Albert Rizzo, M.D.

This month’s Lungcast features a discussion on lung cancer screening guidelines and pulmonary nodule management. 

Lung Cancer Screening: A Decade of Lessons Learned with Mary Pasquinelli, DNP

Lung cancer remains the leading cause of cancer-related death worldwide, accounting for nearly 2 million deaths annually, which is more than those caused by breast, colorectal, and cervical cancers combined. Despite this burden, only 15% of patients survive 5 years post-diagnosis, largely due to late-stage detection in the majority of cases. It has been more than a decade since lung cancer screening guidelines via low-dose CT, based on the USPSTF’s B recommendations, have been put into place. 

In the latest episode of Lungcast, host Albert Rizzo, MD, chief medical officer of the American Lung Association (ALA), discussed this topic on the monthly respiratory health podcast series. Rizzo spoke with Mary Pasquinelli, DNP, a nurse practitioner in the Division of Pulmonary, Critical Care, Sleep, and Allergy at University of Illinois Health. She also serves as the director of the Lung Screening Program at the University of Illinois Chicago.

In this episode of Lungcast, Rizzo and Pasquinelli discussed the guidelines’ ambitions and obstacles. They also discussed pulmonary nodule management, which, while a lifesaving procedure for at-risk individuals, has seen slower than expected the uptake of screening on a population-level, although this is increasing. Pasquinelli also outlined a number of efforts and tools to increase screening rates.

“Screening truly saves lives, and we have all these efforts underway to really enhance screening through refined criteria, risk stratification, integration of emerging tools like biomarkers and AI such as Sybil, which holds really great, great promise for improving early detection and outcomes. So, it's just so important that we remember that anybody with lungs can get lung cancer. And thankfully, the narrative around lung cancer is changing. There's more awareness, there's more innovation, and more, most importantly, there's more hope,” Pasquinelli stressed.

Lungcast is a monthly respiratory news podcast series hosted by Albert Rizzo, MD, chief medical officer of the ALA, and produced by 

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This interview in the latest issue of The Respiratory Report features Jamie Hook, MD, discussing research into targeting the lung and not the virus to treat influenza.

Bolstering Alveolar Defense to Treat Complicated Influenza

Influenza is a major cause of global mortality and a frequent cause of pandemics, with death often resulting from secondary pneumonia by inhaled 

 (SA), especially in children. New research is uncovering how influenza infection disrupts lung defenses and opens the door to deadly bacterial co-infections with SA.

Jaime Hook, MD, Assistant Professor, Division of Pulmonary, Critical Care, and Sleep Medicine, Departments of Medicine and Microbiology, Global Health and Emerging Pathogens Institute, Icahn School of Medicine at Mount Sinai, and her team are studying new therapeutic approaches for influenza lung infection that protect against fatal SA coinfection. 

Hook spoke in the third issue of The Respiratory Report, a quarterly newsletter from 

 that is powered by the American Lung Association Research Institute, on her team’s current research in this area.

Her team found that influenza impairs alveolar defense by blocking CFTR-dependent liquid secretion and activating ENaC-driven absorption, creating an absorptive environment that allows inhaled 

 to cause fatal lung injury and were able to rescue alveolar wall liquid secretion and protect against SA-induced lung injury with the CFTR potentiator drug ivacaftor.

"These findings support CFTR potentiator therapy as a new treatment strategy for flu, SA coinfection, and they also inform the design of new CFTR potentiating therapies that might have more precise alveolar sites of action,  better drug efficacy, fewer side effects, and perhaps resilience in the face of new pandemic viruses and new viral and bacterial mutations that threaten the efficacy of existing drugs," Hook said.

To learn more about Hook's research, view the interview above or read her contribution to the third issue of The Respiratory Report here:

Developing new treatments for influenza that target the lung – not the virus

This interview in the latest issue of The Respiratory Report features Jamie Hook, MD, discussing research into targeting the lung and not the virus to treat influenza.


This interview in the latest issue of The Respiratory Report features Divay Chandra, MD, MSc, discussing lithium's potential enhancement of alveolar repair after injury.

Exploring Lithium: A Potential Disease-Modifying Therapy for Emphysema

While chronic obstructive pulmonary disease (COPD) remains a leading cause of death worldwide, there is still no treatment that reverses or halts its progression.  Recent research is exploring the potential of lithium, a drug commonly used for bipolar disorder, as a candidate to repair lung damage by targeting a key regenerative signaling pathway in the lung.

This study is being led by Divay Chandra, MD, MSc, an associate professor in the Division of Pulmonary, Allergy, Critical Care, and Sleep Medicine, Department of Medicine, at University of Pittsburgh in Pennsylvania. Chandra spoke in the third issue of 

 that is powered by the American Lung Association Research Institute, on his team’s current research in this area.

Chandra and his team analyzed data from large population cohorts to assess whether individuals taking lithium for other conditions had less lung disease and then measured environmental lithium exposure in people not on the drug. They found that both therapeutic and naturally occurring lithium levels were associated with reduced COPD severity, supporting its potential as a disease-modifying agent. The next step in Chandra's research is scaling up their studies to look at longitudinal progression and is enabled by an American Lung Association grant.

"Despite decades of research and multiple clinical trials, as yet, we have not been able to identify a disease modifying agent in COPD. And that is really the frustrating part. We have drugs that can treat symptoms. You know, we have drugs which can treat eosinophilia, which can reduce exacerbations, but we have no drug that can get at the fundamental disease process that drives this lung disease. That is exactly where lithium could play a role," Chandra said.

To learn more about Chandra's research, view the interview above or read his contribution to the third issue of The Respiratory Report here:

Exploring Lithium as a Potential Disease-Modifying Therapy for Emphysema

This interview in the latest issue of The Respiratory Report features Divay Chandra, MD, MSc, discussing lithium's potential enhancement of alveolar repair after injury.



This interview in the latest issue of The Respiratory Report features William Zhang, MD, discussing AM iron accumulation, which may contribute to the well-known phenomenon of AM dysfunction in COPD6.

Investigating COPD Pathogenesis: Abnormal Iron Homeostasis in Alveolar Macrophages

Disruptions in iron metabolism within alveolar macrophages may play a key role in the progression and exacerbation of chronic obstructive pulmonary disease (COPD), according to ongoing research led by William Zhang, MD, Assistant Professor of Medicine at Weill Cornell Medicine. His research aims to better understand the biological mechanisms underlying COPD and address gaps that currently limit the development of targeted therapies.

Zhang and his team used murine models of cigarette smoke exposure and single-cell RNA sequencing to investigate how dysregulated iron metabolism in alveolar macrophages contributes to COPD pathogenesis and exacerbation risk. He found that cigarette smoke induces iron loading in these immune cells, impairing their function, and that disrupting iron regulation may reduce emphysema development but could also weaken infection response. He also discussed proof-of-concept studies in humans the team is conducting.

"To get rid of an important protein that breaks down ferritin and allows the cell to retrieve iron when it needs to, especially when macrophages are fighting infection, I think probably also hampers them to some extent in this infection model. So, I think that the biology behind this is is more complex than we initially hypothesized and not so straightforward," Zhang said.

To learn more about Zhang's research, view the interview above or read his contribution to the third issue of The Respiratory Report here:

Abnormal Iron Homeostasis in Alveolar Macrophages: Implications for COPD Pathogenesis

Albert Rizzo, M.D.

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