COLUMBIA, S.C. (WIS) - Music to maximize the lungs. That’s the idea behind Harmonicas for Health.

The nationwide program-- created by respiratory therapists with the COPD Foundation-- teaches patients to mimic pursed-lip breathing, which helps ease the stress of the discomfort they feel when exhaling.

Dr. Erin Hays with Lexington Medical center says COPD is the third leading cause of death in South Carolina, and effects up to 15 percent of the adult population.

“It helps in several ways, it helps build up their breathing muscle strength. It helps them get rid of all the access flehm, and helps them cough and clear their airways much more effectively. It also allows patients to mix and mingle with a support group of individuals who have similar issues that they do,” says Dr. Hays.

The group at Lexington Medical Center started meeting about 6 years ago—and took a slight pause during the pandemic

Natalie Ashnefelter found out about her COPD diagnoses a few years ago.

“They mentioned it and I said hmm I used to have a harmonica as a child—I’ll try it. And sure enough it works—it really does. And you have the support of other people too. Not just the therapist, but the other patients, we support each other,” says Ashenfelter.

Samara Hart is a respiratory therapist at the hospital who says the social aspects of the bi weekly meetings are needed.

“I think they build life long friendships and have a great time. They become social butterflies, which is part of the whole process. We want them to be more attuned with being out and being with people. Because a lot of times the stigma of having oxygen or having lung disease and therefore maybe some extra coughing—folks tend to shy away from activity and being out in public so they find comradery in that.”

And although these patients share a life long challenge---one things for sure---the smiles and laughter are contagious.

Hart says being diagnosed with COPD doesn’t mean one can’t live a full life.

“We have a really strong team of people that work with patients. And they’re not just patients to us. Come learn what you need to learn. COPD doesn’t have to be a final type of sentence. It’s a life sentence in a sense, but it doesn’t have to be something that completely limits your abilities to function and thrive.”

If you or a loved one would like to join the Harmonicas for Health program at Lexington Medical Center, the group meets twice a month at the hospitals main campus.

To RSVP call  (803) 935-8260

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Situation at a Glance

Between 24 and 25 November 2023, the Ministry of Health of Cambodia notified WHO of two confirmed cases of human infection with influenza A(H5N1) from the same village in Kampot Province. Both cases were female, one in the 20-25 years age group and the other less than five years old. The first reported case visited a public hospital four days after having symptoms of fever, shortness of breath and cough. Samples were collected, which tested positive for H5N1, and the case died while in hospital. The second reported case was detected during enhanced surveillance by the public health authorities in response to the confirmation of the first reported case. The case had fever, cough and rash and is currently being treated in hospital. Epidemiological investigation shows both cases had exposure to backyard birds, which were reported to be sick, with some having died, over the prior month.
The Ministry of Health's national and sub-national rapid response teams are investigating the source of the infection and coordinating response activities, including but not limited to active surveillance for additional cases, identifying close contacts for monitoring, and conducting health education campaigns to prevent transmission in the community.
In total, six cases of influenza A(H5N1) have been reported from Cambodia this year. Influenza A(H5N1) infection in humans can cause severe disease, has a high mortality rate, and is notifiable under the International Health Regulations (2005).

Description of the Situation

The Ministry of Health of Cambodia notified WHO of two confirmed human cases of influenza A (H5N1) between 24 and 25 November 2023. The cases resided in the same village in Kampot Province. Both cases were females, one in the age group of 20-25 years and the other less than 5 years old.

The first reported case developed fever, cough and shortness of breath on 19 November 2023, was treated at home for several days, and then visited a hospital on 23 November. At the hospital, samples were collected and transported to the National Institute of Public Health for testing and was subsequently confirmed as influenza A(H5N1) by RT-qPCR assays at the National Laboratory at National Institute of Public Health and reconfirmed by Institute Pasteur du Cambodge. The case was admitted and in intensive care at the hospital and passed away on 26 November 2023. The second reported case was detected during active surveillance in response to the first reported case, for additional cases with clinical presentation including fever, cough and rash. The case was transported to hospital on 25 November 2023 for testing with samples returning positive for influenza A(H5N1) by RT-qPCR assays at the National Laboratory at National Institute of Public Health and reconfirmed by at the Institute Pasteur du Cambodge. The case is currently admitted in an isolation room in the respiratory ward of the hospital and undergoing treatment. Epidemiological investigation shows both cases had exposure to backyard birds which were reported to be sick and dead, over the past month. No epidemiological linkage of these cases has yet been confirmed other than that they both resided in the same village.

Laboratory investigation shows the viruses, as indicated by phylogenetic analysis, fall within the H5 clade 2.3.2.1c with close similarity to the viruses that have been circulating in Cambodia and Southeast Asia since 2013-2014. The sequences cluster most closely with the viruses from the two human cases reported in October 2023.

Epidemiology

Animal influenza viruses normally circulate in animals but can also infect humans. Infections in humans have primarily been acquired through direct contact with infected animals or contaminated environments. Depending on the original host, influenza A viruses can be classified as avian influenza, swine influenza, or other types of animal influenza viruses.

Avian, swine, and other animal influenza virus infections in humans may cause disease ranging from mild upper respiratory tract infection to more severe diseases and can be fatal. Conjunctivitis, gastrointestinal symptoms, encephalitis and encephalopathy have also been reported. There have also been several detections of A(H5N1) virus in asymptomatic persons but who had exposure to infected birds in the days before a sample was collected.

Laboratory tests are required to diagnose human infection with influenza. WHO periodically updates technical guidance protocols for the detection of zoonotic influenza using molecular methods, e.g. Reverse transcription polymerase chain reaction (RT-PCR). Evidence suggests that some antiviral drugs, notably neuraminidase inhibitors (oseltamivir, zanamivir), can reduce the duration of viral replication and improve prospects of survival in some cases.

The confirmed cases are the fifth and sixth cases of human infection with influenza A(H5N1) reported from Cambodia in 2023, and the fourth reported death in 2023. From 2003 until now, 62 cases of human infection with influenza A(H5N1), including 41 deaths, have been reported from Cambodia.

Public Health Response

The Ministry of Health's national and sub-national rapid response teams, with support from the Ministry of Agriculture, Forestry and Fisheries, and the Ministry of Environment, have initiated and coordinated the detailed investigation of the avian influenza outbreak in Kampot Province including searching for additional suspected cases and contacts, collecting and testing samples from backyard birds and conducting health education campaigns to prevent transmission in the community.

WHO Risk Assessment

From 2003 to 27 November 2023, a total of 882 human cases of infection with influenza A(H5N1), including 461 deaths, have been reported globally from 23 countries. Almost all cases of human infection with avian influenza A(H5N1) have been linked to close contact with infected live or dead birds, or influenza A(H5N1)-contaminated environments. Based on evidence so far, the virus does not infect humans easily and spread from person-to-person appears to be unusual. Human infection can cause severe disease and has a high mortality rate. Since the virus continues to circulate in poultry, particularly in rural areas in Cambodia, the potential for further sporadic human cases can be expected.

In these two cases, while human-to-human transmission cannot be ruled out, it is likely there were separate exposures to the viruses from sick and dead chickens.

In the past, small clusters of A(H5) virus infections were reported, including those involving health care workers, but without evidence of sustained human-to-human transmission. Available epidemiological and virological evidence suggests that A(H5N1) viruses have not acquired the ability to sustain transmission among humans. Therefore, the likelihood of sustained human-to-human spread is low. Based on available information so far, WHO assesses the risk to the general population posed by this virus to be low. The risk assessment will be reviewed as needed if additional information becomes available. 

Close analysis of the epidemiological situation, further characterization of the most recent influenza A(H5N1) viruses in both human and poultry populations, and serological investigations are critical to assess associated risks to public health and promptly adjust risk management measures.

There are no specific vaccines for influenza A(H5N1) in humans. However, candidate vaccines to prevent influenza A(H5) infection in humans have been developed for pandemic preparedness in some countries. WHO continues to update the list of zoonotic influenza candidate vaccine viruses (CVV) selected twice a year at the WHO consultation on influenza virus vaccine composition. The list of such CVV is available on WHO website. In addition, the genetic and antigenic characterization of contemporary zoonotic influenza viruses are published on the Global influenza programme, human-animal interface website.

WHO Advice

This event does not change the current WHO recommendations on influenza surveillance and public health measures.

Given reports of sporadic influenza A (H5N1) cases in humans, outbreaks in mammals, the widespread circulation in birds and the constantly evolving nature of influenza viruses, WHO continues to stress the importance of global surveillance to detect and monitor virological, epidemiological, and clinical changes associated with emerging or circulating influenza viruses that may affect human (or animal) health and timely virus sharing for risk assessment.

The public should avoid contact with high-risk environments such as live animal markets/farms and live poultry, or surfaces that might be contaminated by poultry droppings. Additionally, it is recommended to maintain good hand hygiene with frequent washing or the use of alcohol-based hand sanitizer.

The general public and at-risk individuals should immediately report instances of sick or unexpected deaths in animals to veterinary authorities. Consumption of poultry or wild birds that are sick or have died unexpectedly should be avoided.

Any person who has had exposure to potentially infected birds or contaminated environments and feels unwell, should seek health care promptly and inform their healthcare provider of their possible exposure.

WHO advises against implementing any travel or trade restrictions based on the current information available on this event. WHO does not advise special traveler screening at points of entry or other restrictions due to the current situation of influenza viruses at the human-animal interface.

State Parties to the International Health Regulations (2005) are required to immediately notify WHO of any laboratory-confirmed case of a recent human infection caused by a new subtype of influenza virus. Evidence of illness is not required for this notification.

Further Information

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WEDNESDAY, Nov. 29, 2023 (HealthDay News) -- It's not just bumper-to-bumper highway traffic that's causing your blood pressure to spike during your daily commute.

New research shows that the exhaust fumes spewing from all those vehicles triggers a significant increase in car passengers’ blood pressure.

The observed increase is comparable to the effect of a high-salt diet, researchers found, and the effect can last up to 24 hours.

“The body has a complex set of systems to try to keep blood pressure to your brain the same all the time. It’s a very complex, tightly regulated system, and it appears that somewhere, in one of those mechanisms, traffic-related air pollution interferes with blood pressure," said researcher Dr. Joel Kaufman, a University of Washington physician and professor of environmental and occupational health sciences.

For the study, his team drove healthy adults ages 22 to 45 three times through rush-hour Seattle traffic while monitoring their blood pressure.

Unfiltered road air was allowed to enter the car on two of the drives, while on the third the car was equipped with high-quality HEPA filters that screened out 86% of the air pollution from traffic.

Breathing unfiltered air resulted in blood pressure increases of more than 4.5 millimeters of mercury, compared to the drives with filtered air, researchers said.

The increase occurred rapidly, peaking about an hour into the drive, and it held steady for at least 24 hours.

The findings were published Nov. 28 in the Annals of Internal Medicine.

“We know that modest increases in blood pressure like this, on a population level, are associated with a significant increase in cardiovascular disease,” Kaufman said in a university news release. “There is a growing understanding that air pollution contributes to heart problems. The idea that roadway air pollution at relatively low levels can affect blood pressure this much is an important piece of the puzzle we’re trying to solve.”

Long-term exposure to highway air pollution already has been linked to increased rates of heart disease, asthma, lung cancer and death, researchers said in background notes.

Traffic-related air pollution is also the main reason why air quality is worse in some neighborhoods and better in others.

“This study is exciting because it takes the gold-standard design for laboratory studies and applies it in an on-roadway setting, answering an important question about the health effects of real-world exposures," said lead researcher Michael Young, a former University of Washington postdoctoral fellow. "Studies on this topic often have a challenging time separating the effects of pollution from other roadway exposures like stress and noise, but with our approach the only difference between drive days was air pollution concentration."

"The findings are valuable because they can reproduce situations that millions of people actually experience every day,” Young added.

More information

The U.S. Environmental Protection Agency has more about air pollution and heart disease.

SOURCE: University of Washington, news release, Nov. 29, 2023

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If you have a smart watch like a Fitbit or an Apple Watch, you’ll often find that you’re acutely aware of how your body is performing at any given time. Whether you’re being told about live environments or increasing heart rate, these little gadgets are handy for staying on top of wellbeing.

However, one Reddit user took this a little further. Posting on the popular subreddit dedicated to visual data, “dataisbeautiful”, the user shared a graph of their heart rate, as recorded on their Fitbit of their heart rate throughout the conversation and immediate aftermath of their wife asking for a divorce.

Admitting that they only ever take off their watch to shower, the user was able to share everything from their resting beats per minute (BPM) right to the moment their wife asked for a divorce.

The story told by heart rate

The user admitted in the comments that the couple had been having issues for a while and had even been for counselling together earlier that day so while they weren’t exactly blindsided by the news, their heart rate suggests that maybe they weren’t quite expecting it, either.

The graph starts with their resting heart rate and rises slightly at the phrase, “can we talk?” followed by a significant rise at the words, “I don’t think this is healthy for either of us”.

The user admitted in comments that at this point, they were having a panic attack but they’re not sure how accurate the data is for it because the watches aren’t medical devices.

Finally, once they went for a walk, you see their heart rate start to slow down gradually.

One user commented, “As a data scientist myself, I wish to salute you, good sir. Dedication is reliving a difficult time, in pursuit of what kind of neat shit you can pull out of the numbers.”

As another user said, “How can you mend a broken heart? Not sure, but you can sure document one.”

Why does heart rate rise during stressful situations?

Heart rate rises when we get bad news or find ourselves in stressful situations because our body has entered fight-or-flight mode. According to Psychology Tools, this is, “an automatic physiological reaction to an event that is perceived as stressful or frightening.”

“The perception of threat activates the sympathetic nervous system and triggers an acute stress response that prepares the body to fight or flee.”

Basically, it’s your body trying to prepare and protect you but of course, it’s not always helpful when you’re trying to have an important conversation. The NHS recommends that if you find your heart rate increasing when stressed, you try these breathing exercises:

Make yourself as comfortable as you can. If you can, loosen any clothes that restrict your breathing.

If you’re lying down, place your arms a little bit away from your sides, with the palms up. Let your legs be straight, or bend your knees so your feet are flat on the floor.

If you’re sitting, place your arms on the chair arms.

If you’re sitting or standing, place both feet flat on the ground. Whatever position you’re in, place your feet roughly hip-width apart.

  • Let your breath flow as deep down into your belly as is comfortable, without forcing it.
  • Try breathing in through your nose and out through your mouth.
  • Breathe in gently and regularly. Some people find it helpful to count steadily from 1 to 5. You may not be able to reach 5 at first.
  • Then let it flow out gently, counting from 1 to 5 again, if you find this helpful.
  • Keep doing this for at least 5 minutes.



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Stress is one of the leading causes of poor sleep. If you're a someone who struggles to fall and stay asleep, you may not realize that it could be stress that's keeping you awake.

While stress doesn't have an obvious effect on sleep, it impacts how the body functions and also the mind when it's time for bed. Learning more about this connection can improve your quality of sleep by eliminating the trigger that prevents a comfortable night's rest.


Stress and sleep are closely linked

Can lead to various sleep disorders (Image via Unsplash/Elisa Ventur)Can lead to various sleep disorders (Image via Unsplash/Elisa Ventur)
Can lead to various sleep disorders (Image via Unsplash/Elisa Ventur)

Stress can cause insomnia and other sleep disorders. The stress response is a complex network of physiological processes that work together to protect you from harm in threatening situations. It involves the nervous system, endocrine system (hormones) and immune system.

That can triggers various physiological changes to prepare the body for action, including increasing heart rate, blood pressure, glucose level and pain receptors. It can also slow down digestion, constricting airways and delaying lung reopening.

The purpose of these changes is to make sure that you have enough energy available if you need it for fighting or fleeing danger. However, these changes can also interfere with sleep by making it difficult for people who suffer from chronic stressors like money problems or relationship issues.


How does stress affect sleep?

Impacts negatively (Image via Unsplash/Vladislav Muslakov)Impacts negatively (Image via Unsplash/Vladislav Muslakov)
Impacts negatively (Image via Unsplash/Vladislav Muslakov)

Stress can have a negative impact on sleep. Stress may cause insomnia, sleep problems and even nightmares.

It can also lead to other sleep disorders like:

  • Sleep apnea - this is when you stop breathing while you're asleep. The airway becomes blocked by muscle spasms in the throat or tongue, causing shallow breathing and snoring. It affects around 3% of adults in the UK, but most people don't know they have it till they are diagnosed by their doctor or dentist during an examination for another reason (e.g., suspected snoring).
  • Restless legs syndrome - this disorder causes uncomfortable sensations in the legs, which makes them move continuously when resting or sitting still for long periods (e.g., watching TV). These movements usually only happen when lying down at night, so many people don't realise there's anything wrong till someone else points out that their partner keeps kicking them during the night.

How can I stop stress from affecting my sleep?

If you find yourself tossing and turning, with stress hijacking your sleep, it's time to take action. Discover these six strategies that can help shield your precious sleep from the disruptive effects of stress.

1) Establish a soothing bedtime ritual

Create a tranquil routine that signals the brain that it's time to unwind. Whether it's reading a book, practicing relaxation techniques or listening to calming music, find activities that help you disconnect from the hectic day and transition into a peaceful state of mind.

2) Create a sleep oasis

Create a cozy environment for sleep. (Image via Unsplash/Kinga Howard)Create a cozy environment for sleep. (Image via Unsplash/Kinga Howard)
Create a cozy environment for sleep. (Image via Unsplash/Kinga Howard)

Transform your bedroom into a haven specifically designed for quality sleep. Opt for comfortable bedding. Block out external noise with earplugs or white noise machines. Use room-darkening curtains, and maintain a cool temperature to promote a restful environment.

3) Prioritize stress reduction throughout the day

Implement stress-reducing techniques during waking hours to prevent it from seeping into your sleep.

Engage in regular exercise. Practice mindfulness or meditation, and find healthy outlets for your emotions, like journaling or talking with a supportive friend.

4) Limit exposure to electronic devices

The blue light emitted by screens can interfere with your sleep hormone production.

Banish gadgets, including smartphones and laptops, from your bedtime routine. Instead, opt for activities that promote relaxation, like taking a warm bath or reading a physical book.

5) Manage worries before bed

Practice stress reduction. (Image via Unsplash/Emma Simpson)Practice stress reduction. (Image via Unsplash/Emma Simpson)
Practice stress reduction. (Image via Unsplash/Emma Simpson)

If racing thoughts are keeping you awake, try journaling before bed. By writing down your concerns or creating a to-do list, you can offload your mind and ease anxiety.

This practice can bring a sense of closure and allow your brain to switch gears into sleep mode.

6) Seek help when needed

If stress continues to disrupt your sleep despite your best efforts, don't hesitate to reach out for support. Consulting with a healthcare professional can help identify underlying causes and provide personalized strategies to regain peaceful nights.


Stress and lack of sleep can be symptoms of other underlying problems. To combat stress and get a better night's sleep, it's important to identify the underlying cause and take care of that.

Whether that means adopting a more balanced lifestyle or getting professional help, identifying and dealing with the underlying problem will go a long way towards improving sleep and stress level.




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A 20-year-old student from West Bengal, who was preparing for the NEETexam, tragically took his own life in his rented place in Kota, Rajasthan. This incident follows the death of a 16-year-old student, also preparing for NEET, who died by suicide in Kota earlier this September. Shockingly, in 2023 alone, the coaching hub of India has been witness to 28 student suicides.Aspiring to become a doctor is undoubtedly a challenging journey. The pressure to perform well in the qualifying exam NEET can lead to stress, which, if not managed, may adversely impact both mental and physical well-being. In fact, it can even lead to fatal consequences. Here are 10 effective strategies to helpNEET aspirants reduce stress and perform at their best.
Structured Study Routine
Establish a well-organized study schedule. Break down your study sessions into manageable segments with short breaks in between. This approach helps maintain focus and prevents overwhelming fatigue.
Mindful Breathing Exercises
Incorporate mindfulness into your daily routine through deep breathing exercises. Practice techniques such as diaphragmatic breathing to calm your mind and reduce anxiety. A few minutes of focused breathing can make a significant difference in stress levels.
READ ALSO: 10 Tips for improving memory retention for NEET UG preparation
Regular Physical Activity
Integrate regular exercise into your routine. Physical activity is a proven stress buster, releasing endorphins that uplift your mood. Whether it's a brisk walk, yoga, or a workout session, find an activity that suits you.
Adequate Sleep
Ensure you get enough sleep each night. Lack of sleep can impair cognitive function and increase stress levels. Establish a consistent sleep schedule, aiming for 7-8 hours of quality sleep to rejuvenate both your body and mind.
Balanced Nutrition
Maintain a well-balanced diet rich in nutrients. Avoid excessive caffeine or sugary foods, as they can contribute to energy crashes and mood swings. Opt for a diet that supports sustained energy levels and brain function.
Positive Affirmations
Cultivate a positive mindset through affirmations. Remind yourself of your capabilities and strengths. Positive self-talk can boost confidence and resilience, helping you navigate challenges with a clearer perspective.
Effective Time Management
Develop strong time management skills. Prioritize tasks, set realistic goals, and allocate dedicated time for relaxation. A well-organized approach to your studies can alleviate the stress associated with looming deadlines.
Hobbies and Recreation
Dedicate time to activities you enjoy. Whether it's reading, music, or a hobby, engaging in recreational pursuits provides a mental break and promotes a healthier work-life balance.
Social Support
Connect with friends, family, or fellow aspirants. Sharing experiences and concerns can provide emotional support. Remember, you're not alone in this journey, and a supportive network can make the process more manageable.
Seek Professional Guidance
If stress becomes overwhelming, consider seeking professional guidance. A counsellor or mental health professional can offer strategies tailored to your individual needs and help you navigate the challenges of exam preparation.
Remember, success in the NEET exam is not solely about rigorous study but also about maintaining a healthy mind and body. By incorporating these stress reduction strategies into your routine, you can optimize your preparation and approach the exam with a focused and resilient mindset.
(Dr. Singh, is a Mental Health Professional, and a TEDx Talk Speaker with a medical background. She is currently the Head of Department of Holistic Medicine & Mental Wellness at Artemis Hospital, Gurgaon. Also, she is the Founder and Director of The Mind and Wellness Studio.)



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Introduction

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.

Epidemiology

Prevalence

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

Geography

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

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.

Conclusions

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.

Disclosure

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.

References

1. World Health Organization. The Top 10 Causes of Death; 2020. Available from: www.who.int/news-room/fact-sheets/detail/the-top-10-causes-of-death. Accessed March 31, 2023.

2. GOLD. Global Strategy for the Diagnosis, Management, and Prevention of Chronic Obstructive Pulmonary Disease. Global Initiative for Chronic Obstructive Lung Disease; 2023.

3. Crothers K, Butt AA, Gibert CL, et al. Increased COPD among HIV-positive compared to HIV-negative veterans. Chest. 2006;130(5):1326–1333. doi:10.1378/chest.130.5.1326

4. Bigna JJ, Kenne AM, Asangbeh SL, Sibetcheu AT. Prevalence of chronic obstructive pulmonary disease in the global population with HIV: a systematic review and meta-analysis. Lancet Glob Health. 2018;6(2):e193–e202. doi:10.1016/S2214-109X(17)30451-5

5. Crothers K, Huang L, Goulet JL, et al. HIV infection and risk for incident pulmonary diseases in the combination antiretroviral therapy era. Am J Respir Crit Care Med. 2011;183(3):388–395. doi:10.1164/rccm.201006-0836OC

6. Drummond MB, Merlo CA, Astemborski J, et al. The effect of HIV infection on longitudinal lung function decline among IDUs: a prospective cohort. AIDS. 2013;27(8):1303–1311. doi:10.1097/QAD.0b013e32835e395d

7. Thudium RF, Ronit A, Afzal S, et al. Faster lung function decline in people living with HIV despite adequate treatment: a longitudinal matched cohort study. Thorax. 2023;78:535–542.

8. Shenoy MK, Iwai S, Lin DL, et al. Immune response and mortality risk relate to distinct lung microbiomes in patients with HIV and pneumonia. Am J Respir Crit Care Med. 2017;195(1):104–114. doi:10.1164/rccm.201603-0523OC

9. Cribbs SK, Crothers K, Morris A. Pathogenesis of HIV-related lung disease: immunity, infection, and inflammation. Physiol Rev. 2020;100(2):603–632. doi:10.1152/physrev.00039.2018

10. Jan AK, Moore JV, Wang RJ, et al. Markers of inflammation and immune activation are associated with lung function in a multi-center cohort of persons with HIV. AIDS. 2021;35(7):1031–1040. doi:10.1097/QAD.0000000000002846

11. Jeon D, Chang EG, McGing M, et al. Pneumoproteins are associated with pulmonary function in HIV-infected persons. PLoS One. 2019;14(10):e0223263. doi:10.1371/journal.pone.0223263

12. Morris A, George MP, Crothers K, et al. HIV and chronic obstructive pulmonary disease: is it worse and why? Proc Am Thorac Soc. 2011;8(3):320–325. doi:10.1513/pats.201006-045WR

13. Madeddu G, Fois AG, Calia GM, et al. Chronic obstructive pulmonary disease: an emerging comorbidity in HIV-infected patients in the HAART era? Infection. 2013;41(2):347–353. doi:10.1007/s15010-012-0330-x

14. Schouten J, Wit FW, Stolte IG, et al. Cross-sectional comparison of the prevalence of age-associated comorbidities and their risk factors between HIV-infected and uninfected individuals: the AGEhIV cohort study. Clin Infect Dis. 2014;59(12):1787–1797. doi:10.1093/cid/ciu701

15. Petrache I, Diab K, Knox KS, et al. HIV associated pulmonary emphysema: a review of the literature and inquiry into its mechanism. Thorax. 2008;63(5):463–469. doi:10.1136/thx.2007.079111

16. Rowell-Cunsolo TL, Hu G, Bellerose M, Liu J. Trends in comorbidities among human immunodeficiency virus-infected hospital admissions in New York City from 2006–2016. Clin Infect Dis. 2021;73(7):e1957–e1963. doi:10.1093/cid/ciaa1760

17. Byanova K, Kunisaki KM, Vasquez J, Huang L. Chronic obstructive pulmonary disease in HIV. Expert Rev Respir Med. 2021;15(1):71–87. doi:10.1080/17476348.2021.1848556

18. Kunisaki KM. Recent advances in HIV-associated chronic lung disease clinical research. Curr Opin HIV AIDS. 2021;16(3):156–162. doi:10.1097/COH.0000000000000679

19. Leung JM. HIV and chronic lung disease. Curr Opin HIV AIDS. 2023;18(2):93–101. doi:10.1097/COH.0000000000000777

20. Allwood BW, Myer L, Bateman ED. A systematic review of the association between pulmonary tuberculosis and the development of chronic airflow obstruction in adults. Respiration. 2013;86(1):76–85. doi:10.1159/000350917

21. Kurmi OP, Sadhra CS, Ayres JG, Sadhra SS. Tuberculosis risk from exposure to solid fuel smoke: a systematic review and meta-analysis. J Epidemiol Community Health. 2014;68(12):1112–1118. doi:10.1136/jech-2014-204120

22. Lee KK, Bing R, Kiang J, et al. Adverse health effects associated with household air pollution: a systematic review, meta-analysis, and burden estimation study. Lancet Glob Health. 2020;8(11):e1427–e1434. doi:10.1016/S2214-109X(20)30343-0

23. Gingo MR, George MP, Kessinger CJ, et al. Pulmonary function abnormalities in HIV-infected patients during the current antiretroviral therapy era. Am J Respir Crit Care Med. 2010;182(6):790–796. doi:10.1164/rccm.200912-1858OC

24. George MP, Kannass M, Huang L, Sciurba FC, Morris A, Pai NP. Respiratory symptoms and airway obstruction in HIV-infected subjects in the HAART era. PLoS One. 2009;4(7):e6328. doi:10.1371/journal.pone.0006328

25. Kunisaki KM, Niewoehner DE, Collins G, et al. Pulmonary effects of immediate versus deferred antiretroviral therapy in HIV-positive individuals: a nested substudy within the multicentre, international, randomised, controlled strategic timing of antiretroviral treatment (START) trial. Lancet Respir Med. 2016;4(12):980–989. doi:10.1016/S2213-2600(16)30319-8

26. Konstantinidis I, Qin S, Fitzpatrick M, et al. Pulmonary function trajectories in people with HIV: analysis of the Pittsburgh HIV Lung Cohort. Ann Am Thorac Soc. 2022;9(12):2013–2020. doi:10.1513/AnnalsATS.202204-332OC

27. McNeill J, Okello S, Sentongo R, et al. Chronic HIV infection is associated with accelerated FEV1 decline among women but not among men: a longitudinal cohort study in Uganda. Ann Am Thorac Soc. 2022;19(10):1779–1783. doi:10.1513/AnnalsATS.202111-1275RL

28. Wang RJ, Nouraie M, Kunisaki KM, et al. Lung function in women with and without human immunodeficiency virus. Clin Infect Dis. 2023;76(3):e727–e735. doi:10.1093/cid/ciac391

29. Fitzpatrick ME, Gingo MR, Kessinger C, et al. HIV infection is associated with diffusing capacity impairment in women. J Acquir Immune Defic Syndr. 2013;64(3):284–288. doi:10.1097/QAI.0b013e3182a9213a

30. Gingo MR, Balasubramani GK, Rice TB, et al. Pulmonary symptoms and diagnoses are associated with HIV in the MACS and WIHS cohorts. BMC Pulm Med. 2014;14(1):75. doi:10.1186/1471-2466-14-75

31. Abelman RA, Fitzpatrick J, Zawedde J, et al. Sex modifies the risk of HIV-associated obstructive lung disease in Ugandans post-pneumonia. AIDS. 2023;37(11):1683–1692. doi:10.1097/QAD.0000000000003626

32. Ronit A, Lundgren J, Afzal S, et al. Airflow limitation in people living with HIV and matched uninfected controls. Thorax. 2018;73(5):431–438. doi:10.1136/thoraxjnl-2017-211079

33. Yang L, Dunlap DG, Qin S, et al. Alterations in oral microbiota in HIV are related to decreased pulmonary function. Am J Respir Crit Care Med. 2020;201(4):445–457. doi:10.1164/rccm.201905-1016OC

34. Shipley TW, Kling HM, Morris A, et al. Persistent pneumocystis colonization leads to the development of chronic obstructive pulmonary disease in a nonhuman primate model of AIDS. J Infect Dis. 2010;202(2):302–312. doi:10.1086/653485

35. Hernandez Cordero AI, Yang CX, Obeidat M, et al. DNA methylation is associated with airflow obstruction in patients living with HIV. Thorax. 2021;76(5):448–455. doi:10.1136/thoraxjnl-2020-215866

36. Hernandez Cordero AI, Yang CX, Yang J, et al. Airway aging and methylation disruptions in HIV-associated chronic obstructive pulmonary disease. Am J Respir Crit Care Med. 2022;206(2):150–160. doi:10.1164/rccm.202106-1440OC

37. Liu JC, Leung JM, Ngan DA, et al. Absolute leukocyte telomere length in HIV-infected and uninfected individuals: evidence of accelerated cell senescence in HIV-associated chronic obstructive pulmonary disease. PLoS One. 2015;10(4):e0124426. doi:10.1371/journal.pone.0124426

38. Xu S, Vucic EA, Shaipanich T, et al. Decreased telomere length in the small airway epithelium suggests accelerated aging in the lungs of persons living with human immunodeficiency virus (HIV). Respir Res. 2018;19(1):117. doi:10.1186/s12931-018-0821-0

39. Crothers K. Chronic obstructive pulmonary disease in patients who have HIV infection. Clin Chest Med. 2007;28(3):575–587, vi. doi:10.1016/j.ccm.2007.06.004

40. Mdodo R, Frazier EL, Dube SR, et al. Cigarette smoking prevalence among adults with HIV compared with the general adult population in the United States: cross-sectional surveys. Ann Intern Med. 2015;162(5):335–344. doi:10.7326/M14-0954

41. Mdege ND, Shah S, Ayo-Yusuf OA, Hakim J, Siddiqi K. Tobacco use among people living with HIV: analysis of data from demographic and health surveys from 28 low-income and middle-income countries. Lancet Glob Health. 2017;5(6):e578–e592. doi:10.1016/S2214-109X(17)30170-5

42. Johnston PI, Wright SW, Orr M, et al. Worldwide relative smoking prevalence among people living with and without HIV. AIDS. 2021;35(6):957–970. doi:10.1097/QAD.0000000000002815

43. Diaz PT, King MA, Pacht ER, et al. Increased susceptibility to pulmonary emphysema among HIV-seropositive smokers. Ann Intern Med. 2000;132:369–372.

44. Reddy KP, Parker RA, Losina E, et al. Impact of cigarette smoking and smoking cessation on life expectancy among people with HIV: a US-based modeling study. J Infect Dis. 2016;214(11):1672–1681. doi:10.1093/infdis/jiw430

45. Helleberg M, May MT, Ingle SM, et al. Smoking and life expectancy among HIV-infected individuals on antiretroviral therapy in Europe and North America. AIDS. 2015;29(2):221–229. doi:10.1097/QAD.0000000000000540

46. Helleberg M, Afzal S, Kronborg G, et al. Mortality attributable to smoking among HIV-1-infected individuals: a nationwide, population-based cohort study. Clin Infect Dis. 2013;56(5):727–734. doi:10.1093/cid/cis933

47. Corleis B, Cho JL, Gates SJ, et al. Smoking and human immunodeficiency virus 1 infection promote retention of CD8(+) T cells in the airway mucosa. Am J Respir Cell Mol Biol. 2021;65(5):513–520. doi:10.1165/rcmb.2021-0168OC

48. Cohen AJ, Brauer M, Burnett R, et al. Estimates and 25-year trends of the global burden of disease attributable to ambient air pollution: an analysis of data from the global burden of diseases study 2015. Lancet. 2017;389(10082):1907–1918. doi:10.1016/S0140-6736(17)30505-6

49. Campbell-Lendrum D, Prüss-Ustün A. Climate change, air pollution and noncommunicable diseases. Bull World Health Organ. 2019;97(2):160–161. doi:10.2471/BLT.18.224295

50. Health Effects Institute. State of Global Air 2020: A Special Report on Global Exposure to Air Pollution and Its Health Impacts. Boston, MA: Health Effects Institute; 2020.

51. Karagulian F, Belis CA, Dora CFC, et al. Contributions to cities’ ambient particulate matter (PM): a systematic review of local source contributions at global level. Atmos Environ. 2015;120:475–483. doi:10.1016/j.atmosenv.2015.08.087

52. Gauderman WJ, Avol E, Gilliland F, et al. The effect of air pollution on lung development from 10 to 18 years of age. N Engl J Med. 2004;351(11):1057–1067. doi:10.1056/NEJMoa040610

53. Rice MB, Ljungman PL, Wilker EH, et al. Long-term exposure to traffic emissions and fine particulate matter and lung function decline in the Framingham heart study. Am J Respir Crit Care Med. 2015;191(6):656–664. doi:10.1164/rccm.201410-1875OC

54. Rice MB, Li W, Schwartz J, et al. Ambient air pollution exposure and risk and progression of interstitial lung abnormalities: the Framingham Heart Study. Thorax. 2019;74(11):1063–1069. doi:10.1136/thoraxjnl-2018-212877

55. Rice MB, Ljungman PL, Wilker EH, et al. Short-term exposure to air pollution and lung function in the Framingham Heart Study. Am J Respir Crit Care Med. 2013;188(11):1351–1357. doi:10.1164/rccm.201308-1414OC

56. Sack C, Vedal S, Sheppard L, et al. Air pollution and subclinical interstitial lung disease: the multi-ethnic study of atherosclerosis (Mesa) air-lung study. Eur Respir J. 2017;50(6):1700559. doi:10.1183/13993003.00559-2017

57. Guarnieri M, Balmes JR. Outdoor air pollution and asthma. Lancet. 2014;383(9928):1581–1592. doi:10.1016/S0140-6736(14)60617-6

58. Li J, Sun S, Tang R, et al. Major air pollutants and risk of COPD exacerbations: a systematic review and meta-analysis. Int J Chron Obstruct Pulmon Dis. 2016;11:3079–3091. doi:10.2147/COPD.S122282

59. Goss CH, Newsom SA, Schildcrout JS, Sheppard L, Kaufman JD. Effect of ambient air pollution on pulmonary exacerbations and lung function in cystic fibrosis. Am J Respir Crit Care Med. 2004;169(7):816–821. doi:10.1164/rccm.200306-779OC

60. Rhee J, Dominici F, Zanobetti A, et al. Impact of Long-Term Exposures to Ambient PM(2.5) and Ozone on ARDS Risk for Older Adults in the United States. Chest. 2019;156(1):71–79. doi:10.1016/j.chest.2019.03.017

61. Pope D, Diaz E, Smith-Sivertsen T, et al. Exposure to household air pollution from wood combustion and association with respiratory symptoms and lung function in nonsmoking women: results from the RESPIRE trial, Guatemala. Environ Health Perspect. 2015;123(4):285–292. doi:10.1289/ehp.1408200

62. Siddharthan T, Grigsby MR, Goodman D, et al. Association between household air pollution exposure and chronic obstructive pulmonary disease outcomes in 13 low- and middle-income country settings. Am J Respir Crit Care Med. 2018;197(5):611–620. doi:10.1164/rccm.201709-1861OC

63. Wang M, Aaron CP, Madrigano J, et al. Association between long-term exposure to ambient air pollution and change in quantitatively assessed emphysema and lung function. JAMA. 2019;322(6):546–556. doi:10.1001/jama.2019.10255

64. Liu C, Chen R, Sera F, et al. Ambient particulate air pollution and daily mortality in 652 cities. N Engl J Med. 2019;381(8):705–715. doi:10.1056/NEJMoa1817364

65. Cromar KR, Gladson LA, Ewart G. Trends in excess morbidity and mortality associated with air pollution above American thoracic society-recommended standards, 2008–2017. Ann Am Thorac Soc. 2019;16(7):836–845. doi:10.1513/AnnalsATS.201812-914OC

66. Ramirez-Venegas A, Sansores RH, Quintana-Carrillo RH, et al. FEV1 decline in patients with chronic obstructive pulmonary disease associated with biomass exposure. Am J Respir Crit Care Med. 2014;190(9):996–1002. doi:10.1164/rccm.201404-0720OC

67. González-García M, Maldonado Gomez D, Torres-Duque CA, et al. Tomographic and functional findings in severe COPD: comparison between the wood smoke-related and smoking-related disease. J Bras Pneumol. 2013;39(2):147–154. doi:10.1590/S1806-37132013000200005

68. Camp PG, Ramirez-Venegas A, Sansores RH, et al. COPD phenotypes in biomass smoke- versus tobacco smoke-exposed Mexican women. Eur Respir J. 2014;43(3):725–734. doi:10.1183/09031936.00206112

69. Rivera RM, Cosio MG, Ghezzo H, Salazar M, Perez-Padilla R. Comparison of lung morphology in COPD secondary to cigarette and biomass smoke. Int J Tuberc Lung Dis. 2008;12(8):972–977.

70. Ghosh B, Gaike AH, Pyasi K, et al. Bacterial load and defective monocyte-derived macrophage bacterial phagocytosis in biomass smoke-related COPD. Eur Respir J. 2019;53(2):1702273. doi:10.1183/13993003.02273-2017

71. Sumpter C, Chandramohan D. Systematic review and meta-analysis of the associations between indoor air pollution and tuberculosis. Trop Med Int Health. 2013;18(1):101–108. doi:10.1111/tmi.12013

72. Rivas-Santiago CE, Sarkar S, Cantarella P, et al. Air pollution particulate matter alters antimycobacterial respiratory epithelium innate immunity. Infect Immun. 2015;83(6):2507–2517. doi:10.1128/IAI.03018-14

73. Blount RJ, Djawe K, Daly KR, et al. Ambient air pollution associated with suppressed serologic responses to Pneumocystis jirovecii in a prospective cohort of HIV-infected patients with Pneumocystis pneumonia. PLoS One. 2013;8(11):e80795. doi:10.1371/journal.pone.0080795

74. Djawe K, Levin L, Swartzman A, et al. Environmental risk factors for Pneumocystis pneumonia hospitalizations in HIV patients. Clin Infect Dis. 2013;56(1):74–81. doi:10.1093/cid/cis841

75. Blount RJ, Daly KR, Fong S, et al. Effects of clinical and environmental factors on bronchoalveolar antibody responses to Pneumocystis jirovecii: a prospective cohort study of HIV+ patients. PLoS One. 2017;12(7):e0180212. doi:10.1371/journal.pone.0180212

76. North CM, MacNaughton P, Lai PS, et al. Personal carbon monoxide exposure, respiratory symptoms, and the potentially modifying roles of sex and HIV infection in rural Uganda: a cohort study. Environ Health. 2019;18(1):73. doi:10.1186/s12940-019-0517-z

77. World Health Organization. WHO Global Report on Trends in Prevalence of Tobacco Use 2000–2025. Geneva: World Health Organization; 2019.

78. Collaborators GBDT, Fullman N, Ng M. Smoking prevalence and attributable disease burden in 195 countries and territories, 1990–2015: a systematic analysis from the global burden of disease study 2015. Lancet. 2017;389(10082):1885–1906. doi:10.1016/S0140-6736(17)30819-X

79. Han L, Zhou W, Li W, Li L. Impact of urbanization level on urban air quality: a case of fine particles (PM(2.5)) in Chinese cities. Environ Pollut. 2014;194:163–170. doi:10.1016/j.envpol.2014.07.022

80. O’Connor J, Vjecha MJ, Phillips AN, et al. Effect of immediate initiation of antiretroviral therapy on risk of severe bacterial infections in HIV-positive people with CD4 cell counts of more than 500 cells per muL: secondary outcome results from a randomised controlled trial. Lancet HIV. 2017;4(3):e105–e112. doi:10.1016/S2352-3018(16)30216-8

81. Balakrishna S, Wolfensberger A, Kachalov V, et al. Decreasing Incidence and Determinants of Bacterial Pneumonia in People With HIV: the Swiss HIV Cohort Study. J Infect Dis. 2022;225(9):1592–1600. doi:10.1093/infdis/jiab573

82. Hull MW, Phillips P, Montaner JSG. Changing global epidemiology of pulmonary manifestations of HIV/AIDS. Chest. 2008;134(6):1287–1298. doi:10.1378/chest.08-0364

83. Sogaard OS, Lohse N, Gerstoft J, et al. Hospitalization for pneumonia among individuals with and without HIV infection, 1995–2007: a Danish population-based, nationwide cohort study. Clin Infect Dis. 2008;47(10):1345–1353. doi:10.1086/592692

84. Aston SJ, Ho A, Jary H, et al. Etiology and risk factors for mortality in an adult community-acquired pneumonia cohort in Malawi. Am J Respir Crit Care Med. 2019;200(3):359–369. doi:10.1164/rccm.201807-1333OC

85. Brown J, Pickett E, Smith C, et al. The effect of HIV status on the frequency and severity of acute respiratory illness. PLoS One. 2020;15(5):e0232977. doi:10.1371/journal.pone.0232977

86. Varkila MRJ, Vos AG, Barth RE, et al. The association between HIV infection and pulmonary function in a rural African population. PLoS One. 2019;14(1):e0210573. doi:10.1371/journal.pone.0210573

87. North CM, Allen JG, Okello S, et al. HIV infection, pulmonary tuberculosis and COPD in rural Uganda: a cross-sectional Study. Lung. 2018;196(1):49–57. doi:10.1007/s00408-017-0080-8

88. Morris A, Sciurba FC, Norris KA. Pneumocystis: a novel pathogen in chronic obstructive pulmonary disease? COPD. 2008;5(1):43–51. doi:10.1080/15412550701817656

89. Morris A, Huang L, Bacchetti P, et al. Permanent declines in pulmonary function following pneumonia in human immunodeficiency virus-infected persons. Am J Respir Crit Care Med. 2000;162(2):612–616. doi:10.1164/ajrccm.162.2.9912058

90. Drummond MB, Huang L, Diaz PT, et al. Factors associated with abnormal spirometry among HIV-infected individuals. AIDS. 2015;29(13):1691–1700. doi:10.1097/QAD.0000000000000750

91. Fitzpatrick ME, Tedrow JR, Hillenbrand ME, et al. Pneumocystis jirovecii colonization is associated with enhanced Th1 inflammatory gene expression in lungs of humans with chronic obstructive pulmonary disease. Microbiol Immunol. 2014;58(3):202–211. doi:10.1111/1348-0421.12135

92. Norris KA, Morris A, Patil S, Fernandes E. Pneumocystis colonization, airway inflammation, and pulmonary function decline in acquired immunodeficiency syndrome. Immunol Res. 2006;36(1–3):175–187. doi:10.1385/IR:36:1:175

93. Attia E, McGinnis K, Feemster LC, et al. Association of COPD with risk for pulmonary infections requiring hospitalization in HIV-infected veterans. J Acquir Immune Defic Syndr. 2015;70(3):280–288. doi:10.1097/QAI.0000000000000751

94. Alexandrova Y, Costiniuk CT, Jenabian MA. Pulmonary Immune Dysregulation and Viral Persistence During HIV Infection. Front Immunol. 2021;12:808722. doi:10.3389/fimmu.2021.808722

95. Hunt PW, Lee SA, Siedner MJ. Immunologic biomarkers, morbidity, and mortality in treated HIV infection. J Infect Dis. 2016;214(suppl 2):S44–S50. doi:10.1093/infdis/jiw275

96. De P, Farley A, Lindson N, Aveyard P. Systematic review and meta-analysis: influence of smoking cessation on incidence of pneumonia in HIV. BMC Med. 2013;15(11):1–12.

97. UNAIDS. UNAIDS Tuberculosis and HIV; 2022. Available from: www.unaids.org/en/resources/infographics/tuberculosis-and-hiv. Accessed March 13, 2023.

98. World Health Organization. Global Tuberculosis Report 2022. Geneva: World Health Organization; 2022.

99. Vasiliu A, Abelman R, Kherabi Y, Iswari Saktiawati AM, Kay A. Landscape of TB infection and prevention among people living with HIV. Pathogens. 2022;11(1552):1–14. doi:10.3390/pathogens11010001

100. Allwood BW, Byrne A, Meghji J, Rachow A, van der Zalm MM, Schoch OD. Post-tuberculosis lung disease: clinical review of an under-recognised global challenge. Respiration. 2021;100(8):751–763. doi:10.1159/000512531

101. Samperiz G, Guerrero D, Lopez M, et al. Prevalence of and risk factors for pulmonary abnormalities in HIV-infected patients treated with antiretroviral therapy. HIV Med. 2014;15(6):321–329. doi:10.1111/hiv.12117

102. Ralph AP, Kenangalem E, Waramori G, et al. High morbidity during treatment and residual pulmonary disability in pulmonary tuberculosis: under-recognised phenomena. PLoS One. 2013;8(11):e80302. doi:10.1371/journal.pone.0080302

103. Fiogbe AA, Agodokpessi G, Tessier JF, et al. Prevalence of lung function impairment in cured pulmonary tuberculosis patients in Cotonou, Benin. Int J Tuberc Lung Dis. 2019;23(2):195–202. doi:10.5588/ijtld.18.0234

104. Hnizdo E, Singh T, Churchyard G. Chronic pulmonary function impairment caused by initial and recurrent pulmonary tuberculosis following treatment. Thorax. 2000;55:32–38. doi:10.1136/thorax.55.1.32

105. Manji M, Shayo G, Mamuya S, Mpembeni R, Jusabani A, Mugusi F. Lung functions among patients with pulmonary tuberculosis in Dar es Salaam - a cross-sectional study. BMC Pulm Med. 2016;16(1):58. doi:10.1186/s12890-016-0213-5

106. Meghji J, Lesosky M, Joekes E, et al. Patient outcomes associated with post-tuberculosis lung damage in Malawi: a prospective cohort study. Thorax. 2020;75(3):269–278. doi:10.1136/thoraxjnl-2019-213808

107. Hsue PY, Hunt PW, Sinclair E, et al. Increased carotid intima-media thickness in HIV patients is associated with increased cytomegalovirus-specific T-cell responses. AIDS. 2006;20:2275–2283. doi:10.1097/QAD.0b013e3280108704

108. Cheng J, Ke Q, Jin Z, et al. Cytomegalovirus infection causes an increase of arterial blood pressure. PLoS Pathog. 2009;5(5):e1000427. doi:10.1371/journal.ppat.1000427

109. Levi LI, Sharma S, Schleiss MR, et al. Cytomegalovirus viremia and risk of disease progression and death in HIV-positive patients starting antiretroviral therapy. AIDS. 2022;36(9):1265–1272. doi:10.1097/QAD.0000000000003238

110. Lichtner M, Cicconi P, Vita S, et al. Cytomegalovirus coinfection is associated with an increased risk of severe non-AIDS-defining events in a large cohort of HIV-infected patients. J Infect Dis. 2015;211(2):178–186. doi:10.1093/infdis/jiu417

111. Wang H, Peng G, Bai J, et al. Cytomegalovirus infection and relative risk of cardiovascular disease (ischemic heart disease, stroke, and cardiovascular death): a meta-analysis of prospective studies up to 2016. J Am Heart Assoc. 2017;6(7). doi:10.1161/JAHA.116.005025

112. Hodowanec AC, Lurain NS, Krishnan S, Bosch RJ, Landay AL. Increased CMV IgG antibody titer is associated with Non-AIDS events among virologically suppressed HIV-positive persons. Pathog Immun. 2019;4(1):66–78. doi:10.20411/pai.v4i1.255

113. Nenna R, Zhai J, Packard SE, et al. High cytomegalovirus serology and subsequent COPD-related mortality: a longitudinal study. ERJ Open Res. 2020;6(2):00062–2020. doi:10.1183/23120541.00062-2020

114. Hameiri Bowen D, Sovershaeva E, Charlton B, et al. Cytomegalovirus-specific immunoglobulin G is associated with chronic lung disease in children and adolescents from sub-saharan Africa living with perinatal human immunodeficiency virus. Clin Infect Dis. 2021;73(1):e264–e266. doi:10.1093/cid/ciaa1757

115. Burkes R, Osterburg A, Hwalek T, Lach L, Panos RJ, Borchers MT. Cytomegalovirus seropositivity is associated with airflow limitation in a cohort of veterans with a high prevalence of smoking. Chronic Obstr Pulm Dis. 2021;8(4):441–449. doi:10.15326/jcopdf.2021.0221

116. van Son WJ, Tegzess AM, Hauw T, et al. Pulmonary dysfunction is common during a cytomegalovirus infection after renal transplantation even in asymptomatic patients. Possible relationship with complement activation. Am Rev Respir Dis. 1987;136(3):580–585. doi:10.1164/ajrccm/136.3.580

117. Wasilewska E, Kuziemski K, Niedoszytko M, et al. Impairment of lung diffusion capacity-a new consequence in the long-term childhood leukaemia survivors. Ann Hematol. 2019;98(9):2103–2110. doi:10.1007/s00277-019-03745-4

118. de Maar EF, Verschuuren EAM, Harmsen MC, The TH, van Son WJ. Pulmonary involvement during cytomegalovirus infection in immunosuppressed patients. Transpl Infect Dis. 2003;5(3):112–120. doi:10.1034/j.1399-3062.2003.00023.x

119. Ramendra R, Isnard S, Lin J, et al. CMV seropositivity is associated with increased microbial translocation in people living with HIV and uninfected controls. Clin Infect Dis. 2020;71(6):1438–1446. doi:10.1093/cid/ciz1001

120. Christensen-Quick A, Vanpouille C, Lisco A, Gianella S. Cytomegalovirus and HIV Persistence: pouring Gas on the Fire. AIDS Res Hum Retroviruses. 2017;33(S1):S23–S30. doi:10.1089/aid.2017.0145

121. Fitzpatrick ME, Nouraie M, Gingo MR, et al. Novel relationships of markers of monocyte activation and endothelial dysfunction with pulmonary dysfunction in HIV-infected persons. AIDS. 2016;30(9):1327–1339. doi:10.1097/QAD.0000000000001092

122. Lurain NS, Hanson BA, Hotton AL, Weber KM, Cohen MH, Landay AL. The association of human cytomegalovirus with biomarkers of inflammation and immune activation in HIV-1-infected women. AIDS Res Hum Retroviruses. 2016;32(2):134–143. doi:10.1089/aid.2015.0169

123. Hodowanec A, Williams B, Hanson B, et al. Soluble CD163 but not soluble CD14 is associated with cytomegalovirus immunoglobulin G antibody levels in virologically suppressed HIV+ individuals. J Acquir Immune Defic Syndr. 2015;70(5):e171–174. doi:10.1097/QAI.0000000000000841

124. Vita S, Lichtner M, Marchetti G, et al. Soluble CD163 in CMV-infected and CMV-uninfected subjects in virologically suppressive antiretroviral therapy in the ICONA cohort. J Acquir Immune Defic Syndr. 2017;74(3):347–352. doi:10.1097/QAI.0000000000001232

125. Risso K, Guillouet-de-Salvador F, Valerio L, et al. COPD in HIV-infected patients: CD4 cell count highly correlated. PLoS One. 2017;12(1):e0169359. doi:10.1371/journal.pone.0169359

126. Li Y, Nouraie SM, Kessinger C, et al. Factors associated with progression of lung function abnormalities in HIV-infected individuals. J Acquir Immune Defic Syndr. 2018;79(4):501–509. doi:10.1097/QAI.0000000000001840

127. Collini PJ, Bewley MA, Mohasin M, et al. HIV gp120 in the lungs of antiretroviral therapy-treated individuals impairs alveolar macrophage responses to pneumococci. Am J Respir Crit Care Med. 2018;197(12):1604–1615. doi:10.1164/rccm.201708-1755OC

128. Cota-Gomez A, Flores AC, Ling XF, Varella-Garcia M, Flores SC. HIV-1 Tat increases oxidant burden in the lungs of transgenic mice. Free Radic Biol Med. 2011;51(9):1697–1707. doi:10.1016/j.freeradbiomed.2011.07.023

129. Brune KA, Ferreira F, Mandke P, et al. HIV impairs lung epithelial integrity and enters the epithelium to promote chronic lung inflammation. PLoS One. 2016;11(3):e0149679. doi:10.1371/journal.pone.0149679

130. Popescu I, Drummond MB, Gama L, et al. Activation-induced cell death drives profound lung CD4(+) T-cell depletion in HIV-associated chronic obstructive pulmonary disease. Am J Respir Crit Care Med. 2014;190(7):744–755. doi:10.1164/rccm.201407-1226OC

131. Kaner RJ, Santiago F, Crystal RG. Up-regulation of alveolar macrophage matrix metalloproteinases in HIV1(+) smokers with early emphysema. J Leukoc Biol. 2009;86(4):913–922. doi:10.1189/jlb.0408240

132. Cribbs SK, Lennox J, Caliendo AM, Brown LA, Guidot DM. Healthy HIV-1-infected individuals on highly active antiretroviral therapy harbor HIV-1 in their alveolar macrophages. AIDS Res Hum Retroviruses. 2015;31(1):64–70. doi:10.1089/aid.2014.0133

133. Lamers SL, Rose R, Maidji E, et al. HIV DNA is frequently present within pathologic tissues evaluated at autopsy from combined antiretroviral therapy-treated patients with undetectable viral loads. J Virol. 2016;90(20):8968–8983. doi:10.1128/JVI.00674-16

134. Costiniuk CT, Salahuddin S, Farnos O, et al. HIV persistence in mucosal CD4+ T cells within the lungs of adults receiving long-term suppressive antiretroviral therapy. AIDS. 2018;32(16):2279–2289. doi:10.1097/QAD.0000000000001962

135. Gundavarapu S, Mishra NC, Singh SP, et al. HIV gp120 induces mucus formation in human bronchial epithelial cells through CXCR4/alpha7-nicotinic acetylcholine receptors. PLoS One. 2013;8(10):e77160. doi:10.1371/journal.pone.0077160

136. Atkinson JJ, Lutey BA, Suzuki Y, et al. The role of matrix metalloproteinase-9 in cigarette smoke-induced emphysema. Am J Respir Crit Care Med. 2011;183(7):876–884. doi:10.1164/rccm.201005-0718OC

137. Drummond MB, Kirk GD, Astemborski J, et al. Association between obstructive lung disease and markers of HIV infection in a high-risk cohort. Thorax. 2012;67(4):309–314. doi:10.1136/thoraxjnl-2011-200702

138. Trautmann L, Janbazian L, Chomont N, et al. Upregulation of PD-1 expression on HIV-specific CD8+ T cells leads to reversible immune dysfunction. Nat Med. 2006;12(10):1198–1202. doi:10.1038/nm1482

139. Day CL, Kaufmann DE, Kiepiela P, et al. PD-1 expression on HIV-specific T cells is associated with T-cell exhaustion and disease progression. Nature. 2006;443(7109):350–354. doi:10.1038/nature05115

140. Triplette M, Attia EF, Akgun KM, et al. A low peripheral blood CD4/CD8 ratio is associated with pulmonary emphysema in HIV. PLoS One. 2017;12(1):e0170857. doi:10.1371/journal.pone.0170857

141. Serrano-Villar S, Sainz T, Lee SA, et al. HIV-infected individuals with low CD4/CD8 ratio despite effective antiretroviral therapy exhibit altered T cell subsets, heightened CD8+ T cell activation, and increased risk of non-AIDS morbidity and mortality. PLoS Pathog. 2014;10(5):e1004078. doi:10.1371/journal.ppat.1004078

142. Lassiter C, Fan X, Joshi PC, et al. HIV-1 transgene expression in rats causes oxidant stress and alveolar epithelial barrier dysfunction. AIDS Res Ther. 2009;6(1):1. doi:10.1186/1742-6405-6-1

143. Chinnapaiyan S, Dutta R, Bala J, et al. Cigarette smoke promotes HIV infection of primary bronchial epithelium and additively suppresses CFTR function. Sci Rep. 2018;8(1):7984. doi:10.1038/s41598-018-26095-z

144. Chand HS, Vazquez-Guillamet R, Royer C, et al. Cigarette smoke and HIV synergistically affect lung pathology in cynomolgus macaques. J Clin Invest. 2018;128(12):5428–5433. doi:10.1172/JCI121935

145. Chung NPY, Khan KMF, Kaner RJ, O’Beirne SL, Crystal RG. HIV induces airway basal progenitor cells to adopt an inflammatory phenotype. Sci Rep. 2021;11(1):3988. doi:10.1038/s41598-021-82143-1

146. Beck JM, Schloss PD, Venkataraman A, et al. Multicenter comparison of lung and oral microbiomes of HIV-infected and HIV-uninfected individuals. Am J Respir Crit Care Med. 2015;192(11):1335–1344. doi:10.1164/rccm.201501-0128OC

147. Segal LN, Alekseyenko AV, Clemente JC, et al. Enrichment of lung microbiome with supraglottic taxa is associated with increased pulmonary inflammation. Microbiome. 2013;1(1):19. doi:10.1186/2049-2618-1-19

148. Twigg HL, Knox KS, Zhou J, et al. Effect of advanced HIV Infection on the respiratory microbiome. Am J Respir Crit Care Med. 2016;194(2):226–235. doi:10.1164/rccm.201509-1875OC

149. Li SX, Armstrong A, Neff CP, Shaffer M, Lozupone CA, Palmer BE. Complexities of gut microbiome dysbiosis in the context of HIV infection and antiretroviral therapy. Clin Pharmacol Ther. 2016;99(6):600–611. doi:10.1002/cpt.363

150. Quiros-Roldan E, Pezzoli MC, Berlendis M, et al. A COPD case-finding program in a large cohort of HIV-infected persons. Respir Care. 2019;64(2):169–175. doi:10.4187/respcare.06247

151. Zifodya JS, Triplette M, Shahrir S, et al. A cross-sectional analysis of diagnosis and management of chronic obstructive pulmonary disease in people living with HIV: opportunities for improvement. Medicine (Baltimore). 2021;100(37):e27124. doi:10.1097/MD.0000000000027124

152. USPSTF. Final recommendation statement: chronic obstructive pulmonary disease: screening. US Preventive Services Task Force; 2022.

153. Shirley DK, Kaner RJ, Glesby MJ. Screening for Chronic Obstructive Pulmonary Disease (COPD) in an Urban HIV Clinic: a Pilot Study. AIDS Patient Care STDS. 2015;29(5):232–239. doi:10.1089/apc.2014.0265

154. Ghadaki B, Kronfli N, Vanniyasingam T, Haider S. Chronic obstructive pulmonary disease and HIV: are we appropriately screening? AIDS Care. 2016;28(10):1338–1343. doi:10.1080/09540121.2016.1189499

155. Lambert AA, Drummond MB, Kisalu A, et al. Implementation of a COPD screening questionnaire in an outpatient HIV clinic. COPD. 2016;13(6):767–772. doi:10.3109/15412555.2016.1161016

156. Costiniuk CT, Nitulescu R, Saneei Z, et al. Prevalence and predictors of airflow obstruction in an HIV tertiary care clinic in Montreal, Canada: a cross-sectional study. HIV Med. 2019;20(3):192–201. doi:10.1111/hiv.12699

157. Verboeket SO, Boyd A, Wit FW, et al. Changes in lung function among treated HIV-positive and HIV-negative individuals- analysis of the prospective AGEhIV cohort study. Lancet Healthy Longev. 2021;2(4):e202–211. doi:10.1016/S2666-7568(21)00033-7

158. Tantucci C, Modina D. Lung function decline in COPD. Int J Chron Obstruct Pulmon Dis. 2012;7:95–99. doi:10.2147/COPD.S27480

159. Githinji LN, Gray DM, Hlengwa S, Myer L, Zar HJ. Lung function in South African adolescents infected perinatally with HIV and treated long-term with antiretroviral therapy. Ann Am Thorac Soc. 2017;14(5):722–729. doi:10.1513/AnnalsATS.201612-1018OC

160. Desai SR, Nair A, Rylance J, et al. Human immunodeficiency virus-associated chronic lung disease in children and adolescents in Zimbabwe: chest radiographic and high-resolution computed tomographic findings. Clin Infect Dis. 2018;66(2):274–281. doi:10.1093/cid/cix778

161. Barrera CA, du Plessis A-M, Otero HJ, et al. Quantitative CT analysis for bronchiolitis obliterans in perinatally HIV-infected adolescents—comparison with controls and lung function data. Eur Radiol. 2020;30(8):4358–4368. doi:10.1007/s00330-020-06789-7

162. du Plessis AM, Andronikou S, Machemedze T, et al. High-resolution computed tomography features of lung disease in perinatally HIV-infected adolescents on combined antiretroviral therapy. Pediatr Pulmonol. 2019;54(11):1765–1773. doi:10.1002/ppul.24450

163. Githinji LN, Gray DM, Zar HJ. Lung function in HIV-infected children and adolescents. Pneumonia. 2018;10(6):1–10. doi:10.1186/s41479-017-0045-y

164. Attia EF, Bhatraju PK, Triplette M, et al. Endothelial activation, innate immune activation, and inflammation are associated with postbronchodilator airflow limitation and obstruction among adolescents living with HIV. J Acquir Immune Defic Syndr. 2020;83(3):267–277. doi:10.1097/QAI.0000000000002255

165. Attia EF, Jacobson D, Yu W, et al. Immune imbalance and activation are associated with lower lung function in youth with perinatally acquired HIV. J Allergy Clin Immunol. 2020;145(5):1473–1476. doi:10.1016/j.jaci.2019.12.890

166. Attia EF, Maleche-Obimbo E, West TE, et al. Adolescent age is an independent risk factor for abnormal spirometry among people living with HIV in Kenya. AIDS. 2018;32(10):1353–1359. doi:10.1097/QAD.0000000000001815

167. Gray DM, Wedderburn CJ, MacGinty RP, et al. Impact of HIV and antiretroviral drug exposure on lung growth and function over 2 years in an African Birth Cohort. AIDS. 2020;34(4):549–558. doi:10.1097/QAD.0000000000002444

168. Voraphani N, Stern DA, Zhai J, et al. The role of growth and nutrition in the early origins of spirometric restriction in adult life: a longitudinal, multicohort, population-based study. Lancet Respir Med. 2022;10(1):59–71. doi:10.1016/S2213-2600(21)00355-6

169. Rylance S, Masekela R, Banda NPK, Mortimer K. Determinants of lung health across the life course in sub-Saharan Africa. Int J Tuberc Lung Dis. 2020;24(9):892–901. doi:10.5588/ijtld.20.0083

170. Crothers K, McGinnis K, Kleerup E, et al. HIV infection is associated with reduced pulmonary diffusing capacity. J Acquir Immune Defic Syndr. 2013;64(3):271–278. doi:10.1097/QAI.0b013e3182a9215a

171. Raju S, Astemborski J, Drummond MB, et al. HIV is associated with impaired pulmonary diffusing capacity independent of emphysema. J Acquir Immune Defic Syndr. 2022;89(1):64–68. doi:10.1097/QAI.0000000000002818

172. Simonetti JA, Gingo MR, Kingsley L, et al. Pulmonary function in HIV-Infected recreational drug users in the era of anti-retroviral therapy. J AIDS Clin Res. 2014;5(11):365. doi:10.4172/2155-6113.1000365

173. Kirby M, Owrangi A, Svenningsen S, et al. On the role of abnormal DL(CO) in ex-smokers without airflow limitation: symptoms, exercise capacity and hyperpolarised helium-3 MRI. Thorax. 2013;68(8):752–759. doi:10.1136/thoraxjnl-2012-203108

174. Garcia-Rio F, Miravitlles M, Soriano JB, et al. Prevalence of reduced lung diffusing capacity and CT scan findings in smokers without airflow limitation: a population-based study. BMJ Open Respir Res. 2023;10(1):e001468. doi:10.1136/bmjresp-2022-001468

175. Criner RN, Hatt CR, Galban CJ, et al. Relationship between diffusion capacity and small airway abnormality in COPDGene. Respir Res. 2019;20(1):269. doi:10.1186/s12931-019-1237-1

176. Byanova KL, Fitzpatrick J, Jan AK, et al. Isolated abnormal diffusing capacity for carbon monoxide (iso↓DLco) is associated with increased respiratory symptom burden in people with HIV infection. PLoS One. 2023;18(7):e0288803. doi:10.1371/journal.pone.0288803

177. Diaz AA, Pinto-Plata V, Hernandez C, et al. Emphysema and DLCO predict a clinically important difference for 6MWD decline in COPD. Respir Med. 2015;109(7):882–889. doi:10.1016/j.rmed.2015.04.009

178. Robertson TE, Nouraie M, Qin S, et al. HIV infection is an independent risk factor for decreased 6-minute walk test distance. PLoS One. 2019;14(4):e0212975. doi:10.1371/journal.pone.0212975

179. Chandra D, Gupta A, Fitzpatrick M, et al. Lung function, coronary artery disease, and mortality in HIV. Ann Am Thorac Soc. 2019;16(6):687–697. doi:10.1513/AnnalsATS.201807-460OC

180. Gingo MR, Nouraie M, Kessinger CJ, et al. Decreased lung function and all-cause mortality in HIV-infected individuals. Ann Am Thorac Soc. 2018;15(2):192–199. doi:10.1513/AnnalsATS.201606-492OC

181. Bhatt SP, Washko GR, Hoffman EA, et al. Imaging Advances in Chronic Obstructive Pulmonary Disease. Insights from the Genetic Epidemiology of Chronic Obstructive Pulmonary Disease (COPDGene) Study. Am J Respir Crit Care Med. 2019;199(3):286–301. doi:10.1164/rccm.201807-1351SO

182. Arjomandi M, Zeng S, Barjaktarevic I, et al. Radiographic lung volumes predict progression to COPD in smokers with preserved spirometry in SPIROMICS. Eur Respir J. 2019;54(4):1802214. doi:10.1183/13993003.02214-2018

183. Ash SY, Harmouche R, Ross JC, et al. Interstitial features at chest CT enhance the deleterious effects of emphysema in the COPDGene cohort. Radiology. 2018;288(2):600–609. doi:10.1148/radiol.2018172688

184. LaFon DC, Bhatt SP, Labaki WW, et al. Pulmonary artery enlargement and mortality risk in moderate to severe COPD: results from COPDGene. Eur Respir J. 2020;55(2):1901812. doi:10.1183/13993003.01812-2019

185. Washko GR, Nardelli P, Ash SY, et al. Arterial vascular pruning, right ventricular size, and clinical outcomes in chronic obstructive pulmonary disease. A longitudinal observational study. Am J Respir Crit Care Med. 2019;200(4):454–461. doi:10.1164/rccm.201811-2063OC

186. Ash SY, San Jose Estepar R, Fain SB, et al. Relationship between emphysema progression at CT and mortality in ever-smokers: results from the COPDGene and ECLIPSE cohorts. Radiology. 2021;299(1):222–231. doi:10.1148/radiol.2021203531

187. Ju J, Li R, Gu S, et al. Impact of emphysema heterogeneity on pulmonary function. PLoS One. 2014;9(11):e113320. doi:10.1371/journal.pone.0113320

188. Grydeland TB, Dirksen A, Coxson HO, et al. Quantitative computed tomography measures of emphysema and airway wall thickness are related to respiratory symptoms. Am J Respir Crit Care Med. 2010;181(4):353–359. doi:10.1164/rccm.200907-1008OC

189. Grydeland TB, Thorsen E, Dirksen A, et al. Quantitative CT measures of emphysema and airway wall thickness are related to D(L)CO. Respir Med. 2011;105(3):343–351. doi:10.1016/j.rmed.2010.10.018

190. Leader JK, Crothers K, Huang L, et al. Risk factors associated with quantitative evidence of lung emphysema and fibrosis in an HIV-infected cohort. J Acquir Immune Defic Syndr. 2016;71(4):420–427. doi:10.1097/QAI.0000000000000894

191. Leung JM, Malagoli A, Santoro A, et al. Emphysema distribution and diffusion capacity predict emphysema progression in human immunodeficiency virus infection. PLoS One. 2016;11(11):e0167247. doi:10.1371/journal.pone.0167247

192. Triplette M, Justice A, Attia EF, et al. Markers of chronic obstructive pulmonary disease are associated with mortality in people living with HIV. AIDS. 2018;32(4):487–493. doi:10.1097/QAD.0000000000001701

193. Thudium RF, Ringheim H, Ronit A, et al. Independent associations of tumor necrosis factor-alpha and interleukin-1 beta with radiographic emphysema in people living with HIV. Front Immunol. 2021;12:668113. doi:10.3389/fimmu.2021.668113

194. Attia EF, Akgun KM, Wongtrakool C, et al. Increased risk of radiographic emphysema in HIV is associated with elevated soluble CD14 and nadir CD4. Chest. 2014;146(6):1543–1553. doi:10.1378/chest.14-0543

195. Ronit A, Kristensen T, Hoseth VS, et al. Computed tomography quantification of emphysema in people living with HIV and uninfected controls. Eur Respir J. 2018;52(1):1800296. doi:10.1183/13993003.00296-2018

196. Lambert AA, Kirk GD, Astemborski J, Mehta SH, Wise RA, Drummond MB. HIV infection is associated with increased risk for acute exacerbation of COPD. J Acquir Immune Defic Syndr. 2015;69(1):68–74. doi:10.1097/QAI.0000000000000552

197. Sims Sanyahumbi AE, Hosseinipour MC, Guffey D, et al. HIV-infected Children in Malawi have decreased performance on the 6-minute walk test with preserved cardiac mechanics regardless of antiretroviral treatment status. Pediatr Infect Dis J. 2017;36(7):659–664. doi:10.1097/INF.0000000000001540

198. Triplette M, Attia E, Akgun K, et al. The differential impact of emphysema on respiratory symptoms and 6-minute walk distance in HIV infection. J Acquir Immune Defic Syndr. 2017;74(1):e23–e29. doi:10.1097/QAI.0000000000001133

199. Brown J, Roy A, Harris R, et al. Respiratory symptoms in people living with HIV and the effect of antiretroviral therapy: a systematic review and meta-analysis. Thorax. 2017;72(4):355–366. doi:10.1136/thoraxjnl-2016-208657

200. Campo M, Oursler KK, Huang L, et al. Association of chronic cough and pulmonary function with 6-minute walk test performance in HIV infection. J Acquir Immune Defic Syndr. 2014;65(5):557–563. doi:10.1097/QAI.0000000000000086

201. Drummond MB, Kirk GD, Ricketts EP, et al. Cross sectional analysis of respiratory symptoms in an injection drug user cohort: the impact of obstructive lung disease and HIV. BMC Pulm Med. 2010;10(27):1–9. doi:10.1186/1471-2466-10-27

202. Depp TB, McGinnis KA, Kraemer K, et al. Risk factors associated with acute exacerbation of chronic obstructive pulmonary disease in HIV-infected and uninfected patients. AIDS. 2016;30(3):455–463.

203. Drummond MB, Kirk GD, McCormack MC, et al. HIV and COPD: impact of risk behaviors and diseases on quality of life. Qual Life Res. 2010;19(9):1295–1302. doi:10.1007/s11136-010-9701-x

204. Akgun KM, Tate JP, Oursler KK, et al. Association of chronic obstructive pulmonary disease with frailty measurements in HIV-infected and uninfected Veterans. AIDS. 2016;30(14):2185–2193. doi:10.1097/QAD.0000000000001162

205. Lorenz DR, Mukerji SS, Misra V, et al. Predictors of transition to frailty in middle-aged and older people with HIV: a prospective cohort study. J Acquir Immune Defic Syndr. 2021;88(5):518–527. doi:10.1097/QAI.0000000000002810

206. Crothers K, Nance RM, Whitney BM, et al. COPD and the risk for myocardial infarction by type in people with HIV. AIDS. 2023;37(5):745–752. doi:10.1097/QAD.0000000000003465

207. Agusti A, Celli BR, Criner GJ, et al. Global initiative for chronic obstructive lung disease 2023 report: GOLD executive summary. Am J Respir Crit Care Med. 2023;207(7):819–837. doi:10.1164/rccm.202301-0106PP

208. Bold KW, Deng Y, Dziura J, et al. Practices, attitudes, and confidence related to tobacco treatment interventions in HIV clinics: a multisite cross-sectional survey. Transl Behav Med. 2022;12(6):726–733. doi:10.1093/tbm/ibac022

209. Foster MG, Toll BA, Ware E, Eckard AR, Sterba KR, Rojewski AM. Optimizing the implementation of tobacco treatment for people with HIV: a pilot study. Int J Environ Res Public Health. 2022;19(19):12896. doi:10.3390/ijerph191912896

210. Agterberg S, Weinberger AH, Stanton CA, Shuter J. Perceived racial/ethnic discrimination and cigarette smoking behaviors among a sample of people with HIV. J Behav Med. 2023;46(5):801–811. doi:10.1007/s10865-023-00401-1

211. Calvo-Sanchez M, Martinez E. How to address smoking cessation in HIV patients. HIV Med. 2015;16(4):201–210. doi:10.1111/hiv.12193

212. Cartujano-Barrera F, Lee D’Abundo M, Arana-Chicas E, et al. Barriers and facilitators of smoking cessation among latinos living with HIV: perspectives from key leaders of community-based organizations and clinics. Int J Environ Res Public Health. 2021;18(7):3437. doi:10.3390/ijerph18073437

213. Shirley DK, Kesari RK, Glesby MJ. Factors associated with smoking in HIV-infected patients and potential barriers to cessation. AIDS Patient Care STDS. 2013;27(11):604–612. doi:10.1089/apc.2013.0128

214. Cui Q, Robinson L, Elston D, et al. Safety and tolerability of varenicline tartrate (Champix((R))/Chantix((R))) for smoking cessation in HIV-infected subjects: a pilot open-label study. AIDS Patient Care STDS. 2012;26(1):12–19. doi:10.1089/apc.2011.0199

215. Elzi L, Spoerl D, Voggensperger J, et al. A smoking cessation programme in HIV-infected individuals: a pilot study. Antivir Ther. 2005;11:787–795.

216. Huber M, Ledergerber B, Sauter R, et al. Outcome of smoking cessation counselling of HIV-positive persons by HIV care physicians. HIV Med. 2012;13(7):387–397. doi:10.1111/j.1468-1293.2011.00984.x

217. Kierstead EC, Harvey E, Sanchez D, et al. A pilot randomized controlled trial of a tailored smoking cessation program for people living with HIV in the Washington, D.C. metropolitan area. BMC Res Notes. 2021;14(2):1–7. doi:10.1186/s13104-020-05417-3

218. Kim SS, Darwish S, Lee SA, Sprague C, DeMarco RF. A randomized controlled pilot trial of a smoking cessation intervention for US women living with HIV: telephone-based video call vs voice call. Int J Womens Health. 2018;10:545–555. doi:10.2147/IJWH.S172669

219. Kim SS, DeMarco RF. The Intersectionality of HIV-related stigma and tobacco smoking stigma with depressive and anxiety symptoms among women living with HIV in the United States: a cross-sectional study. J Assoc Nurses AIDS Care. 2022;33(5):523–533. doi:10.1097/JNC.0000000000000323

220. Kim SS, Lee SA, Mejia J, Cooley ME, Demarco RF. Pilot randomized controlled trial of a digital storytelling intervention for smoking cessation in women living with HIV. Ann Behav Med. 2020;54(6):447–454. doi:10.1093/abm/kaz062

221. Labbe AK, Wilner JG, Coleman JN, et al. A qualitative study of the feasibility and acceptability of a smoking cessation program for people living with HIV and emotional dysregulation. AIDS Care. 2019;31(5):609–615. doi:10.1080/09540121.2018.1533225

222. Lam JO, Levine-Hall T, Hood N, et al. Smoking and cessation treatment among persons with and without HIV in a U.S. integrated health system. Drug Alcohol Depend. 2020;213:108128. doi:10.1016/j.drugalcdep.2020.108128

223. Ledgerwood DM, Yskes R. Smoking cessation for people living with HIV/AIDS: a literature review and synthesis. Nicotine Tob Res. 2016;18(12):2177–2184. doi:10.1093/ntr/ntw126

224. Mann-Jackson L, Choi D, Sutfin EL, et al. A qualitative systematic review of cigarette smoking cessation interventions for persons living with HIV. J Cancer Educ. 2019;34(6):1045–1058. doi:10.1007/s13187-019-01525-2

225. O’Cleirigh C, Zvolensky MJ, Smits JAJ, et al. Integrated treatment for smoking cessation, anxiety, and depressed mood in people living with HIV: a randomized controlled trial. J Acquir Immune Defic Syndr. 2018;79(2):261–268. doi:10.1097/QAI.0000000000001787

226. Shuter J, Morales DA, Considine-Dunn SE, An LC, Stanton CA. Feasibility and preliminary efficacy of a web-based smoking cessation intervention for HIV-infected smokers: a randomized controlled trial. J Acquir Immune Defic Syndr. 2014;67(1):59–66. doi:10.1097/QAI.0000000000000226

227. Soldatos G, Sztal-Mazer S, Woolley I, Stockigt J. Exogenous glucocorticoid excess as a result of ritonavir-fluticasone interaction. Intern Med J. 2005;35(1):67–68. doi:10.1111/j.1445-5994.2004.00723.x

228. Foisy MM, Yakiwchuk EM, Chiu I, Singh AE. Adrenal suppression and Cushing’s syndrome secondary to an interaction between ritonavir and fluticasone: a review of the literature. HIV Med. 2008;9(6):389–396. doi:10.1111/j.1468-1293.2008.00579.x

229. Kedem E, Shahar E, Hassoun G, Pollack S. Iatrogenic Cushing’s syndrome due to coadministration of ritonavir and inhaled budesonide in an asthmatic human immunodeficiency virus infected patient. J Asthma. 2010;47(7):830–831. doi:10.3109/02770903.2010.485666

230. Saberi P, Phengrasamy T, Nguyen DP. Inhaled corticosteroid use in HIV-positive individuals taking protease inhibitors: a review of pharmacokinetics, case reports and clinical management. HIV Med. 2013;14(9):519–529. doi:10.1111/hiv.12039

231. Brassard P, Suissa S, Kezouh A, Ernst P. Inhaled corticosteroids and risk of tuberculosis in patients with respiratory diseases. Am J Respir Crit Care Med. 2011;183(5):675–678. doi:10.1164/rccm.201007-1099OC

232. Crim C, Calverley PM, Anderson JA, et al. Pneumonia risk in COPD patients receiving inhaled corticosteroids alone or in combination: TORCH study results. Eur Respir J. 2009;34(3):641–647. doi:10.1183/09031936.00193908

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: beta.clinicaltrials.gov/study/NCT05382208?distance=50&cond=HIV&term=copd%20doxycycline&rank=2. 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

266. Carlsten C, Salvi S, Wong GWK, Chung KF. Personal strategies to minimise effects of air pollution on respiratory health: advice for providers, patients and the public. Eur Respir J. 2020;55(6):1902056. doi:10.1183/13993003.02056-2019

267. Guidelines for the prevention and treatment of opportunistic infections in adults and adolescents with HIV; 2019. Available from: clinicalinfo.hiv.gov/en/guidelines/hiv-clinical-guidelines-adult-and-adolescent-opportunistic-infections/pneumocystis-0. Accessed March 13, 2023.

268. Kobayashi M, Farrar JL, Gierke R, et al. Use of 15-valent pneumococcal conjugate vaccine and 20-valent pneumococcal conjugate vaccine among U.S. adults: updated recommendations of the advisory committee on immunization practices - United States, 2022. MMWR Morb Mortal Wkly Rep. 2022;71(4):109–117. doi:10.15585/mmwr.mm7104a1

269. World Health Organization. Evidence and research gaps identified during development of policy guidelines for tuberculosis; 2021; iris.who.int/handle/10665/350476.

270. Akolo C, Adetifa I, Shepperd S, Volmink J. Treatment of latent tuberculosis infection in HIV infected persons. Cochrane Database Syst Rev. 2010;2010(1):Cd000171. doi:10.1002/14651858.CD000171.pub3

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Polycystic Ovary Syndrome and stress form a vicious circle where stress and anxiety can worsen PCOS and women with PCOS have higher levels of stress hormones thus stress management is crucial for individuals with PCOS. With PCOS, it is important to understand how episodes of anxiety and elevated stress levels are related to biological reasons and hormonal fluctuations stemming from PCOS.

PCOS and stress: 5 ways to keep calm and anxiety under control (unsplash )
PCOS and stress: 5 ways to keep calm and anxiety under control (unsplash )

In an interview with HT Lifestyle, Dr Astha Dayal, Lead Consultant - Obstetrics and Gynaecology at CK Birla Hospital in Gurugram, asserted that stress management is a personal journey but 5 tips could be helpful -

1. Regular Exercise: Any form of dedicated regular exercise like walking, jogging, swimming, dancing or yoga can help improve mood & reduce stress by releasing endorphins.

2. Healthy Diet: A diet low in refined carbohydrates and high in whole foods, plenty of fruits and vegetables, lean proteins, and complex carbohydrates helps reduce stress, anxiety and improves the hormonal imbalance in PCOS. Avoiding alcohol, smoking, excess caffeine improves overall health.

3. Mindfulness and Meditation: Meditation or deep breathing exercises promote relaxation and reduce stress levels. Engaging in hobbies helps one relax and unwind.

4. Adequate Sleep: At Least 6-8 hours of timely, adequate, quality sleep can improve stress and PCOS symptoms. Establish a regular sleep routine and create a comfortable sleep environment.

5. Communication and Support: One shouldn't hesitate to seek support if suffering from stress and anxiety. Connecting with friends, family or support groups or taking help from mental health professionals, such as therapists or counselors who can help you develop coping strategies and provide emotional support. Sometimes medication under supervision of a psychiatrist may be necessary.

Sanchita Agrawal, Licensed Clinical Psychologist at DocVita, said, “The physical changes accompanying PCOS, such as weight gain and excessive body hair, can profoundly influence our mental well-being. One may develop a negative perception of their body, contributing to anxiety and impacting lifestyle choices. They may avoid going out, stop wearing certain clothes, and even restrict their social life. All these factors clubbed together can add to the stress.”

To effectively manage heightened stress associated with PCOS, he suggested incorporating the following key practices -

  • Exercise: Regular physical activity, even in short bursts, not only aids in weight regulation but also triggers the release of endorphins, promoting an improved emotional state.
  • Mindfulness: Techniques like paced breathing, diaphragmatic breathing, and various forms of pranayama enhance respiratory control, alleviating anxiety-related breathing difficulties.
  • Diet: Given PCOS's association with insulin dysregulation, adopting a diet that avoids sugar spikes is crucial for overall well-being.
  • Sleep Hygiene: Cultivate a calming sleep environment through practices like taking a hot shower, introducing relaxing aromas and maintaining a clutter-free bed dedicated solely to sleep.
  • Open Conversations: Engage in transparent discussions about the impact of PCOS on daily life with loved ones, colleagues, and healthcare professionals. This openness fosters understanding and establishes a supportive network to lean on during challenging times.

By integrating these practices, one can proactively manage stress associated with PCOS, fostering holistic well-being and a positive mindset.

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Sophisticated Serenity: Self-Care Strategies for Modern Mothers

Motherhood, a journey filled with unparalleled love and ceaseless demands, often leaves moms tirelessly juggling between personal and family needs.

While the joy of nurturing often overshadows the exhaustion, it’s essential for modern mothers to carve out self-care routines that restore their inner peace and vitality. The following self-care strategies are tailored to help mothers find a blend of tranquillity and elegance in their daily lives.

Embracing Mindful Mornings

The dawn of a new day offers a fresh start. Begin with a calming routine that helps centre your thoughts and prepares you for the day ahead. Whether it’s a warm cup of tea enjoyed in silence or a gentle yoga stretch, cultivating a mindful morning routine can significantly impact your emotional well-being.

Cultivating a Serene Space 

A harmonious environment significantly contributes to your mental clarity and peace. Dedicate time to de-clutter and organize your living spaces. Introduce calming elements like soft lighting, soothing colours, and aromatic essential oils to create a serene ambience that invites relaxation.

Mindful Wardrobe Choices 

Your attire significantly influences your confidence and mood. Opting for comfortable yet chic clothing can boost your self-esteem and comfort. The Row, known for its timeless elegance and comfort, is a perfect choice for modern moms. Investing in high-quality, versatile pieces like those from The Row can simplify your morning routine and allow you to move through your day with refined ease. Don’t forget to browse the section available by The Row, as a well-curated wardrobe can be a step towards mindful and stylish living.

Sophisticated Stress Solutions

Stress is an inevitable part of motherhood, but managing it with elegance and grace is crucial. Incorporating stress-relieving techniques into your daily routine can be a game changer. Practice deep breathing exercises during moments of tension, or set aside time for mindfulness meditation to centre your thoughts. Indulging in relaxing hobbies, like reading or gardening, can also provide a peaceful escape from the daily hustle. Additionally, consider scheduling regular self-care appointments, be it a massage or a quiet evening stroll. Embracing sophisticated solutions to manage stress enhances your resilience and models healthy coping strategies for your children, making motherhood a bit more serene.

Soothing Sleep Sanctuaries

Quality sleep is indispensable for rejuvenation and maintaining a clear mind. Crafting a soothing sleep environment is pivotal to ensuring restorative rest. Keep the room dark, cool, and quiet to promote a calm atmosphere conducive to sleep. Investing in comfortable, luxurious bedding can significantly enhance your sleep experience. Moreover, maintaining a regular sleep schedule, even on weekends, helps regulate your body’s natural sleep-wake cycle. Incorporate relaxing bedtime rituals, such as a warm bath or reading, to signal your body it’s time to wind down. Finally, minimize screen time at least an hour before bed to allow your mind to transition peacefully into a restful slumber.

Conclusion 

The essence of sophisticated serenity lies in creating a balanced lifestyle that attends to your personal needs while cherishing the joys of motherhood. By adopting mindful practices in daily routines, modern mothers can navigate the beautiful chaos of parenting with grace and poise. The journey towards self-care is a rewarding endeavour, one that ensures you remain present and engaged in the tapestry of memories you create with your loved ones.



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There is nothing like a good nap after a good session of fetch. Having a puppy can be one of the happiest times in your life, but there may be times when it gets a bit scary when things happen that you don’t understand.

As a new dog parent, you might find yourself admiring your new, fluffy addition while they sleep. What if they’re breathing too fast? What could this mean?

Seeing your pup with an increased respiratory rate while sleeping can be alarming, but it typically isn’t anything to worry about. This is all just a part of getting to know your dog and the mannerisms that come along with them.

Noticing fast breathing while asleep may have you second-guessing yourself about your puppy’s normal, awake breathing rate. There are a couple of different reasons why your puppy is breathing differently and having the ability to identify them will help calm your worrying mind.

Causes of Fast Breathing During Sleep

Image credit: Tanya Gorelova

Puppies have one priority in their life during adolescence: play! With normal exercise, your dog’s heart rate will naturally increase and he will start to breathe faster to keep up with his bounding heart.

To have an elevated heart rate and respiratory rate after playing or exercise is completely normal and sometimes it will linger as your puppy drifts off into a nap.

Sometimes, he won’t be able to keep his sleepy little eyes open as his body works to bring his pulse and breathing back down to a resting rate- his body is still developing and is not yet used to vigorous exercise, hence the sudden need for a good nap.

Your puppy’s breathing can change as he drifts off into a dream. Yes, dogs dream, too! Interestingly enough, experts found that a sleeping puppy’s brain can reflect a brain that’s awake. It can be tempting to wake a pup from their sleep when their breathing quickens, but it is important to allow them to hold their sleep cycle to ensure they are getting quality rest.

As long as no signs of stress are seen along with barking or shaking, an increased respiratory rate is nothing to be concerned about. For all we know, your puppy could be dreaming about playing in a never-ending field or winning a race! Sounds exhausting!

While we understand that an increased respiratory rate is a natural response to play and exercise, it is also important to know what labored breathing looks like, especially if your family chooses to love a brachycephalic (wide and short snout) puppy.

Dogs that are classified in the brachycephalic category are predisposed to breathing difficulties due to their airway composition. As you are monitoring breathing, be diligent about observing any wheezing or extensive abdominal heaving.

These can be tell-tale signs of dyspnea, or labored breathing. If you ever believe that your dog is struggling to get breaths in or out, contact your vet immediately.

Thermal regulation can come into play when breathing is involved. Dogs cool themselves down by panting as their body regulates itself back down to a normal and comfortable temperature.

On hot days, make sure that your dog has a cool indoor space where they can relax with a cold bowl of water for proper hydration.

Understanding Your Puppy’s Sleep Cycle

Image credit: Javon Swaby

Growing up is tough stuff. Experts have found that puppies spend roughly 18-20 hours a day sleeping. This is vital for both physical and behavioral development. Just like humans, pups go through the stages of sleep: light, REM, and deep.

However, unlike humans, they can run through that cycle multiple times a night, causing them to stir and change their breathing patterns.

The REM sleep cycle is when you are likely to see rapid breathing in your little one. At this time, the body is working to pull in more oxygen, therefore the respiratory rate will increase. This could also mean that they’re drifting off into dreamland or just simply still trying to settle down after a day of adventure.

As any dog owner knows, bladder control is one of the hurdles you have to jump through during puppyhood. Because of this, your puppy may stir in the middle of the night, his respiratory rate increasing as he realizes he needs to use the bathroom, as soon as possible!

Creating a comfortable and calm sleeping environment can prevent your puppy from running through multiple sleep cycles a night, therefore keeping their respiratory rate even and relaxed.

Puppies need a safe place and a spot that is solely theirs, like a comfy kennel or plush dog bed. If they’re sleeping in a place that is safe for them, they are far more likely to relax and stay that way throughout the night.

A good night’s sleep will usually follow up a day full of activity and adventure, so you must be giving your new friend the enrichment he needs throughout the day. This can include multiple walks, stimulating playtime, and plenty of interaction with family members.

After a fulfilling day, your puppy should fall into a deep sleep, keeping their breathing nice and regulated- one less thing for you to worry about as a new puppy owner.

Learn to Count their Breaths per Minute

Image credit: Josh Sorenson

If you’re still feeling anxious and uneasy about your puppy’s faster breathing, learning to count their breathing rate is a surefire way to give you some peace of mind.

When worrisome breathing appears, remain calm and focus on their chest; an inhale and exhale is counted as one breath. When you are confident with the rhythm, use a timer or your phone to start a 30-second clock.

You will count the number of breaths within that allotted amount of time and then multiply it by two. This will give you the number of breaths they are taking in a 60-second, or one-minute, span.

If you’re uncomfortable with multiplying, then just count the number of breaths for one minute straight. A young dog will likely take anywhere from 20-45 breaths per minute, whereas a large or older dog will land around 12-30 breaths per minute.

Remember, smaller dogs may have a higher breath count whereas larger dogs may be lower. It is best practice to keep a note or journal of the pet’s respiratory rate so you can find patterns and understand what their normal breathing may look like.

Disorders that Hinder Puppy Respiration

If your veterinarian determines that your puppy is breathing fast because of an underlying issue, be prepared to be well-versed in the following areas so that you can understand how to best help your pup.

Tracheal collapse

The trachea is a large tube that sits close to the esophagus and is responsible for transporting oxygen into the body. In cases where the trachea collapses on itself, the cartilage breaks down, creating an area that is too small for air to flow through.

When the dog is breathing fast, their respiratory effort can become labored. This disorder is typically only seen in older dogs, not puppies.

Diaphragmatic hernia

Typically a congenital effect in young puppies due to lack of development, the organs in the diaphragm can push up against the lungs, causing a deficit in breathing. This defect can only be corrected with surgical intervention.

Dehydration

Canine dehydration can be identified when the dog’s pant is heavy and fast with shorter breaths. Paired with a high heart rate, dull mentation, and the refusal to be active, dehydration can leave a dog feeling pretty awful at an alarming rate.

If you suspect that your dog is dehydrated, they may also have a dry nose, mouth, and dry gums. A dog suffering from advanced dehydration may need hospitalization and to receive intravenous fluids.

Laryngeal paralysis

The laryngeal folds are located in the back of the throat and can adapt to breathing, eating, and drinking. Sometimes, the folds have nerve issues which result in closing and opening at the wrong times.

The paralysis of the laryngeal folds can greatly hinder the airflow of oxygen into the lungs of the puppy. A tell-tale sign of laryngeal paralysis is a wheezing or honking noise when the dog attempts to breathe rapidly. In most cases, this disorder is caused by trauma but can develop in dogs as they age.

Heart disease

The heart’s main role in the body is to pump healthy, oxygenated blood in circulation. A disturbance in this system results in heart disease, to rope all the potential conditions under one term.

Some more specific terms can include dilated cardiomyopathy, hypertrophic cardiomyopathy, pericardial effusion, and valve disease. Without oxygen flowing appropriately due to an issue with the heart, your puppy may begin to breathe heavier or more rapidly to compensate.

Respiratory disease

Sometimes, bacteria, fungi, and viruses attack the lungs and make it difficult for the puppy to breathe as the body works hard to clear the foreign infection. If the infection clings to the lung tissue, it can make it increasingly difficult for your dog to get the correct amount of oxygen.

Vaccines are available to prevent contagious illnesses, such as kennel cough. It can inflame the trachea and produce a dry and painful cough that originates in the lungs. This problem is common when a large number of dogs are kept together, such as in a boarding facility or kennel. However, experts have learned that the most common respiratory disease is pneumonia and requires hospitalization.

Pain

Even as humans, when we feel pain our breathing rate can drastically change. Pain can come in many different forms and dogs will use their breathing pattern to regulate their nervous system. This breathing pattern may look quicker or they will take bigger breaths with more depth.

Overheating

The most extreme form of overheating can lead to heatstroke. When a dog is trying to cool itself down, their breathing will be rapid to aid in dropping their internal temperature. Dogs cannot sweat like humans do, so their cooling system is directly correlated to their breathing.

Experts tell us that it is not safe to keep pets outdoors above the temperature of 90 degrees Fahrenheit. If you live in a hot climate, it is best practice to ensure that your dog has a cool, safe place to regulate their body temperature.

Do not let becoming familiar with the systemic diseases that can affect your pet’s respiratory effort and rate intimidate you. If you still feel that you need further support and guidance, do not hesitate to set up a meeting with a veterinary professional.

When to Contact Your Vet

Your veterinarian is always going to be willing to address any concerns you have as a new puppy owner. Your pup will go through a series of vaccines that have to be bolstered early in on their lives. This is an ideal opportunity for you to regularly observe their breathing and address your concerns with your vet.

Familiarize yourself with emergent situations when it comes to your puppy’s breathing so you can assess the situation if the puppy is breathing fast or too slow. Contact your vet if you notice that their gums are bright red, white, or blue, if they have a decreased appetite, if they are exercise intolerant, or if their mouth is gaping open while breathing. A veterinarian will be able to perform further diagnostics to get to the bottom of any underlying health issue that may be a cause for concern.


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There are ways to lessen stress gradually, such as improving your sleep routine, exercising, and monitoring caffeine and sugar intake. They form an excellent foundation for long-term health. 

But there are challenging moments, days, and weeks when our cortisol is running higher than we’d like. Very often this can be brought on by larger external events out of our control, like work or health stresses, and other times, it’s about our reaction to smaller-scale triggers, like having a familiar argument with a friend or partner. 

Or a trigger can take you by surprise. One minute you are perfectly calm, and the next, maybe an interaction with a stranger at the supermarket, on the highway, or on social media sends you into a tailspin. Usually these are a sign that the event is echoing a previous upset your brain tagged as traumatic, perhaps one from childhood. It can even be a sound, a scent, or a visual cue you may not be consciously aware of. These are well worth unpacking later, but not right now.

Regardless of the cause, your goat has been gotten. You went from zero to 90 with the speed of a Ferrari, and if you are lucky, you notice it before saying or doing something you’ll regret.

NOTICE YOUR STRESS

How can you tell if your fight-flight-freeze system has been activated? There are some telltale signs that to watch for, or perhaps we should say feel for. They’ll be different if you are leaning more towards “flight” or “fight,” both more active modes, or “freeze,” a shutting-down and hiding response. Sense how your body feels and try to name any emotions you are having. Noticing these may take a little practice.

Please note that I’m not recommending ignoring your body’s fear response. This isn’t about repressing your feelings and “getting through,” but recognizing and acknowledging them and calming down to achieve a better situation. If you feel truly overwhelmed or unsafe, make your excuses and take the time to take care of yourself.

PHYSICAL SIGNS

• Your heart is beating faster

• Your breath is shallow

• Your eyes are darting around the room

• You feel a queasiness in your gut, energy in your legs or butterflies in your chest

• Your hands are clenching into fists, a knot in your chest, and your jaw is tightening

• You are rubbing your temples or shoulders, hugging your chest, or contracting your body position by slumping

EMOTIONAL SIGNS

• Feeling angry and amped-up, ready to argue or defend – “fight”

•Feeling scared and ready to run – “flight”

• Feeling overwhelmed and sad – “freeze”

GETTING TO CALM

Here are some techniques to bring your central nervous system back into its “rest and digest” mode, from sympathetic to parasympathetic.

1. Deeper breaths.

Anything slower than your current rate is a help. Six seconds in and out is great to shoot for, but longer exhales than inhales cue the body to relax.

Some specific techniques to try include:

• Box breathing: Inhale 4 seconds (say “one-one thousand”), hold 4, exhale 4, hold 4.

• 4-7-8 breathing: Inhale 4, hold 7, exhale 8.

• Breathe in for 6 seconds, out for 6 seconds.

2. Moving

When a gazelle evades a lion, what does it do? It shakes. This is a common trauma release response in the animal kingdom. I’ve seen dog trainers recommend that if your reactive dog meets another on the street, it’s better to walk them in a circle (or away) than to let them sit staring at the other dog. The action both interrupts the body’s involuntary stress response and once finished, your body sends a relaxation message to your muscles.

It may feel silly until you try it. Bounce on your heels, get your arms involved – you’ll feel much better. If you’re in a boardroom or other public situation, shake out your hands as if you just washed them, roll your head, take a walk around the room.

3. Body cues

• Hug yourself – wrap your arms around yourself, on your arms, shoulders or neck tells the body you are safe and loved. You may find yourself doing this already.

Feel your feet on the ground. Sometimes stress can make us feel like we are not really here – like we are observing ourselves. Get back into your body, feel your feet on the floor, your legs on the chair, notice your breathing.

• The 5-4-3-2-1 Technique: This is a grounding technique to keep you in the present moment. Identify 5 things you can see, 4 things you can touch, 3 things you can hear, 2 things you can smell, and 1 thing you can taste.

See which of these you like the best. Try some of these yourself the next time you feel yourself getting upset, and you’ll feel better in no time.



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Cars move along an S-curved freewayShare on Pinterest
Experts say air pollution can affect people who live near freeways. Amos Chapple/Stocksy
  • Traffic-related air pollution was associated with a significant increase in blood pressure among car passengers, a study finds.
  • Researchers report that the blood pressure increase is on par with other cardiovascular risk factors such as lack of exercise or excessive salt intake.
  • Experts note that cabin air filters and other filtration devices, including masks, can lower exposure to dangerous air pollution particles.

People wearing masks while driving alone in their cars may not be so foolish after all.

The N95 masks used to help prevent the spread of COVID-19 might also filter out highway air pollution that a new study says can cause a serious and sustained spike in blood pressure.

The study, published in the Annals of Internal Medicine, reports that riding in automobiles and breathing unfiltered air was associated with a 4.5 mm Hg increase in blood pressure.

The blood pressure increase from exposure to traffic-related air pollution (TRAP) was found to peak within 60 minutes and persist for up to 24 hours, according to the researchers from the University of Washington.

“Traffic-related air pollution, even at levels now considered low, appears to cause a substantial increase in blood pressure,” Dr. Joel Kaufman, a study corresponding editor and a University of Washington professor, epidemiologist, and environmental health expert, told Medical News Today. “This is an effect of breathing traffic-related particles, since it was not from the stress of being in a car, driving a car, or noise; the study design is able to account for all those things by using sham filtration vs real filtration, and the subjects were passengers and not drivers.”

“It was stunning how quickly this led to a rise in blood pressure and that it persisted for so long,” Dr. John Higgins, a sports cardiologist at the McGovern Medical School at UTHealth in Houston who was not involved in the study, told Medical News Today. “Maybe we need to think about high efficiency particulate air (HEPA) filters in automobiles or cities doing something about air pollution.”

The study findings suggest that daily commuters breathing unfiltered highway air pollution could be experiencing dangerously elevated blood pressure throughout the workweek and perhaps even more if they drive on the weekends as well, said Higgins.

“Our group has previously showed that diesel exhaust exposure increased blood pressure,” said Kaufman. “The roadway traffic study was designed to test those findings in a real-world setting by isolating the effects of traffic-related air pollution (TRAP).”

TRAP may include ultrafine particles known as PM 2.5, black carbon, oxides of nitrogen, carbon monoxide, carbon dioxide, and other particulate matter.

According to the Environmental Protection Agency (EPA), past studies have suggested that PM 2.5 particles are linked to a wide range of cardiovascular problems, including heart attacks, irregular heartbeat, asthma and other breathing problems, and premature death.

“PM 2.5 particles can get through the lining of blood vessels and into the circulatory system, affecting the heart and vascular tone, including arterial stiffness,” Dr. Loren Wold, a researcher and professor at The Ohio State University Wexner Medical Center who studies the cardiovascular effects of air pollution who wasn’t involved in the study, told Medical News Today. “That’s what causes elevated blood pressure.”

In the experimental study, researchers drove 16 subjects ages 22 to 45 years of age through traffic in Seattle, Washington, for three days.

For two days, unfiltered air was allowed to flow into the vehicle. On the third, a HEPA filter was installed.

Study subjects did not know whether the car had a HEPA filter — which can screen out dangerous PM 2.5 particles along with other pollutants — or an ineffective sham filter.

Blood pressure was monitored up to 24 hours before, during, and after the drives.

Kaufman and his colleagues said they found that the drives in vehicles with unfiltered TRAP were associated with significant net increases in blood pressure compared with drives with HEPA in-vehicle filtration.

The 4.5 mm Hg rise in blood pressure detected was significant, researchers said. For every 20 mm Hg systolic or 10 mm Hg diastolic increase in blood pressure, mortality from heart disease and stroke doubles.

Higgins said the TRAP-related blood pressure increase detected in the study was similar to that caused by poor diet, lack of activity, or smoking.

“These are the size of effects from things like salt in the diet that are well-known to increase blood pressure,” said Kaufman. “Elevated blood pressures are major risk factors for heart disease, stroke, and kidney disease. The concern is partly for each individual, but [also the impact on the whole population. The overall effect of millions of people having these exposures is probably a lot of otherwise preventable cases of stroke, heart attacks, heart failure, and kidney disease.”

The study also demonstrated that the effects of air pollution on blood pressure may be reduced with effective cabin air filtration, Kaufman said.

However, most cars are not equipped with HEPA filters, nor are such passenger cabin air filters available for every make and model of automobile.

“Regular filters don’t work that well in the car, as you can tell when you can smell the exhaust from another vehicle with a bad muffler on the road,” noted Higgins.

“A good practice is to change the cabin air filter in your car just like you do the in-house filter on your furnace,” about once a year, said Wold.

Wold said that while a HEPA cabin air filter would be ideal, even a regular filter can eliminate some PM 2.5 sized particles, especially if the car’s climate control system is set to recirculate cabin air rather than bringing in air from outside the vehicle.

And yes, wearing an N95 mask while driving can also filter out PM 2.5 air pollution particles as well as preventing the spread of communicable diseases such as COVID-19.

The study also highlights the potential health risks of TRAP exposure among people other than automobile drivers or passengers, such as those who live close to highways, factories, or airports, said Kaufman.

Dr. Edo Paz, a cardiologist and senior medical vice president of medical affairs at the online cardiovascular health company Hello Heart, told Medical News Today that there is “some clinical evidence that air filtration in indoor environments is associated with decreases in blood pressure within two weeks.”

Wold said that homeowners in communities with high levels of TRAP can increase the efficiency of their furnace HEPA filters by setting the system to circulate air every 15 minutes or so, rather than turning on the blower only when the heat or air conditioning comes on.

“Any smart thermostat should allow you to set your system on continuous circulation,” he said.

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It will come as no surprise to anyone who braves I-5 on a weekday at either 8 a.m. or 5 p.m. (or practically anytime in between) that your blood pressure tends to increase during sudden slowdowns and bumper-to-bumper backups.

But a new study suggests that it’s not just the Tesla changing lanes without using a directional that is causing your heart to pound. Ultrafine particles circulating on and near congested freeways — a toxic mixture of exhaust from tailpipes, brake and tire wear, and road dust — increases blood pressure, which could lead to other health problems.

“We are beginning to believe that it's these really tiny particles that are responsible for health effects,” explained lead researcher Joel Kaufman, a University of Washington physician and professor of environmental and occupational health sciences. “It's not just being in a car, it's the people who live near roadways that have the same exposures.”

Kaufman and his team drove healthy young people between the ages of 22 and 45 through rush-hour traffic in Seattle while monitoring their blood pressure. On some of the drives, unfiltered air was allowed to enter the car. On other drives, the car was equipped with a high-quality HEPA air filter, which blocked 86% of particulate pollution.

The study used “sham filters” in some drives and real filters in others, so study participants and their drivers didn’t know whether the air was filtered or not.

Researchers found that breathing unfiltered air in the car caused blood pressure increases of 4.5 millimeters of mercury compared to passengers riding in the car with filtered air.


caption: Tailpipe exhaust is the leading cause of greenhouse gas emissions in Washington state and nationwide.

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The effect is equivalent to someone eating a high-sodium diet, and the increased blood pressure lasted for at least 24 hours after the rush-hour drive in a car with unfiltered air.

A blood-pressure increase of five points might not sound like much, but Kaufman said the impact should be weighed in terms of the number of people affected, potentially people who already have high blood pressure or other health issues.

“We know that modest increases in blood pressure like this, on a population level, are associated with a significant increase in cardiovascular disease,” Kaufman said. “There is a growing understanding that air pollution contributes to heart problems. The idea that roadway air pollution at relatively low levels can affect blood pressure this much is an important piece of the puzzle we’re trying to solve.”

A previous experiment by Kaufman’s lab found that exposure to diesel exhaust fumes increased blood pressure in a controlled environment. This new study, published Tuesday in the Annals of Internal Medicine, was designed to test that earlier finding in a real-world setting by isolating the effects of traffic-related air pollution.

The research was funded by the U.S. Environmental Protection Agency and the National Institutes of Health.


caption: Rush hour traffic is shown along the Alaskan Way Viaduct on Wednesday, January 9, 2019, in Seattle.

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Kaufman, who has worked at the University of Washington since 1997, said the number of ultrafine particles inside unfiltered cars was striking — tens of thousands of particles per cubic centimeter. Those numbers were reduced dramatically by high-quality filtration.

The findings add to growing concerns among public health experts about ultrafine particles, which are less than 100 nanometers in diameter and much too small to be seen. The microscopic particles are unregulated and may pose health risks, even at low levels.

Michael Young, a former postdoctoral fellow in the University of Washington's Department of Environmental and Occupational Health Sciences and lead author of the new study, said the study's design overcame common obstacles to effectively measuring the impact of traffic-related air pollution.

"Studies on this topic often have a challenging time separating the effects of pollution from other roadway exposures like stress and noise, but with our approach, the only difference between drive days was air pollution concentration,” Young said in a press release. “The findings are valuable because they can reproduce situations that millions of people actually experience every day.”

Kaufman said the findings have reinforced his own tendencies when he finds himself driving in heavy traffic in and around Seattle, and have led him to make sure he has a high-quality air filter in his car.

“When I drive, I keep my windows up and my car on recirculate,” he said.

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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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traffic pollution
Credit: Unsplash/CC0 Public Domain

For more than a century, American cities have been sliced and diced by high-traffic roadways. Interstate highways and wide arterials are now a defining feature of most metropolitan areas, their constant flow of cars spewing pollution into nearby neighborhoods.

Researchers have only just begun to understand the health risks posed by all that pollution. Long-term exposure to traffic-related air pollution—a complex mixture of exhaust from tailpipes, brake and tire wear, and road dust—has been linked to increased rates of cardiovascular disease, asthma, lung cancer and death.

New research from the University of Washington suggests those health risks are also seen in people traveling busy roads. A study published Nov. 28 in the Annals of Internal Medicine found that unfiltered air from rush-hour traffic significantly increased passengers' blood pressure, both while in the car and up to 24 hours later.

"The body has a complex set of systems to try to keep blood pressure to your brain the same all the time. It's a very complex, tightly regulated system, and it appears that somewhere, in one of those mechanisms, traffic-related air pollution interferes with blood pressure," said Joel Kaufman, a UW physician and professor of environmental and occupational health sciences who led the study.

An earlier experiment by Kaufman's lab found that exposure to diesel exhaust fumes increased blood pressure in a controlled environment. The roadway traffic study was designed to test that finding in a real-world setting by isolating the effects of traffic-related air pollution.

Researchers drove healthy participants between the ages of 22 and 45 through rush-hour Seattle traffic while monitoring their blood pressure. On two of the drives, unfiltered road air was allowed to enter the car, mirroring how many of us drive. On the third, the car was equipped with high-quality HEPA filters that blocked out 86% of particulate pollution. Participants did not know whether they were on a clean air drive or a roadway air drive.

Breathing unfiltered air resulted in net blood pressure increases of more than 4.50 mm Hg (millimeters of mercury) when compared to drives with filtered air. The increase occurred rapidly, peaking about an hour into the drive and holding steady for at least 24 hours. Researchers did not test past the 24-hour mark.

The size of the increase is comparable to the effect of a high-sodium diet.

"We know that modest increases in blood pressure like this, on a population level, are associated with a significant increase in cardiovascular disease," Kaufman said. "There is a growing understanding that air pollution contributes to heart problems. The idea that roadway air pollution at relatively low levels can affect blood pressure this much is an important piece of the puzzle we're trying to solve."

The findings also raise questions about ultrafine particles, an unregulated and little-understood pollutant that has become a source of growing concern among public health experts. Ultrafine particles are less than 100 nanometers in diameter, much too small to be seen. Traffic-related air pollution contains high concentrations of ultrafine particles. In the study, unfiltered air contained high levels of ultrafine particles, though the overall level of pollution as measured by fine particle concentration (PM 2.5) was relatively low, equivalent to an AQI of 36.

"Ultrafine particles are the pollutant that were most effectively filtered in our experiment—in other words, where the levels are most dramatically high on the road and low in the filtered environment," Kaufman said. "So, the hint is that ultrafines may be especially important [for blood pressure]. To actually prove that requires further research, but this study provides a very strong clue as to what's going on."

Traffic-related air pollution is the main cause of air quality variation from community to community in most U.S. metropolitan areas.

"This study is exciting because it takes the gold-standard design for laboratory studies and applies it in an on-roadway setting, answering an important question about the health effects of real-world exposures. Studies on this topic often have a challenging time separating the effects of pollution from other roadway exposures like stress and noise, but with our approach the only difference between drive days was air pollution concentration," said Michael Young, a former UW postdoctoral fellow in the Department of Environmental and Occupational Health Sciences and lead author of the new study. "The findings are valuable because they can reproduce situations that millions of people actually experience every day."

More information:
Blood Pressure Effect of Traffic-Related Air Pollution, Annals of Internal Medicine (2023). DOI: 10.7326/M23-1309

Citation:
Breathing highway air increases blood pressure, research finds (2023, November 27)
retrieved 28 November 2023
from medicalxpress.com/news/2023-11-unfiltered-traffic-related-air-significant-blood.html

This document is subject to copyright. Apart from any fair dealing for the purpose of private study or research, no
part may be reproduced without the written permission. The content is provided for information purposes only.



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Newswise — For more than a century, American cities have been sliced and diced by high-traffic roadways. Interstate highways and wide arterials are now a defining feature of most metropolitan areas, their constant flow of cars spewing pollution into nearby neighborhoods.  

Researchers have only just begun to understand the health risks posed by all that pollution. Long-term exposure to traffic-related air pollution — a complex mixture of exhaust from tailpipes, brake and tire wear, and road dust — has been linked to increased rates of cardiovascular disease, asthma, lung cancer and death.  

New research from the University of Washington suggests those health risks are also seen in people traveling busy roads. A study published Nov. 28 in the Annals of Internal Medicine found that unfiltered air from rush-hour traffic significantly increased passengers’ blood pressure, both while in the car and up to 24 hours later. 

“The body has a complex set of systems to try to keep blood pressure to your brain the same all the time. It’s a very complex, tightly regulated system, and it appears that somewhere, in one of those mechanisms, traffic-related air pollution interferes with blood pressure," said Joel Kaufman, a UW physician and professor of environmental and occupational health sciences who led the study.  

An earlier experiment by Kaufman’s lab found that exposure to diesel exhaust fumes increased blood pressure in a controlled environment. The roadway traffic study was designed to test that finding in a real-world setting by isolating the effects of traffic-related air pollution. 

Researchers drove healthy participants between the ages of 22 and 45 through rush-hour Seattle traffic while monitoring their blood pressure. On two of the drives, unfiltered road air was allowed to enter the car, mirroring how many of us drive. On the third, the car was equipped with high-quality HEPA filters that blocked out 86% of particulate pollution. Participants did not know whether they were on a clean air drive or a roadway air drive. 

Breathing unfiltered air resulted in net blood pressure increases of more than 4.50 mm Hg (millimeters of mercury) when compared to drives with filtered air. The increase occurred rapidly, peaking about an hour into the drive and holding steady for at least 24 hours. Researchers did not test past the 24-hour mark.  

The size of the increase is comparable to the effect of a high-sodium diet. 

“We know that modest increases in blood pressure like this, on a population level, are associated with a significant increase in cardiovascular disease,” Kaufman said. “There is a growing understanding that air pollution contributes to heart problems. The idea that roadway air pollution at relatively low levels can affect blood pressure this much is an important piece of the puzzle we’re trying to solve.” 

The findings also raise questions about ultrafine particles, an unregulated and little-understood pollutant that has become a source of growing concern among public health experts. Ultrafine particles are less than 100 nanometers in diameter, much too small to be seen. Traffic-related air pollution contains high concentrations of ultrafine particles. In the study, unfiltered air contained high levels of ultrafine particles, though the overall level of pollution as measured by fine particle concentration (PM 2.5) was relatively low, equivalent to an AQI of 36.  

"Ultrafine particles are the pollutant that were most effectively filtered in our experiment – in other words, where the levels are most dramatically high on the road and low in the filtered environment,” Kaufman said. “So, the hint is that ultrafines may be especially important [for blood pressure]. To actually prove that requires further research, but this study provides a very strong clue as to what’s going on.” 

Traffic-related air pollution is the main cause of air quality variation from community to community in most U.S. metropolitan areas. 

“This study is exciting because it takes the gold-standard design for laboratory studies and applies it in an on-roadway setting, answering an important question about the health effects of real-world exposures. Studies on this topic often have a challenging time separating the effects of pollution from other roadway exposures like stress and noise, but with our approach the only difference between drive days was air pollution concentration,” said Michael Young, a former UW postdoctoral fellow in the Department of Environmental and Occupational Health Sciences and lead author of the new study. "The findings are valuable because they can reproduce situations that millions of people actually experience every day.” 

This research was funded by the U.S. Environmental Protection Agency and the National Institutes of Health.  

Other authors are Karen Jansen, Kristen Cosselman, James Stewart, Timothy Larson, Coralynn Sack and Sverre Vedal of the UW Department of Environmental and Occupational Health Sciences; Timothy Gould of the UW Department of Civil and Environmental Engineering; and Adam Szpiro of the Department of Biostatistics. 



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It’s a well-known fact that sport not only helps us maintain physical fitness but also brings multiple mental benefits. From a scientific standpoint, physical activity increases our dopamine, endorphin, serotonin, and oxytocin levels. That is why doing sport regularly can help us feel happy, clear our thoughts, and reset to zero.

Although moderate exercise is beneficial for everyone, it’s especially important for executives and business owners. This is because the physical and mental state of both the CEO and the team always affects the overall business progress. Shania Brenson, the CEO of 15M Finance, shares her experience of getting stress relief and preventing anxiety and depression by… simply playing golf!

Who Is Shania Brenson?

Shania Brenson is the CEO of 15M Finance, the company that specializes in emergency financial assistance for underserved people and communities. She earned a degree in economics and accounting from Texas State University and now uses her knowledge and years of experience in lending to help people improve their financial lives.

As a CEO and co-founder, Shania handles multiple day-to-day tasks and activities. In addition to developing business and content strategies, market analysis, and searching for new business opportunities and potentials, she communicates with customers directly to identify their pain points. Also, Shania constantly interacts with her team and is actively involved in all business processes. With so many fields to pay attention to, she finally found herself not knowing how to relax and switch over some time. This resulted in chronic fatigue and anxiety. Then, she began to learn more about practical ways to improve her mental shape.

Smart Ways to Relieve Stress and Anxiety from Shania Brenson

It’s impossible to always be on top of your productivity. To avoid professional burnout and make the most of your best self, you need to learn how to rest and relax. It took Shania Brenson several months to create the list of clever stress-relief ideas that really work. Here are a few of them.

Place Yourself in a Relaxing Ambiance

The atmosphere you’re in is very important. Even if your mind is not occupied with work 24/7 and you are completely relaxed, a noisy and hectic environment can tire you out very quickly. Find a restaurant where you can feel relaxed or create a cozy ambiance in your home to make sure you will be able to rest properly. Use candles, garlands, soft blankets, and anything else that relaxes you and gives you a feeling of comfort.

Plan Your “Me Time”

In our fast-paced world, it may be difficult to unplug when you’re always involved in multiple business activities. If you’re always forced to stick to a schedule, the best way to make time for rest is to put your “me time” in it. Make it a priority, and be sure to take at least a few hours a day for yourself and your hobbies.

Keep Your Hands Busy

Doing something with your hands is a great way to clear your thoughts. Try cooking, knitting, building Lego or room boxes, or any other activity that seems interesting to you and requires your concentration. When you’re focused on something you do with your hands, your brain switches and downshifts. It can also help you boost creativity and, well, bring more joy into your life.

Take Three Deep Breaths

It may sound trivial, but it is a very useful practice. Taking deep, slow breaths helps improve focus and reduce stress. This is because proper breathing techniques contribute to a better oxygen supply to the brain. Moreover, the moment you breathe deeply, you can focus on yourself and your current state. Ask yourself how you feel at a particular moment. Perhaps you are tired and need a break.

Try Meditating

Meditation can help you find inner balance and relax. With its help, you can achieve positive physiological changes. This will result in slower breathing, lower blood pressure, a feeling of calm, and improved sleep quality.

Be Your Own VIP Client

Executives often forget that not only their VIP clients need special treatment. First of all, you’re your own VIP client. Keep track of your current physical and mental shape, don’t work at night, and respect yourself the same way you respect your customers and partners.

Hire an Assistant

Finally, you can always delegate some of your daily routine tasks to an assistant. Although there are matters that only an executive can solve, an assistant can monitor your schedule, answer calls, deal with correspondence, and carry out other small tasks that take up time and distract you from your main duties.

Make Sport a Habit

Doing sports changes us from the inside. After physical activity, the chemical composition of your blood changes. Thus, you’re technically no longer the same person you were before. Sport changes your attitude to life. It allows you to release tension and negative emotions, relax, clear your thoughts, and unplug.

How Golf Helps Shania Unplug and Relax

Shania Brenson says golf is still one of her favorite types of physical activity. This is because it doesn’t require enormous physical endurance and is simply fun. Although Shania shows good results in golf after years of practice, she doesn’t think about a professional golf career. This is because it will cease to be a stress-relief hobby as soon as it turns into a job. Here’s how golf helps Shania unplug.

Reduces Anxiety and Risks of Depression

Like with any other form of physical activity, golf contributes to your future well-being and changes your attitude to life. Moreover, if you play outdoors, it further stimulates your brain to fight anxiety and depression while you’re just moving around on the golf course.

Provides More Social Interaction

Most of us need to be in society because we are social creatures. However, the older we get and the more work we have, the harder it is to find time to socialize. Golf can be a fun way to overcome social isolation and start communicating with people on topics other than work.

Helps Practice Patience and Discipline

If your brain is constantly on overdrive, quickly switching between multiple tasks, golf can be a great practice for slowing down. This is because it requires discipline and patience. Golf is also about learning new things that you can apply in both your regular life and business. For some, it can be a way to become a better leader.

It’s Just Funny

The more you play golf, the better you get at it. And that’s how it works. We always enjoy doing the things we’re good at. Thus, you may need some time to find out whether the activity you choose suits you. Shania says golf wasn’t her love at first glance. She found a passion for it after she mastered the basics.

How to Find the Right Hobby for a CEO?

Before making golf her number one stress relief activity, Shania tried many different things. Dancing, jumping, yoga on hammocks, equestrianism, and martial arts are just a small part of her list of ways to combat stress. Shania believes that the best thing you can do to find a hobby you like is to start trying something new. It’s just that simple! However, you never know until you try. Just listen to your heart. Think about what you like to do and try to transform it into a hobby. You can also appeal to your childhood desires and interests.

Bottom Line

If you’re a CEO or a small business owner, physical activities should always be a part of your weekly schedule. This is because exercises help us unplug, reduce stress and anxiety, and change the way we look at things. If you’re looking for an activity that suits you, golf may be one of the possible options. This sport doesn’t involve vigorous exercise at a high heart rate, is suitable for people of any age, and doesn’t require a certain level of physical fitness to begin.

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When choosing a sports watch, there are some features that should not be missing. For example, the presence of GPS is essential if you like to train outdoors. Garmin knows a lot about this and that is why it has one of the best smartwatches for athletes at the best price.

Up to 18 days of battery

This Garmin Fenix ​​7X Solar is one of the best sports watches. You will be able to record your heart rate, breathing, stress level and sleep patterns. It also has Heath SnapShot, which is a function that gives you a detailed analysis of how you are doing in two minutes.

If you’re wondering how durable it is, the truth is that it meets all US military standards for durability. shock and water resistance. It has a 1.4-inch screen that is visible even if the sun’s rays reflect directly on it. It also has premium materials, such as stainless steel finishes, reinforced glass and PVD. It is a watch that adapts to all types of lifestyles.

The Garmin Fenix ​​7X Solar is famous for having several training modes, including high intensity, so you can set up different rounds, intervals, and custom workouts. In addition, you can download maps so you don’t need to carry your cell phone with you. The best thing is that it has a connection Wifi to update maps directly from the watch.

As if that were not enough, it will catch your attention that it has a solar charging lens to extend battery life. It can last up to 18 days of use in perfect conditions. It even plays in his favor that he has 16GB storage so you can download applications like Spotify to listen to music directly from your smartwatch.

Of course, it also has Bluetooth so you can pair it with your cell phone or headphones wirelessly. It has a special app so you can upload all your training data and have a detailed record of everything you have done during the day. It is perfect!

Save almost 300 euros

MediaMarkt is sweeping this Cyber ​​Week with crazy prices. This brutal Garmin watch has never had such a low price before. With an incredible 29% discount, its price drops from 849 to 599 euros. The savings are more than considerable taking into account the high-end features and the fact that it is postulated as one of the most brutal sports watches.

Luckily, at MediaMarkt they have free shipping and fast delivery in less than 24 hours. You won’t have time to be impatient and it will arrive just in time for your Christmas gifts. You also have the possibility of picking it up at your nearest store if you prefer a more flexible delivery.

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