Pulmonology

Individuals with asthma and chronic obstructive pulmonary disease (COPD) were more vulnerable than healthy controls to epithelial cell changes caused by microplastics exposure, based on data from a new simulation study.

Microplastic fibers present in the ambient air can be inhaled into the lungs and promote a range of complications including oxidative stress, local injury, and cytotoxicity, but data on the effects of microplastic fibers on individuals with obstructive lung diseases are limited, wrote Magdalena Poplinska-Goryca, MD, of the Medical University of Warsaw, Warsaw, Poland, and colleagues. 

In a study published in Scientific Reports, the researchers identified 10 adults aged ≥ 18 years with asthma, eight adults aged ≥ 40 years with COPD, and 11 healthy adult controls. Individuals with more serious conditions such as severe asthma or COPD, unstable or uncontrolled disease, concomitant malignancies, or chronic or acute lung disease were excluded.

The researchers obtained nasal epithelial cells from all participants, and exposed these cells to microplastic fibers created by the researchers in a laboratory setting. Overall, asthmatic and COPD airway epithelial cells showed a different reaction to microplastic fibers stimulation compared to healthy epithelial cells. The most significant response was associated with Th2 inflammation, modulation of stress response, and carcinogenesis. No differences in cytotoxic or minor inflammatory effects on epithelial cells of patients with asthma or COPD were noted compared with healthy controls. 

In addition, flow cytometric analysis showed increased CD24+ epithelial cells in asthma patients compared to controls after microplastics exposure.

“Many of the gene candidates selected from RNA-Seq analysis are related to cancer (upregulated in many cancer types according to the literature), and the activation of CD24 on primarily ciliated asthmatic epithelial cells after microplastic stimulation further supports this theory,” the researchers wrote.

The findings were limited by several factors including the use of nasal rather than bronchial epithelial cells, which would have yielded more information, the researchers noted. Also, patients with severe asthma and COPD were excluded, they said, because of the impact of oral steroid and antibiotic use by this patient group on epithelial cell immunology that could bias the results of epithelial response to microplastic fiber exposure.

However, the results suggest that “the structural impairment of the airway epithelium in obstructive diseases enhances the impact of microplastic particles compared to healthy epithelium,” the researchers concluded.

 

Current and Future Implications

The current study is important in addressing the increasing environmental presence of microplastics and their potential impact on respiratory health, said Seyedmohammad Pourshahid, MD, assistant professor of thoracic medicine and surgery at the Lewis Katz School of Medicine at Temple University, Philadelphia, in an interview.

“By examining how microplastics interact with airway epithelial cells, particularly in individuals with asthma and COPD, the research aims to elucidate mechanisms that could contribute to disease progression or exacerbation,” he said. 

“The study’s findings that microplastics did not induce a strong inflammatory response, unlike other pollutants such as PM2.5, were unexpected; instead, microplastics appeared to influence pathways related to airway remodeling and oxidative stress,” Pourshahid noted. “This suggests that microplastics may affect respiratory health through mechanisms distinct from traditional pollutants,” he said.

“While preliminary, this research highlights the potential role of environmental microplastic exposure in respiratory diseases,” Pourshahid told this news organization. “Clinicians should be aware of emerging environmental factors that could impact patient health, especially in individuals with asthma and COPD. This awareness may inform patient education and advocacy for reducing exposure to airborne microplastics,” he said.

More studies are needed to explore the long-term effects of microplastic exposure on respiratory health, particularly in vulnerable populations, said Pourshahid. Research with in vivo models is necessary to confirm the findings and assess potential clinical implications to confirm these findings and assess potential clinical implications, he said. “Understanding the prevalence and sources of daily microplastic exposure can inform public health strategies to mitigate risks,” he added.

The study was supported by the Jakub Potocki Foundation. Paplińska-Goryca and Pourshahid had no financial conflicts to disclose.

A version of this article first appeared on Medscape.com.

Individuals with asthma and chronic obstructive pulmonary disease (COPD) were more vulnerable than healthy controls to epithelial cell changes caused by microplastics exposure, based on data from a new simulation study.

Microplastic fibers present in the ambient air can be inhaled into the lungs and promote a range of complications including oxidative stress, local injury, and cytotoxicity, but data on the effects of microplastic fibers on individuals with obstructive lung diseases are limited, wrote Magdalena Poplinska-Goryca, MD, of the Medical University of Warsaw, Warsaw, Poland, and colleagues. 

In a study published in Scientific Reports, the researchers identified 10 adults aged ≥ 18 years with asthma, eight adults aged ≥ 40 years with COPD, and 11 healthy adult controls. Individuals with more serious conditions such as severe asthma or COPD, unstable or uncontrolled disease, concomitant malignancies, or chronic or acute lung disease were excluded.

The researchers obtained nasal epithelial cells from all participants, and exposed these cells to microplastic fibers created by the researchers in a laboratory setting. Overall, asthmatic and COPD airway epithelial cells showed a different reaction to microplastic fibers stimulation compared to healthy epithelial cells. The most significant response was associated with Th2 inflammation, modulation of stress response, and carcinogenesis. No differences in cytotoxic or minor inflammatory effects on epithelial cells of patients with asthma or COPD were noted compared with healthy controls. 

In addition, flow cytometric analysis showed increased CD24+ epithelial cells in asthma patients compared to controls after microplastics exposure.

“Many of the gene candidates selected from RNA-Seq analysis are related to cancer (upregulated in many cancer types according to the literature), and the activation of CD24 on primarily ciliated asthmatic epithelial cells after microplastic stimulation further supports this theory,” the researchers wrote.

The findings were limited by several factors including the use of nasal rather than bronchial epithelial cells, which would have yielded more information, the researchers noted. Also, patients with severe asthma and COPD were excluded, they said, because of the impact of oral steroid and antibiotic use by this patient group on epithelial cell immunology that could bias the results of epithelial response to microplastic fiber exposure.

However, the results suggest that “the structural impairment of the airway epithelium in obstructive diseases enhances the impact of microplastic particles compared to healthy epithelium,” the researchers concluded.

 

Current and Future Implications

The current study is important in addressing the increasing environmental presence of microplastics and their potential impact on respiratory health, said Seyedmohammad Pourshahid, MD, assistant professor of thoracic medicine and surgery at the Lewis Katz School of Medicine at Temple University, Philadelphia, in an interview.

“By examining how microplastics interact with airway epithelial cells, particularly in individuals with asthma and COPD, the research aims to elucidate mechanisms that could contribute to disease progression or exacerbation,” he said. 

“The study’s findings that microplastics did not induce a strong inflammatory response, unlike other pollutants such as PM2.5, were unexpected; instead, microplastics appeared to influence pathways related to airway remodeling and oxidative stress,” Pourshahid noted. “This suggests that microplastics may affect respiratory health through mechanisms distinct from traditional pollutants,” he said.

“While preliminary, this research highlights the potential role of environmental microplastic exposure in respiratory diseases,” Pourshahid told this news organization. “Clinicians should be aware of emerging environmental factors that could impact patient health, especially in individuals with asthma and COPD. This awareness may inform patient education and advocacy for reducing exposure to airborne microplastics,” he said.

More studies are needed to explore the long-term effects of microplastic exposure on respiratory health, particularly in vulnerable populations, said Pourshahid. Research with in vivo models is necessary to confirm the findings and assess potential clinical implications to confirm these findings and assess potential clinical implications, he said. “Understanding the prevalence and sources of daily microplastic exposure can inform public health strategies to mitigate risks,” he added.

The study was supported by the Jakub Potocki Foundation. Paplińska-Goryca and Pourshahid had no financial conflicts to disclose.

A version of this article first appeared on Medscape.com.

Individuals with asthma and chronic obstructive pulmonary disease (COPD) were more vulnerable than healthy controls to epithelial cell changes caused by microplastics exposure, based on data from a new simulation study.

Microplastic fibers present in the ambient air can be inhaled into the lungs and promote a range of complications including oxidative stress, local injury, and cytotoxicity, but data on the effects of microplastic fibers on individuals with obstructive lung diseases are limited, wrote Magdalena Poplinska-Goryca, MD, of the Medical University of Warsaw, Warsaw, Poland, and colleagues. 

In a study published in Scientific Reports, the researchers identified 10 adults aged ≥ 18 years with asthma, eight adults aged ≥ 40 years with COPD, and 11 healthy adult controls. Individuals with more serious conditions such as severe asthma or COPD, unstable or uncontrolled disease, concomitant malignancies, or chronic or acute lung disease were excluded.

The researchers obtained nasal epithelial cells from all participants, and exposed these cells to microplastic fibers created by the researchers in a laboratory setting. Overall, asthmatic and COPD airway epithelial cells showed a different reaction to microplastic fibers stimulation compared to healthy epithelial cells. The most significant response was associated with Th2 inflammation, modulation of stress response, and carcinogenesis. No differences in cytotoxic or minor inflammatory effects on epithelial cells of patients with asthma or COPD were noted compared with healthy controls. 

In addition, flow cytometric analysis showed increased CD24+ epithelial cells in asthma patients compared to controls after microplastics exposure.

“Many of the gene candidates selected from RNA-Seq analysis are related to cancer (upregulated in many cancer types according to the literature), and the activation of CD24 on primarily ciliated asthmatic epithelial cells after microplastic stimulation further supports this theory,” the researchers wrote.

The findings were limited by several factors including the use of nasal rather than bronchial epithelial cells, which would have yielded more information, the researchers noted. Also, patients with severe asthma and COPD were excluded, they said, because of the impact of oral steroid and antibiotic use by this patient group on epithelial cell immunology that could bias the results of epithelial response to microplastic fiber exposure.

However, the results suggest that “the structural impairment of the airway epithelium in obstructive diseases enhances the impact of microplastic particles compared to healthy epithelium,” the researchers concluded.

 

Current and Future Implications

The current study is important in addressing the increasing environmental presence of microplastics and their potential impact on respiratory health, said Seyedmohammad Pourshahid, MD, assistant professor of thoracic medicine and surgery at the Lewis Katz School of Medicine at Temple University, Philadelphia, in an interview.

“By examining how microplastics interact with airway epithelial cells, particularly in individuals with asthma and COPD, the research aims to elucidate mechanisms that could contribute to disease progression or exacerbation,” he said. 

“The study’s findings that microplastics did not induce a strong inflammatory response, unlike other pollutants such as PM2.5, were unexpected; instead, microplastics appeared to influence pathways related to airway remodeling and oxidative stress,” Pourshahid noted. “This suggests that microplastics may affect respiratory health through mechanisms distinct from traditional pollutants,” he said.

“While preliminary, this research highlights the potential role of environmental microplastic exposure in respiratory diseases,” Pourshahid told this news organization. “Clinicians should be aware of emerging environmental factors that could impact patient health, especially in individuals with asthma and COPD. This awareness may inform patient education and advocacy for reducing exposure to airborne microplastics,” he said.

More studies are needed to explore the long-term effects of microplastic exposure on respiratory health, particularly in vulnerable populations, said Pourshahid. Research with in vivo models is necessary to confirm the findings and assess potential clinical implications to confirm these findings and assess potential clinical implications, he said. “Understanding the prevalence and sources of daily microplastic exposure can inform public health strategies to mitigate risks,” he added.

The study was supported by the Jakub Potocki Foundation. Paplińska-Goryca and Pourshahid had no financial conflicts to disclose.

A version of this article first appeared on Medscape.com.

TOPLINE: Gulf War Illness (GWI) symptom severity shows negative correlation with predicted binding affinity of anthrax vaccine antigen to Human Leukocyte Antigen (HLA) Class II molecules. Stronger binding affinity is associated with weaker symptoms, with correlation coefficient r = -0.356 (P < .001).

METHODOLOGY: 

•      Researchers analyzed 458 Gulf War veterans: 397 men, 61 women, mean (SD) age 56.3 (0.5) years.
•      The aim was to determine the association between GWI symptom severity and binding affinity of anthrax Protective Antigen to HLA Class II molecules.
•      Analysis included in silico estimation of predicted binding affinity between 750 15-amino acid length subsequences of protective antigen and specific HLA Class II alleles carried by each participant.
•      Investigators assessed GWI symptom severity across 6 domains: fatigue, pain, neurological/cognitive/mood, respiratory, gastrointestinal, and dermatologic symptoms that began during or after Gulf War and lasted > 6 months. 

TAKEAWAY:

•      GWI symptom severity demonstrated significant negative correlation with strength of predicted binding affinity of protective antigen peptides to HLA-II molecules (correlation coefficient [r], −0.356; P < .001), independent of age (partial correlation, −0.376; P < .001).
•      Researchers identified 180 of 750 (24%) 15-mer epitopes with strong binding affinities to HLA-II molecules, suggesting good potential for CD4+ lymphocyte engagement.
•      Analysis revealed that DPB1 (15/31, 48%) and DRB1 (13/44, 30%) alleles showed strong binding affinity with Protective Antigen epitopes, while all DQB1 alleles (18/18, 100%) showed no strong binding.
•      The number of strong binding hits per individual ranged from 3 to 168, indicating wide variability in potential antibody production capability across participants.

IN PRACTICE: "The current findings, demonstrating a robust negative association between HLAanthrax vaccine PA binding and GWI symptom severity, strongly support the hypothesized role of reduced antibody production against anthrax vaccine PA in GWI that most probably underlies the findings supporting anthrax antigen persistence in GWI, in the broader context of antigen persistence in other diseases," Lisa M. James and Apostolos P. Georgopoulos write. 

SOURCE: The study was led by Lisa M. James and Apostolos P. Georgopoulos of the Brain Sciences Center at the Minneapolis Veterans Affairs Health Care System. It was published online on January 18 in Vaccines.

This article was created using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication.

TOPLINE: Gulf War Illness (GWI) symptom severity shows negative correlation with predicted binding affinity of anthrax vaccine antigen to Human Leukocyte Antigen (HLA) Class II molecules. Stronger binding affinity is associated with weaker symptoms, with correlation coefficient r = -0.356 (P < .001).

METHODOLOGY: 

•      Researchers analyzed 458 Gulf War veterans: 397 men, 61 women, mean (SD) age 56.3 (0.5) years.
•      The aim was to determine the association between GWI symptom severity and binding affinity of anthrax Protective Antigen to HLA Class II molecules.
•      Analysis included in silico estimation of predicted binding affinity between 750 15-amino acid length subsequences of protective antigen and specific HLA Class II alleles carried by each participant.
•      Investigators assessed GWI symptom severity across 6 domains: fatigue, pain, neurological/cognitive/mood, respiratory, gastrointestinal, and dermatologic symptoms that began during or after Gulf War and lasted > 6 months. 

TAKEAWAY:

•      GWI symptom severity demonstrated significant negative correlation with strength of predicted binding affinity of protective antigen peptides to HLA-II molecules (correlation coefficient [r], −0.356; P < .001), independent of age (partial correlation, −0.376; P < .001).
•      Researchers identified 180 of 750 (24%) 15-mer epitopes with strong binding affinities to HLA-II molecules, suggesting good potential for CD4+ lymphocyte engagement.
•      Analysis revealed that DPB1 (15/31, 48%) and DRB1 (13/44, 30%) alleles showed strong binding affinity with Protective Antigen epitopes, while all DQB1 alleles (18/18, 100%) showed no strong binding.
•      The number of strong binding hits per individual ranged from 3 to 168, indicating wide variability in potential antibody production capability across participants.

IN PRACTICE: "The current findings, demonstrating a robust negative association between HLAanthrax vaccine PA binding and GWI symptom severity, strongly support the hypothesized role of reduced antibody production against anthrax vaccine PA in GWI that most probably underlies the findings supporting anthrax antigen persistence in GWI, in the broader context of antigen persistence in other diseases," Lisa M. James and Apostolos P. Georgopoulos write. 

SOURCE: The study was led by Lisa M. James and Apostolos P. Georgopoulos of the Brain Sciences Center at the Minneapolis Veterans Affairs Health Care System. It was published online on January 18 in Vaccines.

This article was created using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication.

TOPLINE: Gulf War Illness (GWI) symptom severity shows negative correlation with predicted binding affinity of anthrax vaccine antigen to Human Leukocyte Antigen (HLA) Class II molecules. Stronger binding affinity is associated with weaker symptoms, with correlation coefficient r = -0.356 (P < .001).

METHODOLOGY: 

•      Researchers analyzed 458 Gulf War veterans: 397 men, 61 women, mean (SD) age 56.3 (0.5) years.
•      The aim was to determine the association between GWI symptom severity and binding affinity of anthrax Protective Antigen to HLA Class II molecules.
•      Analysis included in silico estimation of predicted binding affinity between 750 15-amino acid length subsequences of protective antigen and specific HLA Class II alleles carried by each participant.
•      Investigators assessed GWI symptom severity across 6 domains: fatigue, pain, neurological/cognitive/mood, respiratory, gastrointestinal, and dermatologic symptoms that began during or after Gulf War and lasted > 6 months. 

TAKEAWAY:

•      GWI symptom severity demonstrated significant negative correlation with strength of predicted binding affinity of protective antigen peptides to HLA-II molecules (correlation coefficient [r], −0.356; P < .001), independent of age (partial correlation, −0.376; P < .001).
•      Researchers identified 180 of 750 (24%) 15-mer epitopes with strong binding affinities to HLA-II molecules, suggesting good potential for CD4+ lymphocyte engagement.
•      Analysis revealed that DPB1 (15/31, 48%) and DRB1 (13/44, 30%) alleles showed strong binding affinity with Protective Antigen epitopes, while all DQB1 alleles (18/18, 100%) showed no strong binding.
•      The number of strong binding hits per individual ranged from 3 to 168, indicating wide variability in potential antibody production capability across participants.

IN PRACTICE: "The current findings, demonstrating a robust negative association between HLAanthrax vaccine PA binding and GWI symptom severity, strongly support the hypothesized role of reduced antibody production against anthrax vaccine PA in GWI that most probably underlies the findings supporting anthrax antigen persistence in GWI, in the broader context of antigen persistence in other diseases," Lisa M. James and Apostolos P. Georgopoulos write. 

SOURCE: The study was led by Lisa M. James and Apostolos P. Georgopoulos of the Brain Sciences Center at the Minneapolis Veterans Affairs Health Care System. It was published online on January 18 in Vaccines.

This article was created using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication.

A new analysis of long-COVID patients has identified five distinct subtypes that researchers say will help doctors diagnose the condition.

The new five-type index, developed by federal researchers with the National Institutes of Health’s RECOVER COVID Initiative, identified the most common symptoms in 14,000 people with long COVID, with data from an additional 4000 people added to the updated 2024 index.

By using the index, physicians and researchers can better understand the condition, which is difficult to treat and diagnose because no standard definitions or therapies have been developed. Doctors can use the index to offer more targeted care and help patients manage their symptoms more effectively.

The index may also help researchers find more treatments for long COVID. Because long COVID can affect so many different parts of the body, it will take time to fully understand how to treat it, but studies like this are making progress in the right direction, experts said.

This new index uses an updated point system, where points are allotted to each symptom in a list of the 44 most reported symptoms in people with likely long COVID based on how often they occur. Among people in the study with prior COVID infection, 2213 (18%) met the threshold for long COVID.

The 44 most common symptoms were then distributed among 5 subtypes, with each representing a difference in impact on quality of life and overall health. The most common symptoms were fatigue (85.8%), postexertional malaise (87.4%), and postexertional soreness (75.0%) — where persistent fatigue and discomfort occur after physical or mental exertion — dizziness (65.8%), brain fog (63.8%), gastrointestinal symptoms (59.3%), and palpitations (58%).

For those with prior COVID infection, symptoms were more prevalent in all cases.

 

Subtype 1

Those grouped into subtype 1 did not report a high incidence of impact on quality of life, physical health, or daily function. Only 21% of people in subtype 1 reported a “poor or fair quality of life.”

A change in smell or taste — usually a symptom that’s bothersome but doesn’t seriously impact overall health — was most present in subtype 1, with 100% of people in subtype 1 reporting it.

The only other symptoms in over 50% of people with subtype 1— which were 490 of the 2213 with prior COVID infection — were fatigue (66%), postexertional malaise (53%), and postexertional soreness (55%).

Though these two symptoms can certainly impact quality of life, they became much more prevalent in other subtypes.

 

Subtype 2

The prevalence of possibly debilitating symptoms like postexertional malaise (94%), fatigue (81%), and chronic cough (100%) rose dramatically in people grouped into subtype 2. 

Plus, 25% of people in subtype 2 reported a “poor or fair quality of life. Postexertional malaise, I think, is probably one of the most debilitating of the symptoms. When somebody comes in and tells me that they’re tired and I think they might have long COVID, the first thing I try to do is see if it is postexertional malaise vs just postinfectious fatigue,” said Lisa Sanders, MD, medical director of Yale’s Long Covid Multidisciplinary Care Center in New Haven, Connecticut.

Postinfectious fatigue usually resolves much more quickly than postexertional malaise. The latter accounts for several symptoms as also associated with myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS). ME/CFS is a chronic illness that causes severe fatigue and makes it difficult for sufferers to perform routine, daily activities.

“Postexertional malaise is an additive symptom of ME/CFS, and that can take a long time to resolve,” Sanders added.

The similarity between these two symptoms highlights the importance that physicians must place in scrutinizing symptoms to a high degree when they suspect a patient of having long COVID, experts said. By doing so, clinicians can unveil the mask of overlapping symptoms between long COVID symptoms and symptoms of other illnesses.

 

Subtype 3

About 37% of people grouped in subtype 3 reported a poor or fair quality of life, a significant rise from subtypes 1 and 2.

Fatigue symptoms were reported by 92%, whereas 82% reported postexertional soreness, and 70% reported dizziness. Additionally, 100% of people in subtype 3 reported brain fog as a symptom.

Sanders said these symptoms are also common in people with postural orthostatic tachycardia syndrome. This condition results from a reduced volume of blood returning to the heart after standing up, which leads to an abnormally fast heart rate. Palpitations and fainting can then occur.

Brain fog can be especially debilitating in people who are used to multitasking. With brain fog, people accustomed to easily alternating between tasks or doing multiple tasks at once can only do one thing at a time. This can cause stress and an overload of thoughts, even precipitating a change in careers if severe enough.

Though brain fog tends to resolve within 6-9 months after infection, it can last up to 18 months or more. Experts say doctors should always be on the lookout if a patient complains they have trouble concentrating or multitasking in the months after a COVID infection. A neurological exam and cognitive testing can identify abnormalities in brain function.

 

Subtype 4

About 40% of people in the study grouped into subtype 4 reported a poor or fair quality of life, a modest increase from those with subtype 3. About 65% reported symptoms of brain fog and 92% reported palpitations.

Dizziness was also prevalent at 71%, whereas 60% reported gastrointestinal issues, and 36% said they experienced fever, sweats, and chills.

Nearly 700 of the 2213 people fell into this subtype group, by far the highest number.

 

Subtype 5

A whopping 66% of people in subtype 5 reported a poor to fair quality of life. These people usually reported multisystem symptoms.

In terms of prevalence rises across the spectrum of 44 common long-COVID symptoms, 99% reported shortness of breath; 98%, postexertional soreness; 94%, dizziness; 92%, postexertional malaise; 80%, GI problems; 78%, weakness; and 69%, chest pain.

A higher proportion of Hispanic and multiracial participants were classified as having subtype 5. Also, according to the study, “higher proportions of unvaccinated participants and those with SARS-CoV-2 infection before circulation of the Omicron variant were in subtype 5.”

This suggests the severity of the Delta variant of COVID-19 be linked to some of the worst long COVID symptoms, but further study would have to be done to conclusively determine may be just a correlation.

 

When Do Symptoms Resolve?

According to Sanders, around 17 million Americans are thought to have long COVID. Although 90%-100% of people typically recover within 3 years, that still leaves possibly around 5% of those who don’t recover.

“What people usually say is, ‘I got COVID, and I never quite recovered,” Sanders said.

“Five percent of 17 million turns out to be a lot. It’s a lot of suffering,” she added. “I would say that the most common symptoms are fatigue, brain fog, anosmia or dysgeusia, and sleep disorders,” as evidenced by the high percentage of people in certain subtypes of the study reporting a poor quality of life.

A version of this article first appeared on Medscape.com.

A new analysis of long-COVID patients has identified five distinct subtypes that researchers say will help doctors diagnose the condition.

The new five-type index, developed by federal researchers with the National Institutes of Health’s RECOVER COVID Initiative, identified the most common symptoms in 14,000 people with long COVID, with data from an additional 4000 people added to the updated 2024 index.

By using the index, physicians and researchers can better understand the condition, which is difficult to treat and diagnose because no standard definitions or therapies have been developed. Doctors can use the index to offer more targeted care and help patients manage their symptoms more effectively.

The index may also help researchers find more treatments for long COVID. Because long COVID can affect so many different parts of the body, it will take time to fully understand how to treat it, but studies like this are making progress in the right direction, experts said.

This new index uses an updated point system, where points are allotted to each symptom in a list of the 44 most reported symptoms in people with likely long COVID based on how often they occur. Among people in the study with prior COVID infection, 2213 (18%) met the threshold for long COVID.

The 44 most common symptoms were then distributed among 5 subtypes, with each representing a difference in impact on quality of life and overall health. The most common symptoms were fatigue (85.8%), postexertional malaise (87.4%), and postexertional soreness (75.0%) — where persistent fatigue and discomfort occur after physical or mental exertion — dizziness (65.8%), brain fog (63.8%), gastrointestinal symptoms (59.3%), and palpitations (58%).

For those with prior COVID infection, symptoms were more prevalent in all cases.

 

Subtype 1

Those grouped into subtype 1 did not report a high incidence of impact on quality of life, physical health, or daily function. Only 21% of people in subtype 1 reported a “poor or fair quality of life.”

A change in smell or taste — usually a symptom that’s bothersome but doesn’t seriously impact overall health — was most present in subtype 1, with 100% of people in subtype 1 reporting it.

The only other symptoms in over 50% of people with subtype 1— which were 490 of the 2213 with prior COVID infection — were fatigue (66%), postexertional malaise (53%), and postexertional soreness (55%).

Though these two symptoms can certainly impact quality of life, they became much more prevalent in other subtypes.

 

Subtype 2

The prevalence of possibly debilitating symptoms like postexertional malaise (94%), fatigue (81%), and chronic cough (100%) rose dramatically in people grouped into subtype 2. 

Plus, 25% of people in subtype 2 reported a “poor or fair quality of life. Postexertional malaise, I think, is probably one of the most debilitating of the symptoms. When somebody comes in and tells me that they’re tired and I think they might have long COVID, the first thing I try to do is see if it is postexertional malaise vs just postinfectious fatigue,” said Lisa Sanders, MD, medical director of Yale’s Long Covid Multidisciplinary Care Center in New Haven, Connecticut.

Postinfectious fatigue usually resolves much more quickly than postexertional malaise. The latter accounts for several symptoms as also associated with myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS). ME/CFS is a chronic illness that causes severe fatigue and makes it difficult for sufferers to perform routine, daily activities.

“Postexertional malaise is an additive symptom of ME/CFS, and that can take a long time to resolve,” Sanders added.

The similarity between these two symptoms highlights the importance that physicians must place in scrutinizing symptoms to a high degree when they suspect a patient of having long COVID, experts said. By doing so, clinicians can unveil the mask of overlapping symptoms between long COVID symptoms and symptoms of other illnesses.

 

Subtype 3

About 37% of people grouped in subtype 3 reported a poor or fair quality of life, a significant rise from subtypes 1 and 2.

Fatigue symptoms were reported by 92%, whereas 82% reported postexertional soreness, and 70% reported dizziness. Additionally, 100% of people in subtype 3 reported brain fog as a symptom.

Sanders said these symptoms are also common in people with postural orthostatic tachycardia syndrome. This condition results from a reduced volume of blood returning to the heart after standing up, which leads to an abnormally fast heart rate. Palpitations and fainting can then occur.

Brain fog can be especially debilitating in people who are used to multitasking. With brain fog, people accustomed to easily alternating between tasks or doing multiple tasks at once can only do one thing at a time. This can cause stress and an overload of thoughts, even precipitating a change in careers if severe enough.

Though brain fog tends to resolve within 6-9 months after infection, it can last up to 18 months or more. Experts say doctors should always be on the lookout if a patient complains they have trouble concentrating or multitasking in the months after a COVID infection. A neurological exam and cognitive testing can identify abnormalities in brain function.

 

Subtype 4

About 40% of people in the study grouped into subtype 4 reported a poor or fair quality of life, a modest increase from those with subtype 3. About 65% reported symptoms of brain fog and 92% reported palpitations.

Dizziness was also prevalent at 71%, whereas 60% reported gastrointestinal issues, and 36% said they experienced fever, sweats, and chills.

Nearly 700 of the 2213 people fell into this subtype group, by far the highest number.

 

Subtype 5

A whopping 66% of people in subtype 5 reported a poor to fair quality of life. These people usually reported multisystem symptoms.

In terms of prevalence rises across the spectrum of 44 common long-COVID symptoms, 99% reported shortness of breath; 98%, postexertional soreness; 94%, dizziness; 92%, postexertional malaise; 80%, GI problems; 78%, weakness; and 69%, chest pain.

A higher proportion of Hispanic and multiracial participants were classified as having subtype 5. Also, according to the study, “higher proportions of unvaccinated participants and those with SARS-CoV-2 infection before circulation of the Omicron variant were in subtype 5.”

This suggests the severity of the Delta variant of COVID-19 be linked to some of the worst long COVID symptoms, but further study would have to be done to conclusively determine may be just a correlation.

 

When Do Symptoms Resolve?

According to Sanders, around 17 million Americans are thought to have long COVID. Although 90%-100% of people typically recover within 3 years, that still leaves possibly around 5% of those who don’t recover.

“What people usually say is, ‘I got COVID, and I never quite recovered,” Sanders said.

“Five percent of 17 million turns out to be a lot. It’s a lot of suffering,” she added. “I would say that the most common symptoms are fatigue, brain fog, anosmia or dysgeusia, and sleep disorders,” as evidenced by the high percentage of people in certain subtypes of the study reporting a poor quality of life.

A version of this article first appeared on Medscape.com.

A new analysis of long-COVID patients has identified five distinct subtypes that researchers say will help doctors diagnose the condition.

The new five-type index, developed by federal researchers with the National Institutes of Health’s RECOVER COVID Initiative, identified the most common symptoms in 14,000 people with long COVID, with data from an additional 4000 people added to the updated 2024 index.

By using the index, physicians and researchers can better understand the condition, which is difficult to treat and diagnose because no standard definitions or therapies have been developed. Doctors can use the index to offer more targeted care and help patients manage their symptoms more effectively.

The index may also help researchers find more treatments for long COVID. Because long COVID can affect so many different parts of the body, it will take time to fully understand how to treat it, but studies like this are making progress in the right direction, experts said.

This new index uses an updated point system, where points are allotted to each symptom in a list of the 44 most reported symptoms in people with likely long COVID based on how often they occur. Among people in the study with prior COVID infection, 2213 (18%) met the threshold for long COVID.

The 44 most common symptoms were then distributed among 5 subtypes, with each representing a difference in impact on quality of life and overall health. The most common symptoms were fatigue (85.8%), postexertional malaise (87.4%), and postexertional soreness (75.0%) — where persistent fatigue and discomfort occur after physical or mental exertion — dizziness (65.8%), brain fog (63.8%), gastrointestinal symptoms (59.3%), and palpitations (58%).

For those with prior COVID infection, symptoms were more prevalent in all cases.

 

Subtype 1

Those grouped into subtype 1 did not report a high incidence of impact on quality of life, physical health, or daily function. Only 21% of people in subtype 1 reported a “poor or fair quality of life.”

A change in smell or taste — usually a symptom that’s bothersome but doesn’t seriously impact overall health — was most present in subtype 1, with 100% of people in subtype 1 reporting it.

The only other symptoms in over 50% of people with subtype 1— which were 490 of the 2213 with prior COVID infection — were fatigue (66%), postexertional malaise (53%), and postexertional soreness (55%).

Though these two symptoms can certainly impact quality of life, they became much more prevalent in other subtypes.

 

Subtype 2

The prevalence of possibly debilitating symptoms like postexertional malaise (94%), fatigue (81%), and chronic cough (100%) rose dramatically in people grouped into subtype 2. 

Plus, 25% of people in subtype 2 reported a “poor or fair quality of life. Postexertional malaise, I think, is probably one of the most debilitating of the symptoms. When somebody comes in and tells me that they’re tired and I think they might have long COVID, the first thing I try to do is see if it is postexertional malaise vs just postinfectious fatigue,” said Lisa Sanders, MD, medical director of Yale’s Long Covid Multidisciplinary Care Center in New Haven, Connecticut.

Postinfectious fatigue usually resolves much more quickly than postexertional malaise. The latter accounts for several symptoms as also associated with myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS). ME/CFS is a chronic illness that causes severe fatigue and makes it difficult for sufferers to perform routine, daily activities.

“Postexertional malaise is an additive symptom of ME/CFS, and that can take a long time to resolve,” Sanders added.

The similarity between these two symptoms highlights the importance that physicians must place in scrutinizing symptoms to a high degree when they suspect a patient of having long COVID, experts said. By doing so, clinicians can unveil the mask of overlapping symptoms between long COVID symptoms and symptoms of other illnesses.

 

Subtype 3

About 37% of people grouped in subtype 3 reported a poor or fair quality of life, a significant rise from subtypes 1 and 2.

Fatigue symptoms were reported by 92%, whereas 82% reported postexertional soreness, and 70% reported dizziness. Additionally, 100% of people in subtype 3 reported brain fog as a symptom.

Sanders said these symptoms are also common in people with postural orthostatic tachycardia syndrome. This condition results from a reduced volume of blood returning to the heart after standing up, which leads to an abnormally fast heart rate. Palpitations and fainting can then occur.

Brain fog can be especially debilitating in people who are used to multitasking. With brain fog, people accustomed to easily alternating between tasks or doing multiple tasks at once can only do one thing at a time. This can cause stress and an overload of thoughts, even precipitating a change in careers if severe enough.

Though brain fog tends to resolve within 6-9 months after infection, it can last up to 18 months or more. Experts say doctors should always be on the lookout if a patient complains they have trouble concentrating or multitasking in the months after a COVID infection. A neurological exam and cognitive testing can identify abnormalities in brain function.

 

Subtype 4

About 40% of people in the study grouped into subtype 4 reported a poor or fair quality of life, a modest increase from those with subtype 3. About 65% reported symptoms of brain fog and 92% reported palpitations.

Dizziness was also prevalent at 71%, whereas 60% reported gastrointestinal issues, and 36% said they experienced fever, sweats, and chills.

Nearly 700 of the 2213 people fell into this subtype group, by far the highest number.

 

Subtype 5

A whopping 66% of people in subtype 5 reported a poor to fair quality of life. These people usually reported multisystem symptoms.

In terms of prevalence rises across the spectrum of 44 common long-COVID symptoms, 99% reported shortness of breath; 98%, postexertional soreness; 94%, dizziness; 92%, postexertional malaise; 80%, GI problems; 78%, weakness; and 69%, chest pain.

A higher proportion of Hispanic and multiracial participants were classified as having subtype 5. Also, according to the study, “higher proportions of unvaccinated participants and those with SARS-CoV-2 infection before circulation of the Omicron variant were in subtype 5.”

This suggests the severity of the Delta variant of COVID-19 be linked to some of the worst long COVID symptoms, but further study would have to be done to conclusively determine may be just a correlation.

 

When Do Symptoms Resolve?

According to Sanders, around 17 million Americans are thought to have long COVID. Although 90%-100% of people typically recover within 3 years, that still leaves possibly around 5% of those who don’t recover.

“What people usually say is, ‘I got COVID, and I never quite recovered,” Sanders said.

“Five percent of 17 million turns out to be a lot. It’s a lot of suffering,” she added. “I would say that the most common symptoms are fatigue, brain fog, anosmia or dysgeusia, and sleep disorders,” as evidenced by the high percentage of people in certain subtypes of the study reporting a poor quality of life.

A version of this article first appeared on Medscape.com.

TOPLINE: Chronic obstructive pulmonary disease (COPD) guidelines are significantly underutilized in clinical practice, with studies attempting to improve implementation yielding inconsistent results. A team of US Department of Veterans Affairs (VA) researchers developed a pilot program and surveyed both patients and primary care practitioners (PCPs) to better understand the barriers to guideline-based COPD care primary care settings.

METHODOLOGY: 

•      Researchers conducted a pilot study using an implementation design at the Central Arkansas Veterans Healthcare System (CAVHS) to explore implementation gaps in a primary care setting
•      Analysis included semi-structured interviews with 17 respondents, comprising both patients and PCPs, to explore barriers and facilitators to 4 COPD clinical practice guidelines
•      The Consolidated Framework of Implementation Science was used to design interview guides focusing on inhaler education, spirometry, pulmonary rehabilitation, and COPD-specific patient education
•      Primary care teams followed a collaborative model including physicians, advanced practice nurses, nurses, social workers, pharmacists, and administrative staff working together with patients

TAKEAWAY:

•      A total of 17 respondents, including patients and PCPs participated in the study, with the patient sample reflecting the general COPD population at CAVHS
•      Both PCPs and patients consistently rated all assessed COPD clinical practice guidelines as highly important, despite significant practice gaps in implementation
•      PCPs reported very low rates of providing education on inhaler use, citing time constraints, lack of educational resources, and low familiarity as primary barriers
•      The main PCP-related barriers to pulmonary rehabilitation included limited knowledge about the program, unfamiliarity with CAVHS resources, and challenges with the referral process

IN PRACTICE: "Reasons behind this insufficient uptake of COPD guidelines include providers' low familiarity with guidelines, perception of minimal value of guidelines, and time constraints. Studies attempting to improve COPD-CPG uptake have shown mixed results and the best practice to bridge this implementation gap remains unknown," wrote the authors of the study.[Note To Staff: This quote was picked by Plume]

SOURCE: The study was led by Deepa Raghavan, Karen L Drummond, Sonya Sanders, and JoAnn Kirchner at Central Arkansas Veterans Healthcare System. It was published online in Chronic Respiratory Disease.

TOPLINE: Chronic obstructive pulmonary disease (COPD) guidelines are significantly underutilized in clinical practice, with studies attempting to improve implementation yielding inconsistent results. A team of US Department of Veterans Affairs (VA) researchers developed a pilot program and surveyed both patients and primary care practitioners (PCPs) to better understand the barriers to guideline-based COPD care primary care settings.

METHODOLOGY: 

•      Researchers conducted a pilot study using an implementation design at the Central Arkansas Veterans Healthcare System (CAVHS) to explore implementation gaps in a primary care setting
•      Analysis included semi-structured interviews with 17 respondents, comprising both patients and PCPs, to explore barriers and facilitators to 4 COPD clinical practice guidelines
•      The Consolidated Framework of Implementation Science was used to design interview guides focusing on inhaler education, spirometry, pulmonary rehabilitation, and COPD-specific patient education
•      Primary care teams followed a collaborative model including physicians, advanced practice nurses, nurses, social workers, pharmacists, and administrative staff working together with patients

TAKEAWAY:

•      A total of 17 respondents, including patients and PCPs participated in the study, with the patient sample reflecting the general COPD population at CAVHS
•      Both PCPs and patients consistently rated all assessed COPD clinical practice guidelines as highly important, despite significant practice gaps in implementation
•      PCPs reported very low rates of providing education on inhaler use, citing time constraints, lack of educational resources, and low familiarity as primary barriers
•      The main PCP-related barriers to pulmonary rehabilitation included limited knowledge about the program, unfamiliarity with CAVHS resources, and challenges with the referral process

IN PRACTICE: "Reasons behind this insufficient uptake of COPD guidelines include providers' low familiarity with guidelines, perception of minimal value of guidelines, and time constraints. Studies attempting to improve COPD-CPG uptake have shown mixed results and the best practice to bridge this implementation gap remains unknown," wrote the authors of the study.[Note To Staff: This quote was picked by Plume]

SOURCE: The study was led by Deepa Raghavan, Karen L Drummond, Sonya Sanders, and JoAnn Kirchner at Central Arkansas Veterans Healthcare System. It was published online in Chronic Respiratory Disease.

TOPLINE: Chronic obstructive pulmonary disease (COPD) guidelines are significantly underutilized in clinical practice, with studies attempting to improve implementation yielding inconsistent results. A team of US Department of Veterans Affairs (VA) researchers developed a pilot program and surveyed both patients and primary care practitioners (PCPs) to better understand the barriers to guideline-based COPD care primary care settings.

METHODOLOGY: 

•      Researchers conducted a pilot study using an implementation design at the Central Arkansas Veterans Healthcare System (CAVHS) to explore implementation gaps in a primary care setting
•      Analysis included semi-structured interviews with 17 respondents, comprising both patients and PCPs, to explore barriers and facilitators to 4 COPD clinical practice guidelines
•      The Consolidated Framework of Implementation Science was used to design interview guides focusing on inhaler education, spirometry, pulmonary rehabilitation, and COPD-specific patient education
•      Primary care teams followed a collaborative model including physicians, advanced practice nurses, nurses, social workers, pharmacists, and administrative staff working together with patients

TAKEAWAY:

•      A total of 17 respondents, including patients and PCPs participated in the study, with the patient sample reflecting the general COPD population at CAVHS
•      Both PCPs and patients consistently rated all assessed COPD clinical practice guidelines as highly important, despite significant practice gaps in implementation
•      PCPs reported very low rates of providing education on inhaler use, citing time constraints, lack of educational resources, and low familiarity as primary barriers
•      The main PCP-related barriers to pulmonary rehabilitation included limited knowledge about the program, unfamiliarity with CAVHS resources, and challenges with the referral process

IN PRACTICE: "Reasons behind this insufficient uptake of COPD guidelines include providers' low familiarity with guidelines, perception of minimal value of guidelines, and time constraints. Studies attempting to improve COPD-CPG uptake have shown mixed results and the best practice to bridge this implementation gap remains unknown," wrote the authors of the study.[Note To Staff: This quote was picked by Plume]

SOURCE: The study was led by Deepa Raghavan, Karen L Drummond, Sonya Sanders, and JoAnn Kirchner at Central Arkansas Veterans Healthcare System. It was published online in Chronic Respiratory Disease.

Chronic cough remains a common reason for consultation in pulmonology post–COVID-19. But what do we really know about this condition, now 5 years after the pandemic’s onset? This topic was discussed at the recent French-Speaking Pneumology Congress held in Marseille, France, from January 24-26, 2025.

Before discussing post-COVID cough, it is crucial to differentiate between an acute cough, often viral in origin (including those associated with SARS-CoV-2), a subacute cough (lasting 3-8 weeks), and a chronic cough (persisting over 8 weeks).

“This distinction allows us to tailor treatment and prescribe the appropriate investigations, according to the duration and the probability of symptom resolution,” explained Laurent Guilleminault, MD, PhD, pulmonologist at Toulouse University Hospital Centre, Toulouse, France.

In the case of an acute cough, for instance, after a viral infection, the probability of spontaneous resolution is very high. It is often unnecessary to carry out additional examinations or initiate specific treatments because none has proven its effectiveness in shortening this type of cough. On the other hand, when a cough persists beyond 8 weeks, the chance of spontaneous resolution decreases considerably. “This is when an assessment is necessary to identify a possible underlying cause,” Guilleminault noted.

“The absence of coughing during the consultation should not lead to ruling out a diagnosis,” he added.

Neurological Link

A large-scale French study of 70,000 patients examined the demographic profiles of patients with COVID-19. It revealed a lower frequency of coughing among children and older individuals, with a notable prevalence among adults aged 30-60 years.

Furthermore, during the acute phase of COVID, coughing did not appear to indicate severity. A comparison between survivors and nonsurvivors revealed no significant differences in the frequency and severity of coughing. Another study concluded that, contrary to expectations, COVID-related pneumonia, although potentially severe, does not necessarily involve severe cough.

These findings highlight the absence of a direct link between coughing and pulmonary involvement in patients with COVID-19.

“Coughing appears to be more closely linked to neurological dysfunction than to classic respiratory involvement. A distinction that is essential for better understanding the pathophysiology of the disease and guiding therapeutic strategies,” Guilleminault noted.

Cough Mechanism

“The analysis of cough in the context of phylogenetic evolution is fascinating,” explained Guilleminault. “It illustrates how this reflex has provided an advantage to the virus for its propagation.” Studies on the transmission of SARS-CoV-2 have confirmed that coughing plays a key role in the spread of viral particles. However, this mechanism does not involve severe pulmonary damage. The primary goal of the virus is to induce neurological dysfunction in the host by triggering a cough reflex. This neurological activation enables the virus to trigger a cough reflex for dissemination even without significant pulmonary damage. This mechanism provides an evolutionary advantage by enhancing the ability of the virus to spread and colonize new hosts.

The cough mechanism remains partially understood and involves cough hypersensitivity, characterized by increased neural responsivity to a range of stimuli that affect the airways, lungs, and other tissues innervated by common nerve supplies. The cough reflex begins with the activation of sensitive peripheral receptors located mainly in the respiratory tract that detect irritants or abnormalities.

These receptors, such as P2X2, P2X3, and others, transmit information to the brainstem, which coordinates the reflex response. This process is modulated by cortical controls that normally inhibit spontaneous coughing, explaining why we do not cough constantly even in the presence of moderate stimuli.

However, when there is an imbalance in this inhibition mechanism, coughing can be triggered either excessively or uncontrollably. SARS-CoV-2 appears to interact directly with these peripheral receptors, stimulating the cough reflex. The widespread presence and density of these receptors make this mechanism highly effective for the virus’s transmission.

Additionally, the vagus nerve likely plays a central role in triggering cough, particularly in viral infections. Studies of influenza have shown the involvement of sensory cells associated with the vagus nerve.

The virus stimulates the vagus nerve, which activates the cough reflex. Research suggests that neurotropism, neuroinflammation, and neuroimmunomodulation via the vagal sensory nerves, which are involved in SARS-CoV-2 infection, lead to cough hypersensitivity.

One question remains: Could vagus nerve involvement prolong coughing beyond the active phase of viral infection? The data indicate that viral infection significantly increases the sensitivity of the cough reflex, regardless of the level of irritation. The brain areas involved in inhibiting this reflex appear less effective during viral infection, resulting in reduced inhibitory control and easier triggering of cough. This phenomenon reflects temporary dysfunction of the neurological modulation system, which gradually recovers after recovery.

Long-Term Effects

The epidemiology of post-COVID cough and its integration into the framework of the long COVID framework remain subjects of ongoing debate. Early studies have revealed that cough could be either an isolated symptom or associated with other manifestations of long COVID. These studies were often conducted over relatively short periods (14-110 days) and estimated that approximately 19% of patients with long COVID experienced persistent cough. Another study found that 14% of patients reported cough between 3 weeks and 3 months after hospital discharge for COVID-19.

Longer follow-up periods showed a significant decrease in the prevalence of cough over time. For instance, a 1-year study reported that only 2.5% of patients had episodes of chronic cough.

However, a 2023 study published in JAMA found that the prevalence of post-COVID chronic cough exceeded 30% in some groups of patients.

“It is not relevant to wait so long before acting,” Guilleminault said. A reasonable threshold for evaluation and treatment is 8-12 weeks postinfection to begin investigations and consider appropriate treatment. What should be done when a patient presents with “Doctor, I had COVID, I have a cough, and it hasn’t stopped?” These situations are common in clinical practice. In terms of severity, quality of life, and overall impact, patients with chronic post-COVID cough are not significantly different from those with other chronic coughs. Moreover, both conditions involve a real neurological dysfunction.

Same Diagnostic Steps

Management should follow existing guidelines, including the recent French recommendations for chronic cough.

A visual analog scale can be used, and possible complications should be assessed. A chest x-ray is recommended to identify any warning signs, such as cough, although linked to COVID — may coincide with other conditions, such as bronchial cancer. In smokers, chest CT should be considered to rule out neoplastic pathology. The presence of interstitial lesions, particularly fibrosing lesions, suggests that fibrosing interstitial pneumonia requires specialized management.

Smoking, which is an aggravating factor, should be discontinued. Discontinuing angiotensin-converting enzyme inhibitors for 4 weeks can help determine if they contribute to cough.

The three most common causes of chronic cough — rhinosinusitis, asthma, and gastroesophageal reflux disease — should be ruled out. Diagnosis is based on history, physical examination, and specific tests: Nasofibroscopy for rhinosinusitis, spirometry, fractional exhaled nitric oxide for asthma and clinical history of gastroesophageal reflux disease. Studies have indicated that asthma may develop after a COVID infection.

Laryngeal abnormalities are also common in chronic post-COVID cough. One study found that a quarter of patients had increased laryngeal sensitivity or voice changes. “The larynx, a highly cough-producing organ, causes more coughing than the lungs,” Guilleminault explained.

Laryngeal abnormalities are frequently observed. A study found that 63% of patients experienced dysphonia, 56% had a sensation of a foreign body in the larynx, and 10% experienced laryngospasms.

These issues are common in patients with post-COVID cough and are often associated with neurological dysfunction. Innervation of the larynx is complex and can be affected by viruses, leading to hypersensitivity, paresthesia, and other sensory disturbances, which may explain the laryngeal symptoms observed in these patients.

Next Steps

If common causes such as asthma, abnormal imaging findings, or laryngeal pathology are ruled out, the condition may be classified as a chronic refractory or unexplained cough. In these cases, the neurological origin is likely due to nervous system dysfunction. Neuromodulatory treatments including amitriptyline, pregabalin, and gabapentin may be considered in some cases. Corticosteroids are generally ineffective against chronic coughs.

This story was translated from Medscape’s French edition using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication.

Chronic cough remains a common reason for consultation in pulmonology post–COVID-19. But what do we really know about this condition, now 5 years after the pandemic’s onset? This topic was discussed at the recent French-Speaking Pneumology Congress held in Marseille, France, from January 24-26, 2025.

Before discussing post-COVID cough, it is crucial to differentiate between an acute cough, often viral in origin (including those associated with SARS-CoV-2), a subacute cough (lasting 3-8 weeks), and a chronic cough (persisting over 8 weeks).

“This distinction allows us to tailor treatment and prescribe the appropriate investigations, according to the duration and the probability of symptom resolution,” explained Laurent Guilleminault, MD, PhD, pulmonologist at Toulouse University Hospital Centre, Toulouse, France.

In the case of an acute cough, for instance, after a viral infection, the probability of spontaneous resolution is very high. It is often unnecessary to carry out additional examinations or initiate specific treatments because none has proven its effectiveness in shortening this type of cough. On the other hand, when a cough persists beyond 8 weeks, the chance of spontaneous resolution decreases considerably. “This is when an assessment is necessary to identify a possible underlying cause,” Guilleminault noted.

“The absence of coughing during the consultation should not lead to ruling out a diagnosis,” he added.

Neurological Link

A large-scale French study of 70,000 patients examined the demographic profiles of patients with COVID-19. It revealed a lower frequency of coughing among children and older individuals, with a notable prevalence among adults aged 30-60 years.

Furthermore, during the acute phase of COVID, coughing did not appear to indicate severity. A comparison between survivors and nonsurvivors revealed no significant differences in the frequency and severity of coughing. Another study concluded that, contrary to expectations, COVID-related pneumonia, although potentially severe, does not necessarily involve severe cough.

These findings highlight the absence of a direct link between coughing and pulmonary involvement in patients with COVID-19.

“Coughing appears to be more closely linked to neurological dysfunction than to classic respiratory involvement. A distinction that is essential for better understanding the pathophysiology of the disease and guiding therapeutic strategies,” Guilleminault noted.

Cough Mechanism

“The analysis of cough in the context of phylogenetic evolution is fascinating,” explained Guilleminault. “It illustrates how this reflex has provided an advantage to the virus for its propagation.” Studies on the transmission of SARS-CoV-2 have confirmed that coughing plays a key role in the spread of viral particles. However, this mechanism does not involve severe pulmonary damage. The primary goal of the virus is to induce neurological dysfunction in the host by triggering a cough reflex. This neurological activation enables the virus to trigger a cough reflex for dissemination even without significant pulmonary damage. This mechanism provides an evolutionary advantage by enhancing the ability of the virus to spread and colonize new hosts.

The cough mechanism remains partially understood and involves cough hypersensitivity, characterized by increased neural responsivity to a range of stimuli that affect the airways, lungs, and other tissues innervated by common nerve supplies. The cough reflex begins with the activation of sensitive peripheral receptors located mainly in the respiratory tract that detect irritants or abnormalities.

These receptors, such as P2X2, P2X3, and others, transmit information to the brainstem, which coordinates the reflex response. This process is modulated by cortical controls that normally inhibit spontaneous coughing, explaining why we do not cough constantly even in the presence of moderate stimuli.

However, when there is an imbalance in this inhibition mechanism, coughing can be triggered either excessively or uncontrollably. SARS-CoV-2 appears to interact directly with these peripheral receptors, stimulating the cough reflex. The widespread presence and density of these receptors make this mechanism highly effective for the virus’s transmission.

Additionally, the vagus nerve likely plays a central role in triggering cough, particularly in viral infections. Studies of influenza have shown the involvement of sensory cells associated with the vagus nerve.

The virus stimulates the vagus nerve, which activates the cough reflex. Research suggests that neurotropism, neuroinflammation, and neuroimmunomodulation via the vagal sensory nerves, which are involved in SARS-CoV-2 infection, lead to cough hypersensitivity.

One question remains: Could vagus nerve involvement prolong coughing beyond the active phase of viral infection? The data indicate that viral infection significantly increases the sensitivity of the cough reflex, regardless of the level of irritation. The brain areas involved in inhibiting this reflex appear less effective during viral infection, resulting in reduced inhibitory control and easier triggering of cough. This phenomenon reflects temporary dysfunction of the neurological modulation system, which gradually recovers after recovery.

Long-Term Effects

The epidemiology of post-COVID cough and its integration into the framework of the long COVID framework remain subjects of ongoing debate. Early studies have revealed that cough could be either an isolated symptom or associated with other manifestations of long COVID. These studies were often conducted over relatively short periods (14-110 days) and estimated that approximately 19% of patients with long COVID experienced persistent cough. Another study found that 14% of patients reported cough between 3 weeks and 3 months after hospital discharge for COVID-19.

Longer follow-up periods showed a significant decrease in the prevalence of cough over time. For instance, a 1-year study reported that only 2.5% of patients had episodes of chronic cough.

However, a 2023 study published in JAMA found that the prevalence of post-COVID chronic cough exceeded 30% in some groups of patients.

“It is not relevant to wait so long before acting,” Guilleminault said. A reasonable threshold for evaluation and treatment is 8-12 weeks postinfection to begin investigations and consider appropriate treatment. What should be done when a patient presents with “Doctor, I had COVID, I have a cough, and it hasn’t stopped?” These situations are common in clinical practice. In terms of severity, quality of life, and overall impact, patients with chronic post-COVID cough are not significantly different from those with other chronic coughs. Moreover, both conditions involve a real neurological dysfunction.

Same Diagnostic Steps

Management should follow existing guidelines, including the recent French recommendations for chronic cough.

A visual analog scale can be used, and possible complications should be assessed. A chest x-ray is recommended to identify any warning signs, such as cough, although linked to COVID — may coincide with other conditions, such as bronchial cancer. In smokers, chest CT should be considered to rule out neoplastic pathology. The presence of interstitial lesions, particularly fibrosing lesions, suggests that fibrosing interstitial pneumonia requires specialized management.

Smoking, which is an aggravating factor, should be discontinued. Discontinuing angiotensin-converting enzyme inhibitors for 4 weeks can help determine if they contribute to cough.

The three most common causes of chronic cough — rhinosinusitis, asthma, and gastroesophageal reflux disease — should be ruled out. Diagnosis is based on history, physical examination, and specific tests: Nasofibroscopy for rhinosinusitis, spirometry, fractional exhaled nitric oxide for asthma and clinical history of gastroesophageal reflux disease. Studies have indicated that asthma may develop after a COVID infection.

Laryngeal abnormalities are also common in chronic post-COVID cough. One study found that a quarter of patients had increased laryngeal sensitivity or voice changes. “The larynx, a highly cough-producing organ, causes more coughing than the lungs,” Guilleminault explained.

Laryngeal abnormalities are frequently observed. A study found that 63% of patients experienced dysphonia, 56% had a sensation of a foreign body in the larynx, and 10% experienced laryngospasms.

These issues are common in patients with post-COVID cough and are often associated with neurological dysfunction. Innervation of the larynx is complex and can be affected by viruses, leading to hypersensitivity, paresthesia, and other sensory disturbances, which may explain the laryngeal symptoms observed in these patients.

Next Steps

If common causes such as asthma, abnormal imaging findings, or laryngeal pathology are ruled out, the condition may be classified as a chronic refractory or unexplained cough. In these cases, the neurological origin is likely due to nervous system dysfunction. Neuromodulatory treatments including amitriptyline, pregabalin, and gabapentin may be considered in some cases. Corticosteroids are generally ineffective against chronic coughs.

This story was translated from Medscape’s French edition using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication.

Chronic cough remains a common reason for consultation in pulmonology post–COVID-19. But what do we really know about this condition, now 5 years after the pandemic’s onset? This topic was discussed at the recent French-Speaking Pneumology Congress held in Marseille, France, from January 24-26, 2025.

Before discussing post-COVID cough, it is crucial to differentiate between an acute cough, often viral in origin (including those associated with SARS-CoV-2), a subacute cough (lasting 3-8 weeks), and a chronic cough (persisting over 8 weeks).

“This distinction allows us to tailor treatment and prescribe the appropriate investigations, according to the duration and the probability of symptom resolution,” explained Laurent Guilleminault, MD, PhD, pulmonologist at Toulouse University Hospital Centre, Toulouse, France.

In the case of an acute cough, for instance, after a viral infection, the probability of spontaneous resolution is very high. It is often unnecessary to carry out additional examinations or initiate specific treatments because none has proven its effectiveness in shortening this type of cough. On the other hand, when a cough persists beyond 8 weeks, the chance of spontaneous resolution decreases considerably. “This is when an assessment is necessary to identify a possible underlying cause,” Guilleminault noted.

“The absence of coughing during the consultation should not lead to ruling out a diagnosis,” he added.

Neurological Link

A large-scale French study of 70,000 patients examined the demographic profiles of patients with COVID-19. It revealed a lower frequency of coughing among children and older individuals, with a notable prevalence among adults aged 30-60 years.

Furthermore, during the acute phase of COVID, coughing did not appear to indicate severity. A comparison between survivors and nonsurvivors revealed no significant differences in the frequency and severity of coughing. Another study concluded that, contrary to expectations, COVID-related pneumonia, although potentially severe, does not necessarily involve severe cough.

These findings highlight the absence of a direct link between coughing and pulmonary involvement in patients with COVID-19.

“Coughing appears to be more closely linked to neurological dysfunction than to classic respiratory involvement. A distinction that is essential for better understanding the pathophysiology of the disease and guiding therapeutic strategies,” Guilleminault noted.

Cough Mechanism

“The analysis of cough in the context of phylogenetic evolution is fascinating,” explained Guilleminault. “It illustrates how this reflex has provided an advantage to the virus for its propagation.” Studies on the transmission of SARS-CoV-2 have confirmed that coughing plays a key role in the spread of viral particles. However, this mechanism does not involve severe pulmonary damage. The primary goal of the virus is to induce neurological dysfunction in the host by triggering a cough reflex. This neurological activation enables the virus to trigger a cough reflex for dissemination even without significant pulmonary damage. This mechanism provides an evolutionary advantage by enhancing the ability of the virus to spread and colonize new hosts.

The cough mechanism remains partially understood and involves cough hypersensitivity, characterized by increased neural responsivity to a range of stimuli that affect the airways, lungs, and other tissues innervated by common nerve supplies. The cough reflex begins with the activation of sensitive peripheral receptors located mainly in the respiratory tract that detect irritants or abnormalities.

These receptors, such as P2X2, P2X3, and others, transmit information to the brainstem, which coordinates the reflex response. This process is modulated by cortical controls that normally inhibit spontaneous coughing, explaining why we do not cough constantly even in the presence of moderate stimuli.

However, when there is an imbalance in this inhibition mechanism, coughing can be triggered either excessively or uncontrollably. SARS-CoV-2 appears to interact directly with these peripheral receptors, stimulating the cough reflex. The widespread presence and density of these receptors make this mechanism highly effective for the virus’s transmission.

Additionally, the vagus nerve likely plays a central role in triggering cough, particularly in viral infections. Studies of influenza have shown the involvement of sensory cells associated with the vagus nerve.

The virus stimulates the vagus nerve, which activates the cough reflex. Research suggests that neurotropism, neuroinflammation, and neuroimmunomodulation via the vagal sensory nerves, which are involved in SARS-CoV-2 infection, lead to cough hypersensitivity.

One question remains: Could vagus nerve involvement prolong coughing beyond the active phase of viral infection? The data indicate that viral infection significantly increases the sensitivity of the cough reflex, regardless of the level of irritation. The brain areas involved in inhibiting this reflex appear less effective during viral infection, resulting in reduced inhibitory control and easier triggering of cough. This phenomenon reflects temporary dysfunction of the neurological modulation system, which gradually recovers after recovery.

Long-Term Effects

The epidemiology of post-COVID cough and its integration into the framework of the long COVID framework remain subjects of ongoing debate. Early studies have revealed that cough could be either an isolated symptom or associated with other manifestations of long COVID. These studies were often conducted over relatively short periods (14-110 days) and estimated that approximately 19% of patients with long COVID experienced persistent cough. Another study found that 14% of patients reported cough between 3 weeks and 3 months after hospital discharge for COVID-19.

Longer follow-up periods showed a significant decrease in the prevalence of cough over time. For instance, a 1-year study reported that only 2.5% of patients had episodes of chronic cough.

However, a 2023 study published in JAMA found that the prevalence of post-COVID chronic cough exceeded 30% in some groups of patients.

“It is not relevant to wait so long before acting,” Guilleminault said. A reasonable threshold for evaluation and treatment is 8-12 weeks postinfection to begin investigations and consider appropriate treatment. What should be done when a patient presents with “Doctor, I had COVID, I have a cough, and it hasn’t stopped?” These situations are common in clinical practice. In terms of severity, quality of life, and overall impact, patients with chronic post-COVID cough are not significantly different from those with other chronic coughs. Moreover, both conditions involve a real neurological dysfunction.

Same Diagnostic Steps

Management should follow existing guidelines, including the recent French recommendations for chronic cough.

A visual analog scale can be used, and possible complications should be assessed. A chest x-ray is recommended to identify any warning signs, such as cough, although linked to COVID — may coincide with other conditions, such as bronchial cancer. In smokers, chest CT should be considered to rule out neoplastic pathology. The presence of interstitial lesions, particularly fibrosing lesions, suggests that fibrosing interstitial pneumonia requires specialized management.

Smoking, which is an aggravating factor, should be discontinued. Discontinuing angiotensin-converting enzyme inhibitors for 4 weeks can help determine if they contribute to cough.

The three most common causes of chronic cough — rhinosinusitis, asthma, and gastroesophageal reflux disease — should be ruled out. Diagnosis is based on history, physical examination, and specific tests: Nasofibroscopy for rhinosinusitis, spirometry, fractional exhaled nitric oxide for asthma and clinical history of gastroesophageal reflux disease. Studies have indicated that asthma may develop after a COVID infection.

Laryngeal abnormalities are also common in chronic post-COVID cough. One study found that a quarter of patients had increased laryngeal sensitivity or voice changes. “The larynx, a highly cough-producing organ, causes more coughing than the lungs,” Guilleminault explained.

Laryngeal abnormalities are frequently observed. A study found that 63% of patients experienced dysphonia, 56% had a sensation of a foreign body in the larynx, and 10% experienced laryngospasms.

These issues are common in patients with post-COVID cough and are often associated with neurological dysfunction. Innervation of the larynx is complex and can be affected by viruses, leading to hypersensitivity, paresthesia, and other sensory disturbances, which may explain the laryngeal symptoms observed in these patients.

Next Steps

If common causes such as asthma, abnormal imaging findings, or laryngeal pathology are ruled out, the condition may be classified as a chronic refractory or unexplained cough. In these cases, the neurological origin is likely due to nervous system dysfunction. Neuromodulatory treatments including amitriptyline, pregabalin, and gabapentin may be considered in some cases. Corticosteroids are generally ineffective against chronic coughs.

This story was translated from Medscape’s French edition using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication.

TOPLINE:

Better lung function, expressed as higher forced vital capacity (FVC), is associated with a reduced risk for the onset of heart disease, diabetes, and stroke over a follow-up period of approximately 10 years, according to a cross-sectional analysis of a population-based study.

METHODOLOGY:

• Researchers conducted a cross-sectional analysis of a population-based study (the BOLD study) between 2003 and 2016 to investigate the association between lung function and the onset of cardiometabolic diseases by using data from participants across 15 countries.
• Overall, 5916 participants (mean age, 54 years; 55% women) were included, and the mean follow-up duration was 9.5 years.
• Lung function was evaluated as forced expiratory volume in 1 second (FEV1), FVC, and FEV1/FVC ratio, measured using spirometry at baseline, and postbronchodilator values of these measures were expressed as the percent of the predicted values at baseline.
• The onset of cardiometabolic diseases was identified through participant-reported doctor diagnoses of hypertension, heart disease, diabetes, and stroke at follow-up but not at baseline.

TAKEAWAY:

• Each 10% predicted FVC was associated with a 9% reduced risk for the onset of diabetes (adjusted odds ratio [aOR], 0.91; 95% CI, 0.84-0.99), a 14% reduced risk for the onset of heart disease (aOR, 0.86; 95% CI, 0.80-0.92), and a 19% reduced risk for the onset of stroke (aOR, 0.81; 95% CI, 0.73-0.89).
• Each 10% predicted FEV1 was associated with a reduced risk for the onset of heart disease (aOR, 0.88; 95% CI, 0.83-0.94) and stroke (aOR, 0.83; 95% CI, 0.76-0.90).
• A high FEV1/FVC ratio was associated with an increased risk for the onset of diabetes (aOR per 10%, 1.21; 95% CI, 1.08-1.35) but not associated with other cardiometabolic diseases.
• Moderate heterogeneity was observed across study sites regarding the association between high lung function and the risk for the onset of diabetes and stroke.

IN PRACTICE:

“FVC is not included in any risk score for predicting the risk of cardiometabolic events, although data also suggests that FVC predicted mortality more strongly than systolic blood pressure or BMI [body mass index]. Our results and several previous studies suggest that including FVC will improve the precision of risk scores used to predict the onset of diabetes and cardiovascular diseases,” the authors wrote.

SOURCE:

This study was led by Christer Janson, Department of Medical Sciences Respiratory Medicine, Uppsala Universitet, Uppsala, Sweden. It was published online on January 19, 2025, in BMJ Open Respiratory Research.

LIMITATIONS:

The primary limitation of this study was the reliance on the self-reported onset of cardiometabolic diseases, which is particularly challenging in low- and middle-income countries with underdeveloped healthcare systems. The observed outcomes could be the result of an undiagnosed condition. The data did not allow differentiation between various types of heart diseases or strokes.

DISCLOSURES:

The BOLD study received support through grants from the Wellcome Trust and Medical Research Council, and the follow-up study at some centers was supported by an unrestricted grant from AstraZeneca. Four authors reported receiving support from various sources related or unrelated to this work.

This article was created using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication.

TOPLINE:

Better lung function, expressed as higher forced vital capacity (FVC), is associated with a reduced risk for the onset of heart disease, diabetes, and stroke over a follow-up period of approximately 10 years, according to a cross-sectional analysis of a population-based study.

METHODOLOGY:

• Researchers conducted a cross-sectional analysis of a population-based study (the BOLD study) between 2003 and 2016 to investigate the association between lung function and the onset of cardiometabolic diseases by using data from participants across 15 countries.
• Overall, 5916 participants (mean age, 54 years; 55% women) were included, and the mean follow-up duration was 9.5 years.
• Lung function was evaluated as forced expiratory volume in 1 second (FEV1), FVC, and FEV1/FVC ratio, measured using spirometry at baseline, and postbronchodilator values of these measures were expressed as the percent of the predicted values at baseline.
• The onset of cardiometabolic diseases was identified through participant-reported doctor diagnoses of hypertension, heart disease, diabetes, and stroke at follow-up but not at baseline.

TAKEAWAY:

• Each 10% predicted FVC was associated with a 9% reduced risk for the onset of diabetes (adjusted odds ratio [aOR], 0.91; 95% CI, 0.84-0.99), a 14% reduced risk for the onset of heart disease (aOR, 0.86; 95% CI, 0.80-0.92), and a 19% reduced risk for the onset of stroke (aOR, 0.81; 95% CI, 0.73-0.89).
• Each 10% predicted FEV1 was associated with a reduced risk for the onset of heart disease (aOR, 0.88; 95% CI, 0.83-0.94) and stroke (aOR, 0.83; 95% CI, 0.76-0.90).
• A high FEV1/FVC ratio was associated with an increased risk for the onset of diabetes (aOR per 10%, 1.21; 95% CI, 1.08-1.35) but not associated with other cardiometabolic diseases.
• Moderate heterogeneity was observed across study sites regarding the association between high lung function and the risk for the onset of diabetes and stroke.

IN PRACTICE:

“FVC is not included in any risk score for predicting the risk of cardiometabolic events, although data also suggests that FVC predicted mortality more strongly than systolic blood pressure or BMI [body mass index]. Our results and several previous studies suggest that including FVC will improve the precision of risk scores used to predict the onset of diabetes and cardiovascular diseases,” the authors wrote.

SOURCE:

This study was led by Christer Janson, Department of Medical Sciences Respiratory Medicine, Uppsala Universitet, Uppsala, Sweden. It was published online on January 19, 2025, in BMJ Open Respiratory Research.

LIMITATIONS:

The primary limitation of this study was the reliance on the self-reported onset of cardiometabolic diseases, which is particularly challenging in low- and middle-income countries with underdeveloped healthcare systems. The observed outcomes could be the result of an undiagnosed condition. The data did not allow differentiation between various types of heart diseases or strokes.

DISCLOSURES:

The BOLD study received support through grants from the Wellcome Trust and Medical Research Council, and the follow-up study at some centers was supported by an unrestricted grant from AstraZeneca. Four authors reported receiving support from various sources related or unrelated to this work.

This article was created using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication.

TOPLINE:

Better lung function, expressed as higher forced vital capacity (FVC), is associated with a reduced risk for the onset of heart disease, diabetes, and stroke over a follow-up period of approximately 10 years, according to a cross-sectional analysis of a population-based study.

METHODOLOGY:

• Researchers conducted a cross-sectional analysis of a population-based study (the BOLD study) between 2003 and 2016 to investigate the association between lung function and the onset of cardiometabolic diseases by using data from participants across 15 countries.
• Overall, 5916 participants (mean age, 54 years; 55% women) were included, and the mean follow-up duration was 9.5 years.
• Lung function was evaluated as forced expiratory volume in 1 second (FEV1), FVC, and FEV1/FVC ratio, measured using spirometry at baseline, and postbronchodilator values of these measures were expressed as the percent of the predicted values at baseline.
• The onset of cardiometabolic diseases was identified through participant-reported doctor diagnoses of hypertension, heart disease, diabetes, and stroke at follow-up but not at baseline.

TAKEAWAY:

• Each 10% predicted FVC was associated with a 9% reduced risk for the onset of diabetes (adjusted odds ratio [aOR], 0.91; 95% CI, 0.84-0.99), a 14% reduced risk for the onset of heart disease (aOR, 0.86; 95% CI, 0.80-0.92), and a 19% reduced risk for the onset of stroke (aOR, 0.81; 95% CI, 0.73-0.89).
• Each 10% predicted FEV1 was associated with a reduced risk for the onset of heart disease (aOR, 0.88; 95% CI, 0.83-0.94) and stroke (aOR, 0.83; 95% CI, 0.76-0.90).
• A high FEV1/FVC ratio was associated with an increased risk for the onset of diabetes (aOR per 10%, 1.21; 95% CI, 1.08-1.35) but not associated with other cardiometabolic diseases.
• Moderate heterogeneity was observed across study sites regarding the association between high lung function and the risk for the onset of diabetes and stroke.

IN PRACTICE:

“FVC is not included in any risk score for predicting the risk of cardiometabolic events, although data also suggests that FVC predicted mortality more strongly than systolic blood pressure or BMI [body mass index]. Our results and several previous studies suggest that including FVC will improve the precision of risk scores used to predict the onset of diabetes and cardiovascular diseases,” the authors wrote.

SOURCE:

This study was led by Christer Janson, Department of Medical Sciences Respiratory Medicine, Uppsala Universitet, Uppsala, Sweden. It was published online on January 19, 2025, in BMJ Open Respiratory Research.

LIMITATIONS:

The primary limitation of this study was the reliance on the self-reported onset of cardiometabolic diseases, which is particularly challenging in low- and middle-income countries with underdeveloped healthcare systems. The observed outcomes could be the result of an undiagnosed condition. The data did not allow differentiation between various types of heart diseases or strokes.

DISCLOSURES:

The BOLD study received support through grants from the Wellcome Trust and Medical Research Council, and the follow-up study at some centers was supported by an unrestricted grant from AstraZeneca. Four authors reported receiving support from various sources related or unrelated to this work.

This article was created using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication.

In 2016, Brady Scott was in his parents’ home in Garrett, Kentucky, scrolling his Facebook feed when a post from a local newspaper caught his attention. “The article said that if you grew up in the region I grew up in, compared to the richer Central Kentucky region, the life expectancy differed by about 9 years,” he recalled.

The respiratory therapist, then a PhD student at Rush University, Chicago, was struck and began “Googling” to find out why this was the case. Initially, he thought diabetes, smoking, and economic distress — all prevalent problems in the area — were the culprits. However, he soon found that respiratory disease was particularly common in his region.

Now a professor and program director of the Respiratory Care Program at Rush University, Scott has spent several years trying to understand why people in certain regions experience respiratory illness at higher rates than in other places.

 

The Environment as a Determinant of Health

When Scott began his PhD, the prevalence of asthma in Southeast Kentucky, part of the Appalachian region, was already well-documented. He focused his research on uncontrolled asthma and the triggers that drove asthma exacerbations.

Housing quality emerged as an important factor. He found that exposure to mold, mildew, dust mites, pests, and rodents increased the risk for asthma and exacerbated existing cases. Lower-income families, more likely to live in poor-quality housing, were significantly affected, even in single-family homes.

Wanda Phipatanakul, MD, MS, director of the Division of Immunology Research Center at Boston Children’s Hospital and S. Jean Emans professor of Pediatrics at Harvard Medical School, Boston, has found similar results in urban environments. She said cockroach and mouse allergen exposure is disproportionately prevalent in urban, low-income neighborhoods. These exposures, closely tied to housing conditions, contribute to worse asthma and respiratory problems, particularly in children.

Scott and Phipatanakul agreed that the environment surrounding people’s homes can also exacerbate respiratory disease.

Rural areas present unique risks, such as agricultural activities that release pesticides and other particulates into the air, said Scott. In mountainous areas like Appalachia, mining operations are another significant contributor. For example, blasting mountains with dynamite creates large clouds of dust and pollutants that settle in valleys. Coal-hauling roads contribute to air quality issues, too. And houses near these roads may be exposed to increased levels of particulate matter, he said.

In the city, Phipatanakul has found that historical practices like redlining have systematically denied certain neighborhoods access to resources and investment, leaving a legacy of poor infrastructure, limited resources, and higher exposure to environmental risks. Today, these areas have more highways and fewer green spaces and are disproportionately linked with a higher incidence of respiratory illnesses.

The findings of both Scott and Phipatanakul underscore a critical bottom line: Health disparities are deeply influenced by environmental factors, which are themselves shaped by socioeconomic conditions and historical inequities. Poor housing quality, exposure to allergens, and proximity to environmental hazards disproportionately affect underserved and minority communities, whether in rural or urban settings.

 

The Role of Green Spaces in Improving Respiratory Health

Restoring and increasing tree cover and green spaces in urban areas can significantly improve respiratory health by addressing environmental challenges and reducing triggers for respiratory issues. Areas with greater greenness tend to have lower levels of pollutants and fewer environmental infestations, such as mice and cockroaches, explained Phipatanakul. Her research highlights that schools in greener areas have fewer airborne pollutants and particles than those in more urbanized, less green areas, which are usually in poorer suburbs.

Trees absorb pollutants such as particulate matter and sulfur dioxide through dry deposition and stomatal uptake, improving air quality. “The question is whether we can use trees as a public health tool, and this is being done in many cities,” said Alessandro Marcon, PhD, a professor of epidemiology and medical statistics at the University of Verona, Verona, Italy, while speaking at the European Respiratory Society conference held in Vienna last September.

A US analysis showed that existing natural vegetation, such as forests and grasslands, absorbs a large portion of emissions. By restoring land cover, pollution from harmful substances like sulfur dioxide and particulate matter could be reduced by about 30%. This approach is often more cost-effective than technological solutions for managing emissions.

Moreover, tree cover contributes to a healthier air microbiome. Research indicates that urban forest areas have lower pathogenic bacteria and fungi concentrations than nearby urban zones.

Another major advantage is the mitigation of the urban heat island effect. A study conducted in Paris found that municipalities with higher tree coverage experienced 20%-30% lower heat-related mortality than those with less greenery. Increasing tree coverage to 30% could reduce up to 40% of excess mortality associated with urban heat islands. Trees achieve this by providing shade and facilitating evapotranspiration, which cools the surrounding air.

Urban environments, unsurprisingly, often have higher levels of air pollution due to increased traffic and industrial activity. However, despite appearing greener, rural environments may harbor less obvious but significant sources of air pollution. “I live in an urban environment now, but I grew up in a rural environment,” Scott said. “Each has its own issues that affect air quality and health.”

Scott, Phipatanakul, and Marcon reported no relevant financial relationships.

A version of this article first appeared on Medscape.com.

In 2016, Brady Scott was in his parents’ home in Garrett, Kentucky, scrolling his Facebook feed when a post from a local newspaper caught his attention. “The article said that if you grew up in the region I grew up in, compared to the richer Central Kentucky region, the life expectancy differed by about 9 years,” he recalled.

The respiratory therapist, then a PhD student at Rush University, Chicago, was struck and began “Googling” to find out why this was the case. Initially, he thought diabetes, smoking, and economic distress — all prevalent problems in the area — were the culprits. However, he soon found that respiratory disease was particularly common in his region.

Now a professor and program director of the Respiratory Care Program at Rush University, Scott has spent several years trying to understand why people in certain regions experience respiratory illness at higher rates than in other places.

 

The Environment as a Determinant of Health

When Scott began his PhD, the prevalence of asthma in Southeast Kentucky, part of the Appalachian region, was already well-documented. He focused his research on uncontrolled asthma and the triggers that drove asthma exacerbations.

Housing quality emerged as an important factor. He found that exposure to mold, mildew, dust mites, pests, and rodents increased the risk for asthma and exacerbated existing cases. Lower-income families, more likely to live in poor-quality housing, were significantly affected, even in single-family homes.

Wanda Phipatanakul, MD, MS, director of the Division of Immunology Research Center at Boston Children’s Hospital and S. Jean Emans professor of Pediatrics at Harvard Medical School, Boston, has found similar results in urban environments. She said cockroach and mouse allergen exposure is disproportionately prevalent in urban, low-income neighborhoods. These exposures, closely tied to housing conditions, contribute to worse asthma and respiratory problems, particularly in children.

Scott and Phipatanakul agreed that the environment surrounding people’s homes can also exacerbate respiratory disease.

Rural areas present unique risks, such as agricultural activities that release pesticides and other particulates into the air, said Scott. In mountainous areas like Appalachia, mining operations are another significant contributor. For example, blasting mountains with dynamite creates large clouds of dust and pollutants that settle in valleys. Coal-hauling roads contribute to air quality issues, too. And houses near these roads may be exposed to increased levels of particulate matter, he said.

In the city, Phipatanakul has found that historical practices like redlining have systematically denied certain neighborhoods access to resources and investment, leaving a legacy of poor infrastructure, limited resources, and higher exposure to environmental risks. Today, these areas have more highways and fewer green spaces and are disproportionately linked with a higher incidence of respiratory illnesses.

The findings of both Scott and Phipatanakul underscore a critical bottom line: Health disparities are deeply influenced by environmental factors, which are themselves shaped by socioeconomic conditions and historical inequities. Poor housing quality, exposure to allergens, and proximity to environmental hazards disproportionately affect underserved and minority communities, whether in rural or urban settings.

 

The Role of Green Spaces in Improving Respiratory Health

Restoring and increasing tree cover and green spaces in urban areas can significantly improve respiratory health by addressing environmental challenges and reducing triggers for respiratory issues. Areas with greater greenness tend to have lower levels of pollutants and fewer environmental infestations, such as mice and cockroaches, explained Phipatanakul. Her research highlights that schools in greener areas have fewer airborne pollutants and particles than those in more urbanized, less green areas, which are usually in poorer suburbs.

Trees absorb pollutants such as particulate matter and sulfur dioxide through dry deposition and stomatal uptake, improving air quality. “The question is whether we can use trees as a public health tool, and this is being done in many cities,” said Alessandro Marcon, PhD, a professor of epidemiology and medical statistics at the University of Verona, Verona, Italy, while speaking at the European Respiratory Society conference held in Vienna last September.

A US analysis showed that existing natural vegetation, such as forests and grasslands, absorbs a large portion of emissions. By restoring land cover, pollution from harmful substances like sulfur dioxide and particulate matter could be reduced by about 30%. This approach is often more cost-effective than technological solutions for managing emissions.

Moreover, tree cover contributes to a healthier air microbiome. Research indicates that urban forest areas have lower pathogenic bacteria and fungi concentrations than nearby urban zones.

Another major advantage is the mitigation of the urban heat island effect. A study conducted in Paris found that municipalities with higher tree coverage experienced 20%-30% lower heat-related mortality than those with less greenery. Increasing tree coverage to 30% could reduce up to 40% of excess mortality associated with urban heat islands. Trees achieve this by providing shade and facilitating evapotranspiration, which cools the surrounding air.

Urban environments, unsurprisingly, often have higher levels of air pollution due to increased traffic and industrial activity. However, despite appearing greener, rural environments may harbor less obvious but significant sources of air pollution. “I live in an urban environment now, but I grew up in a rural environment,” Scott said. “Each has its own issues that affect air quality and health.”

Scott, Phipatanakul, and Marcon reported no relevant financial relationships.

A version of this article first appeared on Medscape.com.

In 2016, Brady Scott was in his parents’ home in Garrett, Kentucky, scrolling his Facebook feed when a post from a local newspaper caught his attention. “The article said that if you grew up in the region I grew up in, compared to the richer Central Kentucky region, the life expectancy differed by about 9 years,” he recalled.

The respiratory therapist, then a PhD student at Rush University, Chicago, was struck and began “Googling” to find out why this was the case. Initially, he thought diabetes, smoking, and economic distress — all prevalent problems in the area — were the culprits. However, he soon found that respiratory disease was particularly common in his region.

Now a professor and program director of the Respiratory Care Program at Rush University, Scott has spent several years trying to understand why people in certain regions experience respiratory illness at higher rates than in other places.

 

The Environment as a Determinant of Health

When Scott began his PhD, the prevalence of asthma in Southeast Kentucky, part of the Appalachian region, was already well-documented. He focused his research on uncontrolled asthma and the triggers that drove asthma exacerbations.

Housing quality emerged as an important factor. He found that exposure to mold, mildew, dust mites, pests, and rodents increased the risk for asthma and exacerbated existing cases. Lower-income families, more likely to live in poor-quality housing, were significantly affected, even in single-family homes.

Wanda Phipatanakul, MD, MS, director of the Division of Immunology Research Center at Boston Children’s Hospital and S. Jean Emans professor of Pediatrics at Harvard Medical School, Boston, has found similar results in urban environments. She said cockroach and mouse allergen exposure is disproportionately prevalent in urban, low-income neighborhoods. These exposures, closely tied to housing conditions, contribute to worse asthma and respiratory problems, particularly in children.

Scott and Phipatanakul agreed that the environment surrounding people’s homes can also exacerbate respiratory disease.

Rural areas present unique risks, such as agricultural activities that release pesticides and other particulates into the air, said Scott. In mountainous areas like Appalachia, mining operations are another significant contributor. For example, blasting mountains with dynamite creates large clouds of dust and pollutants that settle in valleys. Coal-hauling roads contribute to air quality issues, too. And houses near these roads may be exposed to increased levels of particulate matter, he said.

In the city, Phipatanakul has found that historical practices like redlining have systematically denied certain neighborhoods access to resources and investment, leaving a legacy of poor infrastructure, limited resources, and higher exposure to environmental risks. Today, these areas have more highways and fewer green spaces and are disproportionately linked with a higher incidence of respiratory illnesses.

The findings of both Scott and Phipatanakul underscore a critical bottom line: Health disparities are deeply influenced by environmental factors, which are themselves shaped by socioeconomic conditions and historical inequities. Poor housing quality, exposure to allergens, and proximity to environmental hazards disproportionately affect underserved and minority communities, whether in rural or urban settings.

 

The Role of Green Spaces in Improving Respiratory Health

Restoring and increasing tree cover and green spaces in urban areas can significantly improve respiratory health by addressing environmental challenges and reducing triggers for respiratory issues. Areas with greater greenness tend to have lower levels of pollutants and fewer environmental infestations, such as mice and cockroaches, explained Phipatanakul. Her research highlights that schools in greener areas have fewer airborne pollutants and particles than those in more urbanized, less green areas, which are usually in poorer suburbs.

Trees absorb pollutants such as particulate matter and sulfur dioxide through dry deposition and stomatal uptake, improving air quality. “The question is whether we can use trees as a public health tool, and this is being done in many cities,” said Alessandro Marcon, PhD, a professor of epidemiology and medical statistics at the University of Verona, Verona, Italy, while speaking at the European Respiratory Society conference held in Vienna last September.

A US analysis showed that existing natural vegetation, such as forests and grasslands, absorbs a large portion of emissions. By restoring land cover, pollution from harmful substances like sulfur dioxide and particulate matter could be reduced by about 30%. This approach is often more cost-effective than technological solutions for managing emissions.

Moreover, tree cover contributes to a healthier air microbiome. Research indicates that urban forest areas have lower pathogenic bacteria and fungi concentrations than nearby urban zones.

Another major advantage is the mitigation of the urban heat island effect. A study conducted in Paris found that municipalities with higher tree coverage experienced 20%-30% lower heat-related mortality than those with less greenery. Increasing tree coverage to 30% could reduce up to 40% of excess mortality associated with urban heat islands. Trees achieve this by providing shade and facilitating evapotranspiration, which cools the surrounding air.

Urban environments, unsurprisingly, often have higher levels of air pollution due to increased traffic and industrial activity. However, despite appearing greener, rural environments may harbor less obvious but significant sources of air pollution. “I live in an urban environment now, but I grew up in a rural environment,” Scott said. “Each has its own issues that affect air quality and health.”

Scott, Phipatanakul, and Marcon reported no relevant financial relationships.

A version of this article first appeared on Medscape.com.

Quitting smoking is challenging, particularly when resources are limited. A recent study in the United States confirmed that an intensive program combining behavioral therapy and medication, linked to a lung cancer screening program, offers the highest success rate. However, its long-term success was similar to that of telephone counseling and drug therapy.

Pulmonologist and experienced smoking cessation specialist from Stuttgart, Germany, Alexander Rupp, MD, emphasized the importance of leveraging routine healthcare interactions to encourage smoking cessation. “Although every doctor-patient contact offers the opportunity to discuss the risks of smoking and the opportunities for smoking cessation, the ‘window of opportunity’ is very wide, especially during lung cancer screening,” he said.

Germany is preparing to launch a lung cancer screening program for high-risk individuals, primarily current smokers and former smokers. Following the establishment of radiation protection regulations for such a program last year, the German Federal Joint Committee is currently working on its design. The initiative could be a game-changer for smoking cessation.

Lung cancer screening has been available for smokers in the United States for some time. Paul M. Cinciripini, PhD, and colleagues from the University of Texas MD Anderson Cancer Center, Houston, examined three smoking cessation strategies with decreasing treatment intensity among screening participants.

 

Unique Opportunity

Previous studies have shown that participation in a lung cancer screening program — typically offered only to high-risk individuals — significantly increases motivation to quit smoking.

“Repeated contact with doctors, repeated CT scans, and especially the findings that require monitoring all contribute to this effect,” explained Rupp, who regularly offers smoking cessation courses.

It has long been known how smoking cessation works best. “The gold standard is a combination of behavioral therapy support and drug treatment — if there is an addiction and withdrawal symptoms occur after quitting, which is the case for the majority of smokers,” Rupp explained.

The US study reinforced what is already well known: More intensive treatment approaches lead to higher quit rates.

“We know that the more intensively we look after smokers, the higher the quit rate. This applies in both areas: The more therapy sessions we do and the more often we prescribe medication, the more likely the patients are to succeed in remaining abstinent,” Rupp said.

However, resources for intensive smoking cessation programs are limited. A database maintained by the German Cancer Research Center and the German Federal Center for Health Education lists only 455 providers of smoking cessation courses in Germany, “not all of which even work on an evidence-based basis,” Rupp emphasized. Given that there are around 16 million smokers in Germany, there is an urgent need for smoking cessation programs that are less resource-intensive.

 

Intensity Variations

The US study compared three smoking cessation strategies of varying intensities, integrating behavioral counseling and medication.

Group 1: An integrated program with eight behavioral therapy sessions and 10-12 weeks of nicotine replacement therapy or medication (bupropion or varenicline).

Group 2: Lighter version of the integrated program. It consisted of four telephone consultations, written materials, online support, and 12 weeks of nicotine replacement therapy or medication prescribed by a radiologist.

Group 3: The least intensive approach, with 12 weeks of nicotine replacement therapy alone.

Each strategy was evaluated in 210 lung cancer screening participants aged 55-64 years who smoked an average of 15-20 cigarettes per day.

After 3 months, significantly more participants in the most intensive program (Group 1, 37.1%) had quit smoking than those in the other two groups (Group 2, 27.1%; Group 3, 25.2%).

But after 6 months, the difference between Groups 1 and 2 was not significant. The quit rates were as follows: Group 1, 32.4%; Group 2, 27.6%; and Group 3, 20.5%.

“It can be concluded from these results that the intensity of smoking cessation can be reduced to a certain extent as long as the combination of behavioral counseling and medication is given,” Rupp concluded.

 

Digital Solutions

Another new possibility, which was not examined in the US study, is digital health applications.

Smoke Free is a digital health application that provides behavioral therapy support for smoking cessation and is available in both German and English. Designed to replicate structured smoking cessation programs and offers an accessible alternative for individuals seeking to quit smoking.

Rupp emphasized the potential of digital tools like Smoke Free to expand access to effective smoking cessation strategies, particularly for those unable to attend in-person programs. While traditional cessation programs are limited in availability, digital apps can increase engagement in and adherence to smoking cessation efforts.

However, the biggest hurdle is smokers’ procrastination: “If you make smokers an offer, they usually do not take action afterward because they are caught in their ambivalence about whether they should quit or not.”

 

Policy Implications

This makes smoking cessation a mandatory component of lung cancer screening in the future. “It’s about cancer, and patients are really afraid of that,” Rupp advocated.

In a position paper, the German Respiratory Society, supported by multiple medical societies, has called for smoking cessation to be integrated into lung cancer screening protocols, with full coverage of counseling and medication by health insurance.

“Smoking cessation must be a mandatory component. If a participant in the lung cancer screening does not want this, then he or she must actively object,” stressed Rupp, lead author of the position paper. Also, the costs of smoking cessation, including those of withdrawal-inhibiting medication, must be fully covered by statutory health insurance, which has not been the case to date.

“That’s the only thing that makes sense. You can’t deny an addict access to proven treatments, especially when we know that a smoker who quits spontaneously without support has a relapse rate of 95%-97%, and the medication per se increases the quit rate by a factor of two or three,” Rupp concluded.

This story was translated and adapted from Medscape’s German edition using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication. A version of this article appeared on Medscape.com.

Quitting smoking is challenging, particularly when resources are limited. A recent study in the United States confirmed that an intensive program combining behavioral therapy and medication, linked to a lung cancer screening program, offers the highest success rate. However, its long-term success was similar to that of telephone counseling and drug therapy.

Pulmonologist and experienced smoking cessation specialist from Stuttgart, Germany, Alexander Rupp, MD, emphasized the importance of leveraging routine healthcare interactions to encourage smoking cessation. “Although every doctor-patient contact offers the opportunity to discuss the risks of smoking and the opportunities for smoking cessation, the ‘window of opportunity’ is very wide, especially during lung cancer screening,” he said.

Germany is preparing to launch a lung cancer screening program for high-risk individuals, primarily current smokers and former smokers. Following the establishment of radiation protection regulations for such a program last year, the German Federal Joint Committee is currently working on its design. The initiative could be a game-changer for smoking cessation.

Lung cancer screening has been available for smokers in the United States for some time. Paul M. Cinciripini, PhD, and colleagues from the University of Texas MD Anderson Cancer Center, Houston, examined three smoking cessation strategies with decreasing treatment intensity among screening participants.

 

Unique Opportunity

Previous studies have shown that participation in a lung cancer screening program — typically offered only to high-risk individuals — significantly increases motivation to quit smoking.

“Repeated contact with doctors, repeated CT scans, and especially the findings that require monitoring all contribute to this effect,” explained Rupp, who regularly offers smoking cessation courses.

It has long been known how smoking cessation works best. “The gold standard is a combination of behavioral therapy support and drug treatment — if there is an addiction and withdrawal symptoms occur after quitting, which is the case for the majority of smokers,” Rupp explained.

The US study reinforced what is already well known: More intensive treatment approaches lead to higher quit rates.

“We know that the more intensively we look after smokers, the higher the quit rate. This applies in both areas: The more therapy sessions we do and the more often we prescribe medication, the more likely the patients are to succeed in remaining abstinent,” Rupp said.

However, resources for intensive smoking cessation programs are limited. A database maintained by the German Cancer Research Center and the German Federal Center for Health Education lists only 455 providers of smoking cessation courses in Germany, “not all of which even work on an evidence-based basis,” Rupp emphasized. Given that there are around 16 million smokers in Germany, there is an urgent need for smoking cessation programs that are less resource-intensive.

 

Intensity Variations

The US study compared three smoking cessation strategies of varying intensities, integrating behavioral counseling and medication.

Group 1: An integrated program with eight behavioral therapy sessions and 10-12 weeks of nicotine replacement therapy or medication (bupropion or varenicline).

Group 2: Lighter version of the integrated program. It consisted of four telephone consultations, written materials, online support, and 12 weeks of nicotine replacement therapy or medication prescribed by a radiologist.

Group 3: The least intensive approach, with 12 weeks of nicotine replacement therapy alone.

Each strategy was evaluated in 210 lung cancer screening participants aged 55-64 years who smoked an average of 15-20 cigarettes per day.

After 3 months, significantly more participants in the most intensive program (Group 1, 37.1%) had quit smoking than those in the other two groups (Group 2, 27.1%; Group 3, 25.2%).

But after 6 months, the difference between Groups 1 and 2 was not significant. The quit rates were as follows: Group 1, 32.4%; Group 2, 27.6%; and Group 3, 20.5%.

“It can be concluded from these results that the intensity of smoking cessation can be reduced to a certain extent as long as the combination of behavioral counseling and medication is given,” Rupp concluded.

 

Digital Solutions

Another new possibility, which was not examined in the US study, is digital health applications.

Smoke Free is a digital health application that provides behavioral therapy support for smoking cessation and is available in both German and English. Designed to replicate structured smoking cessation programs and offers an accessible alternative for individuals seeking to quit smoking.

Rupp emphasized the potential of digital tools like Smoke Free to expand access to effective smoking cessation strategies, particularly for those unable to attend in-person programs. While traditional cessation programs are limited in availability, digital apps can increase engagement in and adherence to smoking cessation efforts.

However, the biggest hurdle is smokers’ procrastination: “If you make smokers an offer, they usually do not take action afterward because they are caught in their ambivalence about whether they should quit or not.”

 

Policy Implications

This makes smoking cessation a mandatory component of lung cancer screening in the future. “It’s about cancer, and patients are really afraid of that,” Rupp advocated.

In a position paper, the German Respiratory Society, supported by multiple medical societies, has called for smoking cessation to be integrated into lung cancer screening protocols, with full coverage of counseling and medication by health insurance.

“Smoking cessation must be a mandatory component. If a participant in the lung cancer screening does not want this, then he or she must actively object,” stressed Rupp, lead author of the position paper. Also, the costs of smoking cessation, including those of withdrawal-inhibiting medication, must be fully covered by statutory health insurance, which has not been the case to date.

“That’s the only thing that makes sense. You can’t deny an addict access to proven treatments, especially when we know that a smoker who quits spontaneously without support has a relapse rate of 95%-97%, and the medication per se increases the quit rate by a factor of two or three,” Rupp concluded.

This story was translated and adapted from Medscape’s German edition using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication. A version of this article appeared on Medscape.com.

Quitting smoking is challenging, particularly when resources are limited. A recent study in the United States confirmed that an intensive program combining behavioral therapy and medication, linked to a lung cancer screening program, offers the highest success rate. However, its long-term success was similar to that of telephone counseling and drug therapy.

Pulmonologist and experienced smoking cessation specialist from Stuttgart, Germany, Alexander Rupp, MD, emphasized the importance of leveraging routine healthcare interactions to encourage smoking cessation. “Although every doctor-patient contact offers the opportunity to discuss the risks of smoking and the opportunities for smoking cessation, the ‘window of opportunity’ is very wide, especially during lung cancer screening,” he said.

Germany is preparing to launch a lung cancer screening program for high-risk individuals, primarily current smokers and former smokers. Following the establishment of radiation protection regulations for such a program last year, the German Federal Joint Committee is currently working on its design. The initiative could be a game-changer for smoking cessation.

Lung cancer screening has been available for smokers in the United States for some time. Paul M. Cinciripini, PhD, and colleagues from the University of Texas MD Anderson Cancer Center, Houston, examined three smoking cessation strategies with decreasing treatment intensity among screening participants.

 

Unique Opportunity

Previous studies have shown that participation in a lung cancer screening program — typically offered only to high-risk individuals — significantly increases motivation to quit smoking.

“Repeated contact with doctors, repeated CT scans, and especially the findings that require monitoring all contribute to this effect,” explained Rupp, who regularly offers smoking cessation courses.

It has long been known how smoking cessation works best. “The gold standard is a combination of behavioral therapy support and drug treatment — if there is an addiction and withdrawal symptoms occur after quitting, which is the case for the majority of smokers,” Rupp explained.

The US study reinforced what is already well known: More intensive treatment approaches lead to higher quit rates.

“We know that the more intensively we look after smokers, the higher the quit rate. This applies in both areas: The more therapy sessions we do and the more often we prescribe medication, the more likely the patients are to succeed in remaining abstinent,” Rupp said.

However, resources for intensive smoking cessation programs are limited. A database maintained by the German Cancer Research Center and the German Federal Center for Health Education lists only 455 providers of smoking cessation courses in Germany, “not all of which even work on an evidence-based basis,” Rupp emphasized. Given that there are around 16 million smokers in Germany, there is an urgent need for smoking cessation programs that are less resource-intensive.

 

Intensity Variations

The US study compared three smoking cessation strategies of varying intensities, integrating behavioral counseling and medication.

Group 1: An integrated program with eight behavioral therapy sessions and 10-12 weeks of nicotine replacement therapy or medication (bupropion or varenicline).

Group 2: Lighter version of the integrated program. It consisted of four telephone consultations, written materials, online support, and 12 weeks of nicotine replacement therapy or medication prescribed by a radiologist.

Group 3: The least intensive approach, with 12 weeks of nicotine replacement therapy alone.

Each strategy was evaluated in 210 lung cancer screening participants aged 55-64 years who smoked an average of 15-20 cigarettes per day.

After 3 months, significantly more participants in the most intensive program (Group 1, 37.1%) had quit smoking than those in the other two groups (Group 2, 27.1%; Group 3, 25.2%).

But after 6 months, the difference between Groups 1 and 2 was not significant. The quit rates were as follows: Group 1, 32.4%; Group 2, 27.6%; and Group 3, 20.5%.

“It can be concluded from these results that the intensity of smoking cessation can be reduced to a certain extent as long as the combination of behavioral counseling and medication is given,” Rupp concluded.

 

Digital Solutions

Another new possibility, which was not examined in the US study, is digital health applications.

Smoke Free is a digital health application that provides behavioral therapy support for smoking cessation and is available in both German and English. Designed to replicate structured smoking cessation programs and offers an accessible alternative for individuals seeking to quit smoking.

Rupp emphasized the potential of digital tools like Smoke Free to expand access to effective smoking cessation strategies, particularly for those unable to attend in-person programs. While traditional cessation programs are limited in availability, digital apps can increase engagement in and adherence to smoking cessation efforts.

However, the biggest hurdle is smokers’ procrastination: “If you make smokers an offer, they usually do not take action afterward because they are caught in their ambivalence about whether they should quit or not.”

 

Policy Implications

This makes smoking cessation a mandatory component of lung cancer screening in the future. “It’s about cancer, and patients are really afraid of that,” Rupp advocated.

In a position paper, the German Respiratory Society, supported by multiple medical societies, has called for smoking cessation to be integrated into lung cancer screening protocols, with full coverage of counseling and medication by health insurance.

“Smoking cessation must be a mandatory component. If a participant in the lung cancer screening does not want this, then he or she must actively object,” stressed Rupp, lead author of the position paper. Also, the costs of smoking cessation, including those of withdrawal-inhibiting medication, must be fully covered by statutory health insurance, which has not been the case to date.

“That’s the only thing that makes sense. You can’t deny an addict access to proven treatments, especially when we know that a smoker who quits spontaneously without support has a relapse rate of 95%-97%, and the medication per se increases the quit rate by a factor of two or three,” Rupp concluded.

This story was translated and adapted from Medscape’s German edition using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication. A version of this article appeared on Medscape.com.

In 2016, Brady Scott was in his parents’ home in Garrett, Kentucky, scrolling his Facebook feed when a post from a local newspaper caught his attention. “The article said that if you grew up in the region I grew up in, compared to the richer Central Kentucky region, the life expectancy differed by about 9 years,” he recalled.

The respiratory therapist, then a PhD student at Rush University, Chicago, was struck and began “Googling” to find out why this was the case. Initially, he thought diabetes, smoking, and economic distress — all prevalent problems in the area — were the culprits. However, he soon found that respiratory disease was particularly common in his region.

Now a professor and program director of the Respiratory Care Program at Rush University, Scott has spent several years trying to understand why people in certain regions experience respiratory illness at higher rates than in other places.

The Environment as a Determinant of Health

When Scott began his PhD, the prevalence of asthma in Southeast Kentucky, part of the Appalachian region, was already well-documented. He focused his research on uncontrolled asthma and the triggers that drove asthma exacerbations.

Housing quality emerged as an important factor. He found that exposure to mold, mildew, dust mites, pests, and rodents increased the risk for asthma and exacerbated existing cases. Lower-income families, more likely to live in poor-quality housing, were significantly affected, even in single-family homes.

Wanda Phipatanakul, MD, MS, director of the Division of Immunology Research Center at Boston Children’s Hospital and S. Jean Emans professor of Pediatrics at Harvard Medical School, Boston, has found similar results in urban environments. She said cockroach and mouse allergen exposure is disproportionately prevalent in urban, low-income neighborhoods. These exposures, closely tied to housing conditions, contribute to worse asthma and respiratory problems, particularly in children.

Scott and Phipatanakul agreed that the environment surrounding people’s homes can also exacerbate respiratory disease.

Rural areas present unique risks, such as agricultural activities that release pesticides and other particulates into the air, said Scott. In mountainous areas like Appalachia, mining operations are another significant contributor. For example, blasting mountains with dynamite creates large clouds of dust and pollutants that settle in valleys. Coal-hauling roads contribute to air quality issues, too. And houses near these roads may be exposed to increased levels of particulate matter, he said.

In the city, Phipatanakul has found that historical practices like redlining have systematically denied certain neighborhoods access to resources and investment, leaving a legacy of poor infrastructure, limited resources, and higher exposure to environmental risks. Today, these areas have more highways and fewer green spaces and are disproportionately linked with a higher incidence of respiratory illnesses.

The findings of both Scott and Phipatanakul underscore a critical bottom line: Health disparities are deeply influenced by environmental factors, which are themselves shaped by socioeconomic conditions and historical inequities. Poor housing quality, exposure to allergens, and proximity to environmental hazards disproportionately affect underserved and minority communities, whether in rural or urban settings.

The Role of Green Spaces in Improving Respiratory Health

Restoring and increasing tree cover and green spaces in urban areas can significantly improve respiratory health by addressing environmental challenges and reducing triggers for respiratory issues. Areas with greater greenness tend to have lower levels of pollutants and fewer environmental infestations, such as mice and cockroaches, explained Phipatanakul. Her research highlights that schools in greener areas have fewer airborne pollutants and particles than those in more urbanized, less green areas, which are usually in poorer suburbs.

Trees absorb pollutants such as particulate matter and sulfur dioxide through dry deposition and stomatal uptake, improving air quality. “The question is whether we can use trees as a public health tool, and this is being done in many cities,” said Alessandro Marcon, PhD, a professor of epidemiology and medical statistics at the University of Verona, Verona, Italy, while speaking at the European Respiratory Society conference held in Vienna last September.

A US analysis showed that existing natural vegetation, such as forests and grasslands, absorbs a large portion of emissions. By restoring land cover, pollution from harmful substances like sulfur dioxide and particulate matter could be reduced by about 30%. This approach is often more cost-effective than technological solutions for managing emissions.

Moreover, tree cover contributes to a healthier air microbiome. Research indicates that urban forest areas have lower pathogenic bacteria and fungi concentrations than nearby urban zones.

Another major advantage is the mitigation of the urban heat island effect. A study conducted in Paris found that municipalities with higher tree coverage experienced 20%-30% lower heat-related mortality than those with less greenery. Increasing tree coverage to 30% could reduce up to 40% of excess mortality associated with urban heat islands. Trees achieve this by providing shade and facilitating evapotranspiration, which cools the surrounding air.

Urban environments, unsurprisingly, often have higher levels of air pollution due to increased traffic and industrial activity. However, despite appearing greener, rural environments may harbor less obvious but significant sources of air pollution. “I live in an urban environment now, but I grew up in a rural environment,” Scott said. “Each has its own issues that affect air quality and health.”

Scott, Phipatanakul, and Marcon reported no relevant financial relationships.■

A version of this article first appeared on Medscape.com.

In 2016, Brady Scott was in his parents’ home in Garrett, Kentucky, scrolling his Facebook feed when a post from a local newspaper caught his attention. “The article said that if you grew up in the region I grew up in, compared to the richer Central Kentucky region, the life expectancy differed by about 9 years,” he recalled.

The respiratory therapist, then a PhD student at Rush University, Chicago, was struck and began “Googling” to find out why this was the case. Initially, he thought diabetes, smoking, and economic distress — all prevalent problems in the area — were the culprits. However, he soon found that respiratory disease was particularly common in his region.

Now a professor and program director of the Respiratory Care Program at Rush University, Scott has spent several years trying to understand why people in certain regions experience respiratory illness at higher rates than in other places.

The Environment as a Determinant of Health

When Scott began his PhD, the prevalence of asthma in Southeast Kentucky, part of the Appalachian region, was already well-documented. He focused his research on uncontrolled asthma and the triggers that drove asthma exacerbations.

Housing quality emerged as an important factor. He found that exposure to mold, mildew, dust mites, pests, and rodents increased the risk for asthma and exacerbated existing cases. Lower-income families, more likely to live in poor-quality housing, were significantly affected, even in single-family homes.

Wanda Phipatanakul, MD, MS, director of the Division of Immunology Research Center at Boston Children’s Hospital and S. Jean Emans professor of Pediatrics at Harvard Medical School, Boston, has found similar results in urban environments. She said cockroach and mouse allergen exposure is disproportionately prevalent in urban, low-income neighborhoods. These exposures, closely tied to housing conditions, contribute to worse asthma and respiratory problems, particularly in children.

Scott and Phipatanakul agreed that the environment surrounding people’s homes can also exacerbate respiratory disease.

Rural areas present unique risks, such as agricultural activities that release pesticides and other particulates into the air, said Scott. In mountainous areas like Appalachia, mining operations are another significant contributor. For example, blasting mountains with dynamite creates large clouds of dust and pollutants that settle in valleys. Coal-hauling roads contribute to air quality issues, too. And houses near these roads may be exposed to increased levels of particulate matter, he said.

In the city, Phipatanakul has found that historical practices like redlining have systematically denied certain neighborhoods access to resources and investment, leaving a legacy of poor infrastructure, limited resources, and higher exposure to environmental risks. Today, these areas have more highways and fewer green spaces and are disproportionately linked with a higher incidence of respiratory illnesses.

The findings of both Scott and Phipatanakul underscore a critical bottom line: Health disparities are deeply influenced by environmental factors, which are themselves shaped by socioeconomic conditions and historical inequities. Poor housing quality, exposure to allergens, and proximity to environmental hazards disproportionately affect underserved and minority communities, whether in rural or urban settings.

The Role of Green Spaces in Improving Respiratory Health

Restoring and increasing tree cover and green spaces in urban areas can significantly improve respiratory health by addressing environmental challenges and reducing triggers for respiratory issues. Areas with greater greenness tend to have lower levels of pollutants and fewer environmental infestations, such as mice and cockroaches, explained Phipatanakul. Her research highlights that schools in greener areas have fewer airborne pollutants and particles than those in more urbanized, less green areas, which are usually in poorer suburbs.

Trees absorb pollutants such as particulate matter and sulfur dioxide through dry deposition and stomatal uptake, improving air quality. “The question is whether we can use trees as a public health tool, and this is being done in many cities,” said Alessandro Marcon, PhD, a professor of epidemiology and medical statistics at the University of Verona, Verona, Italy, while speaking at the European Respiratory Society conference held in Vienna last September.

A US analysis showed that existing natural vegetation, such as forests and grasslands, absorbs a large portion of emissions. By restoring land cover, pollution from harmful substances like sulfur dioxide and particulate matter could be reduced by about 30%. This approach is often more cost-effective than technological solutions for managing emissions.

Moreover, tree cover contributes to a healthier air microbiome. Research indicates that urban forest areas have lower pathogenic bacteria and fungi concentrations than nearby urban zones.

Another major advantage is the mitigation of the urban heat island effect. A study conducted in Paris found that municipalities with higher tree coverage experienced 20%-30% lower heat-related mortality than those with less greenery. Increasing tree coverage to 30% could reduce up to 40% of excess mortality associated with urban heat islands. Trees achieve this by providing shade and facilitating evapotranspiration, which cools the surrounding air.

Urban environments, unsurprisingly, often have higher levels of air pollution due to increased traffic and industrial activity. However, despite appearing greener, rural environments may harbor less obvious but significant sources of air pollution. “I live in an urban environment now, but I grew up in a rural environment,” Scott said. “Each has its own issues that affect air quality and health.”

Scott, Phipatanakul, and Marcon reported no relevant financial relationships.■

A version of this article first appeared on Medscape.com.

In 2016, Brady Scott was in his parents’ home in Garrett, Kentucky, scrolling his Facebook feed when a post from a local newspaper caught his attention. “The article said that if you grew up in the region I grew up in, compared to the richer Central Kentucky region, the life expectancy differed by about 9 years,” he recalled.

The respiratory therapist, then a PhD student at Rush University, Chicago, was struck and began “Googling” to find out why this was the case. Initially, he thought diabetes, smoking, and economic distress — all prevalent problems in the area — were the culprits. However, he soon found that respiratory disease was particularly common in his region.

Now a professor and program director of the Respiratory Care Program at Rush University, Scott has spent several years trying to understand why people in certain regions experience respiratory illness at higher rates than in other places.

The Environment as a Determinant of Health

When Scott began his PhD, the prevalence of asthma in Southeast Kentucky, part of the Appalachian region, was already well-documented. He focused his research on uncontrolled asthma and the triggers that drove asthma exacerbations.

Housing quality emerged as an important factor. He found that exposure to mold, mildew, dust mites, pests, and rodents increased the risk for asthma and exacerbated existing cases. Lower-income families, more likely to live in poor-quality housing, were significantly affected, even in single-family homes.

Wanda Phipatanakul, MD, MS, director of the Division of Immunology Research Center at Boston Children’s Hospital and S. Jean Emans professor of Pediatrics at Harvard Medical School, Boston, has found similar results in urban environments. She said cockroach and mouse allergen exposure is disproportionately prevalent in urban, low-income neighborhoods. These exposures, closely tied to housing conditions, contribute to worse asthma and respiratory problems, particularly in children.

Scott and Phipatanakul agreed that the environment surrounding people’s homes can also exacerbate respiratory disease.

Rural areas present unique risks, such as agricultural activities that release pesticides and other particulates into the air, said Scott. In mountainous areas like Appalachia, mining operations are another significant contributor. For example, blasting mountains with dynamite creates large clouds of dust and pollutants that settle in valleys. Coal-hauling roads contribute to air quality issues, too. And houses near these roads may be exposed to increased levels of particulate matter, he said.

In the city, Phipatanakul has found that historical practices like redlining have systematically denied certain neighborhoods access to resources and investment, leaving a legacy of poor infrastructure, limited resources, and higher exposure to environmental risks. Today, these areas have more highways and fewer green spaces and are disproportionately linked with a higher incidence of respiratory illnesses.

The findings of both Scott and Phipatanakul underscore a critical bottom line: Health disparities are deeply influenced by environmental factors, which are themselves shaped by socioeconomic conditions and historical inequities. Poor housing quality, exposure to allergens, and proximity to environmental hazards disproportionately affect underserved and minority communities, whether in rural or urban settings.

The Role of Green Spaces in Improving Respiratory Health

Restoring and increasing tree cover and green spaces in urban areas can significantly improve respiratory health by addressing environmental challenges and reducing triggers for respiratory issues. Areas with greater greenness tend to have lower levels of pollutants and fewer environmental infestations, such as mice and cockroaches, explained Phipatanakul. Her research highlights that schools in greener areas have fewer airborne pollutants and particles than those in more urbanized, less green areas, which are usually in poorer suburbs.

Trees absorb pollutants such as particulate matter and sulfur dioxide through dry deposition and stomatal uptake, improving air quality. “The question is whether we can use trees as a public health tool, and this is being done in many cities,” said Alessandro Marcon, PhD, a professor of epidemiology and medical statistics at the University of Verona, Verona, Italy, while speaking at the European Respiratory Society conference held in Vienna last September.

A US analysis showed that existing natural vegetation, such as forests and grasslands, absorbs a large portion of emissions. By restoring land cover, pollution from harmful substances like sulfur dioxide and particulate matter could be reduced by about 30%. This approach is often more cost-effective than technological solutions for managing emissions.

Moreover, tree cover contributes to a healthier air microbiome. Research indicates that urban forest areas have lower pathogenic bacteria and fungi concentrations than nearby urban zones.

Another major advantage is the mitigation of the urban heat island effect. A study conducted in Paris found that municipalities with higher tree coverage experienced 20%-30% lower heat-related mortality than those with less greenery. Increasing tree coverage to 30% could reduce up to 40% of excess mortality associated with urban heat islands. Trees achieve this by providing shade and facilitating evapotranspiration, which cools the surrounding air.

Urban environments, unsurprisingly, often have higher levels of air pollution due to increased traffic and industrial activity. However, despite appearing greener, rural environments may harbor less obvious but significant sources of air pollution. “I live in an urban environment now, but I grew up in a rural environment,” Scott said. “Each has its own issues that affect air quality and health.”

Scott, Phipatanakul, and Marcon reported no relevant financial relationships.■

A version of this article first appeared on Medscape.com.