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.