A new study shows for the first time that even in the absence of nicotine, vaping directly impairs lung function and the body’s ability to ward off infections. A UNM College of Pharmacy scientist played a key role in the landmark research.
The finding, published in the Journal of Clinical Investigation, comes amid a wave of mysterious vaping-related illnesses (and at least two reported deaths) and growing concern about the rapid spread of e-cigarette use among young people.
The culprit appears not to be the nicotine, but other ingredients used in e-cigarette liquid, says Matthew Campen, PhD, a professor in the Department of Pharmaceutical Sciences and an expert in the health effects of air pollution, such as ozone and smoke.
Campen joined with Dr. Farrah Kheradmand and her colleagues at the Baylor College of Medicine, the University of Texas Health Science Center and the Michael E. DeBakey VA Medical Center in Houston to study how the vaporized chemicals affect the lungs.
The researchers focused on surfactant – the thin layer of lung-lining fluid that is affected by vaping. Surfactant supports alveoli, tiny balloon-shaped sacs in the lungs where oxygen and carbon dioxide cross into blood-carrying capillaries. The alveoli are very delicate, but reinforced by the protein and fat molecules in the surfactant, Campen says.
Macrophages – a type of immune cell – keep the surfactant healthy by finding and “recycling” damaged proteins, as well as killing inhaled viruses and bacteria. ‘That’s their job,” Campen says. “Throughout your life, they’re cleaning things up.”
But the new study finds that the inhaled e-cigarette vapor damages the macrophages, hampering their ability to protect the surfactant – and therefore the lungs, Campen says.
Vaping has been touted as a safer alternative to cigarette smoking, which has a well-documented connection to lung cancer, emphysema and other diseases. E-cigarette liquid is a mixture of the solvents propylene glycol and vegetable glycerin, common food additives.
When vaporized, the liquid does not trigger lung inflammation in the way cigarette smoke does, the study found, but it does trigger changes in the macrophages.
Mice exposed to e-cigarette vapor for months and then exposed to the influenza A virus died at higher-than-usual rates. Vapor exposure “reduces innate immune responsiveness, and long-term exposure impairs the ability of mice to control pulmonary infection with influenza,” the team wrote.
It also disrupts the mechanism for maintaining healthy surfactant in the alveoli. “This study demonstrates an urgent need to better examine the physiological effects of e-cigarette solvents currently in the market,” the authors wrote.
“These changes in the lung-lining fluid and the macrophages may relate to the severe cases of vaping-associated lung injury being seen around the country,” Campen says, adding that further study will be needed to determine which of the e-cigarette liquid ingredients is responsible for the damage, and who might be vulnerable.