in PWH treated with ritonavir or cobicistat.230 In PWH who are receiving ritonavir or cobicistat, an added consequence is the inability to use any combination medication for COPD that includes an ICS as fluticasone- and budesonide-containing combination inhaler therapies are contraindicated and beclomethasone is only available as a single, standalone inhaler. Given the already elevated risk of pulmonary tuberculosis and other pneumonias in this population, additional caution should be applied when using ICS, as they can increase the risk of lung infections in this already vulnerable population.231,232

Modulation of Chronic Inflammation

While no HIV-specific COPD therapies exist, there is an interest in the role of modulating chronic inflammation to improve lung function and clinical outcomes. For example, in a small double-blind pilot clinical RCT of rosuvastatin taken daily for the management of COPD in PWH, Morris et al showed that after 24 weeks of daily rosuvastatin therapy, FEV1 stabilized and DLco improved significantly.233 Another trial studied the role of weekly azithromycin in HIV-related chronic lung disease, defined as an irreversible obstructive defect with minimal radiographic abnormalities, in children and adolescents.234 While the authors found no improvement in lung function parameters after 72 weeks of treatment, they noted an increased time to and fewer total exacerbations. Furthermore, data in the general population have shown benefit of using angiotensin converting enzyme inhibitors (ACEi) or angiotensin receptor blockers (ARBs) in slowing down the progression of emphysema on chest CT in COPD, albeit with no effect on longitudinal lung function on spirometry.235 A randomized controlled trial by MacDonald et al measured pneumoprotein levels as a proxy for lung function decline in PWH with COPD randomized to placebo or losartan treatment, but did not see any significant changes in the pneumoprotein plasma concentrations after 12 months of follow-up.236 Finally, an NHLBI-funded multi-site randomized controlled trial evaluating the influence of twice daily doxycycline on change in DLco among PWH who smoke is currently underway.237 In sum, findings from prior studies suggest that targeting chronic inflammation has the potential to improve lung function of PWH with COPD, but currently there are no definitive data to support any single drug’s use.

Prevention of COPD in PWH

Smoking Cessation

Smoking is perhaps the single most important modifiable risk factor for COPD among PWH. Evidence suggests that PWH may metabolize nicotine more rapidly than HIV-uninfected smokers,238 which could have important implications for the effectiveness of smoking cessation interventions among this population. A growing body of literature is focused on identifying effective smoking cessation interventions among PWH; Table 1 summarizes the randomized controlled trials that have been conducted or have recently completed enrollment on smoking cessation in PWH.218,220,225,226,239–262 For example, O’Cleirigh et al found that among 41 PWH who smoke and reported motivation to quit, those who were randomized to receive cognitive behavioral therapy for smoking cessation and anxiety/depression treatment in addition to nicotine replacement therapy were more likely to quit smoking compared to those who received nicotine replacement therapy alone,225 highlighting the importance of focusing concomitantly on smoking cessation and mental health in this population. A Cochrane review summarizing 14 randomized controlled trials of smoking cessation interventions among PWH in the United States found that pairing behavioral interventions with medications may facilitate short-term abstinence in comparison to medications alone but did not appear to facilitate long-term abstinence.263 Further, a systematic review of smoking cessation interventions among PWH found that successful smoking cessation was most likely when the intervention included cellphone-based technology.264 Although long-term smoking cessation is the goal, any reduction in exposure to tobacco products is likely to have significant health impacts. Using a Monte Carlo microsimulation model, Reddy et al demonstrated that sustained smoking cessation among PWH could result in over 260,000 expected years of life gained.44 This per-person survival gain is more than the life expectancy gained with early ART initiation or improved ART adherence, and among the general population is more than the life expectancy gained by initiating statins for primary cardiovascular disease prevention or clopidogrel for secondary cardiovascular disease prevention. Therefore, encouraging and supporting smoking cessation must remain a priority in the care for PWH.

Table 1 Summary of Randomized Controlled Trials of Smoking Cessation in People with HIV

Air Pollution Mitigation

Interventions aimed at reducing personal air pollution exposure can be categorized into policy-level approaches (regional, national, international) and personal-level approaches. Overall, there is no level of air pollution exposure below which there are no negative health impacts. In fact, evidence suggests that the greatest gains in health per unit reduction in air pollution exposure may occur at the lowest end of the exposure spectrum.265 While attention is being paid to regional and national air quality guidelines, individuals with HIV can adopt behavioral changes that may reduce their personal exposure. Evidence to guide these decisions is still an area of active research. In 2019, Carlsten et al published a summary of 10 key approaches to reduce personal exposure to outdoor and indoor pollution sources, including: using close-fitting face masks when exposure is unavoidable; preferential use of active transport (walking or cycling) rather than motorized transport; choosing travel routes that minimize near-road air pollution exposure; optimizing driving style and vehicle settings when in polluted conditions; moderating outdoor physical activity when and where air pollution levels are high; monitoring air pollution levels to inform when individuals should act to minimize exposure; minimizing exposure to household air pollution by using clean fuels, optimizing household ventilation, and adopting efficient cookstoves where possible; and using portable indoor air cleaners.266 Unfortunately, the data supporting these strategies are not of high quality, which highlights the importance of future work focused on carefully designed studies leveraging implementation science methodology to characterize the feasibility, acceptability, and effectiveness of behavioral interventions focused on improving air pollution-associated lung disease.

Infection Prevention

As pulmonary infections, many of which are preventable, have been implicated in the development of COPD among PWH, infection prevention is important for mitigating COPD risk. First, early ART initiation is imperative, as many pulmonary infections such as PJP are opportunistic infections and develop in the setting of high HIV viral loads and low CD4 counts. Primary prophylaxis for PJP prevention is recommended in PWH with CD4 counts <200 cells/mm3 and considered in those with CD4% <14%.267 Given the high morbidity and mortality associated with pneumococcal infection in PWH, pneumococcal immunization has been recommended in all adults with HIV.268 Consistent with general population recommendations, PWH should also receive annual flu vaccination, as well as the full COVID-19 vaccination series. Given the increased risk of TB disease and its associated mortality among PWH, screening for TB is recommended for all PWH at the time of HIV diagnosis and once a CD4 count ≥200 cells/mm3.269 PWH should be tested annually only if they have a history of a negative test for latent TB infection and are at high-risk for repeated or ongoing exposure to people with active TB disease.269 Among PWH diagnosed with latent TB, TB preventive treatment reduces both mortality and progression to active TB and thus should be offered to all PWH with a positive TB screening test without evidence of active TB disease.269,270

Future Directions

Although progress has been made in understanding the underlying mechanisms of COPD among PWH, significant knowledge gaps remain. For example, there are many cross-sectional studies evaluating the prevalence of COPD among PWH but only limited data on the natural disease course of COPD in PWH and whether it differs from the general population. Additionally, while studies suggest that PWH demonstrate a higher risk of COPD and a higher symptom burden, there are no HIV-specific screening guidelines for COPD in PWH. Further research is also needed on the interplay between risk factors such as mode of HIV transmission, biologic sex, aging, CMV infection, air pollution, and TB, as well as a deeper understanding of the epidemiology, development, and progression of chronic lung disease in PWH. Management strategies designed specifically for PWH with COPD are also warranted. Lastly, while much progress has been made in understanding the mechanistic pathways that render PWH particularly vulnerable to developing COPD, we remain limited in our ability to counteract these pathways and prevent COPD development. These are only a few examples highlighting the multiple avenues for future research, all of which have the potential to substantially improve both our scientific understanding of COPD among PWH and our ability to effectively prevent and treat this deadly, irreversible condition.


COPD is highly prevalent among PWH. With an aging global population of PWH, high rates of cigarette smoking, and air pollution, COPD is a growing health challenge, and improved diagnosis and treatment of COPD in PWH will become increasingly important. Further research is needed to understand the underlying mechanisms driving COPD in PWH, as well as HIV-specific screening and treatment modalities.


Katerina L Byanova and Rebecca Abelman are co-first authors for this study. Dr. Byanova was supported by NIH F32 HL166065. Dr. Abelman was supported by NIH T32 AI060530 and K12 HL143961. Dr. North was supported by NIH K23 HL154863. Dr. Christenson was supported by NIH R01 HL143998, she also reports personal fees from AstraZeneca, Sanofi, Regeneron, GlaxoSmithKline, Amgen, MJH Holdings LLC: Physicians’ Education Resource, Glenmark Pharmaceuticals, and Axon Advisors, outside the submitted work. Dr. Huang was supported by NIH R01 HL128156, R01 HL128156-07S2, and R01 HL143998.


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233. Morris A, Fitzpatrick M, Bertolet M, et al. Use of rosuvastatin in HIV-associated chronic obstructive pulmonary disease. AIDS. 2017;31(4):539–544. doi:10.1097/QAD.0000000000001365

234. Ferrand RA, McHugh G, Rehman AM, et al. Effect of once-weekly azithromycin vs placebo in children with HIV-associated chronic lung disease: the BREATHE randomized clinical trial. JAMA Netw Open. 2020;3(12):e2028484. doi:10.1001/jamanetworkopen.2020.28484

235. Parikh MA, Aaron CP, Hoffman EA, et al. Angiotensin-converting inhibitors and angiotensin II receptor blockers and longitudinal change in percent emphysema on computed tomography. the multi-ethnic study of atherosclerosis lung study. Ann Am Thorac Soc. 2017;14(5):649–658. doi:10.1513/AnnalsATS.201604-317OC

236. MacDonald DM, Collins G, Wendt CH, et al. Short communication: a pilot study of the effects of losartan versus placebo on pneumoproteins in HIV: a secondary analysis of a randomized double blind study. AIDS Res Hum Retroviruses. 2022;38(2):127–130. doi:10.1089/aid.2020.0285

237. Doxycycline for emphysema in people living with HIV (The DEPTH Trial). Weill Medical College of Cornell University; 2023. Available from: Accessed March 1, 2023.

238. Ashare RL, Thompson M, Leone F, et al. Differences in the rate of nicotine metabolism among smokers with and without HIV. AIDS. 2019;33(6):1083–1088. doi:10.1097/QAD.0000000000002127

239. Stanton CA, Papandonatos GD, Shuter J, et al. Outcomes of a tailored intervention for cigarette smoking cessation among latinos living with HIV/AIDS. Nicotine Tob Res. 2015;17(8):975–982. doi:10.1093/ntr/ntv014

240. Tseng TY, Krebs P, Schoenthaler A, et al. Combining text messaging and telephone counseling to increase varenicline adherence and smoking abstinence among cigarette smokers living with HIV: a randomized controlled study. AIDS Behav. 2017;21(7):1964–1974. doi:10.1007/s10461-016-1538-z

241. Gritz ER, Danysh HE, Fletcher FE, et al. Long-term outcomes of a cell phone-delivered intervention for smokers living with HIV/AIDS. Clin Infect Dis. 2013;57(4):608–615. doi:10.1093/cid/cit349

242. Vidrine DJ, Arduino RC, Gritz ER. Impact of a cell phone intervention on mediating mechanisms of smoking cessation in individuals living with HIV/AIDS. Nicotine Tob Res. 2006;8 Suppl 1(1):S103–108. doi:10.1080/14622200601039451

243. Vidrine DJ, Arduino RC, Lazev AB, Gritz ER. A randomized trial of a proactive cellular telephone intervention for smokers living with HIV/AIDS. AIDS. 2006;20(2):253–260. doi:10.1097/01.aids.0000198094.23691.58

244. Vidrine DJ, Marks RM, Arduino RC, Gritz ER. Efficacy of cell phone-delivered smoking cessation counseling for persons living with HIV/AIDS: 3-month outcomes. Nicotine Tob Res. 2012;14(1):106–110. doi:10.1093/ntr/ntr121

245. Ingersoll KS, Cropsey KL, Heckman CJ. A test of motivational plus nicotine replacement interventions for HIV positive smokers. AIDS Behav. 2009;13(3):545–554. doi:10.1007/s10461-007-9334-4

246. Lloyd-Richardson EE, Stanton CA, Papandonatos GD, et al. Motivation and patch treatment for HIV+ smokers: a randomized controlled trial. Addiction. 2009;104(11):1891–1900. doi:10.1111/j.1360-0443.2009.02623.x

247. Moadel AB, Bernstein SL, Mermelstein RJ, Arnsten JH, Dolce EH, Shuter J. A randomized controlled trial of a tailored group smoking cessation intervention for HIV-infected smokers. J Acquir Immune Defic Syndr. 2012;61(2):208–215. doi:10.1097/QAI.0b013e3182645679

248. Cropsey KL, Hendricks PS, Jardin B, et al. A pilot study of screening, brief intervention, and referral for treatment (SBIRT) in non-treatment seeking smokers with HIV. Addict Behav. 2013;38(10):2541–2546. doi:10.1016/j.addbeh.2013.05.003

249. Cropsey KL, Jardin BF, Burkholder GA, Clark CB, Raper JL, Saag MS. An algorithm approach to determining smoking cessation treatment for persons living with HIV/AIDS: results of a pilot trial. J Acquir Immune Defic Syndr. 2015;69(3):291–298. doi:10.1097/QAI.0000000000000579

250. Humfleet GL, Hall SM, Delucchi KL, Dilley JW. A randomized clinical trial of smoking cessation treatments provided in HIV clinical care settings. Nicotine Tob Res. 2013;15(8):1436–1445. doi:10.1093/ntr/ntt005

251. Manuel JK, Lum PJ, Hengl NS, Sorensen JL. Smoking cessation interventions with female smokers living with HIV/AIDS: a randomized pilot study of motivational interviewing. AIDS Care. 2013;25(7):820–827. doi:10.1080/09540121.2012.733331

252. Pengpid S, Peltzer K, Puckpinyo A, et al. Screening and concurrent brief intervention of conjoint hazardous or harmful alcohol and tobacco use in hospital out-patients in Thailand: a randomized controlled trial. Subst Abuse Treat Prev Policy. 2015;10(1):22. doi:10.1186/s13011-015-0018-1

253. Mercie P, Arsandaux J, Katlama C, et al. Efficacy and safety of varenicline for smoking cessation in people living with HIV in France (ANRS 144 Inter-ACTIV): a randomised controlled phase 3 clinical trial. Lancet HIV. 2018;5(3):e126–e135. doi:10.1016/S2352-3018(18)30002-X

254. Mussulman LM, Faseru B, Fitzgerald S, Nazir N, Patel V, Richter KP. A randomized, controlled pilot study of warm handoff versus fax referral for hospital-initiated smoking cessation among people living with HIV/AIDS. Addict Behav. 2018;78:205–208. doi:10.1016/j.addbeh.2017.11.035

255. Ashare RL, Thompson M, Serrano K, et al. Placebo-controlled randomized clinical trial testing the efficacy and safety of varenicline for smokers with HIV. Drug Alcohol Depend. 2019;200:26–33. doi:10.1016/j.drugalcdep.2019.03.011

256. Ditre JW, LaRowe LR, Vanable PA, De Vita MJ, Zvolensky MJ. Computer-based personalized feedback intervention for cigarette smoking and prescription analgesic misuse among persons living with HIV (PLWH). Behav Res Ther. 2019;115:83–89. doi:10.1016/j.brat.2018.10.013

257. Gryaznov D, Chammartin F, Stoeckle M, et al. Smartphone app and carbon monoxide self-monitoring support for smoking cessation: a randomized controlled trial nested into the Swiss HIV cohort study. J Acquir Immune Defic Syndr. 2020;85(1):e8–e11. doi:10.1097/QAI.0000000000002396

258. Shuter J, Chander G, Graham AL, Kim RS, Stanton CA. Randomized trial of a web-based tobacco treatment and online community support for people with HIV attempting to quit smoking cigarettes. J Acquir Immune Defic Syndr. 2022;90(2):223–231. doi:10.1097/QAI.0000000000002936

259. Shuter J, Kim RS, An LC, Abroms LC. Feasibility of a smartphone-based tobacco treatment for HIV-infected smokers. Nicotine Tob Res. 2020;22(3):398–407. doi:10.1093/ntr/nty208

260. Stanton CA, Kumar PN, Moadel AB, et al. A multicenter randomized controlled trial of intensive group therapy for tobacco treatment in HIV-infected cigarette smokers. J Acquir Immune Defic Syndr. 2020;83(4):405–414. doi:10.1097/QAI.0000000000002271

261. Schnall R, Liu J, Alvarez G, et al. A smoking cessation mobile app for persons living with HIV: preliminary efficacy and feasibility study. JMIR Form Res. 2022;6(8):e28626. doi:10.2196/28626

262. Tindle HA, Freiberg MS, Cheng DM, et al. Effectiveness of varenicline and cytisine for alcohol use reduction among people with HIV and substance use: a randomized clinical trial. JAMA Netw Open. 2022;5(8):e2225129. doi:10.1001/jamanetworkopen.2022.25129

263. Pool ER, Dogar O, Lindsay RP, Weatherburn P, Siddiqi K. Interventions for tobacco use cessation in people living with HIV and AIDS. Cochrane Database Syst Rev. 2016;6:CD011120.

264. Moscou-Jackson G, Commodore-Mensah Y, Farley J, DiGiacomo M. Smoking-cessation interventions in people living with HIV infection: a systematic review. J Assoc Nurses AIDS Care. 2014;25(1):32–45. doi:10.1016/j.jana.2013.04.005

265. Pope CA, Cropper M, Coggins J, Cohen A. Health benefits of air pollution abatement policy: role of the shape of the concentration-response function. J Air Waste Manag Assoc. 2015;65(5):516–522. doi:10.1080/10962247.2014.993004

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Patients with mild COPD have higher all-cause mortality and respiratory disease-related death than individuals with normal spirometry, according to systematic review and meta-analysis findings published in Pulmonology.

There is conflicting evidence regarding whether risk of all-cause death in patients with mild COPD is higher than the risk among patients with normal spirometry. Therefore, investigators sought compare rates of all-cause mortality and respiratory-related mortality in individuals with mild COPD vs those with normal spirometry.

The investigators conducted a systematic review and meta-analysis of cohort studies reporting an association between mild COPD and all-cause mortality in adult patients, searching the Web of Science, Embase, and PubMed databases from inception through February 2023. Mild COPD was defined as pre-bronchodilator or post-bronchodilator forced expiratory volume in 1 second (FEV1)/forced vital capacity (FVC) less than 0.70 and FEV1 at least 80% of the predicted value. Normal spirometry was defined as pre- or post-bronchodilator FEV1/FVC at least 0.70 and FEV1 at least 80% of the predicted value.

The investigators found 12 studies published between 2003 and 2023 (all graded as good quality) that met eligibility requirements (N=9973 participants with mild COPD; N=255,527 participants with normal spirometry). All data were adjusted for body mass index and age. Most of the studies used the pre-bronchodilator definition of mild COPD. Average follow-up was less than 10 years in 5 studies and at least 10 years in 7 studies.

[P]atients with mild COPD have higher all-cause mortality and respiratory disease-related mortality than individuals with normal spirometry.

Patients with mild COPD vs those with normal spirometry had higher risk of all-cause mortality (pre-bronchodilator hazard ratio [HR], 1.21; 95% CI, 1.11-1.32; I2=47.1%; P =.023; post-bronchodilator HR, 1.19; 95% CI, 1.02-1.39; I2=0.0%; P =.365).

There was no suggestion of publication bias in funnel plots or Egger’s line regression. Omit-one meta-analysis showed HRs and corresponding CIs were greater than 1.

A higher risk for respiratory disease-related death was noted among individuals with mild COPD vs those with normal spirometry (HR, 1.71; 95% CI, 1.03-2.82; I2=0.0%). No higher risk for cardiovascular disease-related death was found among individuals with mild COPD vs those with normal spirometry (HR, 1.22; 95% CI, 0.87-1.71; I2=27.1%) nor was there a higher risk for cancer-related mortality (HR, 1.19; 95% CI, 0.93-1.51; I2=0.0%).

Among those who currently smoked, risk of all-cause mortality was higher among people with mild COPD vs those with normal spirometry (HR, 1.31; 95% CI, 1.04-1.64; I2=62.0%; P =.021).

In citing limitations their analysis, the researchers noted that most included studies used pre-bronchodilator spirometry to diagnose mild COPD whereas Global Initiative for Chronic Obstructive Lung Disease (GOLD) guidelines recommend use of post-bronchodilator spirometry. Additionally, the number of studies in each subgroup was too small to obtain clear results.

“[P]atients with mild COPD have higher all-cause mortality and respiratory disease-related mortality than individuals with normal spirometry,” the review authors concluded. The investigators wrote, “Further research is required to determine whether early pharmacological or nonpharmacological intervention and treatment are beneficial in mild COPD.”

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Oxygen Cylinders, Concentrators Market is poised to witness robust growth over the forecast period. Increasing geriatric population base will serve as a high impact rendering factor.

In the evolving landscape of healthcare, the Oxygen Cylinders and Concentrators Market is gearing up for substantial growth, with a projected market size of US$ 6.77 billion and a commendable CAGR of 5.15%. Dive into our comprehensive analysis to uncover the driving forces, regional dynamics, and future opportunities in this vital industry.

The Impact of COVID-19:
The global pandemic has cast a unique shadow on the market, affecting leaders, followers, and disruptors differently based on regional variations in lockdown measures. Our detailed report explores the short-term and long-term repercussions, aiding decision-makers in crafting strategic plans adaptable to specific regions and segments.

A Breath of Fresh Growth:
The Oxygen Cylinders and Concentrators Market are on the brink of robust expansion, propelled by factors such as the increasing geriatric population, which is more susceptible to respiratory disorders like COPD. Lifestyle choices, including smoking and exposure to dust particles, are contributing to a surge in respiratory issues, further fuelling market growth.


The Symphony of Market Dynamics: Brewing Growth and Challenges

Healthcare Dominance:
The healthcare segment takes center stage, securing the largest revenue share due to a substantial number of patients reliant on oxygen. Rising cases of respiratory disorders, accidents, and surgeries are driving the demand for oxygen concentrators. Explore how these devices are becoming integral in treating conditions like COPD, chronic hypoxemia, and even severe sleep apnea.

North America Leading the Charge:
In 2017, North America held the highest revenue share, with the U.S. oxygen cylinders and concentrators market claiming over 85% of the regional pie. Factors such as the prevalence of respiratory diseases, early diagnosis, developed healthcare infrastructure, and increasing per capita income are contributing to the region's dominance. Uncover the nuances that make North America a key player in the market's growth.

Oxygen Cylinders, Concentrators Market Segment Analysis:

Healthcare segment of Oxygen Cylinders, Concentrators Market accounted for the largest revenue share in 2017 owing to the substantial number of patients’ dependent on oxygen. Increasing incidence of respiratory disorders such as COPD, asthma will fuel industry growth over the forecast years. Oxygen concentrators are used to deliver supplementary oxygen to individuals suffering from COPD, chronic hypoxemia, and pulmonary enema.

by Product

They are also used in adjunct treatment for severe sleep apnoea. Moreover, oxygen is also required during surgery and intensive care treatment. The increasing number of accidents and fatalities requiring immediate hospitalization and operation along with the rising number of surgeries should further propel demand.

by Application

  • • Healthcare
    • Pharmaceutical &amp
    • Biotechnology
    • Manufacturing
    • Aerospace &amp
    • Automotive
    • Others


Who are Oxygen Cylinders, Concentrators Market Key Players?

  • • Chart Industries
    • Inogen, Invacare
    • Koninklijke Philips N.V.
    • Catalina Cylinders
    • Air Liquide
    • MeBer
    • Tecno Gaz
    • Cramer Decker
    • Cramer Decker
    • Invacare
    • DeVilbiss Healthcare LLC
    • Nidek Medical Products, Inc.
    • O2 Concepts
    • Teijin Limited
    • Royax
    • Jiuxin Medical Technology Co., Ltd.
    • Vygon
    • OSI Systems
    • Smith’s Medical
    • Becton, Dickinson and Company
    • Drägerwerk AG & Co. KGaA
    • Teleflex Incorporated
    • Fisher & Paykel Healthcare Corporation Limited
    • Taiyo Nippon Sanso Corporation

Table of content for the Oxygen Cylinders, Concentrators Market includes:

Part 01: Executive SummaryPart 02: Scope of the Oxygen Cylinders, Concentrators Market ReportPart 03: Oxygen Cylinders, Concentrators Market LandscapePart 04: Oxygen Cylinders, Concentrators Market SizingPart 05: Oxygen Cylinders, Concentrators Market Segmentation by TypePart 06: Five Forces AnalysisPart 07: Customer LandscapePart 08: Geographic LandscapePart 09: Decision FrameworkPart 10: Drivers and ChallengesPart 11: Market TrendsPart 12: Vendor LandscapePart 13: Vendor Analysis


Navigating Regional Dynamics:
Understand the Oxygen Cylinders and Concentrators Market in North America and Asia Pacific by analyzing market segments. Our report provides a clear representation of competitive analysis, guiding investors through factors like type, price, financial position, product portfolio, growth strategies, and regional presence.

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Oxygen Conservation Devices Market

Oxygen Conservation Devices Market

The Oxygen Conservation Devices Market is estimated for 2023 for the forecast period 2023-2030, as highlighted in a new report published by Coherent Market Insights.

Market Overview:

Oxygen conservation devices aid in conserving the flow of oxygen by delivering a controlled amount of oxygen to patients based on their breathing patterns. They help patients breathe more deeply and prolong the use of oxygen tanks.

Market Dynamics:

The oxygen conservation devices market is expected to witness significant growth over the forecast period owing to the rising incidences of chronic respiratory diseases such as COPD and asthma. As per the WHO, around 65 million people suffer from moderate to severe COPD worldwide. Moreover, the increasing healthcare expenditure and better access to healthcare facilities also contributes to market growth. Government initiatives to spread awareness regarding respiratory diseases and availability of reimbursement for oxygen therapy further drives the adoption of oxygen conservation devices. Additionally, technological advancements in oxygen delivery devices have improved patient comfort and compliance, thereby fueling market expansion.

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** Note - This Report Sample Includes:

‣ Brief Overview to the research study.

‣ Table of Contents The scope of the study's coverage

‣ Leading market participants

‣ Structure of the report's research framework

‣ Coherent Market Insights' research approach

Major companies in Oxygen Conservation Devices Market are:

✤ Medline Industries Inc.
✤ Invacare Corporation
✤ Responsive Respiratory Inc.
✤ Drive Medical
✤ DeVilbiss Healthcare Ltd.
✤ Precision Medical Inc.
✤ Hersill S.L.
✤ Inogen Inc.
✤ Essex Industries Inc.

Note: Major Players are sorted in no particular order.

Rising prevalence of chronic respiratory diseases is driving the oxygen conservation devices market

The prevalence of chronic respiratory diseases such as chronic obstructive pulmonary disease (COPD) and asthma is increasing significantly across the world. As per WHO estimates, around 65 million people suffer from moderate to severe COPD globally. COPD is projected to be the third leading cause of death worldwide by 2030. Oxygen conservation devices help these patients reduce their oxygen usage and dependency on oxygen supply, thereby offering significant cost benefits to the healthcare systems. These devices are playing a pivotal role in managing COPD and other respiratory disorders effectively at home, improving patient outcomes and quality of life. Their ability to maximize oxygen therapy is fueling the demand from healthcare providers and patients.

Growing geriatric population is propelling the adoption of oxygen conservation devices

The global geriatric population, aged 65 years or older, is expected to nearly double by 2050. Older adults are more susceptible to developing chronic health conditions like respiratory diseases due to age-related physiological changes and decline in the immune system. With life expectancy rising, the risk of respiratory disorders is also rising among the elderly. As oxygen conserving techniques can help senior citizens minimize supplemental oxygen usage and stay active for longer duration between cylinder replacements, their popularity is surging rapidly. Manufacturers are actively developing innovative products specifically targeting the unique needs of the aging population to further penetrate the market.

Stringent regulatory environment for new product approval is impeding market growth

Medical device companies dealing with oxygen therapy equipment have to comply with stringent regulations of authorities like the U.S. FDA and the European Commission to gain approvals for new products. The approval process involves rigorous clinical testing and documentation which is a costly and time-consuming process. Even minor changes or upgrades in existing devices require prior regulatory clearance. This poses regulatory hurdles, increases the product development cycle and delays the launch of advanced solutions. It hampers quick innovations and technical advancements to meet evolving care needs. Regulatory issues have emerged as a major restraint hampering the development and commercialization of novel oxygen conservation devices.

Advent of 3D printing offers a major opportunity

3D printing or additive manufacturing has emerged as a breakthrough technology that is revolutionizing the medical devices industry. This innovative production method provides significant benefits like reduced cost of production, design customization capability and compact size. Its application in designing oxygen conserving devices can unlock new opportunities. Companies are leveraging 3D printing to develop patient-specific oxygen conserving solution and meet the diverse requirements of individual diseases. This technology brings product miniaturization, making devices more wearable. It also enables mass-customization and rapid prototyping, accelerating the product development cycle. 3D printing is opening up new avenues for producing next-gen portable and integrated devices, giving an impetus to market development.

Adoption of telehealth and remote monitoring trend is gaining traction

With the COVID-19 pandemic accelerating the digital health transformation, telehealth and remote patient monitoring solutions are witnessing tremendous growth. Oxygen conservation device manufacturers are actively developing smart connected versions integrated with mobile apps, sensors and cloud computing. These digital devices monitor patients' vital parameters from home and alert care teams in case of emergencies. The data is available seamlessly to physicians for timely interventions. This technology trend allows continuous supervision of patients, improves adherence to therapy regimens and clinical outcomes. It brings improved access to specialty care and greater independence. As healthcare shifts from institutions to homes, the demand for telehealth-enabled oxygen conservation products is expected to surge dramatically over the coming years.

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Highlights of the global Oxygen Conservation Devices Market report:

→ This analysis provides market size (US$ Million) and compound annual growth rate (CAGR%) for the forecast period (2023-2030), using 2021 as the base year. It also covers the global Oxygen Conservation Devices Market in-depth.

→ It offers enticing investment proposition matrices for this sector and explains the likely future growth of key revenue streams.

→ Additionally, this study offers crucial insights into market forces, limitations, opportunities, new product introductions or approvals, market trends, regional perspective, and competitive tactics used by top rivals.

→ Based on the following factors: company highlights, product portfolio, significant highlights, financial performance, and strategies, it covers key players in the global Oxygen Conservation Devices Market.

→ Marketers and company leaders will be able to make wise decisions about next product launches, type updates, market expansion, and marketing strategies thanks to the insights from this research.

→ A wide spectrum of industry stakeholders are covered by the global Oxygen Conservation Devices Market research, including investors, vendors, product producers, distributors, new entrants, and financial analysts.

→ The many strategy matrices used in researching the global Oxygen Conservation Devices Market will aid stakeholders in making decisions.

The research was developed through the synthesis, analysis, and interpretation of data gathered from multiple sources on the parent market. Additionally, analysis has been done of the economic circumstances and other economic indicators and factors to evaluate their respective impact on the Oxygen Conservation Devices Market, along with the present impact, so as to develop strategic and informed projections about the scenarios in the market. This is mostly due to the developing countries' unmet potential in terms of product pricing and revenue collection.

Key Questions Answered In The Report:

• Which regional market will experience the greatest and most rapid growth?

• Who are the top five Oxygen Conservation Devices Market players?

• How will the Oxygen Conservation Devices Market evolve over the next six years?

• What application and product will dominate the Oxygen Conservation Devices Market?

• What are the market drivers and constraints for Oxygen Conservation Devices Market?

• What will be the Oxygen Conservation Devices Market's CAGR and size during the forecast period?

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Coherent Market Insights is a global market intelligence and consulting organization that provides syndicated research reports, customized research reports, and consulting services. We are known for our actionable insights and authentic reports in various domains including aerospace and defense, agriculture, food and beverages, automotive, chemicals and materials, and virtually all domains and an exhaustive list of sub-domains under the sun. We create value for clients through our highly reliable and accurate reports. We are also committed in playing a leading role in offering insights in various sectors post-COVID-19 and continue to deliver measurable, sustainable results for our clients.

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Chronic Obstructive Pulmonary Disease (COPD) is a progressive respiratory condition that affects nearly 50 million people in India, causing persistent breathing difficulties and reducing the overall quality of life. COPD is an umbrella term which encompasses chronic bronchitis and emphysema and is characterized by persistent airflow limitation and difficulty in breathing. 

COPD often results from long-term exposure to irritating gases or particulate matter, most commonly from cigarette smoke. Additional risk factors of COPD include untreated asthma, exposure to air pollution, exposure to biomass fuel and second-hand smoke.

How Heated Steam Therapy Works

Unsplash/Representational image

While existing COPD treatments aim to alleviate symptoms and improve lung function, they may fall short in repairing the underlying damage to the lung tissue. Moderate to severe cases often require more targeted approaches to address the structural changes and promote healing within the lungs.

Heated steam therapy (Bronchoscopic thermal vapour ablation) via bronchoscope represents a cutting-edge treatment designed to directly target damaged lung tissue. This minimally invasive procedure involves the introduction of heated steam into the airways through a bronchoscope, a thin, flexible tube equipped with a light and camera. While heated steam therapy holds great promise, it is essential to carefully select patients based on the type and severity of their COPD and overall health. The procedure may be most beneficial for individuals with emphysema localized to upper parts of the lung who have not responded optimally to traditional treatments.

The procedure begins with the insertion of a bronchoscope into the patient's airways, allowing the medical professional to visualize the affected areas. Once the bronchoscope is in position, heated steam is carefully delivered to the targeted regions within the lungs. The controlled application of heat aims to promote tissue repair and reduce inflammation.

Benefits of Heated Steam Therapy:


- Precision Targeting: Unlike systemic treatments, heated steam therapy precisely targets the affected areas within the lungs, maximizing its therapeutic impact.

- Minimally Invasive: The procedure is minimally invasive, reducing the risks associated with more invasive surgical interventions. Patients typically experience shorter recovery times and fewer complications.

- Improved Lung Function: By promoting tissue repair and regeneration, heated steam therapy aims to enhance lung function, potentially leading to improved breathing and overall quality of life.

Heated steam therapy (Bronchoscopic thermal vapour ablation) via bronchoscope represents a groundbreaking advancement in the field of COPD treatment. By directly addressing damaged lung tissue this innovative approach offers hope to individuals with moderate to severe COPD who seek not only symptom relief despite optimal medical therapy. 

As research and clinical trials continue to unfold, heated steam therapy (Bronchoscopic thermal vapour ablation) may become a transformative option, heralding a new era in the management of chronic respiratory conditions. Always consult with healthcare professionals to determine the most suitable treatment approach based on individual health circumstances.

About the author: Dr. Vivek Singh is the Director, Respiratory and Sleep Medicine, Medanta, Gurugram. All views/opinions expressed in the article are of the author. 

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JONESBORO, Ark. (Edited News Release/KAIT) - November is COPD Awareness Month—a time to raise awareness, take action, and help make a difference in the lives of people living with chronic obstructive pulmonary disease (COPD).

The disease, which includes chronic bronchitis and emphysema, is long-term, and progressive and makes it hard to breathe.

There is currently no cure for COPD, but the disease is treatable.

As the month comes to a close, the American Lung Association is driving attention to its recently released COPD State Briefs, which include data about prevention, diagnosis, health outcomes, and treatment of the disease for all 50 states and Washington, D.C.

The State Briefs found that Arkansas has one of the highest COPD prevalence rates in the country.

Nationally, approximately 5 percent of adults, or 12.5 million people, are living with COPD in Arkansas:

  • 223,174 adults have been diagnosed with COPD
  • The COPD prevalence rate is 9.6 percent
  • 2,338 people die each year from COPD
  • The annual cost of COPD treatment is $295 million
  • 202,540 days of work are lost each year due to COPD

“Unfortunately, here in Arkansas, we face a higher burden of COPD, but together, we can work to help prevent COPD and support our community members living with the disease to live longer and more active lives,” said Laura Turner, senior manager of advocacy for Arkansas at the American Lung Association.

“The new COPD State Briefs also examine key indicators for COPD in Arkansas, such as air quality, tobacco use, education, income level, and vaccination rate, which can help us determine where to focus our prevention efforts and help those most impacted by the disease.”

The Lung Association recommends the following actions to reduce the burden of COPD in Arkansas:

  • Use a validated COPD screening tool for people who may be at risk of COPD or reporting symptoms
  • Confirm a COPD diagnosis using spirometry, especially in primary care
  • Use evidence-based tobacco prevention and cessation services;
  • Promote recommended vaccinations
  • Recommend pulmonary rehabilitation, COPD education, and a COPD Action Plan

Arkansas is one of 11 states with the highest COPD rates and highest burden in the country.

The other states are Alabama, Indiana, Kentucky, Louisiana, Missouri, Maine, Mississippi, Ohio, Tennessee and West Virginia.

COPD prevalence rates range from 3.7 percent in Hawaii to 13.6 percent in West Virginia.

The goal of the COPD State Briefs is to raise awareness for COPD and empower public health and healthcare professionals to take actionable steps to prevent the onset of illness, reduce health inequities, set goals for earlier diagnosis, and ensure clinical guidelines are used to manage and treat COPD.

The COPD State Briefs were created with support from the Centers for Disease Control and Prevention. Learn more and view the COPD State Briefs at

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Silent killer: India gasps for breath as COPD spreads to rural areas, affects non-smokers.
Silent killer: India gasps for breath as COPD spreads to rural areas, affects non-smokers.

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The irreversible lung disease is affecting a large part of India’s population, especially the elderly. It is the biggest cause of mortality after heart ailments, while the rising number of cases reported among non-smokers in rural India raises an alarm.

Veteran chest surgeon and lung-transplant specialist Arvind Kumar faces a grim reality every day. As he deftly makes incisions to access the lungs of his patients, Kumar loathes the sight that unfolds. With rare exceptions, he finds black deposits scarring patients’ lungs. And much to his dismay, most patients have no history of smoking. Dust emanating from construction sites and smoke-spewing factory chimneys and vehicles are pushing India into

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A State brief from the American Lung Association has released data showing Arkansas has the highest rates of COPD in the country and has recommendations on how to reduce the burden.

The disease known as chronic obstructive pulmonary disease is long-term, includes chronic bronchitis and emphysema, is progressive, and makes it hard to breathe, the brief said.

The ALA stated that the goal of the COPD State Briefs is to raise awareness for COPD and empower public health and healthcare professionals to take actionable steps to prevent the onset of illness, reduce health inequities, set goals for earlier diagnosis, and ensure clinical guidelines are used to manage and treat COPD.

A news release stated that Arkansas is one of 11 states with the highest COPD rates and highest burden in the country. The other states are Alabama, Indiana, Kentucky, Louisiana, Missouri, Maine, Mississippi, Ohio, Tennessee and West Virginia.

“Unfortunately, here in Arkansas, we face a higher burden of COPD, but together we can work to help prevent COPD and support our community members living with the disease to live longer and more active lives,” said Laura Turner, senior manager of advocacy for Arkansas at the American Lung Association. “The new COPD State Briefs also examine key indicators for COPD in Arkansas, such as air quality, tobacco use, education, income level, and vaccination rate, which can help us determine where to focus our prevention efforts and help those most impacted by the disease.”

Nationally, approximately 5 percent of adults, or 12.5 million, people are living with COPD In Arkansas:

  • 223,174 of adults have been diagnosed with COPD;
  • The COPD prevalence rate is 9.6 percent;
  • 2,338 people die each year from COPD;
  • Annual cost of COPD treatment is $295 million; and
  • 202,540 days of work are lost each year due to COPD.

There is currently no cure for COPD, but the disease is treatable.

As November comes to a close, the American Lung Association is driving attention to its recently released COPD State Briefs, which include data about prevention, diagnosis, health outcomes, and treatment of the disease for all 50 states and Washington, D.C.

The Lung Association recommends the following actions to reduce the burden of COPD in Arkansas:

  • Use a validated COPD screening tool for people who may be at risk of COPD or reporting symptoms;
  • Confirm a COPD diagnosis using spirometry, especially in primary care;
  • Use evidence-based tobacco prevention and cessation services;
  • Promote recommended vaccinations; and
  • Recommend pulmonary rehabilitation, COPD education, and a COPD Action Plan.

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By Dr. Greg Zerovnik

Contributing Writer

11/28/2023 at 12:49 PM

SAN BERNARDINO, CALIF. – A new monoclonal antibody and new anti-viral vaccines are coming for the first time to provide protection against RSV, Respiratory Syncytial (sin-SISH-uhl) Virus. LaSalle Medical Associates clinics will be providing these breakthroughs to patients this fall.

“RSV is a cold-like virus that is usually mild but can put some people in the hospital,” says Dr. Cheryl Emoto, Medical Director of LaSalle Medical Associates. “For the first time this fall, young infants and seniors (those with the highest risk for severe disease) now have a way to prevent it.”

The Centers for Disease Control and Prevention notes that “Most people recover in a week or two, but RSV can be serious. Infants and older adults are more likely to develop severe RSV and need hospitalization. Vaccines are available to protect older adults from severe RSV. Monoclonal antibodies are available to protect infants.”

The CDC goes on to note that RSV is “one of the most common causes of childhood illness and is the most common cause of hospitalization among infants [emphasis ours].” It usually starts in the fall and peaks in the winter, but this can vary.

Monoclonal antibodies and vaccines may now prevent RSV. A monoclonal antibody is a clone of a unique white blood cell (white blood cells are the body’s own infection fighters) given to augment and reinforce the body’s natural defenses. It’s the option available for infants who are entering their first RSV season. They are not used when someone already has RSV.

Up until now, almost all children have contracted RSV by the time they reach 24 months, so the new prevention regimen has the potential to prevent illness and potential complications such as bronchitis and pneumonia, making life easier for both infants and their parents or caretakers.

For older adults, the CDC estimates that between 60 to 100 thousand are hospitalized every year. resulting in 6,000 to 10,000 deaths. The most at-risk cohorts are older adults, adults with chronic heart or lung disease, those with weakened immune systems or certain underlying medical conditions and residents in nursing homes or long-term care facilities.

Complications may include asthma, chronic obstructive pulmonary disease (COPD, a chronic disease of the lungs that makes it hard to breathe), and congestive heart failure—when the heart can’t pump enough blood and oxygen through the body.

Additionally, this year, there is now a regimen for pregnant women that keeps the developing fetus safe from infection. Now is the time to contact your healthcare provider to schedule an appointment for preventive care, especially if you are pregnant, have an infant under 8 months of age or are 60 years of age or older.

LaSalle Medical Associates serves more than 350,000 patients in their clinics and statewide Independent Physicians Association Group (IPA) who are covered by Medi-Cal, Medicare, and Covered California, as well as those covered by Blue Cross, Blue Shield, Brand New Day, Molina, Care 1st, Health Net and Inland Empire Health Plan (IEHP).

LaSalle staff also help people who come into a clinic without any insurance to become enrolled for a variety of state and federal health coverage.

For more information call (909) 890-0407 or go online to

Tags: (IEHP)and clinicsand Covered Californiaas well as those covered by Blue CrossasthmaBlue ShieldBrand New DayCare 1stCDCchronic obstructive pulmonary diseaseCOPDdelivering high-quality patient caredoctorsFresnoHealth NethospitalsInland Empire Health PlanKingsLos AngelesMaderamedi-calmedicareMolinaRespiratory Syncytial VirusriversideRSVSan BernardinoSan Bernardino and Tulare counties.

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pulmonary rehabilitation

For people living with chronic obstructive pulmonary disease (COPD), doing everything it takes to breathe properly is a priority. While you’ll have a medication protocol to follow, your doctor might also suggest undergoing pulmonary rehabilitation. This is a form of treatment that can be essential to living a full life with COPD. 

What’s Pulmonary Rehabilitation?

Pulmonary rehabilitation is a medically supervised program that helps people with lung diseases live more fulfilling lives. This program generally includes learning about breathing exercises, maintaining fitness, adjusting your daily behavior, and improving your overall nutrition.

When enrolled in the program, you may work with doctors, nurses, physical therapists, respiratory therapists, exercise specialists, and dietitians. It also encourages taking part in group activities so you’ll get support and advice from those who are dealing with similar situations. 

Who Qualifies For This Treatment

Usually, anyone who has had COPD for more than a year can qualify for pulmonary rehabilitation. All that’s required is for your doctor to refer you to a program of your choice. Of course, your doctor might have their own criteria for giving you a referral. These criteria can include having worsening symptoms and not responding to medication as well as you used to. 

RELATED: Improving Lung Function: 10 Things to Know About Pulmonary Rehab

How Rehabilitation Can Help You

Pulmonary rehabilitation is designed to be a well-rounded program that can help you regain your strength, carry out your daily activities, work, and remain social. It does this by combining exercises, breathing techniques, a nutrition program, support, education about your medication regimen, and stress management. 

Some of the exercises that you can expect include leg exercises like walking or climbing stairs, upper body exercises like turning cranks, and strength training like weight lifting.

Breathing techniques are also used to steadily increase your lung capacity, help you remove mucus from your lungs, and improve your lung function. These alone can help you carry out your job and other everyday activities more easily with COPD. 

For some people, managing their weight will be essential to maintaining proper lung function so having a personalized nutrition plan can help with that. Given that studies show how having COPD can negatively affect your mental health, having the support of therapists and your peers can have a positive impact as well. In fact, people who have that kind of support are less likely to suffer from the anxiety and depression that are associated with COPD. 

It’s important to note that working out with a physical therapist or another medical professional can still have its risks. Sometimes, the suggested exercises can put a strain on your muscles and bones. In that case, the team will stop the routine to

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COPD, as the sixth leading cause of death in the US, is widely seen as a preventable epidemic. However, shortcomings in public policy and healthcare hinder access to timely and accurate diagnosis, as well as effective specialty care. We must prioritize expanding access to early screening, diagnosis, and continuous care to mitigate disease progression and save lives. November’s National COPD Awareness Month is the perfect time to propose a 4-point plan to support patients and accelerate early diagnosis.

The silent epidemic

COPD is known to be a ‘silent epidemic’: impacting over 25 million adults in the U.S. Data shows that up to 50% are living without a proper diagnosis, meaning they’re going overlooked and untreated by the healthcare system.  There are several reasons why the disease hasn’t been addressed on a national scale:

  • Public policy shortcomings: COPD is one of the leading causes of preventable death and disability, yet public policy does not prioritize access to affordable COPD medications, pulmonary rehabilitation programs, or sufficient funding for COPD awareness and education.
  • Lack of access to spirometry: The lack of widespread use of spirometry, the diagnostic test used to confirm COPD, results in underdiagnosis or misdiagnosis. Consequently, undiagnosed individuals may not realize they have COPD until it has reached a more severe stage, resulting in more acute symptoms, complex cases, and worse outcomes.
  • Costly comorbidities: COPD tends to occur more frequently in patients over the age of 65, and over 80% of people with COPD have at least one comorbidity. When comorbidities are present, medical costs are five times higher for COPD patients, and as patients age, the comorbidities often become more complex. One of the most commonly occurring comorbidities is heart failure, which is closely linked to COPD exacerbations. Thus, it’s not surprising that both COPD and heart failure represent the top fourth and second diagnoses. respectively, for hospital readmissions.
  • Declining number of specialists: As physician retirements increase across the board, there is a particularly concerning shortage of pulmonary specialists.  As a result, patients in areas without convenient access to pulmonologists may have to travel up to 100 miles and wait up to four months for an appointment.
  • Access to care in rural markets: Americans in rural areas face a variety of challenges when it comes to accessing healthcare. For COPD in particular, rural Americans face higher diagnosis and mortality rates, due to difficulties traveling to, affording, and consistently accessing timely and high-quality specialty care.

The four-point plan to address COPD

  1. Drive more awareness:  The first step in addressing the silent epidemic of COPD is to raise awareness. Organizations like the COPD Foundation are instrumental to educating the public about the risk factors and symptoms of COPD. They emphasize the importance of early diagnosis and treatment, shedding light on a condition often overshadowed by more high-profile health concerns.  However, there remains a critical need for robust anti-smoking campaigns, clean air regulations, and increased funding for COPD awareness and education. It’s time for public policy to prioritize adequate reimbursement for spirometry testing, including home based testing, affordable COPD medications, remote pulmonary rehab, remote self management programs, and other evidence based COPD care.
  2. Prioritize Diagnosis and Screening:  To address the diagnostic shortfall in COPD, we must improve access to and utilization of spirometry so that physicians and individuals alike can assess and confirm the condition before it progresses. Just last month, the American Lung Association issued a new COPD State Brief recommending the use of a COPD screening tool and spirometry to confirm diagnosis. In recent years, there has been significant investment in at-home solutions for spirometry that can produce high-quality readings without the need for a clinic. We have seen an increase in the ability to do spirometry from the home environment, often producing equally high quality readings as seen in clinic. Combining home-based spirometry with the CAPTURE screening tool, which uses a combination of questions and peak expiratory flow (PEF) rate, will empower providers and patients to diagnose and care for COPD from home.
  3. Leverage monitoring devices and wearables: As we embrace a future of connected healthcare, monitoring devices and wearables play a pivotal role in managing chronic conditions like COPD. These devices enable healthcare providers to keep a close eye on a patient’s conditions, tracking important metrics, and intervening promptly when necessary. By incorporating, Bluetooth connected devices such as spirometers, pulse oximeters, and inhaler trackers into clinical management, we can empower patients to take a more active role in their own care. Regular monitoring of patient’s conditions can detect exacerbations while uncovering rising risk, helping to prevent hospital admissions and readmissions while improving overall quality of life. In a world increasingly reliant on technology, we must harness these tools to address COPD comprehensively.
  4. Embrace Virtual Care: The emergence of the Covid- 19 pandemic accelerated the adoption of  telehealth services and virtual care practices. COPD patients, who are often elderly or living in rural areas, benefit immensely from the accessibility and convenience that virtual care provides, including telehealth appointments and ongoing disease monitoring. Likewise, telehealth can mitigate the shortage of pulmonologists and the extended waiting times for specialist appointments. Virtual care not only ensures timely access to care but also enables continuous monitoring and early intervention. Patients can receive timely check-ups, participate in pulmonary rehabilitation programs, and seek advice, all from the comfort of their homes, eliminating the burden of transportation costs and time. This trend in virtual care must continue to expand to ensure that all COPD patients receive the care they deserve.

Urgent action is necessary

To summarize, the silent COPD epidemic demands urgent recognition and action. The four-point plan offers a holistic strategy for tackling this critical public health issue through increased awareness, emphasis on diagnosis and screening, utilization of monitoring devices, and the adoption of virtual care. In this way, we can revolutionize the landscape of COPD management, slowing disease’s progression and potentially saving numerous lives.. The time for decisive action has arrived.

Photo: milan2099, Getty Images

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Chronic obstructive pulmonary disease (COPD) is a chronic respiratory disease characterized by irreversible and progressive airflow obstruction and chronic airway inflammation.1 The latest data show that an age-standardized incidence rate of COPD is 200.49 per 100,000 people worldwide, with smoking being a major environmental risk factor.2 The pathogenesis of COPD is still not fully understood and could be attributed to the overexpression of inflammatory mediators and cytokines, activation of inflammatory signaling pathways, protease/anti-protease imbalance and oxidation-antioxidant imbalance.3 An FEV1/FVC ratio less than 0.70 is considered diagnostic of COPD according to the Global Initiative for Obstructive Lung Disease (GOLD).4 It has been noted that the emergence of some novel COPD markers has improved clinical decision-making.5–8 The specific mechanisms that underlie the development and progression of COPD should therefore be investigated.

Increasing evidence indicates that lipid metabolic disorders are associated with COPD onset and progression. It has been reported that the levels of free alpha-linolenic acid, linoleic acid and eicosapentaenoic acid in the sputum of patients with stable COPD are significantly lower than those in the control group.9 The lipid metabolism profile during acute exacerbations of COPD exhibits a unique characteristic.10 It has been demonstrated that phospholipididylcholine 34:3 levels are positively correlated with COPD progression and lung function decline in FEV1.11 In COPD patients with acute exacerbations, a predictive model developed using the three lipid metabolites had excellent discriminatory power in distinguishing eosinophilic and non-eosinophilic inflammatory subtypes, with an area under the receiver operating characteristic (ROC) curve (AUC) of 0.834.12 Smoking and oxidative stress may contribute to the development of lipid-metabolism abnormalities in COPD, with smokers having elevated serum triglyceride concentrations and reduced plasma high-density lipoprotein and high-density lipoprotein cholesterol.13 A high level of high-density lipoprotein cholesterol is associated with an increased risk of COPD mortality.14 Exposure to cigarette smoke causes lipid peroxidation in bronchial epithelial cells and leads to the redistribution of various lipid components, resulting in the accumulation of lipids in the cytoplasm.15 During smoking, the continuous process of lipid metabolism in respiratory tract cells is disrupted.16 It also reduces the fluidity of the plasma membrane of alveolar macrophages, leading to changes in lipid composition.17 In addition, lipids can also act as a second messenger in cell signaling to modulate host inflammatory responses. Lipid molecules play a critical role in regulating inflammation generation and resolution by balancing pro-inflammatory and anti-inflammatory mediators.18

Lipid metabolism-related genes (LMRGs) are essential molecules involved in lipid production and metabolism, playing a vital role in tumors, immune disorders and inflammatory diseases.19,20 A growing body of research has also revealed the importance of LMRGs in COPD. It has been shown that cholesterol overload intensifies inflammation in cigarette smoke-treated bronchial epithelial cells and causes mitochondrial dysfunction mediated by StAR-related lipid transfer domain-3 (STARD3).21 In lung epithelial cells exposed to cigarette smoke, the family with sequence similarity 13 member A (FAM13A) induces the expression of carnitine palmitoyltransferase 1A (CPT1A) to enhance fatty acid oxidation, resulting in an accumulation of reactive oxygen species and cell death.22

In this study, the diagnostic characteristics of LMRGs in COPD were established by analyzing transcriptional profile data from multiple databases. Further cytological validation identified BCHE and PLA2G7 as potential COPD biomarkers associated with lipid metabolism.

Materials and Methods

Data Collection

The expression profiles of datasets GSE76925 and GSE8581 were downloaded from the Gene Expression Omnibus (GEO) database ( The two datasets contain genome-wide information derived from lung tissue samples. R software (version 3.5.1) was used to preprocess the data, box plots were used to verify sample standardization, PCA plots and UMAP plots were used to check clustering between sample groups, and the “Limma” package was used to identify differentially expressed genes (DEGs). DEGs are defined as gene expression differences greater than twofold between two groups with adjusted p-values less than 0.05. Visualization of the data was accomplished using the ggplot2 package (version 3.3.3) and the ComplexHeatmap package (version 2.2.0).

Subject Characteristics

We included 38 control samples and 111 samples of COPD in GSE76925. According to GOLD criteria, COPD was diagnosed as FEV1/FVC<70%. Compared with healthy controls, FEV1/FVC values were significantly lower in the COPD group, as well as FEV1%pred. There were no statistically significant differences in gender and age between COPD patients and controls. Patients with COPD smoked significantly more pack-years and had a lower BMI compared with healthy controls, which is consistent with the clinical features of the disease. The demographic characteristics of dataset GSE76925 are shown in Table 1. In the validation set GSE8581, 18 control samples and 16 samples with COPD were included, and there was no statistical difference in age or gender between the two groups (Supplementary Table 1).

Table 1 Demographic and Baseline Characteristics of the Samples in GSE76925

Extraction of Genes in Lipid Metabolism

The Kyoto Encyclopedia of Genes and Genomes (KEGG) database ( and Molecular Signature Database (MSigDB, version 7.4) ( were used to search for lipid metabolism pathways. We summarized major lipid metabolism-related gene sets from the KEGG database (including hsa00061, hsa00062, hsa00071 and other lipid metabolism-related gene sets) and the GSEA database (including Hallmark fatty acid metabolism, KEGG glycerophospholipid metabolism, and lipid raft), and extracted LMRGs from the main lipid metabolism-related gene sets. By removing duplicate, nonsense and ambiguous gene annotations, we identified a total of 1102 LMRGs for further analysis (Supplementary Table 2).

Functional Annotation of Differentially Expressed Genes

Gene ontology (GO) analysis and KEGG enrichment analysis of DEGs were performed using the “clusterProfiler” package in R language. GO enrichment analysis can explain the biophysical properties of the overall gene, mainly including three aspects: cellular components, molecular functions and biological processes. KEGG analysis provides an overview of metabolic pathways as well as functionally related databases of gene expression information in cells. P<0.05 was set as the cutoff criterion. Gene set enrichment analysis (GSEA) is a computational procedure that examines gene expression profiles at the level of entire gene sets to better understand candidate gene sets or pathways associated with disease. The clusterprofiler package was used to perform GSEA analysis, as well as normalized enrichment scores (|NES|>1) and adjusted p-values of 0.05 were set as threshold levels.

Protein-Protein Interaction (PPI) Network Construction

STRING ( is an online database that holds information on all known and predicted proteins and can be used to construct functional protein association networks. To obtain the interaction information between differentially expressed lipid metabolism-related genes (DeLMRGs) and proteins, we used the STRING database and assigned a confidence score of 0.4 for the medium confidence score. PPI networks were constructed and visualized using Cytoscape software (version 3.9.1), a general open-source software platform for network biology analysis and visualization. With default parameters, the CytoHubba plug-in was used to identify hub genes with five core algorithms.

Competing Endogenous RNA (ceRNA) Regulatory Network Construction

To predict miRNA targets of selected DeLMRGs, online databases including TargetScan ( and miRDB ( databases were used. Using the VEEN graph, the targeted miRNAs were obtained by intersecting the miRNAs of the same DeLMRGS in the two databases. Starbase database ( was selected for predicting miRNA-targeted long non-coding RNAs (lncRNAs), with a screening condition of CLIP data high stringency (clipExpNum≥3). Data visualization was performed using Cytoscape.

Cigarette Smoke Extract (CSE) Preparation

Non-filtered cigarettes (tar: 11 mg, nicotine: 1.0 mg, carbon monoxide: 14 mg/cigarette; Furong Brand; Hunan China Tobacco Industrial Co., Ltd.) were burned, one end of the cigarette was connected to a 50mL centrifuge tube containing 5 mL PBS solution and the other end was connected to a 50 mL syringe. Take three cigarettes each time, and the smoke was directed through the tube and fully dissolved in 5 mL of PBS solution. OD values were detected at 320 nm and adjusted to 12±0.5 as the original CSE (100% concentration). Then the 100% CSE solution was filtered with a 0.22 μm filter (Merck-Millipore, USA) to remove bacteria and was used within 30 mins. Depending on the experimental group, 100% CSE was diluted to the required concentration using culture medium.

Cell Culture and Treatment

The Mouse macrophage cell line RAW264.7 and the Human mononuclear macrophage cell line THP-1 were obtained from the American Type Culture Collection (ATCC, USA). Among them, RAW264.7 cell line was cultured in DMEM medium (Gibco, China) containing 10% fetal bovine serum (Procell, Wuhan, China) and 1% penicillin/streptomycin (Ecotop, Guangzhou, China); THP-1 cell line in RPMI-1640 medium (Gibco, Shanghai, China) containing 10% fetal bovine serum (Procell, Wuhan, China) and 1% penicillin/streptomycin (Ecotop, Guangzhou, China), and cultured at 37°C in an incubator with 5% CO2. THP-1 monocytes were transformed into adherent macrophages in 6-well plates treated with 100 nM phobolol 12-myristate 13-acetate (PMA) final concentration for 48h. THP-1 cells and RAW264.7 cells were seeded to 6-well plates and stimulated with 0–3% (final concentration) CSE for 24h or 48h. Finally, cells were collected to extract proteins and RNA for subsequent analysis.

CCK8 Assay for Cell Viability

A cell viability assay was performed using the cell counting kit 8 (CCK-8; ECOTOP, Guangzhou, China) according to the manufacturer’s instructions. THP-1 cells (3×104 / well) and RAW264.7 cells (2×104 / well) were incubated with different concentrations of CSE in 96-well plates for 24h or 48h. Subsequently, the supernatant was collected, and 100ul DMEM or RPMI-1640 containing 10% CCK-8 solution was added. The cells were further incubated for 60 mins at 37°C. A microplate reader (Bio-TEK; USA) was used to measure the absorbance (Ab) value at 450 nm wavelength. Cell activity (%) = (Ab value of treated well – Ab value of blank well)/(Ab value of control well – Ab value of blank well) × 100 (Supplementary Figure 1).

Enzyme-Linked Immunosorbent Assay (ELISA)

Briefly, THP-1 cells and RAW264.7 cells were seeded in a 6-well culture plate at a concentration of 5×105 per well and treated according to established experimental grouping. The supernatant of each group was collected after 24h or 48h, followed by centrifugation at 1000 × g for 20 mins. PLA2G7 (LP-PLA2) and BCHE expression levels were measured according to the ELISA assay kit instructions (RenJie Biotechnology, Shanghai, China). Mouse (RJ23239, China) and human (RJ14515, China) PLA2G7, and Mouse (RJ17076, China) and human (RJ24172, China) BCHE ELISA kits.

Statistical Analysis

Statistical analysis was performed using R software (version 3.6.2) and SPSS 26.0. Data with a normal distribution were expressed as mean ± standard error of the mean (SEM), and Student’s t-test were used to compare the mean of two groups. Data that did not fit the normal distribution were expressed as interquartile ranges, and Mann–Whitney U-test were applied to compare the two groups. Comparisons between groups were made using the Chi-square test with count data expressed in n (%). Correlations between DeLMRGs expressions were analyzed using Pearson correlation analysis. Pearson’s correlation coefficient is between 0.5 and 1, indicating a strong correlation. The ROC curve analysis was used for determining the predictive value of the hub gene in Validation set for the diagnosis of COPD, with AUC>0.7 indicating a high diagnostic value. P -value < 0.05 was considered statistically significant.


Identification of DEGs and DeLMRGs in COPD

According to the flow chart, the entire study was conducted (Figure 1). For gene expression profiling, 111 severe COPD cases and 38 smoking controls with normal lung function were selected from GSE76925 in the GEO database, all of whom underwent surgical removal for lung tissue sampling. The difference analysis between the two groups was performed and 587 DEGs were found with a 2-fold difference between the two groups and adjusted P values less than 0.05, including 62 genes upregulated and 525 genes downregulated (Figure 2A and B). The intersection of 587 DEGs with 1102 LMRGs led to the identification of 20 DeLMRGs, including 1 up-regulated and 19 down-regulated genes (Figure 2C).

Figure 1 A flowchart of the study.

Abbreviations: GEO, Gene Expression Omnibus; KEGG, Kyoto Encyclopedia of Genes and Genomes; MsigDB, Molecular Signatures Database; LMRGs, lipid metabolism-related genes; DEGs, differentially expressed genes; DeLMRGs, differentially expressed lipid metabolism-related genes; GO, Gene Ontology; ROC, receiver operating characteristic; BCHE, butyrylcholinesterase; PLA2G7, phospholipase A2 Group VII; ELISA, Enzyme linked immunosorbent assay.

Figure 2 Identification of DeLMRGs in COPD patients. (A) Volcano plot of COPD-related DEGs, graphed with log2FoldChange on the abscissa and -log10 on the ordinate (adjusted P value): Nodes in red represent DEGs up-regulated, nodes in blue represent DEGs down-regulated, and nodes in gray represent genes not significantly differentially expressed. (B) Heat map of top 20 COPD-related DEGs: disease samples are indicated by group1, normal control samples by group2, and high gene expression is indicated by red with low gene expression by blue; (C) Venn diagram of DeLMRGs derived from DEGs and LMRGs intersection: green represents LMRGs, blue represents upregulated DEGs and pink represents downregulated DEGs.

Abbreviations: DEGs, differentially expressed genes; LMRGs, lipid metabolism-related genes; DeLMRGs, differentially expressed lipid metabolism-related genes.

Enrichment Analysis of DEGs and DeLMRGs in COPD

To better understand the biological functions and pathways underlying the 587 differential genes associated with COPD, we performed GO and KEGG enrichment analysis (Figure 3A). Biological processes associated with these DEGs include mitotic nuclear division, nuclear division, and sister chromatid segregation. Spindle, mitotic spindle, and centromeric regions are the major cell components associated with these DEGs. The main molecular functions of these DEGs include microtubule attachment, tubulin attachment, and microtubule motor activity. According to the KEGG pathway analysis, the cell cycle, oocyte meiosis, and cellular senescence are the most closely related pathways. Using GSEA analysis, concordant differences between disease and normal states were detected or the distribution trend of DEGs was examined. Results revealed that these DEGs were strongly associated with matrisome, extracellular matrix organization, membrane trafficking and vesicle mediated transport (Figure 3B).

Figure 3 Enrichment analysis of DEGs and DeLMRGs in COPD patients. (A) GO and KEGG enrichment analysis of 587 DEGs. (B) KEGG analysis of 587 DEGs. (C) GO enrichment analysis of 20 DeLMRGs. (D) KEGG enrichment analysis of 20 DeLMRGs.

Abbreviations: DEGs, differentially expressed genes; DeLMRGs, differentially expressed lipid metabolism-related genes; GO, gene ontology; KEGG, kyoto encyclopedia of genes and genomes.

Similarly, we performed GO and KEGG enrichment analysis on these screened 20 DeLMRGs. GO analysis revealed that these DeLMRGs were primarily involved in biological processes such as unsaturated fatty acid metabolism, fatty acid derivative metabolism, fatty acid metabolism, ammonium ion metabolism, fatty acid derivative biosynthesis, protein-lipid complex, phospholipase activity, phospholipase A2 activity, lipase activity, carboxylate hydrolase activity and calcium-dependent phospholipase A2 activity (Figure 3C). KEGG pathway analysis showed that these DeLMRGs primarily function in signaling pathways such as arachidonic acid metabolism, ether lipid metabolism, α-linolenic acid metabolism, adipocytokine signaling pathway and linoleic acid metabolism (Figure 3D).

PPI Network Construction and Hubgene Screening

To investigate the relationship between DeLMRGs, these 20 DeLMRGs were imported into Cytoscape to construct a PPI network (Figure 4A) and 10 hub genes were obtained by screening with the cytohubba plug-in (details about the genes are provided in Table 2). Among them, PLA2G7 was the only gene that was up-regulated, followed by PLA2G4A, HPGDS, LEP, PTGES3, LEPR, PLA2G2D, MED21, SPTLC1, and BCHE, which were the nine genes down-regulated (Figure 4B).

Table 2 Table of Detailed Information About 10 Hub DeLMRGs

Figure 4 PPI network of DeLMRGs. (A) PPI network of 20 DeLMRGs: upregulated genes are shown in red, while downregulated genes are shown in blue. (B) PPI network of 10 hub DeLMRGs: The darker the color, the greater the contribution of genes to the PPI network. The black line indicates the presence of genes that interact.

Abbreviations: DeLMRGs, differentially expressed lipid metabolism-related genes; PPI, Protein-Protein Interaction.

Verification of Diagnostic Biomarkers

Validation of the identified 10 DeLMRGs was carried out using the dataset GSE8581 which includes gene expression profiles of lung tissues from 16 COPD patients and 18 controls with normal lung function. A total of 9 DeLMRGs (except MED21) were found in the validation set (Figure 5A–I), in which BCHE and PLA2G7 expression levels were statistically different between the two groups. In comparison with normal controls, patients with COPD had lower expressions of BCHE (P<0.01, Figure 5A), as well as higher expressions of PLA2G7 (P<0.01, Figure 5G). Meanwhile, we generated the ROC curves for 9 DeLMRGs. A high diagnostic value was found for both BCHE (with an AUC of 0.753) and PLA2G7 (with an AUC of 0.760) in predicting the development of COPD (Supplementary Figure 2).

Figure 5 Validation of 9 hub DeLMRGs between COPD and controls in GSE8581. (A) The expressions of BCHE in validation sets. (B) The expressions of HPDGS in validation sets. (C) The expressions of LEP in validation sets. (D) The expressions of LEPR in validation sets. (E) The expressions of PLA2G2D in validation sets. (F) The expressions of PLA2G4A in validation sets. (G) The expressions of PLA2G7 in validation sets. (H) The expressions of PTGES3 in validation sets. (I) The expressions of SPTLC1 in validation sets. *P< 0.05, **P < 0.01.

Abbreviations: DeLMRGs, differentially expressed lipid metabolism-related genes; BCHE, Butyrylcholinesterase; HPDGS, hematopoietic prostaglandin D synthase; LEP, leptin; LEPR, leptin receptor; PLA2G2D, phospholipase A2 group IID; PLA2G4A, phospholipase A2 group IVA; PLA2G7, phospholipase A2 group VII; PTGES3, prostaglandin E synthase 3; SPTLC1, serine palmitoyltransferase long chain base subunit 1.

Construction of ceRNA Regulatory Network

CeRNA plays a crucial role in gene expression regulation, as ceRNA molecules (mRNA, lncRNA, pseudogene, etc.) can modulate gene expression by competing with miRNA response elements. To explore possible interactions among lncRNAs, miRNAs, and DeLMRGs in COPD, BCHE and PLA2G7 ceRNA regulatory networks were constructed. We collected 57 miRNAs in this study, including hsa-miR-342-3p, hsa-miR-3145-3p, and hsa-miR-218-5p (Figure 6A and B). The starbase database was used to map the above 57 miRNAs and find their target lncRNAs. A total of 20 lncRNAs were examined for interactions with seven of the 57 miRNAs in the Starbase database. The ceRNA regulatory network was then constructed and visualized by CytoScape (Figure 6C).

Figure 6 CeRNA regulatory network of lncRNA-miRNA-DeLMRG. (A) Venn diagram showing that 40 miRNAs from TargetScan and miRDB interact with BCHE. (B) Venn diagram showing that 17 miRNAs from TargetScan and miRDB interact with PLA2G7. (C) CeRNA network of BCHE and PLA2G7: red diamonds represent protein-coding genes, blue circles represent miRNAs, green rectangles represent lncRNAs, and black lines represent the interactions between lncRNAs, miRNAs, and mRNAs.

Abbreviations: BCHE, butyrylcholinesterase; PLA2G7, phospholipase A2 Group VII; ceRNA, competing endogenous RNA; lncRNA, long non-coding RNA; miRNA, microRNA; DeLMRG, differentially expressed lipid metabolism-related genes.

Verification of BCHE and PLA2G7 Expression in Cell Experiment

To verify the bioinformatics results, we detected the expression of PLA2G7 and BCHE in macrophages treated with different concentrations of CSE. CSE-induced groups showed significant decreases in the expression of BCHE (Figure 7) and increases in the expression of PLA2G7 (Figure 8), indicating the analysis was reliable and PLA2G7 and BCHE may contribute to the development of COPD.

Figure 7 The expression levels of BCHE in macrophages treated with different concentrations of CSE by ELISA. (A) Expression levels of BCHE after different concentrations of CSE treated RAW264.7 cells for 24h. (B) Expression levels of BCHE after different concentrations of CSE treated RAW264.7 cells for 48h. (C) Expression levels of BCHE after different concentrations of CSE treated THP-1 cells for 24h. (D) Expression levels of BCHE after different concentrations of CSE treated THP-1 cells for 48h. Data are presented as mean±sem and differences between groups were assessed by one-way ANOVA. *Indicates the comparison between different CSE administration (0.5–3%) with the blank control group, and *p<0.05; **p<0.01; NS: no significant (P > 0.05).

Abbreviations: BCHE, butyrylcholinesterase; CSE, cigarette smoke extract.

Figure 8 The expression levels of PLA2G7 in macrophages treated with different concentrations of CSE by ELISA. (A) Expression levels of PLA2G7 after different concentrations of CSE treated RAW264.7 cells for 24h. (B) Expression levels of PLA2G7 after different concentrations of CSE treated RAW264.7 cells for 48h. (C) Expression levels of PLA2G7 after different concentrations of CSE treated THP-1 cells for 24h. (D) Expression levels of PLA2G7 after different concentrations of CSE treated THP-1 cells for 48h. Data are presented as mean±sem and differences between groups were assessed by one-way ANOVA. *Indicates the comparison between different CSE administration (0.5–3%) with the blank control group, and *p<0.05; **p<0.01; ***p<0.001; ****p < 0.0001.

Abbreviations: PLA2G7, phospholipase A2 Group VII; CSE, cigarette smoke extract.


Advances in proteomics and metabolomics have greatly contributed to the understanding of disease. The metabolic alteration of the lungs and even the exhaled breath can be used as indicators of lung disease.23,24 As a common metabolic process, lipid metabolism is not only significant for energy production, but also for biosynthesis, redox homeostasis, and the regulation of intercellular communication.25 Numerous studies have demonstrated that lipid metabolism disorders contribute to the development of diseases, including cancer,26 autoimmune diseases27 and chronic inflammatory conditions.28 Lipid metabolism is active in the lungs, particularly in the alveoli. In the lung, surfactants are typical lipid complexes that regulate the homeostasis of each respiratory cycle.29 Lipids are not only important surfactants and energy storage compounds in the lungs, but they also contribute to the development of diseases such as pulmonary fibrosis and COPD by acting as signaling molecules in a variety of physiological and pathophysiological processes.30,31 As a common chronic inflammatory airway disease, COPD has been found to be associated with lipid metabolic disorders.32 Tobacco smoking is a major risk factor for COPD due to its significant effects on lung cell function, surfactant composition and lung lipid composition (particularly phospholipids, cholesterol, and fatty acids).33

Supported by the close association of altered lipid metabolism with disease, specific lipid profiles are emerging as unique disease biomarkers with diagnostic, prognostic and predictive potential. Our study explored this specific lipid profile between COPD patients and normal ones. The results identified PLA2G4A, HPGDS, LEP, PTGES3, LEPR, PLA2G2D, MED21, SPTLC1, PLA2G7, and BCHE as lipid molecules that strongly associated with COPD development. The hematopoietic prostaglandin D synthase (HPGDS) is a σ-like glutathione transferase that participates in the arachidonic acid metabolic pathway and catalyzes the production of prostaglandin D2, which is an important mediator of inflammation and malignant tumor growth. According to Shao et al34 mutations of HPGDS promote lung cancer cell migration by upregulating the expression of ACSL1 and ACC, important enzymes involved in lipid metabolism. In type 2 diabetic mice, HPGDS was significantly downregulated in wounds, and its deficiency delayed normal wound healing.35 Overexpression of HPGDS in adipose-derived mesenchymal stem cells reduced inflammation and improved wound healing. Leptin (LEP) is a product of the obesity gene, synthesized and secreted by white adipocytes. Besides regulating food intake and body weight, LEP and leptin receptors (LEPRs) also play an integral role in fetal growth, pro-inflammatory immune responses, angiogenesis and lipolysis.36–38 Accordingly, elevated levels of LEP during lung inflammation and the presence of functional LEPR in the lungs suggest that LEP/LEPR play an important role in respiratory immune responses and the development of inflammatory respiratory diseases.39 Among patients with moderate COPD, Broekhuizen et al40 found that leptin levels were detected in induced sputum and were significantly correlated with C-reactive protein and total TNF-α. Hansel et al41 found that genetic variants in the LEPR gene were significantly associated with reduced lung function in COPD patients who smoked, by genotyping 36 single nucleotide polymorphisms in LEPR. Wang et al42 suggested that the mutations of the LEPR gene Gln223Arg site may worsen chronic bronchitis by inhibiting the biological effects of leptin, although not directly affecting LEP levels. The molecular chaperone P23, also known as prostaglandin E synthase 3 (PTGES3), is an important component of the Hsp90 molecular chaperone machinery. Gao et al43 found that PTGES3 was highly expressed in lung, cholangiocarcinoma, and breast invasive carcinoma samples, and overexpression was associated with poor overall survival in lung adenocarcinomas. Adekeye et al44 showed that PTGES3 can be a prognostic marker in breast cancer. Mediator Complex Subunit 21 (MED21) is a subunit of the Arabidopsis Mediator, which can interact with the human RNA polymerase II holoenzyme and participate in the transcriptional regulation of the RNA polymerase II transcriptional gene.45 Tan et al46 have demonstrated that all members of the MED family, including MED21, are highly expressed in hepatocellular carcinoma, and that expression levels correlate with pathological stages. Nikas et al47 found that MED21 may be a diagnostic marker for prostate cancer. Serine palmitoyl transferase (SPT) is the rate-limiting enzyme in the de novo synthesis of sphingolipids (SL) and is essential for embryonic development, physiological homeostasis, and stress response.48 SPT long chain subunits 1 (SPTLC1) is a key subunit in the enzymatic activity of the SPT complex and is closely associated with vascular development and systemic sphingolipid homeostasis.49 Jiang et al50 found that inhibition of SPTLC1 expression in lung microvascular endothelial cells significantly reduced SPT expression and inhibited LPS-induced ceramide production, thereby inducing endothelial barrier dysfunction. Medler et al51 found that inhibition of SPTLC1 expression in lung endothelial cells inhibited TNF-α (plus actinomycin) induced apoptosis. Gorshkova et al52 found that inhibition of SPTLC1 downregulated sphingosine kinase 1 expression and thereby delayed the onset of radiation-induced pulmonary fibrosis. Accordingly, these findings support our conclusion that lipid-related molecules are predictive of COPD development.

The results of the enrichment analysis suggest that the biological processes in which these genes are mainly involved include polyunsaturated fatty acids (PUFA) metabolism, fatty acid derivative metabolism and fatty acid metabolism as the molecular pathways in which these genes are mainly involved. PUFA metabolism plays a crucial role in COPD development. Cigarette smoke may contribute directly to an alteration in epithelial PUFA metabolism, promoting the remodeling of airway epithelium. Significant differences in PUFA metabolism have been observed in COPD patients, with further changes occurring during acute exacerbations.9 Increasing the intake of PUFA may reduce the risk of COPD due to its antioxidant and anti-inflammatory properties.30,53 Rutting et al54 found that supplementation with the ω-6 polyunsaturated fatty acid arachidonic acid resulted in impaired cytokine release from fibroblasts and inhibition of extracellular matrix protein expression in COPD patients. Atlantis et al55 found that supplementation with omega-3 fatty acids (eicosapentaenoic acid, docosahexaenoic acid or alpha-linolenic acid) significantly improved exercise capacity in COPD patients. According to Lee-Sarwar et al56 dietary intake and plasma levels of PUFA were negatively associated with asthma and recurrent wheezing at age three. Many respiratory diseases are associated with the metabolism of fatty acids and their derivatives. The impaired metabolism of fatty acids in cystic fibrosis, characterized by an increase in arachidonic acid-derived metabolites and a decrease in docosahexaenoic acid-derived metabolites, may be partially corrected by supplementation with docosahexaenoic acid.57 Linoleic acid-derived lipid mediators are associated with an increased risk of COPD in women, including the cytochrome P450-derived epoxide product of linoleic acid (leukotoxin) and its corresponding soluble epoxide hydrolase (sEH)-derived product (leukotoxin diol).58 Cigarette smoke may be involved in COPD development by reducing fatty acid catabolism in pulmonary microvascular endothelial cells, leading to apoptosis of pulmonary endothelial cells.59 There is some evidence that exogenous supplementation of fatty acids and their derivatives may have a beneficial effect on lung disease. When short-chain fatty acids are supplemented, inflammation and oxidative stress are reduced in the lungs of aging mice, as well as the increased inflammatory signal in acute lung injury in these mice.60 A fatty acid derivative of quercetin-3-O-glucoside prevents cigarette smoke extract-induced cell death and membrane lipid peroxidation in human fetal lung fibroblasts.61 As a result of these studies, lipids and their derivatives have been implicated as a critical pathogenic factor in COPD and other lung diseases.

The ceRNA network regulatory mechanism also plays a crucial role in the regulation of COPD onset and progression. Liu et al62 showed that overexpression of LncRNA CASC2 is involved in the development of COPD by targeting the miR-18a-5p/IGF1 axis to inhibit bronchial epithelial cell apoptosis and inflammation. Shen et al63 found that LncRNA SNHG5 attenuated the pro-apoptotic and pro-inflammatory effects of cigarette smoke extracts on bronchial epithelial cells via the miR-132/PTEN axis. Comprehensive analysis of COPD-related coding and non-coding RNA transcriptome expression profiles and the construction of competing endogenous RNA networks facilitates visualization of the interactions between these RNAs, providing a more comprehensive insight into the pathology of COPD.64,65 Our study constructs a ceRNA network comprising lipid metabolism-related molecules, which partially serves as a foundation for exploring therapeutic targets associated with COPD-related lipid metabolism.

We identified PLA2G7 and BCHE as lipid metabolism diagnostic molecules in COPD. Lp-PLA2, formerly known as plasma platelet-activating factor acetylhydrolase, is encoded by the PLA2G7 gene located on chromosome 6p12-21. In respiratory diseases, PLA2G7 is secreted by macrophages and circulates in the blood as a complex with lipoproteins.66 Deng et al67 found that Lp-PLA2 levels were upregulated in COPD patients and that significantly associated with FEV1/FVC, CAT scores, mMRC scores and 6-minute walk test in COPD patients. Zhao et al68 found that PLA2G7 promotes the progression of COPD by promoting the expansion of myeloid-derived suppressor cells and inhibiting their function. Woodruff et al69 found increased expression of PLA2G7 in alveolar macrophages of cigarette smoke-treated mice. Butyrylcholinesterase (BCHE), also known as plasma cholinesterase, is synthesized in the liver and secreted into the plasma as an enzyme that catalyzes the hydrolysis of the neurotransmitter acetylcholine to acetate, thus restoring resting cholinergic neurons.70 Halu et al71 suggest that BCHE may be involved in the common pathogenesis of COPD and idiopathic pulmonary fibrosis. Sicinska et al72 observed a significant reduction in plasma BCHE activity in COPD patients and that this reduction was associated with increased lipid peroxidation and reduced total antioxidant capacity. However, Ben et al73 showed that BCHE activity was increased in COPD patients compared to healthy controls, and in COPD smokers, plasma BCHE activity was positively correlated with levels of several protein oxidative damage biomarkers, including total protein carbonyl compounds and advanced oxidative protein products These findings imply a potential role of PLA2G7 and BCHE in the pathogenesis of COPD, however, further investigations are warranted to validate their pathological mechanisms.

By developing a ceRNA network of lipid metabolism molecules, our study provides comprehensive investigation of lipid metabolism-related molecular markers associated with COPD. We aim to establish a foundation for therapeutic strategies targeting lipid metabolism pathways in COPD. However, there are some limitations to our study. Firstly, we were unable to analyze the relationship between these key genes and patient prognosis due to the lack of prognostic information in the public databases. A second factor that may have influenced our experimental results was the lack of nutrition-related data such as obesity level and weight information for these patients.


In summary, through bioinformatics analysis, we have identified two lipid metabolism-related factors closely associated with the occurrence of COPD. PLA2G7 expression was up-regulated while BCHE expression was down-regulated. Our study also involved the lipid metabolism molecules PLA2G7 and BCHE in the construction of a comprehensive ceRNA network. Our findings provide valuable insights into the pathophysiological mechanisms underlying COPD at the level of lipid metabolism, offering potential therapeutic targets and paving new avenues for disease prediction and intervention.

Data Sharing Statement

The underlying data support the results of the present study and can be obtained from the corresponding author upon reasonable request.


This study was supported by National Key R&D Program of China (2020YFC2008605 and 2020YFC2008600).


The authors declare that they have no conflicts of interest in this work.


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55. Atlantis E, Cochrane B. The association of dietary intake and supplementation of specific polyunsaturated fatty acids with inflammation and functional capacity in chronic obstructive pulmonary disease: a systematic review. Int J Evid Based Healthc. 2016;14(2):53–63. doi:10.1097/xeb.0000000000000056

56. Lee-Sarwar K, Kelly RS, Lasky-Su J, et al. Dietary and plasma polyunsaturated fatty acids are inversely associated with asthma and atopy in early childhood. J Allergy Clin Immunol Pract. 2019;7(2):529–538.e528. doi:10.1016/j.jaip.2018.07.039

57. Teopompi E, Risé P, Pisi R, et al. Arachidonic acid and docosahexaenoic acid metabolites in the airways of adults with cystic fibrosis: effect of docosahexaenoic acid supplementation. Front Pharmacol. 2019;10:938. doi:10.3389/fphar.2019.00938

58. Balgoma D, Yang M, Sjödin M, et al. Linoleic acid-derived lipid mediators increase in a female-dominated subphenotype of COPD. Eur Respir J. 2016;47(6):1645–1656. doi:10.1183/13993003.01080-2015

59. Gong J, Zhao H, Liu T, et al. Cigarette smoke reduces fatty acid catabolism, leading to apoptosis in lung endothelial cells: implication for pathogenesis of COPD. Front Pharmacol. 2019;10:941. doi:10.3389/fphar.2019.00941

60. Hildebrand CB, Lichatz R, Pich A, et al. Short-chain fatty acids improve inflamm-aging and acute lung injury in old mice. Am J Physiol Lung Cell Mol Physiol. 2023;324(4):L480–L492. doi:10.1152/ajplung.00296.2022

61. Warnakulasuriya SN, Rupasinghe H. Novel long chain fatty acid derivatives of quercetin-3-O-glucoside reduce cytotoxicity induced by cigarette smoke toxicants in human fetal lung fibroblasts. Eur J Pharmacol. 2016;781:128–138. doi:10.1016/j.ejphar.2016.04.011

62. Liu P, Zhang H, Zeng H, et al. LncRNA CASC2 is involved in the development of chronic obstructive pulmonary disease via targeting miR-18a-5p/IGF1 axis. Ther Adv Respir Dis. 2021;15:17534666211028072. doi:10.1177/17534666211028072

63. Shen Q, Zheng J, Wang X, et al. LncRNA SNHG5 regulates cell apoptosis and inflammation by miR-132/PTEN axis in COPD. Biomed Pharmacother. 2020;126:110016. doi:10.1016/j.biopha.2020.110016

64. Liu P, Wang Y, Zhang N, et al. Comprehensive identification of RNA transcripts and construction of RNA network in chronic obstructive pulmonary disease. Respir Res. 2022;23(1):154. doi:10.1186/s12931-022-02069-8

65. Feng X, Dong H, Li B, et al. Integrative analysis of the expression profiles of whole coding and non-coding RNA transcriptomes and construction of the competing endogenous RNA networks for chronic obstructive pulmonary disease. Front Genet. 2023;14:1050783. doi:10.3389/fgene.2023.1050783

66. Dua P, Mishra A, Reeta KH. Lp-PLA2 as a biomarker and its possible associations with SARS-CoV-2 infection. Biomark Med. 2022;16(10):821–832. doi:10.2217/bmm-2021-1129

67. Deng M, Yin Y, Zhang Q, et al. Identification of inflammation-related biomarker Lp-PLA2 for patients with COPD by comprehensive analysis. Front Immunol. 2021;12:670971. doi:10.3389/fimmu.2021.670971

68. Zhao X, Yue Y, Wang X, et al. Bioinformatics analysis of PLA2G7 as an immune-related biomarker in COPD by promoting expansion and suppressive functions of MDSCs. Int Immunopharmacol. 2023;120:110399. doi:10.1016/j.intimp.2023.110399

69. Woodruff PG, Ellwanger A, Solon M, et al. Alveolar macrophage recruitment and activation by chronic second hand smoke exposure in mice. COPD. 2009;6(2):86–94. doi:10.1080/15412550902751738

70. Gok M, Cicek C, Sari S, et al. Novel activity of human BChE: lipid hydrolysis. Biochimie. 2023;204:127–135. doi:10.1016/j.biochi.2022.09.008

71. Halu A, Liu S, Baek SH, et al. Exploring the cross-phenotype network region of disease modules reveals concordant and discordant pathways between chronic obstructive pulmonary disease and idiopathic pulmonary fibrosis. Hum Mol Genet. 2019;28(14):2352–2364. doi:10.1093/hmg/ddz069

72. Sicinska P, Bukowska B, Pajak A, et al. Decreased activity of butyrylcholinesterase in blood plasma of patients with chronic obstructive pulmonary disease. Arch Med Sci. 2017;13(3):645–651. doi:10.5114/aoms.2016.60760

73. Ben Anes A, Ben Nasr H, Garrouch A, et al. Alterations in acetylcholinesterase and butyrylcholinesterase activities in chronic obstructive pulmonary disease: relationships with oxidative and inflammatory markers. Mol Cell Biochem. 2018;445(1–2):1–11. doi:10.1007/s11010-017-3246-z

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Breathing Easy: Unveiling Dynamics in Italy's Respiratory


The respiratory devices market in Sweden is experiencing substantial growth, primarily attributed to the increasing prevalence of respiratory disorders such as Chronic Obstructive Pulmonary Disease (COPD), Tuberculosis (TB), Asthma, and Sleep Apnea. Despite significant advancements in device technologies improving treatment effectiveness, the market faces challenges related to the high cost of these devices.

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Key Features:

Prevalence of Respiratory Diseases: A report by Gianluigi Ferrante et al., published in the European Journal of Public Health 2017, revealed a 7% prevalence of Chronic Respiratory Diseases in Sweden. Among these, 3.4% accounted for asthma, 2.6% for COPD, and 1.0% for Asthma-COPD Crossover Syndrome. This escalating prevalence is a primary driver for the increased demand for respiratory devices in the country.

Technological Advancements: Swift technological advancements in respiratory devices have positively impacted the population by providing access to new and more effective technologies. This has significantly contributed to the market's growth, allowing patients to benefit from state-of-the-art solutions for managing respiratory conditions.

Cost-Related Market Constraints: Despite the evident demand, the high cost associated with respiratory devices and instruments has been a hindrance to market expansion. This factor needs careful consideration to ensure broader accessibility to these essential medical devices.

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Key Market Trends:

Inhalers as Therapeutic Devices: Chronic obstructive pulmonary disease (COPD) stands as a leading cause of death in Italy, particularly prevalent among the elderly population. A report by Francesco Blasi et al. in the Journal of Human Vaccines and Immunotherapeutics indicated COPD prevalence ranging from 3.3% in adults aged 20 to 44 years to 13.3% in those aged 65 to 84 years. Inhalers play a pivotal role in COPD treatment, and their demand is expected to surge, contributing significantly to market growth.
Competitive Landscape:

Italy, as a developed nation with a well-structured healthcare system, attracts numerous global players in the respiratory devices market. The competitive landscape is robust, featuring both international and domestic players. This dynamic market scenario creates an environment where innovative solutions and strategic market positioning are crucial for success.

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Conclusion: "Breathing Easy in Italy's Respiratory Devices Market"

In conclusion, Italy's respiratory devices market is at the forefront of providing innovative solutions to combat the rising prevalence of respiratory disorders, notably COPD. While technological advancements have ushered in new possibilities for patient care, the high cost remains a challenge. The emphasis on inhalers as therapeutic devices aligns with the critical need for effective COPD management.

Italy's competitive landscape, characterized by the presence of global and domestic players, underscores the importance of continuous innovation and strategic market approaches. As the geriatric population increases, addressing respiratory health challenges becomes paramount, making Italy's respiratory devices market a vital sector for healthcare advancements.

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Oxidative stress is the imbalance between the body's production of free radicals and their neutralization by antioxidants. Oxidative stress can lead to problems in the body, including organ and tissue damage.

Free radicals are harmful compounds produced by biological processes in the body, such as digesting food, breathing, turning fats into energy, and metabolizing alcohol and drugs.

Free radicals can cause problems within the body, including blocking the action of major enzymes, destroying cell membranes, preventing cellular processes the body needs to function properly, preventing normal cell division, blocking energy generation, and destroying DNA. They can also promote inflammation.

Antioxidants neutralize free radicals and help minimize the damage they cause.

This article will discuss why oxidative stress and free radicals matter, the symptoms and long-term effects of oxidative stress, what raises oxidative stress, how to lower oxidative stress, and small changes that can make a big impact on oxidative stress.

Kseniya Ovchinnikova / Getty Images

Oxidative Stress and Free Radicals: Why Do They Matter?

Free radicals are unstable molecules created when oxygen is metabolized in the body. They vary in shape, size, and chemical configuration.

Free radicals "steal" electrons from other molecules. This changes the other molecules' structure or function, causing damage such as altering instructions coded in DNA, changing a cell's membrane (affecting the flow of what enters and leaves the cell), and other effects.

At low or moderate levels, free radicals can play beneficial, even vital, roles within the body. In the right amount, they are crucial to maintaining human health.

Antioxidants help keep free radicals in check by neutralizing them. When there is an imbalance between the free radicals being produced and their elimination by antioxidants, oxidative stress occurs.

Oxidative stress can harm cellular structures such as:

  • Membranes
  • Lipids
  • Proteins
  • Lipoproteins
  • DNA

If not controlled, oxidative stress can be associated with:

  • Chronic and degenerative medical conditions
  • Speeding up the body's aging process
  • Acute medical problems (such as stroke)

What Are Antioxidants?

Antioxidants are molecules that neutralize free radicals by giving them electrons. They also help repair DNA and maintain the health of cells.

Hundreds to thousands of substances work as antioxidants. They aren't interchangeable. They have a different makeup, perform different roles, and are believed to work as parts of a network.

Certain foods contain antioxidants. Nutrient antioxidants include vitamins A, C, and E and copper, zinc, and selenium minerals. Non-nutrient antioxidants include other dietary food compounds, such as phytochemicals found in plants like tomatoes and cranberries.

Antioxidants may be water-soluble. These are best absorbed by the body but are rapidly eliminated through urine. Polyphenols and vitamin C are examples of water-soluble antioxidants.

Antioxidants can also be fat-soluble. Fats must be present for the body to absorb and use these antioxidants. Because they are not easily removed from the body, they can accumulate to levels that are too high. Vitamin E is one fat-soluble antioxidant.

Oxidative Stress Symptoms and Long-Term Effects 

Oxidative stress contributes to cellular damage. Over time, this can play a role in the development of a wide range of medical conditions, some of which include:

  • Chronic obstructive pulmonary disease (COPD)
  • Atherosclerosis (thickening or hardening of the arteries due to a build-up of plaque)
  • Alzheimer's disease
  • Heart disease (free radicals prompt low-density lipoprotein, or LDL, cholesterol to stick to artery walls)
  • Liver disease
  • Certain cancers (such as oral, esophageal, stomach, and bowel cancers)
  • Arthritis
  • Vision loss (from deterioration of the eye lens)
  • Parkinson's disease (and other conditions arising from damage to nerve cells in the brain)
  • Accelerating the aging process
  • Potentially neuropsychiatric disorders such as anxiety and depression (more research is needed)

Conditions Associated With Higher Oxidative Stress

Research has found links (of varying degrees) between oxidative stress and the onset and/or progression of a variety of medical conditions, including:

  • Cardiovascular diseases (atherosclerosis, ischemia, hypertension, cardiomyopathy, cardiac hypertrophy, and congestive heart failure)
  • Pulmonary diseases (like asthma and COPD)
  • Neurocognitive/neurological disorders (such as Alzheimer's disease, Parkinson's disease, amyotrophic lateral sclerosis (ALS), multiple sclerosis (MS), depression, and memory loss)
  • Metabolic disorders (like diabetes)
  • Certain cancers
  • Rheumatoid arthritis
  • Problems with kidney function

What Raises Oxidative Stress?

Oxidative stress can arise when there are more free radicals than the body can neutralize. Free radicals can be generated from endogenous (originating in the body) sources and exogenous (originating outside the body) sources.

Endogenous free radical production can stem from sources such as:

  • Immune cell activation
  • Inflammation
  • Infection
  • Cancer
  • Ischemia (restricted blood flow/oxygen to a part of the body)
  • Excessive exercise
  • Mental stress
  • Aging

Exogenous free radical production can result from sources such as:

  • Environmental pollutants
  • Heavy metals
  • Certain medications (such as cyclosporine, tacrolimus, gentamicin, and bleomycin)
  • Certain products from cooking (such as used oil, excessive consumption of polyunsaturated fatty acids, food additives, and smoked meat)
  • Tobacco smoke
  • Alcohol
  • Exposure to radiation (including ultraviolet, or UV, radiation/sunlight)
  • Pesticides and other chemicals
  • Ozone
  • Allergens

How to Lower Oxidative Stress 

Eating a diet rich in antioxidants can help prevent or reduce damage caused by oxidation and reduce the risk of several conditions, such as heart disease and certain cancers.

Antioxidants can be found in fruits, vegetables, whole grains, nuts, and some meats, fish, and poultry.

Good sources of antioxidants include:

  • Cruciferous vegetables: Like broccoli, cauliflower, and cabbage
  • Leafy green vegetables: Like spinach
  • Other vegetables: Like corn, tomatoes, carrots, eggplant, pumpkin, red capsicum, and sweet potatoes
  • Alliums: Like leeks, onions, and garlic
  • Fruits: Such as apricots, watermelon, pink grapefruit, mangoes, grapes, berries, citrus fruits, apples, oranges, black currants, kiwi, and avocado
  • Legumes: Like soybeans, tofu, lentils, and peas
  • Nuts and seeds: Such as sesame
  • Herbs: Like parsley
  • Whole grains: Such as bran
  • Tea: Including green tea
  • Vegetable oils: Like wheatgerm oil
  • Milk
  • Seafood
  • Lean meat

These foods offer many different types of antioxidants, and eating a variety of them is important. Research suggests antioxidants work best when combined with other nutrients, plant chemicals, and other antioxidants.

Increasing evidence suggests antioxidants are more effective when consumed as part of whole foods rather than when isolated from a food or as a supplement.

Consuming antioxidant vitamins or minerals at significantly higher levels than the recommended dietary amounts can prompt them to act as pro-oxidants and cause damage. Talk to a healthcare provider or registered dietitian before taking supplements.

Eating foods rich in antioxidants is part of a healthful lifestyle plan, but they are not a substitute for overall healthy lifestyle choices.

Small Changes That Make a Big Impact on Oxidative Stress

Preventing oxidative stress is all about balance. More doesn't always mean better, especially when it comes to supplements. Focus on overall balanced lifestyle choices, like:

  • Eat a balanced diet with a variety of nutrient-rich foods, including those that are sources of antioxidants.
  • Talk to a registered dietitian about developing a healthful eating plan that works for you.
  • Get plenty of exercise without overdoing it.
  • Don't smoke.


Free radicals can cause damage within the body. Antioxidants neutralize free radicals and help prevent or minimize the damage from them. Oxidative stress is when there is an imbalance between the production of free radicals and the body's ability to neutralize them.

Oxidative stress is linked to several health conditions, such as cardiovascular disease, pulmonary disease, and neurological conditions.

Free radicals can be created from processes within the body or exposure to factors outside the body, such as pollution, cigarette smoke, and UV radiation.

Antioxidants can be found in many foods, particularly fruits, vegetables, whole grains, nuts, and some seafood, meats, and poultry. Research suggests antioxidants are more effective when they come as part of a variety of whole foods rather than in isolation or as a supplement.

Preventing oxidative stress is more about balance than consuming large amounts of antioxidants. Aim for a balanced diet with a variety of nutrient-rich foods, and practice other healthful lifestyle habits.

Verywell Health uses only high-quality sources, including peer-reviewed studies, to support the facts within our articles. Read our editorial process to learn more about how we fact-check and keep our content accurate, reliable, and trustworthy.
  1. Poladian N, Navasardyan I, Narinyan W, Orujyan D, Venketaraman V. Potential role of glutathione antioxidant pathways in the pathophysiology and adjunct treatment of psychiatric disorders. Clinics and Practice. 2023;13(4):768-779. doi:10.3390/clinpract13040070

  2. Sharifi-Rad M, Anil Kumar NV, Zucca P, et al. Lifestyle, oxidative stress, and antioxidants: back and forth in the pathophysiology of chronic diseases. Front Physiol. 2020;11:694. doi:10.3389/fphys.2020.00694

  3. Hussain T, Tan B, Yin Y, Blachier F, Tossou MC, Rahu N. Oxidative stress and inflammation: what polyphenols can do for us? Oxid Med Cell Longev. 2016;2016:7432797. doi:10.1155/2016/7432797

  4. Better Health. Antioxidants.

  5. Harvard T.H. Chan. Antioxidants.

  6. Pizzino G, Irrera N, Cucinotta M, et al. Oxidative stress: harms and benefits for human health. Oxidative Medicine and Cellular Longevity. 2017;2017:1-13. doi:10.1155/2017/8416763

  7. Forman HJ, Zhang H. Targeting oxidative stress in disease: promise and limitations of antioxidant therapy. Nat Rev Drug Discov. 2021;20(9):689-709. doi:10.1038/s41573-021-00233-1

By Heather Jones

Heather M. Jones is a freelance writer with a strong focus on health, parenting, disability,
and feminism. 

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Alpha-1 antitrypsin (AAT) is a glycoprotein serine protease inhibitor (coded by the SERPINA1 gene). AAT is mainly synthesized in the liver and released into serum. The main physiological function of AAT is to protect the lung from damage by inhibiting neutrophil elastase but also has anti-inflammatory, immunomodulatory, and anti-infective properties on a wide range of cell types.1,2 The allele coding for the normal AAT protein is designated as M and the homozygous Pi*MM genotype is present in 85–90% of individuals, which leads to the production of serum levels of functional AAT between 90 and 200 mg/dL.3

Alpha-1 antitrypsin deficiency (AATD) is a chronic, autosomal co-dominant hereditary condition characterized by decreased serum AAT levels, which may potentially lead to a loss of pulmonary function, emphysema, and development of liver disease, panniculitis, and vasculitis.4,5 So far, more than 150 mutations of the SERPINA1 gene have been identified, in which 40% of them are responsible for causing AATD.6 The risk for lung disease due to AATD depends on the AAT genotype, the AAT serum levels, and environmental exposures to hazardous agents.4,7 The two most common deficiency mutations are the S and Z alleles, which result in five deficiency genotypes: MS, SS, MZ, SZ, and ZZ.3 The homozygous Pi*ZZ genotype is characterized by a reduction in AAT levels below the protective threshold of 11 µM,8 and predisposes the carriers to develop lung disease (emphysema and premature onset of chronic obstructive pulmonary disease [COPD]) and liver disease (cirrhosis in children and adults, cholestasis, and hepatocarcinoma).9 The remaining deficient AAT genotypes are grouped as rare variants, such as Pi*I and Pi*M malton, and null variants, in which no serum AAT levels are detected.10

Clinical practice guidelines recommend that all symptomatic patients with COPD, emphysema, or asthma with airflow obstruction and relatives of someone with AATD or COPD should undergo specific testing for AATD.4,5,11,12 However, AATD is still a highly underdiagnosed disorder, with less than 10% of patients diagnosed.3 This is often due to the fact that a confirmatory testing needs to be conducted in specialized centers.13,14 Early identification of patients with AATD is recommended because delayed diagnosis worsens clinical status, including COPD-related symptoms.15

Overall, it is estimated that 3.4 million individuals worldwide have one of the deficient allele combinations. When reviewing the epidemiology of the disease, AATD frequency varies markedly among countries worldwide. Specifically, the mean prevalence of Pi*ZZ genotype in Europe is 1 in 35,702, being higher in north-western countries and decreasing gradually from west to east, and in America, the Pi*ZZ prevalence is 1 in 26,002 patients.3 Therefore, there are approximately 74,000 individuals in the European countries and 44,000 in North America with severe AATD of the Pi*ZZ genotype.3 In addition, differences in the risk for developing AATD have been reported depending on the ethnic of the individuals.2 Of note is that mutations rarely described in European patients may be predominantly detected in other countries.16 In some regions of the Mediterranean area, such as southern Italy and central Tunisia, the frequency of rare variant PI*M malton has been described over Pi*Z.16,17

In Turkey, there are limited data on the frequency of AATD and the presence of rare variants.18,19 Considering that prevalence data may differ greatly among countries, regions, and ethnicities, targeted screening programs are needed in countries such as Turkey to identify carriers of AATD variants. Therefore, the aims of the study were to identify AATD as a genetic underlying cause of lung disease in patients with COPD, bronchiectasis, or asthma and to report the frequency of AATD alleles in Turkey.

Materials and Methods

This was a non-interventional, multicenter, prospective study conducted at eight sites in Turkey between October 2021 and June 2022. The study was based on analysis of clinical data obtained under standard clinical practice conditions and enrolled patients with documented COPD or other reasons for AATD testing, such as a relative in whom AATD has been diagnosed.


Patients were selected on the basis of the following inclusion criteria: male or female adult (≥18) of any ethnic origin with documented respiratory symptoms, ie, COPD, bronchiectasis, or asthma, or another reason for wanting to exclude or confirm AATD (for example, liver symptoms or AATD in family members), and willingness to participate in the study. Patients were excluded if they had been previously tested for AATD. Screening of COPD patients in search of AATD was carried out following the ATS-ERS AATD Guidelines.4,5

The protocol was reviewed and approved by the independent ethics committee from the Aydin Adnan Menderes University Medical Faculty and submitted to the national regulatory health authorities (approval number E-66175679-514.05.04–443436) prior to patient enrollment. All patients signed a written informed consent form before the study was initiated, and all study procedures were compliant with the ICH standards for Good Clinical Practice (GCP). The study was conducted in full conformance with applicable local and national laws and regulations and the Declaration of Helsinki.


At screening, demographic and clinical characteristics of patients were recorded (age, sex, ethnicity, and family members with known AATD or COPD), liver disease history (neonatal hepatitis, or a diagnosis with any liver disease), diagnosis of pulmonary disease (COPD, emphysema, bronchiectasis, or asthma), pulmonary function tests (forced expiratory volume in 1 sec % [FEV1], forced vital capacity [FVC], FEV1/FVC), smoking history, respiratory symptoms (chronic cough, sputum production, or shortness of breath), number of COPD exacerbations during the last year, and the number hospitalizations due to exacerbations during the last 2 years. Data from patients were collected on a case report form (CRF).

AAT levels were measured by nephelometry.20 AAT levels should not be measured when patients have an infection since AAT levels would be increased as an acute-phase reaction. Adverse events (AEs) were recorded during the study visit including up to at least 30 minutes after the collection of blood samples. This study was conducted with an in vitro device with no direct contact with the patient except for the blood draw.

Genotyping Test

Whole blood samples were collected as dried blood spots (DBS) by finger stick capillary blood on filter paper for AATD genotyping testing. The diagnostic test also allowed sampling from oral mucosa with a buccal swab. However, that procedure was not approved by health authorities when the study was conducted. Genomic DNA was extracted from whole-blood sample and the allele-specific genotyping was carried out with the validated A1AT Genotyping Test (Progenika, a Grifols company, Derio, Spain). This was a qualitative, PCR, and hybridization-based in vitro diagnostic test (FDA cleared, and CE marked). It relies on allele-specific probes attached to color-coded microspheres, which hybridize specifically to the labelled PCR products. A subsequent fluorescent labelling step allows detection and quantification of the hybridization signal with the Luminex 200TM (Diasorin, Saluggia, Italy) instrument for the simultaneous detection and identification of 14 allelic variants and their associated alleles found in the AAT codifying gene SERPINA1: PI*F, PI*I, PI*S, PI*Z, PI*M procida, PI*M malton, PI*S iiyama, PI*Q0 granite falls, PI*Q0 west, PI*Q0 bellingham, PI*P lowell, PI*Q0 mattawa, PI*Q0 clayton, and PI*M heerlen. The absence of any of the 14 alleles included in the analysis was interpreted, with over 99% of probability, as an M/M genotype.

The AAT allelic variant genotypes and associated allele results, when used in conjunction with clinical findings and other laboratory tests, are intended as an aid in the diagnosis of individuals with AATD.

Statistical Analysis

A sample size of approximately 1000 patients was planned anticipating 10% AATD gene carriers and between three and five cases of severe AATD in that population.3,21 Continuous variables were summarized using the following standard descriptive statistics: number of observations, mean, standard deviation, or median and minimum and maximum ranges, as applicable. Categorical data are described using absolute and relative frequencies. All patients with genotyping analysis results were analyzed. Statistical analysis was descriptive by calculating the different percentages to obtain the frequencies of each AATD genotype. No inferential statistical analysis was conducted.


Study Patients’ Characteristics and Disease Activity

A total of 1090 patients were enrolled during the study period. Two of them (0.18%) did not meet eligibility criteria and were excluded from the analysis. Baseline patient characteristics were available for a total of 1087 patients. The majority were male (85.6%), with a mean age of 61.7 years, and current smokers (32.2%). Patients were diagnosed with COPD (92.7%), bronchiectasis (20.7%) or asthma (19.2%). Some patients had overlapping diagnoses with two or more conditions. The most frequent respiratory symptoms were shortness of breath in 855 (78.7%), sputum production in 683 (68.2%) and chronic cough in 628 (57.8%) patients (Table 1).

Table 1 Demographic and Clinical Data of Assessable Patients Included in the Study. Data Were Available for n=1087 Patients

When patients were stratified by the presence or absence of AATD mutation, no relevant differences between groups were observed in respirometry, smoking habits, or workplace exposure to dust, fumes, or gases. Likewise, no differences were observed in the percentage of patients diagnosed with COPD or emphysema. Liver disease was slightly more common in the group containing AATD mutation than in the non-AATD group (5.9% vs 2.1%). In the AATD group, 35% of the patients had exacerbations in the last year, compared with the 47% in the non-AATD group, although the mean number of exacerbations was the same (Table 1).

AAT serum levels were available for 168 (15%) of patients, with a mean (range) of 1.78 (0.2–20.1) g/L. As expected, AAT serum levels in AATD patients were lower (1 [0.2–1.94] g/L) than in patients without AATD (1.8 [1.3–20.1] g/L).

No adverse events (AEs) or any other safety signal were reported. This was an in vitro device with no direct contact of the device with the patient and no patient contact except for the blood draw.

AATD Genotyping results

The distribution of mutations is shown in Figure 1. Overall, there were 1037 patients (95%) carrying no mutations and 51 (5%) patients with a AATD mutation of any type. Of the patients with mutations, 15 (29.4%) showed the well-known mutations S or Z, whereas 36 patients (70.6%) carried rare alleles (Pi*M malton, Pi*I, Pi*P lowell, Pi*M heerlen, and Pi*S iiyama). The most frequent combinations reported were Pi*M/Z (n=12, 24%), followed by Pi*M/M malton (n=11, 22%). The percentage of patients carrying two deficiency alleles, was 19.6% (n=10 patients): two of them with Pi*Z/Z genotype, seven had a severe deficiency associated with the M malton allele (Pi*M malton/M malton and Pi*Z/M malton), and one had the genotype Pi*Z/M Heerlen (Figure 1).

Figure 1 Distribution of AATD mutations in the study cohort. Data are expressed as absolute values with percentages in parenthesis: the first percentage is referred to the total number of patients with mutations (n=51 patients); the second percentage is referred to the total number of patients in the study cohort (n=1088 patients).

Eighteen (35.3%) patients presented with the Pi*Z mutation. Most of them were former or current smokers (n=17) and had COPD (n=16). Moreover, evidence of advanced COPD (post-bronchodilator FEV1 of 60% or lower) was reported in 10 patients, with the following genotypes: Pi*Z/Z (n=2), Pi*Z/M malton (n=2), Pi*Z/M heerlen (n=1), and Pi*M/Z (n=5).

Rare Genotypes

In this study, AATD mutation Pi*M malton was observed in 18 patients (35.3% of the total mutations), achieving the same frequency as the Z allele. Of those patients with one or two M malton alleles, 11 (61%) had the diagnosis COPD, and all of them were former or current smokers. Three patients with genotypes Pi*M malton/M malton (n=2) and Pi*Z/M malton (n=1) had a post-bronchodilator FEV1 below 30%, indicating severe COPD and emphysema. Six patients were diagnosed with the M malton mutation without having major respiratory symptoms, and one patient was diagnosed with the severe genotype Pi*M malton/M malton who suffered from COPD and was a relative of an individual with AATD.

The heterozygous genotypes P*M/I and P*M/P lowell were identified in eight (16%) and seven (14%) patients, respectively. All of them were current or former smokers who suffered from COPD. The Pi*M heerlen mutation was detected in two (4%) patients. One had the combination with the Z allele (Pi*Z/M heerlen) and had severe AATD. The other was heterozygous with one normal allele (Pi*M/M heerlen). Both patients were former smokers and suffered from severe COPD (FEV1 of 36% and 22%, respectively) with AAT serum levels of 0.44 g/L and 1.03 g/L, respectively. The heterozygous genotypes Pi*M/S and Pi*M/S iiyama corresponded to former smokers with advanced COPD (post-bronchodilator FEV1% of 44%) and emphysema.

The geographic distribution of AATD alleles in Turkey is shown in Figure 2. Geographic data were available for 46 out of 51 patients (90.2%). Most of the AATD mutations (n=24, 52%) were documented in the Eastern Black Sea region of Turkey, whereas in the south (Mediterranean region), no AATD mutations were reported. Of note is that many of the patients diagnosed with an M malton allele came from the Black Sea region (Rize, n=8) and Eastern Anatolia (Erzurum, n=2).

Figure 2 Geographic distribution of AATD mutations among the seven geographical regions of Turkey: Black Sea, Marmara, Aegean, Central Anatolia, Eastern Anatolia, Southeastern Anatolia and Mediterranean. Out of n=51 patients with AATD mutations, data about their geographic origin was available for n=46 patients. Map obtained from

AAT Levels in Patients with AATD Mutation

AAT serum levels were available in 11 (21.1%) patients with AATD mutation and varied according to the mutation. The highest AAT level (1.94 g/L) corresponded to a patient with the Pi*M/I genotype and a FEV1 of 82%, whereas the lowest AAT level (0.21 g/L) was associated with a patient with two deficiency alleles, Pi*Z/M malton and a FEV1 of 60% (Table 2).

Table 2 Alpha-1 Antitrypsin (AAT) Serum Levels (g/L) and Clinical Phenotype Based on Each Genotype in Patients with AATD. AAT Levels Were Available for n=11 (21.6%) Patients with AATD Mutations


This prospective study conducted under standard clinical practice conditions described the frequency of each AATD genotype in a selected sample population of Turkish individuals with pulmonary disease. Specifically, this study was designed to identify patients who were previously diagnosed with COPD, bronchiectasis, or asthma that have a mutation in the SERPINA1 gene, a potential underlying genetic cause of lung disease.

Despite knowing that early diagnosis could help manage patients with AATD, this condition remains widely underdiagnosed.4,11 The present study evidenced that AATD was detected in 5% of patients with COPD, bronchiectasis, and asthma. Interestingly, this percentage was similar to two recent studies, which reported genetic AAT mutations in 7.1% and 3.5% of Turkish patients with COPD.18,19 Similarly, these results were aligned with previous studies that evaluated AATD distribution in patients with other pulmonary diseases,22,23 and reinforced the utility of routine screening for AATD in these patients. The percentage of male patients in our study (85.6%) was unusually high when compared with the COPD and AATD series from other countries, but it was similar to values reported in other Turkish studies (80.6%, 90.5%).18,19 It is possible that cultural reasons in Turkey keep women more hesitant to consult a doctor regarding pulmonary and other diseases.24

Family members of patients with AATD are expected to have more AATD mutations, and a targeted approach for this subgroup usually yields a higher AATD detection rate.25 We identified seven AATD patients with a family history of AATD, six of whom had no respiratory symptoms. This result emphasizes the importance of early testing for AATD in adults with first-degree relatives with severe AATD, regardless of respiratory symptoms, as an important test targeting strategy. Altogether, more extensive screening for AATD could prevent certain clinical consequences by allowing patients to receive early therapeutic intervention or at least smoking prevention or cessation counseling.

The prevalence of AATD mutations in European countries has been extensively evaluated, but there is limited evidence in Turkey. In Finland, the allele frequencies were 19.7 per 1000 habitants for Pi*Z and 10.2 cases per 1000 habitants for Pi*S.26 Similarly, Poland reported a frequency of 17.5 per 1000 for the Pi*S allele and 10.5 per 1000 habitants for the Pi*Z allele.27 The highest frequency of the S allele was observed in the Iberian Peninsula (100–200 cases per 1000 habitants).28

In the present study, we observed a considerably lower frequency for the Pi*S genotype (0.09%) compared with these studies. These differences between geographic areas are to be expected since the distribution of Pi*Z and Pi*S alleles is different among countries and even within different regions of the same country.28 Interestingly, the proportions of the Pi*Z and Pi*S mutations in our Turkish population (35.3% and 2%, respectively) were consistent with the percentages obtained in a feasibility study of the A1AT genotyping test that evaluated the percentage of these mutations in Turkey (36.4% and 5%, respectively).29

The use of AATD genotyping testing is also useful to analyze the most prevalent rare variants in each region. In Turkey, we identified a total of 36 patients who carried rare alleles (Pi*M malton, Pi*I, Pi*P lowell, Pi*M heerlen, and Pi*S iiyama). This high frequency of rare alleles has been previously detected in other countries, evidencing that the so-called rare AATD alleles may not be as rare as expected.10 In Italian patients with AATD, the prevalence of rare AAT genotypes was 11%.17 Similarly, in Switzerland, rare AAT alleles represented 7%,30 and in Japan, the most common deficient variant is the PI*S iiyama, a rare variant present in most patients with AATD.31

Regarding the worldwide geographic distribution of AATD, the highest frequency of Pi*ZZ is located in the Atlantic region of Europe. Then, it decreases gradually from west to east, and in the most remote regions of the south of the continent, until it almost disappears in Asia.28,32 Here, we observed a similar geographic distribution in the frequency of AATD variants since a higher percentage of mutations was observed in the north and decreasing gradually to the south of Turkey.

This study revealed the high frequency of rare AAT variants in Turkey, especially the Pi*M malton, being the most frequent mutation detected. Thirty-five percent of all AATD mutations were associated with the Pi*M malton rare allele, which has the same frequency as the most prevalent mutation (Z allele) in other regions. This finding is in agreement with previous research in which the rare variant Pi*M malton prevails over Z and S alleles in particular regions of the Mediterranean area, such as southern Italy,17 central Tunisia, and North Africa.16,33 Human migrations, commercial purposes, and ethnic relationships between these countries have been proposed to be responsible for spreading rare AATD variants in these regions.16,19,33 The Pi*M malton mutations and other rare AATD variants seem to be widespread in regions in which the frequency of Pi*ZZ is lower.16,17 In the current study, the geographic distribution of patients carrying the rare AATD variant Pi*M malton were mainly located in the Black Sea region in northern Turkey. More importantly, individuals with the Pi*M malton may develop pulmonary emphysema and polymeric intrahepatic inclusions like in AATD patients with Pi*ZZ genotype.10 Indeed, it has been shown that rare AATD mutations could be identified in up to 17% of clinical cases.34 In the present study, most of the reported Pi*M malton cases presented with pulmonary emphysema. Since rare AATD variants remain unexplored in many regions worldwide, targeted screening programs could be recommended even in countries in which a high prevalence of the disease has been reported.

One of the potential benefits of conducting extensive AATD genetic testing is to consider providing early lifestyle interventions, such as smoking prevention, and to prevent delayed introduction of augmentation therapy to preserve lung parenchyma in patients with emphysema. The S iiyama allele is another extremely rare variant mainly identified among Japanese patients that has very rarely been found outside of Japan.31 It was found in the study cohort in a heterozygous Pi*M/S iiyama variant patient who was a former smoker with advanced COPD. Altogether, more than 150 mutations of the SERPINA-1 gene have been described in the literature,34 and new mutations are currently being identified.35 Evidence is emerging that rare AATD mutations may play an important role in Turkey. For example, Pi*M malton was found to have the same frequency as Pi*Z and lead to comparable clinical symptoms.

AATD is characterized by a diverse clinical expression and prognosis. Augmentation therapy with AAT is indicated for patients with severe AATD, in which serum AAT levels are below the protective threshold of 11 µM (or 0.5 g/L),4 and who have evidence of advanced lung disease. Early identification of those patients with extremely low AAT levels is paramount since they are more prone to developing COPD and emphysema.8,36 In our analysis, only three patients were documented to have AAT serum levels below the protective threshold: 0.33 g/L (Pi*ZZ genotype), 0.21 g/L (Pi*Z/M malton) and 0.44 g/L (Pi*Z/M heerlen). AAT serum levels were not routinely available in the study centers. It would be important to better establish AAT serum-level testing in Turkey for the future.

One of the limitations of this study is that the real AATD prevalence was overestimated since this was a highly selected population in which patients with family members known to have AATD disease were included. This could have increased the probability of identifying a patient with AATD. AATD prevalence in a whole-population-based study is usually lower compared to a study conducted in a targeted population.37 Additional limitations are that AAT serum levels were only available for a small number of patients because it was not routinely collected and that female patients were underrepresented. The inclusion of these patients would have strengthened the generalizability of the study results.


In conclusion, our results confirm AATD as a genetic underlying cause of lung disease and determine the frequencies of different AATD alleles in a selected population of Turkish individuals.

Data Sharing Statement

The data that support the findings of this study are available from the corresponding author upon reasonable request.


Eugenio Rosado, PhD, and Jordi Bozzo, PhD CMPP (Grifols), are acknowledged for medical writing and editorial support in the preparation of this manuscript. The authors wish to thank all the patients who contributed to this study.

Author Contributions

All authors made a significant contribution to the work reported, whether that is in the conception, study design, execution, acquisition of data, analysis and interpretation, or in all these areas and took part in drafting, revising, or critically reviewing the article. MP: conceptualization, study design, methodology, resources, data acquisition, data curation, investigation, writing – review and editing. STO, SA, NS, MÇ, DK, AŞ, BPY, NK, SAB, and SKC: study design, methodology, resources, data acquisition, data curation, validation, investigation, writing – review and editing. AN and BD: conceptualization, formal analysis, project administration, supervision, validation, visualization, writing – review and editing. All authors critically revised, edited, agreed, and approved the final version of the article before submission, and during the revision, of the manuscript. Authors agreed in the journal to which the article is submitted, take responsibility, and are accountable for the contents of the article.


This study was funded by Grifols, manufacturer of A1AT Genotyping Test and plasma-derived alpha-1 antitrypsin medicinal products.


AN and BD are full-time employees of Grifols. DK reports honoraria paid to her institution, as speaker, from AstraZeneca, Abdi İbrahim, Novartis and Grifols, outside the submitted work. The remaining authors have no conflicts of interest to declare for this work.


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7. Mayer AS, Stoller JK, Bucher Bartelson B, James Ruttenber A, Sandhaus RA, Newman LS. Occupational exposure risks in individuals with PI*Z alpha(1)-antitrypsin deficiency. Am J Respir Crit Care Med. 2000;162(2 Pt 1):553–558. doi:10.1164/ajrccm.162.2.9907117

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9. Patel D, Teckman JH. Alpha-1-Antitrypsin Deficiency Liver Disease. Clin Liver Dis. 2018;22(4):643–655. doi:10.1016/j.cld.2018.06.010

10. Rodriguez-Frias F, Miravitlles M, Vidal R, Camos S, Jardi R. Rare alpha-1-antitrypsin variants: are they really so rare? Ther Adv Respir Dis. 2012;6(2):79–85. doi:10.1177/1753465811434320

11. Sandhaus RA, Turino G, Brantly ML, et al. The Diagnosis and Management of Alpha-1 Antitrypsin Deficiency in the Adult. Chronic Obstr Pulm Dis. 2016;3(3):668–682. doi:10.15326/jcopdf.3.3.2015.0182

12. Casas F, Blanco I, Martínez MT, et al. Indications for active case searches and intravenous alpha-1 antitrypsin treatment for patients with alpha-1 antitrypsin deficiency chronic pulmonary obstructive disease: an update. Arch Bronconeumol. 2015;51(4):185–192. doi:10.1016/j.arbres.2014.05.008

13. Miravitlles M, Nuñez A, Torres-Durán M, et al. The Importance of Reference Centers and Registries for Rare Diseases: the Example of Alpha-1 Antitrypsin Deficiency. Copd. 2020;17(4):346–354. doi:10.1080/15412555.2020.1795824

14. Gurevich S, Daya A, Da Silva C, Girard C, Rahaghi F. Improving Screening for Alpha-1 Antitrypsin Deficiency with Direct Testing in the Pulmonary Function Testing Laboratory. Chronic Obstr Pulm Dis. 2021;8(2):190–197. doi:10.15326/jcopdf.2020.0179

15. Tejwani V, Nowacki AS, Fye E, Sanders C, Stoller JK. The Impact of Delayed Diagnosis of Alpha-1 Antitrypsin Deficiency: the Association Between Diagnostic Delay and Worsened Clinical Status. Respir Care. 2019;64(8):915–922. doi:10.4187/respcare.06555

16. Denden S, Zorzetto M, Amri F, et al. Screening for Alpha 1 antitrypsin deficiency in Tunisian subjects with obstructive lung disease: a feasibility report. Orphanet J Rare Dis. 2009;4:12. doi:10.1186/1750-1172-4-12

17. Ferrarotti I, Baccheschi J, Zorzetto M, et al. Prevalence and phenotype of subjects carrying rare variants in the Italian registry for alpha1-antitrypsin deficiency. J Med Genet. 2005;42(3):282. doi:10.1136/jmg.2004.023903

18. Çörtük M, Demirkol B, Arslan MA, et al. Frequency of alpha-1 antitrypsin deficiency and unexpected results in COPD patients in Turkey; rare variants are common. Turk J Med Sci. 2022;52(5):1478–1485. doi:10.55730/1300-0144.5486

19. Önür ST. Initial alpha-1 antitrypsin screening in Turkish patients with chronic obstructive pulmonary disease. Turk J Med Sci. 2023;53(4):1012–1018.

20. Ferrarotti I, Scabini R, Campo I, et al. Laboratory diagnosis of alpha-1-antitrypsin deficiency. Transl Res. 2007;150(5):267–274. doi:10.1016/j.trsl.2007.08.001

21. Greulich T, Rodríguez-Frias F, Belmonte I, Klemmer A, Vogelmeier CF, Miravitlles M. Real world evaluation of a novel lateral flow assay (AlphaKit® QuickScreen) for the detection of alpha-1-antitrypsin deficiency. Respir Res. 2018;19(1):151. doi:10.1186/s12931-018-0826-8

22. Carreto L, Morrison M, Donovan J, et al. Utility of routine screening for alpha-1 antitrypsin deficiency in patients with bronchiectasis. Thorax. 2020;75(7):592–593. doi:10.1136/thoraxjnl-2019-214195

23. Veith M, Tüffers J, Peychev E, et al. The Distribution of Alpha-1 Antitrypsin Genotypes Between Patients with COPD/Emphysema, Asthma and Bronchiectasis. Int J Chron Obstruct Pulmon Dis. 2020;15:2827–2836. doi:10.2147/copd.S271810

24. Tackett S, Young JH, Putman S, Wiener C, Deruggiero K, Bayram JD. Barriers to healthcare among Muslim women: a narrative review of the literature. Women’s Studies International Forum. 2018;69:190–194.

25. Brantly M, Campos M, Davis AM, et al. Detection of alpha-1 antitrypsin deficiency: the past, present and future. Orphanet J Rare Dis. 2020;15(1):96. doi:10.1186/s13023-020-01352-5

26. Häggblom J, Kettunen K, Karjalainen J, Heliövaara M, Jousilahti P, Saarelainen S. Prevalence of PI*Z and PI*S alleles of alpha-1-antitrypsin deficiency in Finland. Eur Clin Respir J. 2015;2:28829. doi:10.3402/ecrj.v2.28829

27. Kaczor MP, Sanak M, Libura-Twardowska M, Szczeklik A. The prevalence of alpha(1)-antitrypsin deficiency in a representative population sample from Poland. Respir Med. 2007;101(12):2520–2525. doi:10.1016/j.rmed.2007.06.032

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30. Zorzetto M, Russi E, Senn O, et al. SERPINA1 gene variants in individuals from the general population with reduced α1-antitrypsin concentrations. Clin Chem. 2008;54(8):1331–1338. doi:10.1373/clinchem.2007.102798

31. Seyama K, Nukiwa T, Souma S, Shimizu K, Kira S. Alpha 1-antitrypsin-deficient variant Siiyama (Ser53[TCC] to Phe53[TTC]) is prevalent in Japan. Status of alpha 1-antitrypsin deficiency in Japan. Am J Respir Crit Care Med. 1995;152(6 Pt 1):2119–2126. doi:10.1164/ajrccm.152.6.8520784

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Ziva offers a wide range of sessions, programs, lessons, wearable tracking, heart rate measurement through your phone’s camera, and modules for improving HRV (Heart Rate Variability) to help elevate sleep quality, reduce stress, enhance focus, find inner calm, ease anxiety, and unlock peak performance. In this interview with TechBullion, Dr. Michael Kurisu, Chief Health Officer at Ziva Health, shows us how Ziva Health brings breathwork and holistic wellness expertise to the market.

Please tell us more about yourself? How excited are you with your new role as Chief Health Officer at Ziva?

I am Dr. Michael Kirusu, a board-certified Osteopathic Physician specializing in Family and holistic medicine. My approach to healthcare emphasizes precision, merging expertise in holistic wellness with extensive experience in remotely monitoring patient data through wearable technology.

Amid the pandemic, I undertook a pioneering initiative in San Diego by providing Apple Watches and Oura Rings to my patients. This allowed me to closely monitor their sleep patterns, resting heart rates, HRV, and respiratory rates. These wearable devices provided valuable insights into their activity levels and movement patterns.

My methodology involves a data-centric approach to wearable technology, coupled with a profound understanding of holistic medicine principles.

I hold a significant role in Project Apollo, an innovative endeavor transforming healthcare through data-driven strategies, prioritizing patients, and fostering collaborative communities.

Ziva takes a unique approach, particularly emphasizing breathing as a key tool for enhancing overall wellness. Additionally, Ziva integrates with wearables to gather activity and physiological data, establishing valuable trends. The proactive monitoring of these trends and the personalized wellness recommendations from Ziva are what generate the most excitement to me.

What is  Ziva Health and what unique solutions do you provide?

Ziva is a digital health and wellness company dedicated to enhancing mental well-being. Our focus is on using the power of breathing to reduce stress, foster calmness, and alleviate anxiety. Through Ziva’s effective breathing module, we aim to influence the body’s physiological responses, activating Vagal stimulation to transition from a sympathetic to a parasympathetic state.

Notable unique features:

  • Utilizes wearable technology like the Apple Watch, integrated into our platform for enhanced tracking and improved overall health outcomes.
  • Harnesses both physiological and psychological user data to offer personalized suggestions through AI coaching.
  • Provides specialized modules scientifically designed for HRV training.
  • Tailors programs targeting better sleep, stress reduction, improved breathing, weight management, along with personalized routine recommendations.

Interview with Dr. Michael Kurisu, Chief Health Officer at Ziva HealthInterview with Dr. Michael Kurisu, Chief Health Officer at Ziva Health

Could you give us an overview of the breathwork market and why Ziva Health is in demand for the digital health and wellness industry?

Breathwork, utilizing various breathing techniques, is known for its profound impact on both physical and mental well-being. These techniques are instrumental in reducing stress, alleviating anxiety and depression, improving sleep quality, promoting relaxation, enhancing HRV (heart rate variability), and even enhancing athletic performance. The market for breathwork is expanding due to several contributing factors:

  • Rising Awareness: There’s a growing understanding of the benefits associated with breathwork, leading to increased interest and adoption.
  • Scientific Validation: Ongoing scientific research is validating the effectiveness of breathwork in healthcare, garnering more recognition and support.
  • Popularity of Mindfulness: The surging popularity of mindfulness and meditation practices has brought attention to the significance of breath in overall wellness.
  • Mental Health Concerns: With the increasing prevalence of mental health conditions, people are turning to alternative therapies like breathwork for support and relief.
  • Demand for Holistic Therapies: There’s a growing preference for natural and holistic approaches to health, driving the interest in breathwork as a complementary therapy.

Can you explain how breathwork stimulates the nervous and cardiovascular systems, leading to enhanced physical and mental health?

Breathwork techniques can stimulate the nervous system in several ways. One way is by activating the vagus nerve, which is the longest cranial nerve in the body. The vagus nerve plays a key role in the parasympathetic nervous system, which is responsible for relaxation and digestion. When the vagus nerve is activated, it sends signals to the brain that help to calm the body and mind.

Breathwork can also stimulate the nervous system by increasing the production of endorphins, which are hormones that have pain-relieving and mood-boosting effects. Breathwork techniques can also have a positive impact on the cardiovascular system. Slow, deep breathing can help to lower blood pressure and heart rate.

Interview with Dr. Michael Kurisu, Chief Health Officer at Ziva HealthInterview with Dr. Michael Kurisu, Chief Health Officer at Ziva Health

What specific techniques or exercises does Ziva Health’s breathing platform utilize for easing anxiety and reducing stress?

The Ziva platform uses slow, controlled, deep breathing techniques that emphasize using the diaphragm to inhale through the nose and exhale through the mouth. The objective in each exercise is to extend the exhale duration more than the inhale to stimulate the parasympathetic nervous system. Additionally, a brief breath hold is included to elevate carbon dioxide (CO2) levels, which can induce a calming effect on the body. This elevation prompts the release of neurotransmitters that aid in relaxing blood vessels and muscles, fostering a sense of calmness.

Are there any scientific studies or research that supports the effectiveness of Ziva Health’s breathing platform in improving medical conditions?

Numerous studies explore the use of breathwork to enhance various medical conditions like insomnia, COPD, and hypertension. However, the Ziva Health platform itself hasn’t conducted its own study on this matter yet.

Interview with Dr. Michael Kurisu, Chief Health Officer at Ziva HealthInterview with Dr. Michael Kurisu, Chief Health Officer at Ziva Health

What kind of results can users expect from regularly utilizing Ziva Health’s breathing platform for their wellness needs, does Ziva Health offer any personalized guidance or recommendations based on individual needs when using their breathing platform?

Users of Ziva Health can expect  range of benefits for their wellness journey, including:

  • Improved heart rate variability (HRV)
  • Better respiratory and resting heart rates
  • Enhanced emotional regulation
  • Optimized nervous and cardiovascular systems

Ziva Health initiates user engagement by tailoring personalized recommendations according to their health conditions and goals. Over time, these recommendations evolve as we gather data from wearables and refine our AI models to better suit individual needs.

How does Ziva Health incorporate digital health technology into its unique approach to breathwork and what sets Ziva Health apart from other digital health and wellness companies in terms of its approach to enhancing mental wellness?

Ziva links up with wearable devices to monitor various physiological metrics such as heart rate variability (HRV), stress levels, resting heart rate, sleep patterns, and respiratory rate. This offers added insights into users’ wellness journeys.

What distinguishes Ziva is its AI-powered recommendation system. This system harnesses wearable physiological data with the user’s own psychological input data to offer personalized suggestions, track trends, and provide wellness coaching tailored to individual needs.

We are onboarding partners now which is after our beta launch. Visit the website Ziva Health to find out more.

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COPD Includes Chronic Lung Diseases Like Emphysema, Some Types of Asthma, and Chronic Bronchitis

Smoking is Main Cause of COPD; Support for Those Who Want to Quit is Available & Affordable in NYS

ALBANY, N.Y. (November 27, 2023) – The New York State Department of Health recognizes November as Chronic Obstructive Pulmonary Disease (COPD) Awareness Month. COPD describes chronic lung diseases that include emphysema, chronic bronchitis, and some types of refractory (severe) asthma. Chronic lower respiratory diseases, including COPD and asthma, were the fifth leading cause of death in New York State in 2020, according to the most recent 2022 Behavioral Risk Factor Surveillance System (BRFSS) report.

"Chronic Obstructive Pulmonary Disease, COPD, is a serious lung disease that can permanently damage the lungs, making early diagnosis and treatment even more important," State Health Commissioner Dr. James McDonald said. "The most important thing people can do to prevent COPD is to quit smoking, even better, never start smoking. For those who need help quitting, I encourage you to reach out to a doctor and learn about smoking cessation options available in New York State."

About 15.7 million adults in the U.S. have been diagnosed with COPD, with more than 900,000 of those living in New York State. COPD is commonly misdiagnosed and many people who have COPD may not be diagnosed until the disease is advanced. Smoking – both current smoking and smoking in the past – is the main cause of COPD.

Data from the most recent 2022 Behavioral Risk Factor Surveillance System (BRFSS) and the Centers for Disease Control and Prevention (CDC) estimates that 5.3 percent of adult New Yorkers have COPD, while the median national prevalence was 6.7 percent. Data from that BRFSS report also found COPD prevalence varies by smoking status, with 13.1 percent among people who currently smoke, 9.5 percent among people who used to smoke, and 2 percent among those who never smoked.

While smoking is the main cause of COPD, it's not the only cause. As many as one in four people with COPD never smoked. Other risk factors for COPD include long-term exposure to air pollution including secondhand smoke, and occupational exposure to chemical fumes dust. Certain respiratory infections may also contribute to diagnosed cases, as well as a rare, inherited disorder called alpha-1-antitrypsin deficiency (AATD). People with COPD are at increased risk of developing heart disease, lung cancer, and a variety of other conditions.

Symptoms of COPD can develop slowly over time. As symptoms worsen, they can limit the ability to do everyday activities.

COPD symptoms include the following:

  • Chronic or frequent coughing and wheezing
  • Excess phlegm, mucous, or sputum production
  • Shortness of breath or chest tightness, especially with physical activity
  • Extreme fatigue
  • Difficulty taking a deep breath
  • Frequent respiratory infections

Lifestyle choices and treatment may slow down the progression of COPD, however, the damage to the lungs is permanent and cannot be reversed. For those who smoke, the most important thing they can do is quit.

For information and assistance with quitting smoking, vaping, and other tobacco products, contact the New York State Smokers' Quitline at 1-866-NYQUITS (1-866-697-8487), or text 'Quit Now' to 333888.

It's also important for people with COPD to avoid lung infections and stay up to date on recommended respiratory vaccines to prevent the flu, COVID, and pneumonia. There is a vaccine available for adults 60 years and older to protect against Respiratory Syncytial Virus (RSV), which can be administered in New York pharmacies without a prescription.

More information on COPD can be found here.

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Long-term treatment with Olympus’ Spiration Valve System (SVS) safely led to sustained improvements in lung function — and in life quality — among people with severe emphysema, a form of chronic obstructive pulmonary disease (COPD).

That’s according to two-year follow-up data from the EMPOWER trial, which had tested the approved treatment with an eye toward any potential adverse effects due to its use.

These findings point “to the significant and positive long-term impact SVS treatment can have on the day-to-day functions of emphysema patients,” John de Csepel, MD, chief medical officer at Olympus, said in a company press release.

“Meaningful improvement in breathing can mean fuller lives for patients for activities as simple as the ability to go on daily walks or enjoying time with grandchildren,” deCsepel added.

The long-term data were detailed in a study, “Sustained Clinical Benefits of Spiration Valve System in Severe Emphysema Patients: 24-Month Follow-Up of EMPROVE,” published in the journal Annals of the American Thoracic Society.

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An illustration shows a close-up view of damaged and inflamed lungs.

SVS found to improve life quality in severe emphysema patients

Emphysema is a progressive form of COPD characterized by damage to the small air sacs, or alveoli, of the lungs. Such damage reduces the lungs’ elasticity and causes chronic shortness of breath, or dyspnea.

As a result, patients’ ability to perform physical tasks and their quality of life typically are impaired.

The Spiration Valve System, known as SVS for short, was approved in the U.S. in late 2018 as a minimally invasive treatment to improve breathing and quality of life in people with severe emphysema.

It is a small, umbrella-shaped device that works by rerouting air circulating inside the airways into healthier parts of the lungs. In so doing, it diverts air away from damaged regions that risk becoming overinflated due to the stiffening of damaged lung tissue.

The SVS is placed in damaged lung areas using a bronchoscope — a small, flexible tube that is inserted into the patient’s throat — in a procedure that is considered minimally invasive.

Its regulatory approval was based on positive data from the EMPROVE trial (NCT01812447), which enrolled 172 people, ages 40 and older, with severe emphysema and severe dyspnea. The trial was conducted at sites across the U.S. and Canada.

Participants were randomly assigned to receive the SVS device — 113 patients — or standard medical management alone, as part of a control group. A total of 59 patients served as controls.

SVS-treated patients showed significant and sustained improvements in lung function after six and 12 months relative to controls. Lung function was assessed with a validated measure called the mean forced expiratory volume in 1 second, or FEV1.

The SVS group also showed significantly greater reductions in lung overinflation and dyspnea, as well as life quality improvements, as compared with those on standard management.

The benefits [of SVS] compared to the control group at 24 months are long lasting, statistically significant and clinically meaningful. … SVS treatment offers an important opportunity to improve a patient’s lung function and quality of life.

Still, this approach may be associated with potential adverse events, which may include COPD exacerbations, or periods of sudden symptom worsening, and pneumothorax, or a collapsed lung due to air leaking into the space between the lung and chest wall.

To that end, researchers tracked patients over a 24-month period.

The newly published follow-up data showed that the SVS group continued to show significantly greater FEV1 improvements compared with the control group after two years.

Significant dyspnea reductions with SVS also were sustained with longer follow-up, as were significant improvements in several health-related quality of life measures, including the St. George’s Respiratory Questionnaire and the COPD Assessment Test.

Importantly, the rate of adverse events was similar between the SVS and control groups. Acute COPD exacerbations occurred in 13.7% of SVS-treated patients versus 15.6% of those in the control group. One patient in the SVS group and none in the control group developed a pneumothorax.

These results highlight that “SVS treatment resulted in statistically significant and clinically meaningful durable improvements in lung function, respiratory symptoms, and [qualify of life], as well as a statistically significant reduction in dyspnea, for at least 24 months, while maintaining an acceptable safety profile,” the researchers wrote.

Gerard Criner, MD, the director of Temple University’s Temple Lung Center and lead investigator of the trial, said that “the results from the EMPROVE trial demonstrate the positive impact the Spiration Valve can have on emphysema patients.”

“The benefits compared to the control group at 24 months are long lasting, statistically significant and clinically meaningful,” and the “SVS treatment offers an important opportunity to improve a patient’s lung function and quality of life,” Criner added.

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Rick Scroggins has worked hard and played hard throughout his 75 years. So, it didn't sit well with him when severe emphysema and chronic obstructive pulmonary disease (COPD) forced him to slow down and rely on oxygen treatment to handle even minor daily tasks. In fact, it was so bad, that it took him minutes to climb the 12 steps to his home office, while having to stop and rest at each landing after four steps. "I've gone 110 miles per hour my whole life," he says. "It's very difficult for me to have to slow down."

Thanks to the experts at The Christ Hospital Physicians – Pulmonary Medicine, and a breakthrough minimally-invasive treatment called The Zephyr Valve, Rick is back to enjoying long periods of physical activity, usually without the need for external oxygen.

Zephyr Valve - A groundbreaking and “breath-giving” procedure

The lungs of patients with COPD are often damaged and can get clogged with or blocked by phlegm, which restricts airflow and can cause air to be trapped in the damaged lobes. This restricts the ability for other lobes to inflate properly, causing shortness of breath and restricting the intake of air/oxygen, which can lead to many other health concerns such as heart problems, weakened muscles and brittle bones, and depression and anxiety.

The Zephyr Valve is a minimally invasive treatment qualifying patients with COPD and emphysema that involves the insertion of valves through the airway and into a lung with no incision required. They make it easier for patients to breathe by deflating and restricting airflow to the more damaged lobe(s), which lessens the restriction on the healthier adjacent lobes.

Eligible patients are typically those with moderate to severe emphysema, and stage three or four COPD, according to Vishal Jivan, MD, the pulmonologist with The Christ Hospital Physicians-Pulmonary Medicine who implanted the five valves in Rick’s lungs. Patients undergo a series of testing and scans to determine if the valves will work for them, and to identify the best location to implant them.

“We’re looking to deflate the part of the lung that has the most emphysema, and the lowest amount of blood supply,” Dr. Jivan says. “This diverts the airflow to the healthier lobes which were impeded by the lobe with more emphysema and allows them to supply more oxygen to the blood, which gives the patient more energy.”

Some patients, including Rick, see a significant reduction in the need for the use of external oxygen, but Dr. Jivan reminds his patients that isn’t the case for everyone. Still, he says, even if they still need oxygen, the differences in their breathing, energy, and stamina are noticeable.

“We’re looking for a difference in tolerance for exercise and physical activity,” he says. “Even for those who still require oxygen, they’re going to notice a big difference in that tolerance. I recently spoke with a patient who was excited to be able to walk around a county fair for four hours, where before, he couldn’t walk for more than an hour.”

What to expect after a Zephyr Valve procedure

The procedure to implant the valves is minimally invasive with little physical stress on the patient, and according to Dr. Jivan, patients can notice an immediate difference, and continue to feel better in the weeks after receiving the implants. However, he points out that the valve does require a minimum three night stay for observation.

“There is a minor risk for a collapsed lung during the first three days, and it’s important for us to monitor for that during that period,” he says.

There is also a risk for the valves to come loose after they are implanted, often from the patient coughing. This isn’t a major concern, however, and Dr. Jivan points out that the procedure to remove and replace the loose valve is the same simple procedure as the original.

“It’s not a medical emergency and there’s very little risk to the patient when the valve comes loose,” Dr. Jivan says. “But they do experience a return of their original symptoms, so we like to move quickly to get them feeling better as soon as possible.”

Rick has experienced a valve coming loose from coughing. “It’s no big deal,” he says. “It’s the same easy procedure and well worth it.”

A lifesaving scan

Zephyr Valve implants require ongoing follow-up scans. When Rick went for a follow-up after having a loose valve replaced, the results indicated that a small nodule that had been previously detected during scans had grown. Rick had lung cancer.

Rick wasn’t going to lose his new-found momentum, however, and began the journey to beat the cancer.

“I had some help,” he says. “My wife and my daughter, who happens to be a nurse, were with me for every visit. I always tell me people, ‘I have my nurse and my bodyguard with me, I’ll be OK.”

Julian Guitron-Roig, MD, a thoracic and cardiac surgeon with The Christ Hospital Physicians – Heart & Vascular, successfully removed the top lobe Rick’s right lung that contained the cancer. Then began the road to recovery, that was admittedly longer and more challenging than recovery from the valve implants, but after about a month of inpatient care, Rick’s back to enjoying his active life, but he wants people to know that he had help.

“The people at The Christ Hospital are great,” he says. “There are none better. And that’s not just Dr. Jivan, Dr. Guitron and the other doctors. That’s everybody from the nurses in the endoscopy department to the nurses in the stepdown unit after cancer surgery. In fact, I’ve told Katie, a nurse in the endoscopy department, ‘Your bubbly personality and positive attitude make this easier. You can take somebody having a terrible day and having to go through with this and make them feel like they are having the best day ever.”

Back to 110 miles per hour

Rick’s procedure did reduce the need for oxygen and he’s back to enjoying some his favorite activities with his family. “I’m not out here running any races,” he says, “but I’m comfortable to cover a lot of ground.”

He and his wife of more than 50 years have two adult daughters and four grown grandchildren, and they’ve always enjoyed travelling with their family. Rick is happy to be back to travel activities such as walking for miles on the beach in Florida or hiking in the mountains of Tennessee with his wife. He also enjoys helping out for hours at a time at the farm owned by his oldest daughter and her husband.

“It’s amazing what I can do that I couldn’t do before,” Rick says. “There’s no way I could have done any of this before those valves.”

Current patients can ask their primary pulmonologist if they believe they may be a candidate for a Zephyr Valve, or call our office at 513-241-5489 for more information. Ask your primary care provider about a referral if you believe you may be a candidate but if you are not an existing patient of The Christ Hospital Physicians - Pulmonary Medicine.

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If you have been coughing and wheezing a lot lately, you may be wondering whether you have chronic obstructive pulmonary disease (COPD). Symptoms of COPD may be similar to other conditions affecting your lungs and breathing, such as asthma and bronchitis. But there are differences between these conditions. Knowing what to look for and when to seek medical attention can help you better manage this condition.

COPD Symptoms

The most common symptom of COPD is a cough that doesn’t go away. The cough may be accompanied by wheezing, chest tightness and mucus production and may cause you to feel short of breath. Below is a list of COPD symptoms, but keep in mind that symptoms may not appear to be very bothersome until COPD has progressed to the point where significant lung damage has occurred.

  1. A chronic cough
  2. Shortness of breath
  3. Mucus/phlegm/sputum production
  4. Wheezing
  5. Chest tightness
  6. Frequent respiratory infections
  7. Fatigue/lack of energy
  8. Weight loss with no known cause
  9. Swelling in feet, ankles or legs

Symptoms may occasionally become worse for periods of time (called exacerbations) before they are under control again. The most common cause of exacerbation is due to infection in the lungs or airways.

Who is most at risk for COPD?

Anyone can develop COPD, but your risk increases if:

  • You are a current or former smoker
  • You are exposed to secondhand smoke, air pollution, dust, fumes or chemicals on a regular basis, such as at work

The most common cause of COPD is long-term exposure to smoke, irritating gases or particulate matter. People who experience chronic bronchitis or emphysema are more likely to develop COPD. People over age 40 are also more likely to develop the condition. But if you experience symptoms of COPD, don’t assume it’s just due to age. See a doctor for further evaluation. A doctor can perform a simple breathing test, called spirometry. This measures the amount of air you blow out and how fast you blow it out. It can determine whether you have COPD.

Does COPD get worse over time?

COPD is a progressive disease, meaning it usually gets worse over time. Although there is no cure for the disease, the condition is treatable and treatment is aimed at managing symptoms. This can improve your quality of life and makes it less likely you will experience complications from related health issues.

The sooner COPD is diagnosed, the sooner treatment can begin. This can prevent further damage to the lungs or loss of lung function.

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