Pulmonology

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.

TOPLINE:

Tumor necrosis factor (TNF) inhibitors led to no significant difference in survival or respiratory-related hospitalizations, compared with non-TNF inhibitors, in patients with rheumatoid arthritis–associated interstitial lung disease (RA-ILD).

METHODOLOGY:

• Guidelines from the American College of Rheumatology and the American College of Chest Physicians conditionally advise against the use of TNF inhibitors for treating ILD in patients with RA-ILD, with persisting uncertainty about the safety of TNF inhibitors.
• Researchers conducted a retrospective cohort study using data from the US Department of Veterans Affairs, with a focus on comparing outcomes in patients with RA-ILD who initiated TNF or non-TNF inhibitors between 2006 and 2018.
• A total of 1047 US veterans with RA-ILD were included, with 237 who initiated TNF inhibitors propensity matched in a 1:1 ratio with 237 who initiated non-TNF inhibitors (mean age, 68 years; 92% men).
• The primary composite outcome was time to death or respiratory-related hospitalization over a follow-up period of up to 3 years.
• The secondary outcomes included all-cause mortality, respiratory-related mortality, and respiratory-related hospitalization, with additional assessments over a 1-year period.

TAKEAWAY:

• No significant difference was observed in the composite outcome of death or respiratory-related hospitalization between the TNF and non-TNF inhibitor groups (adjusted hazard ratio, 1.21; 95% CI, 0.92-1.58).
• No significant differences in the risk for respiratory-related hospitalization and all-cause or respiratory-related mortality were found between the TNF and non-TNF inhibitor groups. Similar findings were observed for all the outcomes during 1 year of follow-up.
• The mean duration of medication use prior to discontinuation, the time to discontinuation, and the mean predicted forced vital capacity percentage were similar for both groups.
• In a subgroup analysis of patients aged ≥ 65 years, those treated with non-TNF inhibitors had a higher risk for the composite outcome and all-cause and respiratory-related mortality than those treated with TNF inhibitors. No significant differences in outcomes were observed between the two treatment groups among patients aged < 65 years.

IN PRACTICE:

“Our results do not suggest that systematic avoidance of TNF inhibitors is required in all patients with rheumatoid arthritis–associated ILD. However, given disease heterogeneity and imprecision of our estimates, some subpopulations of patients with rheumatoid arthritis–associated ILD might benefit from specific biological or targeted synthetic DMARD [disease-modifying antirheumatic drug] treatment strategies,” the authors wrote.

SOURCE:

The study was led by Bryant R. England, MD, PhD, University of Nebraska Medical Center, Omaha It was published online on January 7, 2025, in The Lancet Rheumatology.

LIMITATIONS:

Administrative algorithms were used for identifying RA-ILD, potentially leading to misclassification and limiting phenotyping accuracy. Even with the use of propensity score methods, there might still be residual selection bias or unmeasured confounding. The study lacked comprehensive measures of posttreatment forced vital capacity and other indicators of ILD severity. The study population, predominantly men and those with a smoking history, may limit the generalizability of the findings to other groups.

DISCLOSURES:

The study was primarily funded by the US Department of Veterans Affairs. Some authors reported having financial relationships with pharmaceutical companies unrelated to the submitted work.

This article was created using several editorial tools, including artificial intelligence, as part of the process. Human editors reviewed this content before publication. A version of this article first appeared on Medscape.com.

TOPLINE:

Tumor necrosis factor (TNF) inhibitors led to no significant difference in survival or respiratory-related hospitalizations, compared with non-TNF inhibitors, in patients with rheumatoid arthritis–associated interstitial lung disease (RA-ILD).

METHODOLOGY:

• Guidelines from the American College of Rheumatology and the American College of Chest Physicians conditionally advise against the use of TNF inhibitors for treating ILD in patients with RA-ILD, with persisting uncertainty about the safety of TNF inhibitors.
• Researchers conducted a retrospective cohort study using data from the US Department of Veterans Affairs, with a focus on comparing outcomes in patients with RA-ILD who initiated TNF or non-TNF inhibitors between 2006 and 2018.
• A total of 1047 US veterans with RA-ILD were included, with 237 who initiated TNF inhibitors propensity matched in a 1:1 ratio with 237 who initiated non-TNF inhibitors (mean age, 68 years; 92% men).
• The primary composite outcome was time to death or respiratory-related hospitalization over a follow-up period of up to 3 years.
• The secondary outcomes included all-cause mortality, respiratory-related mortality, and respiratory-related hospitalization, with additional assessments over a 1-year period.

TAKEAWAY:

• No significant difference was observed in the composite outcome of death or respiratory-related hospitalization between the TNF and non-TNF inhibitor groups (adjusted hazard ratio, 1.21; 95% CI, 0.92-1.58).
• No significant differences in the risk for respiratory-related hospitalization and all-cause or respiratory-related mortality were found between the TNF and non-TNF inhibitor groups. Similar findings were observed for all the outcomes during 1 year of follow-up.
• The mean duration of medication use prior to discontinuation, the time to discontinuation, and the mean predicted forced vital capacity percentage were similar for both groups.
• In a subgroup analysis of patients aged ≥ 65 years, those treated with non-TNF inhibitors had a higher risk for the composite outcome and all-cause and respiratory-related mortality than those treated with TNF inhibitors. No significant differences in outcomes were observed between the two treatment groups among patients aged < 65 years.

IN PRACTICE:

“Our results do not suggest that systematic avoidance of TNF inhibitors is required in all patients with rheumatoid arthritis–associated ILD. However, given disease heterogeneity and imprecision of our estimates, some subpopulations of patients with rheumatoid arthritis–associated ILD might benefit from specific biological or targeted synthetic DMARD [disease-modifying antirheumatic drug] treatment strategies,” the authors wrote.

SOURCE:

The study was led by Bryant R. England, MD, PhD, University of Nebraska Medical Center, Omaha It was published online on January 7, 2025, in The Lancet Rheumatology.

LIMITATIONS:

Administrative algorithms were used for identifying RA-ILD, potentially leading to misclassification and limiting phenotyping accuracy. Even with the use of propensity score methods, there might still be residual selection bias or unmeasured confounding. The study lacked comprehensive measures of posttreatment forced vital capacity and other indicators of ILD severity. The study population, predominantly men and those with a smoking history, may limit the generalizability of the findings to other groups.

DISCLOSURES:

The study was primarily funded by the US Department of Veterans Affairs. Some authors reported having financial relationships with pharmaceutical companies unrelated to the submitted work.

This article was created using several editorial tools, including artificial intelligence, as part of the process. Human editors reviewed this content before publication. A version of this article first appeared on Medscape.com.

TOPLINE:

Tumor necrosis factor (TNF) inhibitors led to no significant difference in survival or respiratory-related hospitalizations, compared with non-TNF inhibitors, in patients with rheumatoid arthritis–associated interstitial lung disease (RA-ILD).

METHODOLOGY:

• Guidelines from the American College of Rheumatology and the American College of Chest Physicians conditionally advise against the use of TNF inhibitors for treating ILD in patients with RA-ILD, with persisting uncertainty about the safety of TNF inhibitors.
• Researchers conducted a retrospective cohort study using data from the US Department of Veterans Affairs, with a focus on comparing outcomes in patients with RA-ILD who initiated TNF or non-TNF inhibitors between 2006 and 2018.
• A total of 1047 US veterans with RA-ILD were included, with 237 who initiated TNF inhibitors propensity matched in a 1:1 ratio with 237 who initiated non-TNF inhibitors (mean age, 68 years; 92% men).
• The primary composite outcome was time to death or respiratory-related hospitalization over a follow-up period of up to 3 years.
• The secondary outcomes included all-cause mortality, respiratory-related mortality, and respiratory-related hospitalization, with additional assessments over a 1-year period.

TAKEAWAY:

• No significant difference was observed in the composite outcome of death or respiratory-related hospitalization between the TNF and non-TNF inhibitor groups (adjusted hazard ratio, 1.21; 95% CI, 0.92-1.58).
• No significant differences in the risk for respiratory-related hospitalization and all-cause or respiratory-related mortality were found between the TNF and non-TNF inhibitor groups. Similar findings were observed for all the outcomes during 1 year of follow-up.
• The mean duration of medication use prior to discontinuation, the time to discontinuation, and the mean predicted forced vital capacity percentage were similar for both groups.
• In a subgroup analysis of patients aged ≥ 65 years, those treated with non-TNF inhibitors had a higher risk for the composite outcome and all-cause and respiratory-related mortality than those treated with TNF inhibitors. No significant differences in outcomes were observed between the two treatment groups among patients aged < 65 years.

IN PRACTICE:

“Our results do not suggest that systematic avoidance of TNF inhibitors is required in all patients with rheumatoid arthritis–associated ILD. However, given disease heterogeneity and imprecision of our estimates, some subpopulations of patients with rheumatoid arthritis–associated ILD might benefit from specific biological or targeted synthetic DMARD [disease-modifying antirheumatic drug] treatment strategies,” the authors wrote.

SOURCE:

The study was led by Bryant R. England, MD, PhD, University of Nebraska Medical Center, Omaha It was published online on January 7, 2025, in The Lancet Rheumatology.

LIMITATIONS:

Administrative algorithms were used for identifying RA-ILD, potentially leading to misclassification and limiting phenotyping accuracy. Even with the use of propensity score methods, there might still be residual selection bias or unmeasured confounding. The study lacked comprehensive measures of posttreatment forced vital capacity and other indicators of ILD severity. The study population, predominantly men and those with a smoking history, may limit the generalizability of the findings to other groups.

DISCLOSURES:

The study was primarily funded by the US Department of Veterans Affairs. Some authors reported having financial relationships with pharmaceutical companies unrelated to the submitted work.

This article was created using several editorial tools, including artificial intelligence, as part of the process. Human editors reviewed this content before publication. A version of this article first appeared on Medscape.com.

Children with asthma scored significantly lower than those without asthma on measures of episodic memory, based on longitudinal data from nearly 500 individuals.

Animal models have shown associations between asthma and memory problems, but data for children are lacking, wrote Nicholas J. Christopher-Hayes, MA, of the University of California, Davis, and colleagues.

“Asthma is very frequent among children, and there is mounting evidence from rodent models that asthma may result in neural injury in the hippocampus, which in turn may cause memory loss,” Christopher-Hayes said in an interview. “Although there is also a good amount of research with older adults, very little research has been done with children, the period that is most frequently linked to asthma onset,” he said. Therefore, the researchers leveraged a large national study on child development to examine development of memory as a function of asthma exposure.

In this study published in JAMA Network Open, the researchers conducted both a longitudinal and cross-sectional analysis of data from the Adolescent Brain Cognitive Development Study, which began in 2015. Children were enrolled at ages 9-10 years with a follow-up assessment 1-2 years later.

The participants were categorized as early childhood-onset asthma (asthma at baseline and follow-up), later childhood-onset asthma (asthma at follow-up only), or no asthma history. The primary outcome of the longitudinal analysis was episodic memory. Approximately half of the participants were boys, and slightly more than half were White.

Among 474 children reviewed in the longitudinal analysis, 135 had early-onset asthma, 102 had later-onset asthma, and 237 had no asthma and served as control individuals. Overall, those with early-onset asthma showed significantly lower rates of longitudinal memory improvements at follow-up compared with the comparison group (P < .01).

Developmental memory improvement in children with later-onset asthma was not significantly different from the control individuals. 

Secondary outcomes included processing speed and inhibition, and attention. In a cross-sectional analysis with a larger sample of 2062 children from the same database (1031 with any asthma), those with asthma scored significantly lower on measures not only of episodic memory but also processing speed and inhibition/attention than children with no asthma, with P values of .04, .01, and .02, respectively.

The results were limited by several factors, including the reliance on parent reports for indicators of asthma and the lack of data on the potential effect of prescription corticosteroid use on neurocognitive development, the researchers noted.

The mechanism behind the association remains unclear; the inflammation associated with asthma may disrupt neural processing and manifest as cognitive dysfunction, as has been seen in rodent models of asthma, the researchers wrote. “It is possible that associations between asthma and developmental trajectories emerge earlier for memory, perhaps due to its sensitivity to subtle hippocampal injury,” they noted.

Longer follow-up studies are needed to fully understand how childhood asthma predicts memory declines or difficulties in childhood and beyond, said Christopher-Hayes. “We also need additional studies to understand why children who were diagnosed earlier and had asthma for longer seem to be particularly affected,” he said.

The results of this study were consistent with previous findings and therefore not surprising, senior author Simona Ghetti, PhD, a professor of psychology at the University of California, Davis, said in an interview. However, the finding that the extent of exposure to asthma was associated with slower memory improvement in childhood was striking, she said. That children with an earlier asthma onset who had disease indicators for a longer period showed a slower development of memory over time, suggests that asthma exposure may affect the developmental trajectory of memory, Ghetti noted. 

“Recommendations to clinicians are premature because we need a better understanding of the boundary conditions, such as the minimal level of asthma exposure that might generate memory difficulties,” said Ghetti.

“Nevertheless, our results underscore the importance of looking at asthma as a potential source of cognitive difficulty in children,” she said.

 

Asthma’s Extensive Effect

Evidence is mounting that a diagnosis of asthma may have implications outside the pulmonary system, Diego J. Maselli, MD, professor and chief of the Division of Pulmonary Diseases & Critical Care at UT Health, San Antonio, said in an interview. 

“Asthmatics may be at risk of nasal polyps, allergic rhinitis, and other allergic conditions, but there is emerging of evidence inflammation associated with asthma may affect other organ systems,” said Maselli, who was not involved in the study.

“For example, chronic inflammation in asthmatics may increase the risk of cardiovascular disease,” he said.

Although less is known about the effects of asthma on the nervous system, animal models suggest that inflammation associated with asthma may result in neuronal injury and potential effects on memory, said Maselli.

The findings of this study provide evidence of potential detrimental effects on the memory of children with asthma but should be interpreted with caution, Maselli said. “Children with chronic medical conditions may have an inherent disadvantage compared with their peers due to the burden of their disease, medication utilization and side effects, absenteeism from school, physical limitations, and other disease-specific circumstances,” he noted.

“Uncontrolled asthma, in particular, has strong links to low socioeconomic factors that are closely tied to access to adequate medical care, nutrition, educational institutions, and other relevant contributors to normal cognitive development,” Maselli said. Although the authors account for some of these socioeconomic factors by evaluating income and race, other variables may have influenced the results, he added.

Overall, this study’s findings suggested that the diagnosis of asthma in children may be associated with memory deficits and may influence neurodevelopment; however, more research is needed to determine whether the findings are replicated in other cohorts, said Maselli. “In particular, evaluating the effects of the severity of asthma and different asthma endotypes would be crucial to identify children with a higher risk of memory or cognitive deficits and confirm these associations,” he said.

This study was funded by the Memory and Plasticity Program at the University of California, Davis, and by a Learning, Memory, and Plasticity Training Program Fellowship grant from the National Institutes of Health. The researchers and Maselli had no financial conflicts to disclose. 

 

A version of this article appeared on Medscape.com.

Children with asthma scored significantly lower than those without asthma on measures of episodic memory, based on longitudinal data from nearly 500 individuals.

Animal models have shown associations between asthma and memory problems, but data for children are lacking, wrote Nicholas J. Christopher-Hayes, MA, of the University of California, Davis, and colleagues.

“Asthma is very frequent among children, and there is mounting evidence from rodent models that asthma may result in neural injury in the hippocampus, which in turn may cause memory loss,” Christopher-Hayes said in an interview. “Although there is also a good amount of research with older adults, very little research has been done with children, the period that is most frequently linked to asthma onset,” he said. Therefore, the researchers leveraged a large national study on child development to examine development of memory as a function of asthma exposure.

In this study published in JAMA Network Open, the researchers conducted both a longitudinal and cross-sectional analysis of data from the Adolescent Brain Cognitive Development Study, which began in 2015. Children were enrolled at ages 9-10 years with a follow-up assessment 1-2 years later.

The participants were categorized as early childhood-onset asthma (asthma at baseline and follow-up), later childhood-onset asthma (asthma at follow-up only), or no asthma history. The primary outcome of the longitudinal analysis was episodic memory. Approximately half of the participants were boys, and slightly more than half were White.

Among 474 children reviewed in the longitudinal analysis, 135 had early-onset asthma, 102 had later-onset asthma, and 237 had no asthma and served as control individuals. Overall, those with early-onset asthma showed significantly lower rates of longitudinal memory improvements at follow-up compared with the comparison group (P < .01).

Developmental memory improvement in children with later-onset asthma was not significantly different from the control individuals. 

Secondary outcomes included processing speed and inhibition, and attention. In a cross-sectional analysis with a larger sample of 2062 children from the same database (1031 with any asthma), those with asthma scored significantly lower on measures not only of episodic memory but also processing speed and inhibition/attention than children with no asthma, with P values of .04, .01, and .02, respectively.

The results were limited by several factors, including the reliance on parent reports for indicators of asthma and the lack of data on the potential effect of prescription corticosteroid use on neurocognitive development, the researchers noted.

The mechanism behind the association remains unclear; the inflammation associated with asthma may disrupt neural processing and manifest as cognitive dysfunction, as has been seen in rodent models of asthma, the researchers wrote. “It is possible that associations between asthma and developmental trajectories emerge earlier for memory, perhaps due to its sensitivity to subtle hippocampal injury,” they noted.

Longer follow-up studies are needed to fully understand how childhood asthma predicts memory declines or difficulties in childhood and beyond, said Christopher-Hayes. “We also need additional studies to understand why children who were diagnosed earlier and had asthma for longer seem to be particularly affected,” he said.

The results of this study were consistent with previous findings and therefore not surprising, senior author Simona Ghetti, PhD, a professor of psychology at the University of California, Davis, said in an interview. However, the finding that the extent of exposure to asthma was associated with slower memory improvement in childhood was striking, she said. That children with an earlier asthma onset who had disease indicators for a longer period showed a slower development of memory over time, suggests that asthma exposure may affect the developmental trajectory of memory, Ghetti noted. 

“Recommendations to clinicians are premature because we need a better understanding of the boundary conditions, such as the minimal level of asthma exposure that might generate memory difficulties,” said Ghetti.

“Nevertheless, our results underscore the importance of looking at asthma as a potential source of cognitive difficulty in children,” she said.

 

Asthma’s Extensive Effect

Evidence is mounting that a diagnosis of asthma may have implications outside the pulmonary system, Diego J. Maselli, MD, professor and chief of the Division of Pulmonary Diseases & Critical Care at UT Health, San Antonio, said in an interview. 

“Asthmatics may be at risk of nasal polyps, allergic rhinitis, and other allergic conditions, but there is emerging of evidence inflammation associated with asthma may affect other organ systems,” said Maselli, who was not involved in the study.

“For example, chronic inflammation in asthmatics may increase the risk of cardiovascular disease,” he said.

Although less is known about the effects of asthma on the nervous system, animal models suggest that inflammation associated with asthma may result in neuronal injury and potential effects on memory, said Maselli.

The findings of this study provide evidence of potential detrimental effects on the memory of children with asthma but should be interpreted with caution, Maselli said. “Children with chronic medical conditions may have an inherent disadvantage compared with their peers due to the burden of their disease, medication utilization and side effects, absenteeism from school, physical limitations, and other disease-specific circumstances,” he noted.

“Uncontrolled asthma, in particular, has strong links to low socioeconomic factors that are closely tied to access to adequate medical care, nutrition, educational institutions, and other relevant contributors to normal cognitive development,” Maselli said. Although the authors account for some of these socioeconomic factors by evaluating income and race, other variables may have influenced the results, he added.

Overall, this study’s findings suggested that the diagnosis of asthma in children may be associated with memory deficits and may influence neurodevelopment; however, more research is needed to determine whether the findings are replicated in other cohorts, said Maselli. “In particular, evaluating the effects of the severity of asthma and different asthma endotypes would be crucial to identify children with a higher risk of memory or cognitive deficits and confirm these associations,” he said.

This study was funded by the Memory and Plasticity Program at the University of California, Davis, and by a Learning, Memory, and Plasticity Training Program Fellowship grant from the National Institutes of Health. The researchers and Maselli had no financial conflicts to disclose. 

 

A version of this article appeared on Medscape.com.

Children with asthma scored significantly lower than those without asthma on measures of episodic memory, based on longitudinal data from nearly 500 individuals.

Animal models have shown associations between asthma and memory problems, but data for children are lacking, wrote Nicholas J. Christopher-Hayes, MA, of the University of California, Davis, and colleagues.

“Asthma is very frequent among children, and there is mounting evidence from rodent models that asthma may result in neural injury in the hippocampus, which in turn may cause memory loss,” Christopher-Hayes said in an interview. “Although there is also a good amount of research with older adults, very little research has been done with children, the period that is most frequently linked to asthma onset,” he said. Therefore, the researchers leveraged a large national study on child development to examine development of memory as a function of asthma exposure.

In this study published in JAMA Network Open, the researchers conducted both a longitudinal and cross-sectional analysis of data from the Adolescent Brain Cognitive Development Study, which began in 2015. Children were enrolled at ages 9-10 years with a follow-up assessment 1-2 years later.

The participants were categorized as early childhood-onset asthma (asthma at baseline and follow-up), later childhood-onset asthma (asthma at follow-up only), or no asthma history. The primary outcome of the longitudinal analysis was episodic memory. Approximately half of the participants were boys, and slightly more than half were White.

Among 474 children reviewed in the longitudinal analysis, 135 had early-onset asthma, 102 had later-onset asthma, and 237 had no asthma and served as control individuals. Overall, those with early-onset asthma showed significantly lower rates of longitudinal memory improvements at follow-up compared with the comparison group (P < .01).

Developmental memory improvement in children with later-onset asthma was not significantly different from the control individuals. 

Secondary outcomes included processing speed and inhibition, and attention. In a cross-sectional analysis with a larger sample of 2062 children from the same database (1031 with any asthma), those with asthma scored significantly lower on measures not only of episodic memory but also processing speed and inhibition/attention than children with no asthma, with P values of .04, .01, and .02, respectively.

The results were limited by several factors, including the reliance on parent reports for indicators of asthma and the lack of data on the potential effect of prescription corticosteroid use on neurocognitive development, the researchers noted.

The mechanism behind the association remains unclear; the inflammation associated with asthma may disrupt neural processing and manifest as cognitive dysfunction, as has been seen in rodent models of asthma, the researchers wrote. “It is possible that associations between asthma and developmental trajectories emerge earlier for memory, perhaps due to its sensitivity to subtle hippocampal injury,” they noted.

Longer follow-up studies are needed to fully understand how childhood asthma predicts memory declines or difficulties in childhood and beyond, said Christopher-Hayes. “We also need additional studies to understand why children who were diagnosed earlier and had asthma for longer seem to be particularly affected,” he said.

The results of this study were consistent with previous findings and therefore not surprising, senior author Simona Ghetti, PhD, a professor of psychology at the University of California, Davis, said in an interview. However, the finding that the extent of exposure to asthma was associated with slower memory improvement in childhood was striking, she said. That children with an earlier asthma onset who had disease indicators for a longer period showed a slower development of memory over time, suggests that asthma exposure may affect the developmental trajectory of memory, Ghetti noted. 

“Recommendations to clinicians are premature because we need a better understanding of the boundary conditions, such as the minimal level of asthma exposure that might generate memory difficulties,” said Ghetti.

“Nevertheless, our results underscore the importance of looking at asthma as a potential source of cognitive difficulty in children,” she said.

 

Asthma’s Extensive Effect

Evidence is mounting that a diagnosis of asthma may have implications outside the pulmonary system, Diego J. Maselli, MD, professor and chief of the Division of Pulmonary Diseases & Critical Care at UT Health, San Antonio, said in an interview. 

“Asthmatics may be at risk of nasal polyps, allergic rhinitis, and other allergic conditions, but there is emerging of evidence inflammation associated with asthma may affect other organ systems,” said Maselli, who was not involved in the study.

“For example, chronic inflammation in asthmatics may increase the risk of cardiovascular disease,” he said.

Although less is known about the effects of asthma on the nervous system, animal models suggest that inflammation associated with asthma may result in neuronal injury and potential effects on memory, said Maselli.

The findings of this study provide evidence of potential detrimental effects on the memory of children with asthma but should be interpreted with caution, Maselli said. “Children with chronic medical conditions may have an inherent disadvantage compared with their peers due to the burden of their disease, medication utilization and side effects, absenteeism from school, physical limitations, and other disease-specific circumstances,” he noted.

“Uncontrolled asthma, in particular, has strong links to low socioeconomic factors that are closely tied to access to adequate medical care, nutrition, educational institutions, and other relevant contributors to normal cognitive development,” Maselli said. Although the authors account for some of these socioeconomic factors by evaluating income and race, other variables may have influenced the results, he added.

Overall, this study’s findings suggested that the diagnosis of asthma in children may be associated with memory deficits and may influence neurodevelopment; however, more research is needed to determine whether the findings are replicated in other cohorts, said Maselli. “In particular, evaluating the effects of the severity of asthma and different asthma endotypes would be crucial to identify children with a higher risk of memory or cognitive deficits and confirm these associations,” he said.

This study was funded by the Memory and Plasticity Program at the University of California, Davis, and by a Learning, Memory, and Plasticity Training Program Fellowship grant from the National Institutes of Health. The researchers and Maselli had no financial conflicts to disclose. 

 

A version of this article appeared on Medscape.com.

A few items bring back unpleasant memories of COVID-19, such as masks. However, they are among the simplest and most effective ways to prevent the spread of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). If everyone had worn them correctly, the transmission could have been reduced as much as ninefold, according to a theoretical study published in Physical Review E by Richard P. Sear, PhD, from the University of Surrey, Guildford, England.

Study Overcomes Limitations

This study aimed to address the limitations of epidemiological investigations of masks, which can be complex and error-prone. Sear used data obtained from the UK’s COVID-19 app, totaling 7 million contacts, to create a mathematical model of virus transmission, focusing on the correlation between contact duration and infection. The model estimates that if all UK residents had worn masks during every potential exposure, virus transmission would have been approximately nine times lower.

Although this is a mathematical model, it adds to the growing evidence that supports the benefits of masks. Masks are among the best strategies for treating SARS-CoV-2. This conclusion has been supported by several systematic reviews and additional statistical studies. Conversely, the decision to relax and eliminate mask regulations has had consequences that have received little attention.

As expected, removing the mask mandate leads to increased virus transmission, resulting in more hospitalizations and deaths. A 2024 study estimated that in Japan, where cultural factors lead to much higher mask use in public than in Europe, the decline in mask use from 97% of the population in 2022 to 63% in October 2023 may have caused an additional 3500 deaths.

 

Impact Beyond SARS-CoV-2

One remarkable effect of non-pharmaceutical interventions during the pandemic was the probable extinction of an entire influenza strain (B/Yamagata), which could improve future influenza vaccines and significantly reduce the spread of respiratory syncytial virus. While this was not solely caused by masks, it was also influenced by emergency measures such as lockdowns and social distancing. These behavioral changes can positively alter the landscape of infectious diseases.

Masks play a role in reducing influenza transmission during pandemics. Their effectiveness has been supported by several studies and systematic reviews on a wide range of respiratory viruses. A randomized clinical trial involving 4647 Norwegian participants from February to April 2023, published in May 2024 by the British Medical Journal, suggested that wearing a mask reduces the incidence of respiratory symptoms. Specifically, 8.9% of those who wore masks reported respiratory symptoms during the study period compared with 12.2% of those who did not, representing a relative risk reduction of 27%.

Widespread mask use could also protect against other factors such as fine particulate matter, indirectly reducing the risk for various health conditions. A retrospective study involving 7.8 million residents in the Chinese city of Weifang, published in December 2024 by BMC Public Health, suggested that mask use during the pandemic may have also protected the population from pollution, reducing the number of stroke cases by 38.6% over 33 months of follow-up.

Although there are still voices in bioethics calling for the reintroduction of mask mandates in public places, it is unlikely that, barring emergencies, mask mandates are politically and socially acceptable today. Mask use is also considered a politically polarizing topic in several Western countries. Nevertheless, it is worth considering whether, as we move away from the acute phase of the COVID-19 pandemic, we can more objectively promote the use of masks in public places.

Communicating the importance of public health initiatives and persuading people to support them is a well-known challenge. However, scientific literature offers valuable insights. These include encouraging people to rely on rational thinking rather than emotions and providing information on how masks protect those around them. The fact that East Asian cultures tend to have a more positive relationship with the use of masks shows that, in principle, it is possible to make them acceptable. Data from studies suggest that, as we prepare for potential future pandemics, it may be time to move past polarization and reintroduce masks — not as a universal mandate but as an individual choice for many.

This story was translated from Univadis Italy 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.

A few items bring back unpleasant memories of COVID-19, such as masks. However, they are among the simplest and most effective ways to prevent the spread of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). If everyone had worn them correctly, the transmission could have been reduced as much as ninefold, according to a theoretical study published in Physical Review E by Richard P. Sear, PhD, from the University of Surrey, Guildford, England.

Study Overcomes Limitations

This study aimed to address the limitations of epidemiological investigations of masks, which can be complex and error-prone. Sear used data obtained from the UK’s COVID-19 app, totaling 7 million contacts, to create a mathematical model of virus transmission, focusing on the correlation between contact duration and infection. The model estimates that if all UK residents had worn masks during every potential exposure, virus transmission would have been approximately nine times lower.

Although this is a mathematical model, it adds to the growing evidence that supports the benefits of masks. Masks are among the best strategies for treating SARS-CoV-2. This conclusion has been supported by several systematic reviews and additional statistical studies. Conversely, the decision to relax and eliminate mask regulations has had consequences that have received little attention.

As expected, removing the mask mandate leads to increased virus transmission, resulting in more hospitalizations and deaths. A 2024 study estimated that in Japan, where cultural factors lead to much higher mask use in public than in Europe, the decline in mask use from 97% of the population in 2022 to 63% in October 2023 may have caused an additional 3500 deaths.

 

Impact Beyond SARS-CoV-2

One remarkable effect of non-pharmaceutical interventions during the pandemic was the probable extinction of an entire influenza strain (B/Yamagata), which could improve future influenza vaccines and significantly reduce the spread of respiratory syncytial virus. While this was not solely caused by masks, it was also influenced by emergency measures such as lockdowns and social distancing. These behavioral changes can positively alter the landscape of infectious diseases.

Masks play a role in reducing influenza transmission during pandemics. Their effectiveness has been supported by several studies and systematic reviews on a wide range of respiratory viruses. A randomized clinical trial involving 4647 Norwegian participants from February to April 2023, published in May 2024 by the British Medical Journal, suggested that wearing a mask reduces the incidence of respiratory symptoms. Specifically, 8.9% of those who wore masks reported respiratory symptoms during the study period compared with 12.2% of those who did not, representing a relative risk reduction of 27%.

Widespread mask use could also protect against other factors such as fine particulate matter, indirectly reducing the risk for various health conditions. A retrospective study involving 7.8 million residents in the Chinese city of Weifang, published in December 2024 by BMC Public Health, suggested that mask use during the pandemic may have also protected the population from pollution, reducing the number of stroke cases by 38.6% over 33 months of follow-up.

Although there are still voices in bioethics calling for the reintroduction of mask mandates in public places, it is unlikely that, barring emergencies, mask mandates are politically and socially acceptable today. Mask use is also considered a politically polarizing topic in several Western countries. Nevertheless, it is worth considering whether, as we move away from the acute phase of the COVID-19 pandemic, we can more objectively promote the use of masks in public places.

Communicating the importance of public health initiatives and persuading people to support them is a well-known challenge. However, scientific literature offers valuable insights. These include encouraging people to rely on rational thinking rather than emotions and providing information on how masks protect those around them. The fact that East Asian cultures tend to have a more positive relationship with the use of masks shows that, in principle, it is possible to make them acceptable. Data from studies suggest that, as we prepare for potential future pandemics, it may be time to move past polarization and reintroduce masks — not as a universal mandate but as an individual choice for many.

This story was translated from Univadis Italy 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.

A few items bring back unpleasant memories of COVID-19, such as masks. However, they are among the simplest and most effective ways to prevent the spread of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). If everyone had worn them correctly, the transmission could have been reduced as much as ninefold, according to a theoretical study published in Physical Review E by Richard P. Sear, PhD, from the University of Surrey, Guildford, England.

Study Overcomes Limitations

This study aimed to address the limitations of epidemiological investigations of masks, which can be complex and error-prone. Sear used data obtained from the UK’s COVID-19 app, totaling 7 million contacts, to create a mathematical model of virus transmission, focusing on the correlation between contact duration and infection. The model estimates that if all UK residents had worn masks during every potential exposure, virus transmission would have been approximately nine times lower.

Although this is a mathematical model, it adds to the growing evidence that supports the benefits of masks. Masks are among the best strategies for treating SARS-CoV-2. This conclusion has been supported by several systematic reviews and additional statistical studies. Conversely, the decision to relax and eliminate mask regulations has had consequences that have received little attention.

As expected, removing the mask mandate leads to increased virus transmission, resulting in more hospitalizations and deaths. A 2024 study estimated that in Japan, where cultural factors lead to much higher mask use in public than in Europe, the decline in mask use from 97% of the population in 2022 to 63% in October 2023 may have caused an additional 3500 deaths.

 

Impact Beyond SARS-CoV-2

One remarkable effect of non-pharmaceutical interventions during the pandemic was the probable extinction of an entire influenza strain (B/Yamagata), which could improve future influenza vaccines and significantly reduce the spread of respiratory syncytial virus. While this was not solely caused by masks, it was also influenced by emergency measures such as lockdowns and social distancing. These behavioral changes can positively alter the landscape of infectious diseases.

Masks play a role in reducing influenza transmission during pandemics. Their effectiveness has been supported by several studies and systematic reviews on a wide range of respiratory viruses. A randomized clinical trial involving 4647 Norwegian participants from February to April 2023, published in May 2024 by the British Medical Journal, suggested that wearing a mask reduces the incidence of respiratory symptoms. Specifically, 8.9% of those who wore masks reported respiratory symptoms during the study period compared with 12.2% of those who did not, representing a relative risk reduction of 27%.

Widespread mask use could also protect against other factors such as fine particulate matter, indirectly reducing the risk for various health conditions. A retrospective study involving 7.8 million residents in the Chinese city of Weifang, published in December 2024 by BMC Public Health, suggested that mask use during the pandemic may have also protected the population from pollution, reducing the number of stroke cases by 38.6% over 33 months of follow-up.

Although there are still voices in bioethics calling for the reintroduction of mask mandates in public places, it is unlikely that, barring emergencies, mask mandates are politically and socially acceptable today. Mask use is also considered a politically polarizing topic in several Western countries. Nevertheless, it is worth considering whether, as we move away from the acute phase of the COVID-19 pandemic, we can more objectively promote the use of masks in public places.

Communicating the importance of public health initiatives and persuading people to support them is a well-known challenge. However, scientific literature offers valuable insights. These include encouraging people to rely on rational thinking rather than emotions and providing information on how masks protect those around them. The fact that East Asian cultures tend to have a more positive relationship with the use of masks shows that, in principle, it is possible to make them acceptable. Data from studies suggest that, as we prepare for potential future pandemics, it may be time to move past polarization and reintroduce masks — not as a universal mandate but as an individual choice for many.

This story was translated from Univadis Italy 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.

MRI-invisible prostate lesions. It sounds like the stuff of science fiction and fantasy, a creation from the minds of H.G. Wells, who wrote The Invisible Man, or J.K. Rowling, who authored the Harry Potter series.

But MRI-invisible prostate lesions are real. And what these lesions may, or may not, indicate is the subject of intense debate.

MRI plays an increasingly important role in detecting and diagnosing prostate cancer, staging prostate cancer as well as monitoring disease progression. However, on occasion, a puzzling phenomenon arises. Certain prostate lesions that appear when pathologists examine biopsied tissue samples under a microscope are not visible on MRI. The prostate tissue will, instead, appear normal to a radiologist’s eye.

Why are certain lesions invisible with MRI? And is it dangerous for patients if these lesions are not detected? 

Some experts believe these MRI-invisible lesions are nothing to worry about.

If the clinician can’t see the cancer on MRI, then it simply isn’t a threat, according to Mark Emberton, MD, a pioneer in prostate MRIs and director of interventional oncology at University College London, England.

Laurence Klotz, MD, of the University of Toronto, Ontario, Canada, agreed, noting that “invisible cancers are clinically insignificant and don’t require systematic biopsies.”

Emberton and Klotz compared MRI-invisible lesions to grade group 1 prostate cancer (Gleason score ≤ 6) — the least aggressive category that indicates the cancer that is not likely to spread or kill. For patients on active surveillance, those with MRI-invisible cancers do drastically better than those with visible cancers, Klotz explained.

But other experts in the field are skeptical that MRI-invisible lesions are truly innocuous.

Although statistically an MRI-visible prostate lesion indicates a more aggressive tumor, that is not always the case for every individual, said Brian Helfand, MD, PhD, chief of urology at NorthShore University Health System, Evanston, Illinois.

MRIs can lead to false negatives in about 10%-20% of patients who have clinically significant prostate cancer, though estimates vary.

In one analysis, 16% of men with no suspicious lesions on MRI had clinically significant prostate cancer identified after undergoing a systematic biopsy. Another analysis found that about 35% of MRI-invisible prostate cancers identified via biopsy were clinically significant.

Other studies, however, have indicated that negative MRI results accurately indicate patients at low risk of developing clinically significant cancers. A recent JAMA Oncology analysis, for instance, found that only seven of 233 men (3%) with negative MRI results at baseline who completed 3 years of monitoring were diagnosed with clinically significant prostate cancer.

When a patient has an MRI-invisible prostate tumor, there are a couple of reasons the MRI may not be picking it up, said urologic oncologist Alexander Putnam Cole, MD, assistant professor of surgery, Harvard Medical School, Boston, Massachusetts. “One is that the cancer is aggressive but just very small,” said Cole.

“Another possibility is that the cancer looks very similar to background prostate tissue, which is something that you might expect if you think about more of a low-grade cancer,” he explained.

The experience level of the radiologist interpreting the MRI can also play into the accuracy of the reading.

But Cole agreed that “in general, MRI visibility is associated with molecular and histologic features of progression and aggressiveness and non-visible cancers are less likely to have aggressive features.”

The genomic profiles of MRI-visible and -invisible cancers bear this out.

According to Todd Morgan, MD, chief of urologic oncology at Michigan Medicine, University of Michigan, Ann Arbor, the gene expression in visible disease tends to be linked to more aggressive prostate tumors whereas gene expression in invisible disease does not.

In one analysis, for instance, researchers found that four genes — PHYHD1, CENPF, ALDH2, and GDF15 — associated with worse progression-free survival and metastasis-free survival in prostate cancer also predicted MRI visibility.

“Genes that are associated with visibility are essentially the same genes that are associated with aggressive cancers,” Klotz said.

 

Next Steps After Negative MRI Result

What do MRI-invisible lesions mean for patient care? If, for instance, a patient has elevated PSA levels but a normal MRI, is a targeted or systematic biopsy warranted?

The overarching message, according to Klotz, is that “you don’t need to find them.” Klotz noted, however, that patients with a negative MRI result should still be followed with periodic repeat imaging.

Several trials support this approach of using MRI to decide who needs a biopsy and delaying a biopsy in men with normal MRIs.

The recent JAMA Oncology analysis found that, among men with negative MRI results, 86% avoided a biopsy over 3 years, with clinically significant prostate cancer detected in only 4% of men across the study period — four in the initial diagnostic phase and seven in the 3-year monitoring phase. However, during the initial diagnostic phase, more than half the men with positive MRI findings had clinically significant prostate cancer detected.

Another recent study found that patients with negative MRI results were much less likely to upgrade to higher Gleason scores over time. Among 522 patients who underwent a systematic and targeted biopsy within 18 months of their grade group 1 designation, 9.2% with negative MRI findings had tumors reclassified as grade group 2 or higher vs 27% with positive MRI findings, and 2.3% with negative MRI findings had tumors reclassified as grade group 3 or higher vs 7.8% with positive MRI findings.

These data suggest that men with grade group 1 cancer and negative MRI result “may be able to avoid confirmatory biopsies until a routine surveillance biopsy in 2-3 years,” according to study author Christian Pavlovich, MD, professor of urologic oncology at the Johns Hopkins University School of Medicine, Baltimore.

Cole used MRI findings to triage who gets a biopsy. When a biopsy is warranted, “I usually recommend adding in some systematic sampling of the other side to assess for nonvisible cancers,” he noted.

Sampling prostate tissue outside the target area “adds maybe 1-2 minutes to the procedure and doesn’t drastically increase the morbidity or risks,” Cole said. It also can help “confirm there is cancer in the MRI target and also confirm there is no cancer in the nonvisible areas.” 

According to Klotz, if imaging demonstrates progression, patients should receive a biopsy — in most cases, a targeted biopsy only. And, Klotz noted, skipping routine prostate biopsies in men with negative MRI results can save thousands of men from these procedures, which carry risks for infections and sepsis.

Looking beyond Gleason scores for risk prediction, MRI “visibility is a very powerful risk stratifier,” he said.

A version of this article appeared on Medscape.com.

MRI-invisible prostate lesions. It sounds like the stuff of science fiction and fantasy, a creation from the minds of H.G. Wells, who wrote The Invisible Man, or J.K. Rowling, who authored the Harry Potter series.

But MRI-invisible prostate lesions are real. And what these lesions may, or may not, indicate is the subject of intense debate.

MRI plays an increasingly important role in detecting and diagnosing prostate cancer, staging prostate cancer as well as monitoring disease progression. However, on occasion, a puzzling phenomenon arises. Certain prostate lesions that appear when pathologists examine biopsied tissue samples under a microscope are not visible on MRI. The prostate tissue will, instead, appear normal to a radiologist’s eye.

Why are certain lesions invisible with MRI? And is it dangerous for patients if these lesions are not detected? 

Some experts believe these MRI-invisible lesions are nothing to worry about.

If the clinician can’t see the cancer on MRI, then it simply isn’t a threat, according to Mark Emberton, MD, a pioneer in prostate MRIs and director of interventional oncology at University College London, England.

Laurence Klotz, MD, of the University of Toronto, Ontario, Canada, agreed, noting that “invisible cancers are clinically insignificant and don’t require systematic biopsies.”

Emberton and Klotz compared MRI-invisible lesions to grade group 1 prostate cancer (Gleason score ≤ 6) — the least aggressive category that indicates the cancer that is not likely to spread or kill. For patients on active surveillance, those with MRI-invisible cancers do drastically better than those with visible cancers, Klotz explained.

But other experts in the field are skeptical that MRI-invisible lesions are truly innocuous.

Although statistically an MRI-visible prostate lesion indicates a more aggressive tumor, that is not always the case for every individual, said Brian Helfand, MD, PhD, chief of urology at NorthShore University Health System, Evanston, Illinois.

MRIs can lead to false negatives in about 10%-20% of patients who have clinically significant prostate cancer, though estimates vary.

In one analysis, 16% of men with no suspicious lesions on MRI had clinically significant prostate cancer identified after undergoing a systematic biopsy. Another analysis found that about 35% of MRI-invisible prostate cancers identified via biopsy were clinically significant.

Other studies, however, have indicated that negative MRI results accurately indicate patients at low risk of developing clinically significant cancers. A recent JAMA Oncology analysis, for instance, found that only seven of 233 men (3%) with negative MRI results at baseline who completed 3 years of monitoring were diagnosed with clinically significant prostate cancer.

When a patient has an MRI-invisible prostate tumor, there are a couple of reasons the MRI may not be picking it up, said urologic oncologist Alexander Putnam Cole, MD, assistant professor of surgery, Harvard Medical School, Boston, Massachusetts. “One is that the cancer is aggressive but just very small,” said Cole.

“Another possibility is that the cancer looks very similar to background prostate tissue, which is something that you might expect if you think about more of a low-grade cancer,” he explained.

The experience level of the radiologist interpreting the MRI can also play into the accuracy of the reading.

But Cole agreed that “in general, MRI visibility is associated with molecular and histologic features of progression and aggressiveness and non-visible cancers are less likely to have aggressive features.”

The genomic profiles of MRI-visible and -invisible cancers bear this out.

According to Todd Morgan, MD, chief of urologic oncology at Michigan Medicine, University of Michigan, Ann Arbor, the gene expression in visible disease tends to be linked to more aggressive prostate tumors whereas gene expression in invisible disease does not.

In one analysis, for instance, researchers found that four genes — PHYHD1, CENPF, ALDH2, and GDF15 — associated with worse progression-free survival and metastasis-free survival in prostate cancer also predicted MRI visibility.

“Genes that are associated with visibility are essentially the same genes that are associated with aggressive cancers,” Klotz said.

 

Next Steps After Negative MRI Result

What do MRI-invisible lesions mean for patient care? If, for instance, a patient has elevated PSA levels but a normal MRI, is a targeted or systematic biopsy warranted?

The overarching message, according to Klotz, is that “you don’t need to find them.” Klotz noted, however, that patients with a negative MRI result should still be followed with periodic repeat imaging.

Several trials support this approach of using MRI to decide who needs a biopsy and delaying a biopsy in men with normal MRIs.

The recent JAMA Oncology analysis found that, among men with negative MRI results, 86% avoided a biopsy over 3 years, with clinically significant prostate cancer detected in only 4% of men across the study period — four in the initial diagnostic phase and seven in the 3-year monitoring phase. However, during the initial diagnostic phase, more than half the men with positive MRI findings had clinically significant prostate cancer detected.

Another recent study found that patients with negative MRI results were much less likely to upgrade to higher Gleason scores over time. Among 522 patients who underwent a systematic and targeted biopsy within 18 months of their grade group 1 designation, 9.2% with negative MRI findings had tumors reclassified as grade group 2 or higher vs 27% with positive MRI findings, and 2.3% with negative MRI findings had tumors reclassified as grade group 3 or higher vs 7.8% with positive MRI findings.

These data suggest that men with grade group 1 cancer and negative MRI result “may be able to avoid confirmatory biopsies until a routine surveillance biopsy in 2-3 years,” according to study author Christian Pavlovich, MD, professor of urologic oncology at the Johns Hopkins University School of Medicine, Baltimore.

Cole used MRI findings to triage who gets a biopsy. When a biopsy is warranted, “I usually recommend adding in some systematic sampling of the other side to assess for nonvisible cancers,” he noted.

Sampling prostate tissue outside the target area “adds maybe 1-2 minutes to the procedure and doesn’t drastically increase the morbidity or risks,” Cole said. It also can help “confirm there is cancer in the MRI target and also confirm there is no cancer in the nonvisible areas.” 

According to Klotz, if imaging demonstrates progression, patients should receive a biopsy — in most cases, a targeted biopsy only. And, Klotz noted, skipping routine prostate biopsies in men with negative MRI results can save thousands of men from these procedures, which carry risks for infections and sepsis.

Looking beyond Gleason scores for risk prediction, MRI “visibility is a very powerful risk stratifier,” he said.

A version of this article appeared on Medscape.com.

MRI-invisible prostate lesions. It sounds like the stuff of science fiction and fantasy, a creation from the minds of H.G. Wells, who wrote The Invisible Man, or J.K. Rowling, who authored the Harry Potter series.

But MRI-invisible prostate lesions are real. And what these lesions may, or may not, indicate is the subject of intense debate.

MRI plays an increasingly important role in detecting and diagnosing prostate cancer, staging prostate cancer as well as monitoring disease progression. However, on occasion, a puzzling phenomenon arises. Certain prostate lesions that appear when pathologists examine biopsied tissue samples under a microscope are not visible on MRI. The prostate tissue will, instead, appear normal to a radiologist’s eye.

Why are certain lesions invisible with MRI? And is it dangerous for patients if these lesions are not detected? 

Some experts believe these MRI-invisible lesions are nothing to worry about.

If the clinician can’t see the cancer on MRI, then it simply isn’t a threat, according to Mark Emberton, MD, a pioneer in prostate MRIs and director of interventional oncology at University College London, England.

Laurence Klotz, MD, of the University of Toronto, Ontario, Canada, agreed, noting that “invisible cancers are clinically insignificant and don’t require systematic biopsies.”

Emberton and Klotz compared MRI-invisible lesions to grade group 1 prostate cancer (Gleason score ≤ 6) — the least aggressive category that indicates the cancer that is not likely to spread or kill. For patients on active surveillance, those with MRI-invisible cancers do drastically better than those with visible cancers, Klotz explained.

But other experts in the field are skeptical that MRI-invisible lesions are truly innocuous.

Although statistically an MRI-visible prostate lesion indicates a more aggressive tumor, that is not always the case for every individual, said Brian Helfand, MD, PhD, chief of urology at NorthShore University Health System, Evanston, Illinois.

MRIs can lead to false negatives in about 10%-20% of patients who have clinically significant prostate cancer, though estimates vary.

In one analysis, 16% of men with no suspicious lesions on MRI had clinically significant prostate cancer identified after undergoing a systematic biopsy. Another analysis found that about 35% of MRI-invisible prostate cancers identified via biopsy were clinically significant.

Other studies, however, have indicated that negative MRI results accurately indicate patients at low risk of developing clinically significant cancers. A recent JAMA Oncology analysis, for instance, found that only seven of 233 men (3%) with negative MRI results at baseline who completed 3 years of monitoring were diagnosed with clinically significant prostate cancer.

When a patient has an MRI-invisible prostate tumor, there are a couple of reasons the MRI may not be picking it up, said urologic oncologist Alexander Putnam Cole, MD, assistant professor of surgery, Harvard Medical School, Boston, Massachusetts. “One is that the cancer is aggressive but just very small,” said Cole.

“Another possibility is that the cancer looks very similar to background prostate tissue, which is something that you might expect if you think about more of a low-grade cancer,” he explained.

The experience level of the radiologist interpreting the MRI can also play into the accuracy of the reading.

But Cole agreed that “in general, MRI visibility is associated with molecular and histologic features of progression and aggressiveness and non-visible cancers are less likely to have aggressive features.”

The genomic profiles of MRI-visible and -invisible cancers bear this out.

According to Todd Morgan, MD, chief of urologic oncology at Michigan Medicine, University of Michigan, Ann Arbor, the gene expression in visible disease tends to be linked to more aggressive prostate tumors whereas gene expression in invisible disease does not.

In one analysis, for instance, researchers found that four genes — PHYHD1, CENPF, ALDH2, and GDF15 — associated with worse progression-free survival and metastasis-free survival in prostate cancer also predicted MRI visibility.

“Genes that are associated with visibility are essentially the same genes that are associated with aggressive cancers,” Klotz said.

 

Next Steps After Negative MRI Result

What do MRI-invisible lesions mean for patient care? If, for instance, a patient has elevated PSA levels but a normal MRI, is a targeted or systematic biopsy warranted?

The overarching message, according to Klotz, is that “you don’t need to find them.” Klotz noted, however, that patients with a negative MRI result should still be followed with periodic repeat imaging.

Several trials support this approach of using MRI to decide who needs a biopsy and delaying a biopsy in men with normal MRIs.

The recent JAMA Oncology analysis found that, among men with negative MRI results, 86% avoided a biopsy over 3 years, with clinically significant prostate cancer detected in only 4% of men across the study period — four in the initial diagnostic phase and seven in the 3-year monitoring phase. However, during the initial diagnostic phase, more than half the men with positive MRI findings had clinically significant prostate cancer detected.

Another recent study found that patients with negative MRI results were much less likely to upgrade to higher Gleason scores over time. Among 522 patients who underwent a systematic and targeted biopsy within 18 months of their grade group 1 designation, 9.2% with negative MRI findings had tumors reclassified as grade group 2 or higher vs 27% with positive MRI findings, and 2.3% with negative MRI findings had tumors reclassified as grade group 3 or higher vs 7.8% with positive MRI findings.

These data suggest that men with grade group 1 cancer and negative MRI result “may be able to avoid confirmatory biopsies until a routine surveillance biopsy in 2-3 years,” according to study author Christian Pavlovich, MD, professor of urologic oncology at the Johns Hopkins University School of Medicine, Baltimore.

Cole used MRI findings to triage who gets a biopsy. When a biopsy is warranted, “I usually recommend adding in some systematic sampling of the other side to assess for nonvisible cancers,” he noted.

Sampling prostate tissue outside the target area “adds maybe 1-2 minutes to the procedure and doesn’t drastically increase the morbidity or risks,” Cole said. It also can help “confirm there is cancer in the MRI target and also confirm there is no cancer in the nonvisible areas.” 

According to Klotz, if imaging demonstrates progression, patients should receive a biopsy — in most cases, a targeted biopsy only. And, Klotz noted, skipping routine prostate biopsies in men with negative MRI results can save thousands of men from these procedures, which carry risks for infections and sepsis.

Looking beyond Gleason scores for risk prediction, MRI “visibility is a very powerful risk stratifier,” he said.

A version of this article appeared on Medscape.com.