Acute vaping exacerbates microbial pneumonia due to calcium (Ca2+) dysregulation.

As electronic cigarette (E-cig) use, also known as "vaping", has rapidly increased in popularity, data regarding potential pathologic effects are recently emerging. Recent associations between vaping and lung pathology have led to an increased need to scrutinize E-cigs for adverse health impacts. Our previous work (and others) has associated vaping with Ca2+-dependent cytotoxicity in cultured human airway epithelial cells.

Vaping Exacerbates Coronavirus-Related Pulmonary Infection in a Murine Model.

Though the current preponderance of evidence indicates the toxicity associated with the smoking of tobacco products through conventional means, less is known about the role of "vaping" in respiratory disease. "Vaping" is described as the use of electronic cigarettes (E-Cigarettes or E-Cigs), which has only more recently been available to the public (∼10 years) but has quickly emerged as a popular means of tobacco consumption worldwide. The World Health Organization (WHO) declared the SARS-CoV-2 outbreak as a global pandemic in March 2020.

JUUL e-liquid exposure elicits cytoplasmic Ca responses and leads to cytotoxicity in cultured airway epithelial cells.

Rationale: The popularity of new and emerging tobacco products such as E-cigarettes (E-cigs) is rapidly expanding worldwide. However, uncertainties surrounding the potential health consequences due to the use of such products exist and warrant further study.

Methods: Cultured A549 and Calu-3 airway epithelia were exposed to three out of the eight types of JUUL brand e-liquids ("Mint", "Virginia Tobacco" and "Menthol", all containing 3% nicotine at 1% and 3% (vol/vol) dilutions) and assessed for viability using a resazurin-based assay.