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Electronic cigarette (e-cigarette) use is rapidly increasing worldwide, especially among teenagers and young adults. Vaping, the inhalation of aerosol from e-cigarettes, has become a common practice, no longer limited to niche groups, said Neena Chandrasekaran, MD, a pulmonologist and critical care physician in Florida, in a video on Medscape.com.

Once considered a harmless alternative to smoking, vaping has become a global health concern with serious and, at times, permanent consequences. One of the most dangerous is e-cigarette or vaping product use-associated lung injury (EVALI), a potentially life-threatening condition.

Vaping can cause serious and permanent pulmonary damage, as seen in the case of David, a 17-year-old student from the US. He had planned to join the Navy, but that dream ended after he developed a severe pulmonary illness associated with vaping. He was diagnosed with EVALI caused by inhaling a homemade liquid containing tetrahydrocannabinol (THC) and vitamin E acetate.

David is not alone. In 2020, approximately 2600 individuals in the US were hospitalized with EVALI, and the number has continued to rise. To date, approximately 50 people have died from this condition nationwide.

In Europe, additives in e-liquids are more strictly regulated, and no similar cases of widespread EVALI have been reported. However, doctors should remain aware of the symptoms, as the condition can still occur, particularly among individuals who mix their own vaping liquids.

Toxic Contents

e-Cigarettes function by heating a liquid containing various additives, producing an aerosol that users inhale. Although this may seem harmless, inhaling certain ingredients can cause serious lung damage.

Vitamin E acetate is a common and extensively studied additive that is potentially harmful when inhaled. A study published in The New England Journal of Medicine found vitamin E acetate in the bronchoalveolar lavage fluid of patients with EVALI.

The authors suggested that vitamin E acetate irritates the lung mucous membranes when inhaled, even though it is considered safe when taken orally.

THC, a psychoactive component of cannabis, is also thought to contribute to the development of EVALI. In many cases, high concentrations of THC have been detected in the bronchoalveolar lavage fluid.

This suggests that the risk is linked not only to vaping but also to the chemical composition of the inhaled liquid.

The diagnosis of EVALI remains challenging. This clinicopathologic syndrome mimics other pulmonary conditions and often resembles atypical viral pneumonia.

Common symptoms include shortness of breath, cough, chest pain, and fever. Physical examination often reveals hypoxemia and tachycardia.

When patients present with hypoxemia and ground-glass opacities on chest imaging, clinicians often suspect COVID-19 or other viral respiratory infections.

EVALI should be considered in differential diagnosis, particularly when patients present with typical viral symptoms but no identifiable infectious pathogens and report using e-cigarettes. 

Identifying the specific components of inhaled products, such as THC or vitamin E acetate, is essential for accurate diagnosis and appropriate treatment planning.

Before confirming a diagnosis of EVALI, other causes must be carefully excluded, including influenza, Streptococcus pneumoniae, Legionella species, and Mycoplasma pneumoniae infections. However, this diagnostic process can be challenging.

Certain indications of EVALI include leukocytosis with neutrophil predominance and elevated inflammatory markers, such as C-reactive protein, erythrocyte sedimentation rate, and procalcitonin. Chest radiography is suitable for the initial evaluation; however, CT with or without contrast is often required to identify characteristic imaging findings.

Typical CT findings include bilateral ground-glass opacities resembling those seen in pneumonia or diffuse alveolar damage. Differentiation can be difficult because similar imaging patterns are present in various pulmonary diseases. In uncertain cases, bronchoscopy or lung biopsy may be necessary to confirm the diagnosis of vaping-associated lung injury.

Treatment and Prognosis

The initial management of EVALI generally includes empirical antibiotic treatment as a precautionary measure for community-acquired pneumonia. Systemic corticosteroids are commonly administered concurrently and have demonstrated efficacy in reducing the inflammatory response in the lungs and oxidative stress at the cellular level. Most patients show rapid improvement in oxygen saturation and resolution of pulmonary infiltrates after steroid treatment.

In severe cases, such as acute respiratory failure, mechanical ventilation may be required to maintain oxygenation. One case series reported that 56% of hospitalized patients required intensive care, with 27% requiring mechanical ventilation. Approximately 1 in 4 patients developed acute respiratory distress syndrome and required extracorporeal membrane oxygenation in some cases.

Despite the potential for severe illness, the overall prognosis is favorable, provided that the diagnosis is made early and e-cigarette use is discontinued immediately.

EVALI is a serious but treatable pulmonary condition that should be included in the differential diagnosis of acute respiratory symptoms in individuals with a history of e-cigarette use. Early recognition and prompt cessation of treatment are essential for recovery.

This story was translated from Medscape’s German edition.

In a new discovery, researchers at the Icahn School of Medicine at Mount Sinai have developed new insights into how a critical brain receptor works at the molecular level. This could eventually lead to the development of more targeted antidepressant medications.

The study, published in Science Advances, focuses on the 5-HT1A serotonin receptor – a major component in regulating mood and a common target for traditional antidepressants. Despite its clinical importance, this receptor has remained poorly understood, with many of its molecular and pharmacological properties hugely understudied – until now.

A molecular ‘control panel’ for brain function

“This receptor is like a control panel that helps manage how brain cells respond to serotonin, a key chemical involved in mood, emotion and cognition,” says senior author Dr Daniel Wacker, Assistant Professor of Pharmacological Sciences and Neuroscience, at the Icahn School of Medicine at Mount Sinai. “Our findings shed light on how that control panel operates – what switches it flips, how it fine-tunes signals and where its limits lie. This deeper understanding could help us design better therapies for mental health conditions like depression, anxiety and schizophrenia.”

Using new lab techniques, the research team found that the 5-HT1A receptor is inherently wired to favour certain cellular signalling pathways over others – regardless of the drug used to target it. However, drugs can still influence the strength with which those pathways are activated.

Cryo-EM sheds light on key interactions

To explore these mechanisms in more detail, the researchers combined experiments in lab-grown cells with high-resolution cryo-electron microscopy (cryo-EM) – an imaging technology that reveals molecular structures at near-atomic resolution. Their work focused on how various drugs activate the 5-HT1A receptor and how the receptor interacts with internal signalling proteins known as G proteins.

Different signalling pathways controlled by the 5-HT1A receptor are linked to different aspects of mood, perception and pain. As scientists better understand which pathways are activated, they can more precisely design drugs that treat specific symptoms or conditions without unwanted side effects.

“Our work provides a molecular map of how different drugs ‘push buttons’ on this receptor – activating or silencing specific pathways that influence brain function,” says study first author Dr Audrey L Warren, a former student in Dr Wacker’s lab who is now a postdoctoral researcher at Columbia University. “By understanding exactly how these drugs interact with the receptor, we can start to predict which approaches might lead to more effective or targeted treatments and which ones are unlikely to work. It’s a step toward designing next-generation therapies with greater precision and fewer side effects.”

A hidden ‘co-pilot’ molecule

In a surprising finding, the researchers discovered that a phospholipid – a type of fat molecule found in cell membranes – plays a major role in steering the receptor’s activity, almost like a hidden co-pilot. This is the first time a role like this has been observed among the more than 700 known receptors of this type in the human body.

While current antidepressants often take weeks to work, scientists hope this new understanding of 5-HT1A signalling could help explain those delays and lead to faster-acting alternatives.

“This receptor may help explain why standard antidepressants take long to work,” says Dr Wacker. “By understanding how it functions at a molecular level, we have a clearer path to designing faster, more effective treatments, not just for depression, but also for conditions like psychosis and chronic pain. It’s a key piece of the puzzle.”

Looking ahead: from the lab to clinic

Next, the researchers plan to dig deeper into the role of the phospholipid ‘co-factor’ and to test how their lab-based findings hold up in more complex experiments. They are also working on turning these discoveries into real-world compounds that could become future psychiatric medications, building on their earlier success with drug candidates derived from psychedelics.

This breakthrough not only broadens scientific understanding of brain signalling but could also enable the design of mental health treatments that are faster, more precise and have fewer side effects.