Respiratory effects
Among e-cigarettes adverse health effects, respiratory impact is by far
the most extensively studied. In the same way as conventional cigarettes
smokers, vapers’ pulmonary epithelium is typically damaged73 and bronchial mucosa chronically
inflamed74. Proteomics of e-cigarette users’ sputum
document higher levels of myeloperoxidase, neutrophil elastase and
proteinase-3, indicative of neutrophil activation. Furthermore, chronic
vapers’ neutrophils display a greater propensity for NET formation when
compared to cigarette smokers or non-smokers62.
Bronchial inflammation result in a higher respiratory impedance and flow
resistance75 (evidenced by a lower
FEV1 and FEV1/FVC 76)
as well as a significant decrease in fractional exhaled Nitrogen
Oxide77, both observed in e-cig users.
From a clinical perspective, these pathophysiological alterations could
underlie the considerable increase in asthma and bronchitic symptoms
reported by e-cigarettes users, especially adolescents. According to
various studies involving high school students, vapers have a twofold
higher risk of chronic cough, phlegm or dyspnea, together with a greater
incidence of asthma78,79. A higher prevalence of
e-cigarette use is reported among adults living with a child affected by
asthma80, whose risk of acute exacerbation can
increase by 30%81. Schoolwork is indirectly affected
too, as a result of absenteeism secondary to the aforementioned
symptoms82. Preclinical studies83suggest also a detrimental effect on mucociliary clearance which,
coupled with a decreased cough sensitivity84 and the
overexpression of PAF-R (pneumococci’s receptor 85),
predispose vapers to increased rates of pneumonia86.
In parallel to the increasingly wide distribution of e-cigarette, a
growing number of cases helped characterize a new nosological entity,
which is now referred to as E-cigarette or Vaping Associated Lung Injury
(EVALI). It is a diagnosis of exclusion that requires use of
e-cigarettes and related products 90 days prior to symptom onset in
addition to pulmonary infiltrates on imaging87. The
prevalence seems higher in youth: indeed, the median age of the
initially reported cases was 1988. The hypothesized
causative agent of lung injury is vitamin E acetate, which may be found
in cartridges of THC flavored e-cigarettes, widespread among high school
students89. Its aerosolization generates ketene, that
is irritant to airways and disrupts phospholipid bilayer decreasing
surfactant effectiveness90. EVALI can occur with
shortness of breath, cough, tachycardia, tachypnea, pleuritic pain and
rarely hemoptysis. Nausea and abdominal pain, as well as fevers and
chills are not infrequent. Up to 30% of the affected require mechanical
ventilation and up to 70% the admission to intensive care
units90–92. Bilateral lower-lobe predominant ground
glass and consolidative opacities with subpleural sparing are the most
typical findings at chest imaging. Other possible radiographic patterns
include dense consolidative opacities (as in Acute Respiratory Distress
Syndrome), diffuse patchy and confluent consolidative opacities (as in
Cryptogenic Organizing Pneumonia) or upperlobe ground glass opacities
with air trapping (as in hypersensitivity
pneumonitis)92,93. After ruling out other respiratory
infections (viral panel, urine antigen testing, sputum and blood
cultures), a bronchoscopy with
Bronchoalveolar Lavage and, if
possible, transbronchial biopsies, should be performed unless clinical
severity precludes it90,94. Steroids should be started
concomitantly with antibiotics, especially in patients with respiratory
failure; in less severe presentations they can be delayed after
infectious causes are ruled out. Response to methylprednisolone is
generally excellent91. Based on the severity of the
clinical picture, patients can benefit from high-flow oxygen therapy,
noninvasive ventilation or require mechanical
ventilation88,91,95.
Case reports point out an association between e-cigarette smoking and
lipoid pneumonia, acute eosinophilic pneumonia, subacute bronchial
toxicity and even reversible cerebral vasoconstriction
syndrome96–99.