A full guide to vape aerosols: Post 9, environmental aerosols (part 2)
This is the ninth Substack post. It is the second one of a series of 3 posts dealing with environmental vape aerosols.
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This 9th Substack post expands the previous 8th post by reviewing the results of two studies: one looking at the chemical composition of exhaled vape aerosol, the other discussing biomarkers of exposed bystanders. So far, all studies (even those methodologically questionable) do not provide robust evidence of concerning aerosol toxicity or health effects from bystander exposure to aerosol exhaled by vapers.
The take away message: the effects of indoor vaping in non-smoking environments is almost the same (and is hard to distinguish) from same environments if vaping had not happened.
Summary of previous posts:
Post 1. Basics: what is an aerosol? Vapes and kettles. Byproducts of the heating process. Post 2. Physical processes in vaping. Essentials of laboratory testing. Optimal Regime. Post 3. Overheating: exponential production of toxic byproducts and the “dry puff”. Post 4. Laboratory testing. The CORESTA standard and the evolution of the vape market. Post 5 Metals. Post 6: Organic byproducts. Post 7: vape exposure in preclinic studies. Post 8, basics of environmental vape aerosols
Environmental vape aerosols.
Post 9: Part II, chemistry & biomarkers
NOTE ON NOMENCLATURE. I will not use the adjective “second hand” to denote aerosols that originate from users’ exhalations (ie “second hand smoke” or “second hand aerosol”). Instead, I will refer to them as environmental tobacco smoke (ETS) and exhaled vape aerosol (EVA)
Quick summary of Post 8
Environmental Tobacco Smoke (ETS) does not originate only from the smoker exhalation, it is a chemically complex air diluted mixture of the exhaled smoke (mainstream emission), the smoke coming from the smoldering tip of the cigarette (side stream emission) and environmental pollutants. The gas phase is a complex mixture of volatile gases (including CO), while Its particulates have small diameters around 300 nm (ultra-fine), can be liquid or solid and are not volatile, hence they do not evaporate and remain long time airborne. ETS involves a hazardous and prolonged (not intermittent) exposure to hundreds of toxins and carcinogens.
Exhaled vape aerosol. There is no side-stream in vaping, only the user exhaled aerosol is released to the environment. It is very diluted in air, since users retain around 90% of the aerosol (in both phases and including almost 100% of aldehydes). The, “particulates” are liquid ultra-fine droplets made of the same compounds (almost 100% of PG, VG, nicotine and water) as the gas phase and the inhaled aerosol (the aerosol only undergoes physical changes during inhalation). Once exhaled, PG and nicotine in the droplets rapidly evaporate into the gas phase, which rapidly disperses in the surrounding air in less than a minute (per puff). Therefore, exhaled vape aerosol involves an intermittent, short lived exposure to PG, VG, nicotine and negligible traces of byproducts that were not retained.
Motivation for Post 9.
The aerosol exhaled by vapers is just one of the many anthropogenic (human made) aerosols we are all exposed to in indoor environments: environmental tobacco smoke (ETS), cooking aerosols, odorizers, outdoor pollution penetrating indoors, vacuum cleaners and electronic appliances, paintings, cosmetics, even paper walls, rugs and furniture emit aerosols, additionally we are also exposed to biological aerosols from respiratory activities and/or airborne bacteria and fungus. The health risks these “household” aerosols pose depend on the physical and chemical properties of the specific particulates and gas (typically air).
The properties and effects from exposure to ETS have been extensively researched. There is even a branch of research dedicated to that chemical ghost known as “third hand smoke” (THS): residual chemicals (typically nicotine and its metabolites) that deposited in walls and surfaces of rooms where someone smoked, found in negligible quantities of a few nanograms per square meter. Nevertheless, there is no doubt that ETS involves a hazardous and prolonged exposure to a toxic indoor pollutant that poses concerning risks to bystanders, specially to vulnerable individuals (though harms from outdoor exposure to ETS have no empiric basis). .
Traditionally, exposure to ETS has been the comparative reference to assess exposure to exhaled vape aerosol, since after all vapes are substitute products of cigarettes and the assessment of risks from ETS has played a major role in the adoption of smoke-free policies. However, when considering ETS as comparative reference, it is important (as explained in detail in Post 8) to consider the empiric evidence proving that exhaled vape aerosol is a considerably (orders of magnitude) weaker and less hazardous pollutant than ETS.
Therefore, I argue in this post that since all public spaces are gradually (and increasingly) becoming smoke-free, we need to adopt smoke-free indoor atmospheres as an updated and more useful comparative reference. To discuss this comparative reference, I examine two studies conducted under more realistic environmental smoke-free conditions, showing negligible differences in air quality and abundance of polluting compounds when vaping takes place and when it is absent.
Some limitations of the current literature
I will examine in detail in the follow up Substack post the available literature on exhaled vape aerosols. Meanwhile, I emphasize that there are only few studies in the current literature that are appropriate for a comparison with smoke-free and vape-free atmospheres, as the overwhelming majority of available studies examine health effects in studies in these three types:
Cross sectional and cohort studies recalling self-reported health effects from exposure to exhaled vape aerosols. These studies provide very weak evidence, not only from the recall bias in self-reported data from questionnaires, but simply because: reported health effects are vaguely described and/or cannot be verified and it is impossible to rule out that vaping was not the cause, also the description of exposure levels is too uncertain. Some of these studies examined small samples and subjects that were also exposed to ETS. A representative study is Constantino et al (2024) a one year retrospective study on the association between children subjected to passive vaping and asthma symptoms (54 children, 27 exposed, 27 non-exposed). Their assessment of passive vaping is as follows
A study-specific questionnaire was administered to all participants.Participants were classified as “unexposed” if their parents reported never using e-cigarettes and “exposed” if their parents reported using e-cigarettes for at least one day in the last year. Furthermore, the frequency of exposure to SHA within the household in the last year was evaluated by asking parents about their daily consumption of e-cigarettes/ENDSs with the following questions: “How many e-cigarettes/ENDS do you smoke per day?” and “How many current users of e-cigarette/ENDS live in your home?”
The weakness of the evidence is evident: the small sample and the weak assessment of the exposure. Although the questionnaire asked parents about the frequency of their vaping, this data is not used in the analysis. It is impossible in self-reported questionnaires to assess the effect of many other pollutants (air pollution, household aerosols) that children are exposed to, besides exhaled vape aerosols.Idealized and (mostly) unrealistic chamber studies. A volunteer vapes in a small closed room (30-40 m3) exposing one or several non-users. In some studies vaping is ad libitum and in others it follows a predetermined puffing sequences. A representative example is the study by Tzorti et al, whose experimented consisted of
”40 healthy non-smoking adults were exposed to e-cigarette aerosols for 30 min in a 35 m3 room. Second-hand e-cigarette aerosol (SHA) was produced by an experienced e-cigarette user using a standardized topography and two resistance settings”.
The standardized topography was one puff every 20-30 seconds, which implies 60-90 puffs in 30 minutes (when vapers puff on average 200 times per day). Gross overexposure is evident, thus it is not surprising that subjects reported burning, dryness, sore throat, cough, breathlessness and headache, with significant increase of ocular, nasal, throat-respiratory symptoms that took more than 1 hour to return to normal. This is clearly an extremely unrealistic and irrelevant experiment.Studies merely counting “particles”. Some idealized chamber studies use their data on exhaled aerosol “particulates” as input in simplified lung deposition models. These studies emphasize that vape “particulates” have very small ultra-fine diameters and thus they deposit deeply in the alveoli when breathed, which involves concerning risks (as is argued regarding PM2.5 of air pollution). However, authors disregard the fact that these “particulates” are not related to air pollution PM2.5, but are liquid droplets made almost 100% of PG, VG, nicotine and water.
To avoid these limitations, it is necessary to consider studies based on vaping atmospheres in larger non-smoking environments, with vapers and bystanders around them not subjected to any regimented protocol.
The chemistry of a vaping atmosphere
A comprehensive study of the chemical composition of exhaled vape aerosol in an indoor atmosphere was accomplished by van Drooge et al in 2018
The experiments involved non-vaping (n = 5) and vaping (n = 5) volunteers staying 12 hours together, with vapers vaping ad libitum their own devices (the “vaping day”), in a room (146 m3) without external ventilation. For comparison the same experiment was repeated in non-vaping days with all volunteers but without vaping (but with prior ventilation). The study analyzed the chemical composition and distribution of particulates (vaping droplets and PM from indoor pollution) and the gas phase. Nicotine was quantified separately in both phases. Concentrations of volatile organic compounds (VOCs), polycyclic aromatic hydrocarbons (PAHs) and exhaled breath of participants were compared in vaping and non-vaping days.
The study detected during the vaping period an increase of droplet sizes and mass densities, which for vaping droplets is due to hygroscopic coagulation (water absorption). Particle sizes of all particles were stratified as PM10, PM2.5 and PM1, with the numbers denoting maximal diameter in micrometers. Nicotine was found predominantly in the particulate phase. Minute increase of VOCs, PAHs and formaldehyde were observed in vaping days, while no change was detected in typical air pollution compounds (toluene, xylenes, benzene, ethylbenzene, and naphthalene).
On the vaping day before the vaping period particle mass densities were the same as in the previous non-vaping day: 25, 10, 6 micrograms/m3 for PM10, PM2.5, PM1. During the 12 hours of vaping PM10 increased to 60 micrograms/m3, while PM2.5 and PM1 slightly increased to 20 and 14 micrograms/m3. After the 12 hour vaping period PM10 recovered the initial density 25 micrograms/m3., while PM2.5 and PM1 showed a slight increase with respect to initial densities (16 and 12 micrograms/m3).
These findings simply show the fact that fewer larger PM10 with diameters between 2.5 and 10 micrometers (including vaping droplets) are 100-1000 of times more massive than smaller ones PM2.5 and PM1, but the smaller ones are far more numerous and dominate the diameter distribution. The fact that PM10 returned to their initial density shows that evaporation had a minimal effect on the few large vaping droplets that grew from hygroscopic coagulation.
Regarding smaller droplets, chamber studies (see Zhao et al) focused on vape droplets show that after a single puff (or sequences of single puffs separated by 1-5 minutes) evaporation produces a rapid decaying of number and mass densities to background levels (that include particles not originating from vaping) .
However, the experiment of van Drooge et al shows a marked increase of PM10 in a vaping period that involved continuous aerosol emission by 5 vapers during in 12 hours, a continuous aerosol emission that balances the effect of evaporation of smaller (but numerous) vaping droplets. This explains why vaping only produce minor density changes in PM2.5 and PM1 mass density
The following picture illustrates the change in droplet mass density in the experiment compared with the WHO air quality standard and in various venues in Barcelona (where the study took place)
The obtained mass density in the 12 hour continuous vaping exceeds the WHO indoor standard, but this standard is not conceived for 12 continuous hours of an aerosol generating activity (for example cooking or candles lighting). However, the WHO standard is also surpassed in schools and in non-smoking bars. Normal home conditions normally involve one or two users vaping with sufficiently long inter-puff lapses to allow for an efficient droplet evaporation.
However, the only way to disentangle vaping droplets from non-vaping particulates is through the chemical composition in vaping and non vaping days. This information is supplied by the following figure taken from the van Drooge et al study
We notice that concentrations of compounds in the particles common to indoor air pollution that would be present without vaping show a negligible increase during the vaping period, but still remain negligible (nanograms/m3). The only compounds showing massive 20x increase are nicotine (from 0.1 to 16 ng/m3) and glycerol (from 170 to 3300 ng/m3), but these two compounds are inherent markers that unequivocally distinguishes the exhaled vape aerosol from any other pollutant in a smoke free atmosphere. In fact, glycerol and nicotine are the main residual chemical signature of the particulate phase of the exhaled aerosol after 12 hours of continuous vaping. Propylene glycol in the droplets was not detected because it is very volatile and most likely evaporated into the gas phase.
The table displayed in Figure 2 shows a relatively high concentration of 52 ng/m3 of Levoglucosan that was not significantly different from 35 ng/m3 in the no vaping days. These concentrations are typical in winter pollution readings in Barcelona. Levoglucosan is an environmental pollutant not related to vaping, it is a dehydration monosaccharide primarily released from the pyrolysis of plant cellulose and hemicellulose, typically in combustion of plants at temperatures above 300°C. Its two isomers are used as molecular markers for tracing vegetation fire emissions in Climate and Earth science studies (see You et al).
Regarding the gas phase, Black Carbon in the study days strongly correlated with outdoor readings in Barcelona and thus was not influenced by vaping. PAHs increased in the vaping day from 0.53 ng/m3 to 1.5 ng/m3, sill below average of 1.7 ng/m3 measured in schools and well below readings in bars and restaurants (20-840 ng/m3). Table 4 of van Drooge et al lists the 9 main VOCs, including 3 of the major indoor pollutants listed by the WHO: formaldehyde, benzene and naphtalene:
Notice that of the 9 VOCs, only formaldehyde a significant 2x increase (from 7.4 to 14 micrograms/m3) in the vaping period. This value is well below the WHO reference value of 100 micrograms/m3 to avoid harm and is equivalent to formaldehyde readings in German (1.5-50) and Austrian (3.1-46) schools and in non-smoking indoor environments in the UK (22-170).
Finally, exhaled breath of vapers and exposed non-vapers showed no change in vaping and non-vaping days
Comparison of vaping and non-vaping homes
A study involving 26 authors published in 2023 (see Amalia et al) provides a good assessment of the effects of bystander exposure to exhaled vape aerosols under quite realistic conditions
To examine the exposure of bystanders to exhaled vape aerosol, the authors selected 29 homes in Athens, Milan, Barcelona and Edinburgh with two residents: an e-cigarette user and a non-user of any tobacco or nicotine product. As a control, they selected 21 homes with no one vaping or using any tobacco or nicotine product. The authors measured PM and airborne nicotine, obtained salivary biomarker concentrations of 10 organic compounds relevant to vaping (Table 3) and urinary biomarkers of metals (Supplementary File). The study took place between June and September 2019 and was developed by the TackSHS project funded by the European Union.
The results of this study confirms (despite the opposite narrative of the authors) that exhaled vape aerosol is a very weak pollutant and benign, not only in comparison with ETS, but in reference to indoor air pollution and cooking aerosols. Notice that: airborne nicotine in the homes of vapers was barely above detection limits, and PM levels did not differ in vaping and non-vaping homes. Regarding salivary and urinary biomarkers, subjects passively exposed in vaping homes showed higher levels than controls only in cotinine, 3-OH-cotinine, propylene glycol (1,2-propanediol) and glycerol (in saliva) and cobalt (urine). While increase of these compounds is an expected signature of passive vaping, higher cobalt concentrations in biomarkers from passive vaping is not expected.
However, the data in the table in the Supplementary file clearly shows that higher cobalt levels in non-users in vaping homes does not originate from their passive exposure to vaping. While these subjects had indeed higher cobalt levels than controls (0.60 m/L vs 0.22 m/L), the controls (without any exposure to the aerosols) had cobalt levels of 0.20 m/L, which are practically the same as e-cigarette users who had the most intense exposure. Therefore, despite the suggestion by Amalia et al, their study does not prove any cause-effect relation between cobalt and passive vaping.
Evidently, cotinine levels in non-user subjects in the vaping homes must be a consequence of their passive exposure to nicotine from e-cigarettes. The authors’ Table 3 reports for these subjects only very slightly higher levels of salivary and urinary cotinine: 0.24 ng/mL (0.09-0.60), while for controls 0.00 ng/mL (0.00-0.12). The authors’ description of these numbers as a “significant” increase is misleading, since urine cotinine levels below 1 ng/mL are also below the lower end of the cut-off in the range of levels of urinary cotinine of 2.03 ng/mL (interquartile interval: 0.43–8.60) in non-smokers mildly exposed to environmental tobacco smoke (see Goniewica et al), In fact these cotinine levels are even below levels of non-smokers exposed to outdoor smoking in bars and terraces (see St Helen et al).
Also, it is important to remark that non-users in vaping homes in this study live in countries with relatively high levels of passive exposure to smoking (Greece, Italy and Spain), hence we cannot rule out that occasional exposure to environmental smoke in local bars and restaurants could have contributed to cotinine levels barely above controls. In practice, non-users in vaping homes are almost indistinguishable from average non-smokers and non-vapers.
Table 3 identifies the biomarkers of propylene glycol (1,2-PD) and glycerol as the only ones that provide a clear signature of passive exposure to vaping aerosols, as these are the only two biomarkers in their Table 3 that are present in significant higher levels in non-users in vaping homes in comparison with controls homes. The presence in the samples of 1,3-propanediol (1,2-PD), a compound not used in e-liquids, can be explained by its use as solvent and in cosmetics.
Amalia et al did not analyze the chemistry of the aerosols, but the dominant presence of propylene glycol and glycerol in passive vaping biomarkers is consistent with their presence reported in the chemistry of the PMs in the study by van Drooge et al that I discussed before. However, there are some differences between the two studies: van Drooge et al analyzed aerosols generated by 5 volunteers vaping 12 hours in the same place, a large closed room of 146 m3, while Amalia et al considered a larger volume of a home with only one vaper generating aerosol. This differences in emission and volume explains why van Drooge et al found an increase of PMs above background during vaping, but Amalia et all did not find significant PM differences in vaping and non-vaping homes.
Authors downplaying their own empiric findings.
The narrative of Amalia et al is extremely precautionary and negative with respect to potential harm from environmental vape aerosols, this despite the fact that their own results suggests aerosols exhaled by vapers are quite benign in comparison, not only with ETS, but with common household aerosols (cooking) and other indoor pollutants. They state in their conclusion that their study shows that exhaled vape aerosol “impairs” air quality. Towards the end of the article they emit the following recommendation:
”Our findings support the importance of comprehensively assessing the consequences of e-cigarette use at home for air quality and bystanders while recommending banning e-cigarette use in the presence of other people.”
This suggestion is an unacceptable request for a state intervention that infringes individual liberties and private lives of e-cigarette users. Amalia et al also take at face value questionable results of various chamber studies that examined passive vaping under unrealistic conditions. For example, they take the study by Tzorti et al that I commented before, as an example that “short term passive exposure can cause burning, dryness, sore throat, cough, breathlessness and headache, with significant increase of ocular, nasal, throat-respiratory symptoms”, ignoring the fact that such effects were produced by a gross overexposure. The study by Tzorti et has several common coauthors with Amalia et al, it was also produced by the TsckSHS project). It is unfortunate that Amalia et al plays down their own empiric results (I discuss this issue in my next Substack post).
Conclusions & further posts.
I have examined and discussed the results from two good quality studies on exhaled vape aerosols in non-smoking environments.
Environmental properties of a vaping atmosphere. van Drooge et al analyzed the exhaled aerosol from five vapers vaping 12 hours in a closed indoor space, outcomes were compared with same space without vaping. Particle “PM” mass and numbers increased when vaping with respect to background levels. However, the chemical analysis shows that the extra particle mass is almost entirely made of glycerol, propylene glycol and nicotine, the compounds that make almost 100% of the released vaping droplets (the “particles” of vaping). Soon after the 12 hour period PM levels return to background levels. The only environmental trace left by vaping is the presence of residual glycerol and nicotine, with all other compounds at same level as if vaping never happened.
Exhaled vape aerosol in homes with and without vaping. Amalia et al examined and compared passive exposure of non-users in vaping homes with exposure in non-vaping homes In non-smoking home environments where vaping take place its long term (1 week) effect on those passively exposed cannot be detected by environmental variables (particulates, gaseous pollutants remain the same as in non-vaping homes). It can only be found from biomarkers of compounds inherent to vaping in passively exposed non-users. Cotinine levels slightly increase but remain within the ranges that characterize non-smokers, while biomarkers of glycerol and propylene glycol are higher than in homes without vaping. All other tested biomarkers were not affected by passive exposure to vaping.
Therefore: the environmental effects that distinguish vaping from non-vaping indoor environments are minute and not concerning (traces of glycerol and nicotine). Biomarkers of those passively exposed differ from those not exposed only in moderately higher levels of glycerol and propylene glycol, with slightly higher cotinine still on the range of non-smokers.
Comment on policies. Potential risks from bystanders exposure is determinant in drafting public policy and regulations on vaping, but these policies must be based on evidence and on pragmatic trade offs that optimize the common good, not on ideological impulse, or on tobacco control inertia bent on applying to environmental vaping same policies as applied to ETS. There is no empiric evidence behind the claim that harms from exhaled vape aerosol justifies applying to vaping the same comprehensive smoke-free regulations applied to smoking.
However, public policies must also protect the right of bystanders to avoid involuntarily exposure, which justifies allowing vaping only in indoor public spaces where exposure is voluntary, specially in hospitality venues that serve adults and owners agree to allow for vaping to take place. This balance of policies is analogous to what is an acceptable regulation to exposure to loud music: involuntary exposure is annoying and can be harmful to vulnerable individuals, but there must be public venues for those enjoying voluntarily listening to Heavy Metal Rock, loud bands or symponies at high decibels.
This is the second of a series of 3 posts looking at environmental vape aerosol. In the upcoming post I will provide a critical summary and review of the literature of studies that have examined exhaled vape aerosols. Unfortunately, most “independent” studies (publicly funded and authored by public health academics) are of questionable quality. Industry studies are of much better quality.