Chapter 18 E-cigarettes and other alternative nicotine products

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Winnall, W |Greenhalgh, EM |Scollo, MM. 18.6.5 E-cigarette use and the risk of non-infectious respiratory diseases. In Greenhalgh, EM |Scollo, MM |Winstanley, MH [editors]. Tobacco in Australia: Facts and issues. Melbourne : Cancer Council Victoria; 2019. Available from https://www.tobaccoinaustralia.org.au/chapter-18-e-cigarettes/18-6-the-health-effects-of-e-cigarette-use/18-6-5-e-cigarette-use-and-the-risk-of-non-infectious-respiratory-diseases
Last updated: June 2024

18.6.5 E-cigarette use and the risk of non-infectious respiratory diseases

This section describes the risk of non-infectious respiratory diseases as well as damage to the respiratory system associated with e-cigarette use. Infections of the airways are discussed in Section 18.6.6 and the risk of cancer in the airways, such as lung cancer, in Section 18.6.4.

18.6.5.1 Exposure of the respiratory system to chemicals during e-cigarette use

Frequent exposure to fine and ultrafine particles, such as tobacco smoke, can contribute to pulmonary inflammatory and increase the risk of respiratory diseases. 1 E-cigarette emissions are aerosols made of chemicals such as propylene glycol and glycerol, with nicotine and many other chemicals at lower levels. 2 , 3 A 2022 review by the National Health and Medical Research Council identified 42 chemicals found in e-liquids and aerosols that are harmful or potentially harmful by inhalation (see Section 18.5.5.2). 4 Most of these chemicals were present at relatively low levels. 4 However, a regular e-cigarette user will expose their lungs to a mix of chemicals hundreds of times a day, every day, for years or decades.

The long-term effects of such exposure to a mix of chemicals are not well understood. However, recent longitudinal studies have provided some evidence of increased risk of respiratory diseases, such as chronic obstructive pulmonary disease, which are commonly associated with long-term exposure to inhaled chemicals (see below in 18.6.5.2).

18.6.5.2 Chronic obstructive pulmonary disease

Chronic obstructive pulmonary disease (COPD) is characterised by persistent respiratory symptoms and airflow limitation that is usually progressive. The chronic airflow limitation is caused by a mix of small airways disease (obstructive bronchitis) and destruction of the alveoli (fine surfaces of the lung) due to chronic inflammation, also referred to as emphysema. 5 Poor lung function and chronic respiratory symptoms may precede this airway obstruction. COPD is more prevalent among middle-aged and older people, at which stage it has important interactions with many other acute and chronic illnesses. The causes of COPD include tobacco smoking, exposure to secondhand smoke, genetic factors and exposure to some chemicals and pollutants. 5

A number of cross-sectional studies have found an association between COPD and e-cigarette use in adults. 6-9 However, the design of these studies means that they cannot determine whether vaping causes COPD.

The results of some longitudinal studies support an association between COPD and sole e-cigarette use — an indication that e-cigarette use may be causing COPD — however, there are some inconsistencies in the evidence. 10-12 , 14 , 15 Most of these studies have used data from the longitudinal Population Assessment of Tobacco and Health (PATH study), a nationally representative, population-based, longitudinal study involving approximately 49,000 people aged 12 years and above. Data has been collected in various waves (waves 1; 2013 to 2014, wave 2; 2014 to 2015, wave 3; 2015 to 2016, wave 4; 2016 to 2017; wave 5: 2018 to 2019) with plans up to wave 8 collection starting in 2024. 13

One study that used PATH data did not find significant associations between e-cigarette use at wave 1 and incident COPD at waves 2 and 3; though the small number of incidents meant the study was likely underpowered to detect increased risk. 10 A study of pooled data up to wave 4 found 6.5-fold increased odds of having ever been diagnosed with COPD among e-cigarette users compared to non-users/non-smokers, after adjusting for other conditions and potentially confounding variables (though former smokers were included in the exclusive vaping group). 11 Another study using the same waves of data—this time examining the relationships longitudinally and adjusting for smoking history—found a significant but smaller association of one and a half times increased odds of developing COPD among e-cigarette users compared to non-users/non-smokers. 12

As COPD incidence increases as people age, some studies included only people aged 40+ using PATH study data. Two such studies from waves 1 to 5 have not found evidence of an association between sole e-cigarette use and COPD incidence after controlling for smoking history. 14 , 15 However exclusive vaping is relatively rare among middle-aged and older adults, which limits examination of health risks among this group.

18.6.5.3 Asthma

Asthma is a common chronic respiratory disease characterised by airways obstruction (narrowing) that leads to wheezing, shortness of breath, coughing, chest tightness or fatigue. 13 Asthma is often first diagnosed in childhood and becomes less frequent over time. However, it may continue for some people, reoccur, or begin later in life. These time periods can mean that it is difficult to determine whether a specific exposure, such as tobacco smoke or e-cigarette use, has preceded the disease onset, which complicates studies of causality. While cigarette smoking is certainly a risk factor for asthma, the 2014 US Surgeon General’s report concluded that the available evidence was suggestive, but is insufficient to conclude, that smoking causes asthma in adults and adolescents. 16 However, smoking is known to exacerbate asthma in adults and leads to poor asthma control (see Section 3.2.5.1 for more about tobacco use and asthma). 16

Numerous studies have concluded that e-cigarette use is associated with asthma, however these are mostly restricted to cross-sectional studies. 9 , 17-19 A meta-analysis from 2024 combined 42 studies and found that vaping was associated with 24% higher odds of asthma or wheeze/cough compared to non-users. 18 Dual use did not appear to be a higher risk than cigarette use. However, most of the studies in this meta-analysis were cross-sectional, which cannot establish causation.

Several longitudinal studies, which are more appropriate for determining causation, have examined the association between e-cigarette use and subsequent asthma onset or exacerbation. 10 , 11 , 20 Most of these studies use data from the longitudinal US PATH study, with some finding an increased risk of asthma among people who vape, 10 , 12 and others finding no association. 11 The two most recent of these studies, both of which controlled for COPD and smoking history, produced conflicting findings. One found no increased risk of asthma among those who used e-cigarettes 1–2 years later, 20 while another examined 6 waves of data over 9 years and found that e-cigarette use increased the risk of asthma onset at earlier ages among adults. 21

A 2022 Australian review concluded that there was insufficient evidence to support an association of e-cigarette use and asthma, 22 but this review not include most of the recent PATH study data discussed above.

There are also inconsistencies in the evidence for an association of asthma and e-cigarette use among adolescents 23 , 24 (see Section 18.6.2 for more information).

18.6.5.4 EVALI (E-cigarette Vaping associated Acute Lung Injury)

An outbreak of serious acute lung injury associated with e-cigarette use began in the US in July 2019, peaking in August and gradually declining from September 2019. The Centers for Disease Control and Prevention (CDC) reported 2,807 instances of hospitalisation and 68 deaths from EVALI in the US from August 2019 until February 2020, when data collection stopped due to the COVID pandemic. 25 EVALI is also referred to as Vaping-Associated Pulmonary Injury (VAPI), and has also been referred to as acute lipoid pneumonia in case reports. 22

Symptoms of EVALI include shortness of breath, fever, cough, vomiting and diarrhoea, occurring in the absence of infection or other lung injury. EVALI is difficult to diagnose as there is no confirmatory diagnostic test and the symptoms are similar to other respiratory diseases such as influenza. The lungs of people with EVALI are inflamed and contain abnormally high numbers of inflammatory cells. 26

Case reports have indicated that EVALI more often occurred in healthy white males who were adolescents or young adults, usually using e-cigarettes containing tetrahydrocannabinol (THC; the major psychoactive ingredient of cannabis) and the additive vitamin E acetate (VEA). E-cigarettes used by these people were more likely to come from illicit sources. 26

A recent, comprehensive review from Australia found conclusive evidence that e-cigarette use causes EVALI in smokers and non-smokers. 22 The exact mechanisms by which e-cigarettes are causing EVALI are unknown. The strong association of EVALI with recent use of e-cigarettes containing THC and VEA indicates that either VEA, or another chemical often present in THC/VEA e-cigarettes, may be triggering this disease. 25 VEA is found in the lung fluid of 94% of people with EVALI, but not people without EVALI. 27 Increased awareness of the potential dangers of VEA as an ingredient in illicit THC cigarettes and the removal of VEA from some products may have contributed to the steady decline in the number of people diagnosed with EVALI. 28

While VEA (or a contaminate or breakdown product of VEA) is a strong candidate for a cause of EVALI, it may not be the only cause. Not all people with EVALI were recent users of THC/VEA e-cigarettes. In one study, 51% of people with EVALI reported recent use of both THC and nicotine e-cigarettes and 17% reported sole use of nicotine e-cigarettes. 26 Furthermore, a study of 17 EVALI cases from a range of countries outside the US found that each person had used nicotine e-cigarettes, and that only 24% of these people had used cannabis, mixed with nicotine. 29 A study that measured chemicals in the lung fluid from EVALI patients in the US reported that 94% contained THC and 64% contained nicotine or its breakdown products (metabolites). 27 Taken together, these studies indicate that between 6% and 76% of people with EVALI were not recent users of THC-containing e-cigarettes.

VEA is a synthetic form of vitamin E that was developed to improve its stability. 30 Its safety for use in food and cosmetics is well-established. If VEA is a trigger for EVALI in some people, the mechanism by which this happens has not been identified. Some potential mechanisms have been proposed, including VEA forming toxic breakdown products such as ketene gas once heated, or VEA disrupting the pulmonary surfactant surface tension that protects the lining of the lungs. Whether these or other mechanisms may underlie the effects of VEA and EVALI are not yet known. 30 , 31

18.6.5.5 Other acute respiratory effects

There is convincing evidence that the acute, and sometimes fatal, lung condition known as EVALI (e-cigarette vaping-induced lung injury) is caused by e-cigarette use, discussed in Section 18.6.5.4 above. There is evidence for lung damage, including inflammation, and subclinical measures of respiratory function, as well as case reports of rare conditions that are potentially associated with e-cigarette use. 22 , 32

Subclinical measures of lung function, such as spirometry, are useful predictors of disease state. These measures are important for predicting the health effects of e-cigarette use, as clinical outcomes such as asthma and COPD may take many years to develop. 22 Measures of exhaled carbon monoxide and nitric oxide are also used as markers of lung inflammation. 22

Multiple reviews have found evidence for a decrease in lung function (based on spirometry and other tests) for non-smokers in the two hours after using an e-cigarette. 22 , 33 , 34 However, the evidence comes from small trials and may be considered ‘limited’. 22 There is also limited evidence that e-cigarette use leads to decreased lung function and respiratory inflammation in healthy and asthmatic people who smoke up to 30 minutes after exposure. 22 , 33 , 34

Numerous trials have tested the effects of substituting e-cigarettes for tobacco cigarettes on the respiratory system. A systematic review of these examined studies of lung function (mostly spirometry) in people who had switched to e-cigarette use. 35 The results of these studies varied considerably. Nine trials found improvements of lung function with switching, 14 found declines in lung function, and 43 found no significant differences after switching to e-cigarettes. Many of these studies were small in size and had risks of bias. Overall, these results do not provide convincing evidence that switching from tobacco cigarettes to e-cigarettes leads to an improvement in lung function. 35

Use of nicotine-containing e-cigarettes may be associated with short-term increases in the urge to cough and cough sensitivity. However these data come mostly from studies described as ‘fair’ quality, so higher quality studies are needed for firmer conclusions. 22 , 33

Including those related to the EVALI outbreak in 2019, described above, a considerable number of case reports and case series have indicated the potential for some acute respiratory diseases in e-cigarette users—see here for a compilation of those that have been published in scientific literature to date. These include diagnoses of eosinophilic pneumonia, hypersensitivity pneumonitis, organising pneumonia, diffuse alveolar haemorrhage and giant cell foreign body reaction. 32 These pneumonia diagnoses appeared to involve lung damage in the absence of infection. Some of these conditions may have been early cases of EVALI. Common to EVALI and many of the earlier case reports are the presence in the lungs of immune cells called macrophages that had engulfed copious lipids (fats), consistent with a deposit of chemicals in the lungs. However, it is not known whether the actions of these cells are part of a pathological mechanism leading to the disease, or if they are actually inhibiting lung pathology. 32 One study found that dual users of cigarettes and e-cigarettes reported poorer general health and greater breathing difficulty in the past month compared to those who smoked only cigarettes. 36 Since these studies come from case studies and case reports, larger studies are necessary before concluding that e-cigarette use is associated with an increased risk from these conditions (except for EVALI, for which the evidence is strong).

Bronchiolitis obliterans (‘popcorn lung’) is a rare inflammatory disease of the small airways of the lungs (bronchioles) that results in obstruction and permanent scar tissue in the lungs. This irreversible lung damage leads to shortness of breath and a dry cough. The name “popcorn lung” came about due to the disease sometimes being caused by inhalation of the artificial butter flavouring chemical diacetyl, which is used to flavour popcorn. Diacetyl, added to some e-liquids, and another chemical called methylglyoxal that also causes bronchiolitis obliterans, have been detected in the emissions from e-cigarettes. 37-39 Although these chemicals are present in very low amounts in e-cigarette emissions, one study has estimated that diacetyl levels in the emissions of some e-cigarettes exceed the proposed safe levels of exposure. 38 However, aside from three case studies involving six people, 40-42 there little evidence of widespread bronchiolitis obliterans in people who use e-cigarettes.

18.6.5.6 Other chronic respiratory conditions

Based on long-term exposure to the chemicals that damage the respiratory system and the emerging evidence for a risk of short-term inflammation and decreased lung function, e-cigarettes have the potential to cause chronic respiratory diseases such as chronic obstructive pulmonary disease (COPD), chronic bronchitis, emphysema and asthma. There are also carcinogens (cancer-causing chemicals) at low levels in e-cigarette aerosols, which have the potential to cause cancer in the respiratory tract, discussed in Section 18.5.5.2

E-cigarette use may be leading to conditions such as bronchitis and chronic cough. Analysis of youth (12–17 years) data from waves 1 to 5 of the longitudinal PATH study show that exclusive users of e-cigarettes had a 1.5-fold increased risk of being diagnosed with a chronic respiratory disease such as bronchitis, chronic cough or pneumonia compared to non-users/non-smokers. 43 In this study, dual-users of e-cigarettes and tobacco cigarettes had a 2.7-fold increased risk, which was higher than tobacco smokers, whose risk was 1.8-fold higher. 43

18.6.5.7 Animal studies of exposure to e-cigarettes

Experimental studies using rodents exposed to e-cigarette emissions indicate the potential of e-cigarette use to damage the lungs, consistent with a risk for respiratory disease in humans. These studies have detected inflammation 44-46 and oxidative damage 47 in the lungs of mice or rats exposed to e-cigarette aerosols. Also detected was the disruption of the protective pulmonary surfactant, a protective coating of fatty proteins in the alveoli. 48

One experiment using mice found that substituting 50% of daily cigarette smoke with e-cigarette emissions did not result in significant attenuation of acute lung injury, as measured by inflammatory markers, infiltration of inflammatory cells and markers of oxidative stress. 49

Relevant news and research

For recent news items and research on this topic, click  here. ( Last updated December 2024)

References 

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Intro
Chapter 2