Vapers are vulnerable to pneumonia

The vapor from e-cigarettes seems to help pneumonia-causing bacteria stick to the cells that line the airways. The study included experiments with cells mice and humans. It showed that e-cigarette vapor had an effect similar to the reported effects of traditional cigarette smoke or particulate matter from fossil-fuel pollution, both of which are known to increase susceptibility to lung infection with pneumococcal bacteria.

Lead researcher, Jonathan Grigg, Professor of Paediatric Respiratory and Environmental Medicine at Queen Mary University of London, said the study indicates that vaping, especially in the long term, could raise the risk of bacterial lung infection. Pneumococcal bacteria can exist in human airways without causing illness. However, in some cases, they can invade the lining cells causing pneumonia or septicaemia. Exposure to traditional cigarette smoke helps these bacteria stick to airway lining cells, increasing the risk of infection.

The research examined the effects of e-cigarette vapor on a molecule produced by the cells that line the airways, called platelet-activating factor receptor (PAFR). Previous research by Professor Grigg's group has shown that pneumococcal bacteria use PAFR to help them stick to airway cells, which in turn increases the ability of bacteria to invade body tissues and cause disease. Research has also shown that PAFR levels increase in response to smoking, passive smoking, pollution and welding fumes.

Researchers examined human nose lining cells in the lab. They exposed some cells to e-cigarette vapor, some containing nicotine and some without, while other cells were not exposed. Cells exposed to either nicotine-containing or nicotine-free vapor produced levels of PAFR that were three times higher. When researchers introduced pneumococcal bacteria to these cells, they found that exposure to either nicotine-containing or nicotine-free vapor doubled the amount of bacteria that stuck to airway cells.

They tested the effect of e-cigarette vapor in mice and found that inhaled exposure to e-cigarette vapor also increased levels of PAFR on airway lining cells and increased the number of pneumococcal bacteria in the respiratory tract after infection, making mice more susceptible to disease. The team studied PAFR levels in cells lining the nose of 17 people. Of these, ten were regular users of nicotine-containing e-cigarettes, one used nicotine-free e-cigarettes, and six were not vapers.

First, PAFR levels in the airways of all 17 volunteers were measured. Then, vapers were asked to take at least ten puffs on their e-cigarettes over five minutes. One hour after vaping, PAFR levels on airway cells increased three-fold. The result shows that vaping makes the airways more vulnerable to bacteria sticking to airway lining cells. If this occurs when a vaper gets exposed to the pneumococcal bacterium, this could increase the risk of infection.
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