Scheer Report - Was steckt dahinter Teil 12

Hallo Liebe Leser,

Heute kommt der zwölfte Teil der Anmerkungen zum Scheer Report. Also die Dinge die mir zum Scheer Report aufgefallen ist und welche man als Anregung für eine Mail an die Abgeordneten mitnehmen kann.

Vorab liste ich Euch wie schon im vorigen Teil alle bisherigen Artikel dieser Serie auf:

Wie auch im Teil vorher werde ich mich nur auf die Bereiche im Scheer Report beschränken, welche nicht explicit in den vorigen Artikeln behandelt wurden, es sei denn ich habe neue Anmerkungen dazu gefunden. Daher fangen wir auch mit Seite 55 des Scheer Reportes an.

6.5.5.2 Dose metrics in the risk assessment of electronic cigarettes

In risk assessment, the hazard information preferably needs to show an exposure regimen close to that of the exposure scenario under investigation. The dose metric to be used depends on the mode of action of the chemical, its toxicokinetics and the dynamics of the chemical in the aerosol and could be the concentration in the aerosol in different regions of the respiratory tract, the inhaled dose per time interval, the absorbed dose per time interval, or a cumulative dose over partial or total lifetime. In a review on toxicokinetics and dynamics of use of electronic cigarettes, Bos et al. (2020) applied this concept to the electronic cigarette. The daily exposure to aerosol from an electronic cigarette is a compilation of multiple peak exposures with irregular time intervals. An increase in the dose is achieved by an increase in puffing frequency and duration whereas, at the same time, the exposure concentration will not or hardly change. Bos et al. performed simulations in which the exposure scenario was compared with that for the general population (continuous exposure of 24 hours per day) starting from the same total inhaled daily dose. It was shown that peak air concentrations during a puff can be easily two orders of magnitude higher than the inhaled concentration of the general population, be it with regular non-exposures between sessions.

From this, it was concluded by Bos et al. that direct risks could not be assessed based on health based guidance values (HBGVs) as also noted by USDHHS (2016). Since there are no HBGVs for smoking or using electronic cigarettes and existing HBGVs are not applicable to the electronic cigarette use scenario, it was advised to perform a risk assessment in which chemical-specific information that is relevant for the scenario (i.e., intensity, duration, and frequency) is taken into account. Because the available hazard information, often based on animal experiments, will mostly be obtained with an exposure regimen that also will significantly differ from the electronic cigarette use scenario, a direct comparison of exposure and hazard characteristics will generally not be possible. Farsalinos and Gillman (2018) also point out that reporting carbonyl emissions as mg/m3 could be relevant to environmental emissions (second-hand exposure) but is problematic when assessing exposure to users due to the intermittent nature of electronic cigarette use.

As a pragmatic alternative, the Margin of Exposure (MoE) approach may be applied. A MoE is the ratio of a reference point (the Point of Departure or PoD), often taken from an animal experiment and corresponding to an exposure that causes a low but measurable response, and the exposure estimate in humans (EFSA, 2005). This approach offers the possibility to take the specific exposure characteristics into account. The minimal value required for the MoE to come to a conclusion of no or low concern depends on the hazard information available and on the exposure characteristics and thus will be different for different scenarios. In general, only interspecies and inter-individual differences in susceptibility need to be taken into account in the evaluation of the MoE if no adverse effects are observed at the PoD. Typically, a MOE of minimally a factor of 100 is then considered to be required for non-carcinogenic effects. If the exposure scenario from which the PoD is derived significantly differs from the human exposure scenario under consideration, these differences need to be bridged by taking them into account in the evaluation of whether a MoE is sufficient to reach a conclusion of low concern.

6.5.5.3 Risk assessment based on modelled topography of electronic cigarette consumption and second-hand exposure scenarios

Assessment for electronic cigarette users
Because of the extremely variable individual differences in the levels of exposure, to ingredients in liquids and aerosol Visser et al. (2014 and 2015a) performed a risk assessment based upon three pre-defined exposure scenarios for daily users. They used the aerosol analysis data for two out of the 12-17 e-liquid samples shown in Section 6.5.2, table 3 and the calculations explained in the previous section. The risk assessment was done for all substances in table 3 except metals. Fragrances were also not included in this analysis. The use topography information used for this assessment was derived from scientific literature and was supplemented with market survey data on the frequency and nature of electronic cigarette use. The following three exposure scenarios were defined:
Light user: fifteen inhalations per day, 1 puff per 4 minutes, with a total daily use duration of sixty minutes.
Average user: sixty inhalations per day, 1 puff per 2 minutes, with a total daily use duration of 120 minutes.
Heavy user: five hundred inhalations per day, 2 puffs per minute with a total daily use duration of 240 minutes.

Given the use topography discussion in section 6.5.1, it can be concluded that the heavy use scenario seems realistic, but maybe is not worst case with regard to the average puff volumes of 70 ml (can run up to 118 ml) which determines the dose inhaled. On the other hand, the number of puffs per day, determining the exposure duration, seems very high.

For local effects on the respiratory tract, the MoE was based on the estimated maximum alveolar concentration calculated from the puff dose, the volume per puff (70 ml), a low absorption rate (30%) and the dilution rate in the lungs. With respect to the latter: the aerosol concentration in the respiratory tract will be lowered since, together with the puff, also air will be inhaled. For systemic effects, the MoE was based on the calculated total absorbed daily dose. On the hazard side a suitable animal experiment was chosen to derive the PoD.
It was concluded for the e-liquid samples considered that:
Exposure to the polyols brings a high risk of irritative damage to the respiratory tract in heavy smokers of electronic cigarettes (MoEs 0.27 – 16, no MoE for diethylene-glycol) and that this risk cannot be excluded in light and average users (MoEs 0.6- 36). It was considered likely that the mechanism by which the various polyols damage the respiratory epithelium is the same in all cases and therefore that cumulative effects are likely. The possibility of heavy users experiencing systemic effects (reduced lymphocyte count) as a result of exposure to propylene glycol cannot be excluded (MoEs 6.7-30). There was no risk for systemic effects from polyols for other scenarios for use of electronic cigarettes.
Exposure to nicotine may induce effects on the respiratory tract since the alveolar concentrations calculated are higher than (effects likely) or comparable to (effects cannot be excluded) effect concentrations in human volunteer studies. Systemic effects on the cardiovascular system are considered possible since the alveolar concentrations calculated are higher than effect concentrations in human volunteer studies. There may be a risk for adverse effects on the foetus for heavy users since the absorbed doses calculated were slightly lower than effect concentrations in a study with monkeys. Nicotine dependence and addiction will be discussed in Section 6.6.
Exposure to the tobacco-specific nitrosamines (e.g. NNK) will increase the risk of tumour development in the respiratory tract in heavy users (MoEs 24-766); in light and average users, the additional tumour risk may vary between negligible (typical MoE 1685) and increased (typical MoE 54) depending on the type of liquid
With regard to aldehydes: formaldehyde, acrolein and diacetyl were present in concentrations sufficient for potential damage to the respiratory tract for heavy users (MoEs 0.11-34), while the risk was considered not to be excluded (MoEs 0.24 – 0.9) or uncertain for average and light users (MoEs 5 -75). It was noted that formaldehyde-induced damage to the respiratory epithelium can be a precursor to tumour formation and that in a few cases, the formaldehyde concentrations were 54 sufficient to create a risk of tumour development in the respiratory tract, maybe exacerbated by the presence of acetaldehyde, acrolein and diacetyl. No definite conclusion was drawn. Other systemic risks were considered low for these substances.

Cumulative assessment groups can be identified for irritative effects on the respiratory tract and for carcinogenicity. In an additive approach, the total exposure to polyols, aldehydes and nicotine will lead to a very low MoE and adverse effects on the respiratory tract will be very likely. Carcinogenic effects can be expected to occur due to exposures to nitrosamines and formaldehyde. The assessment above already takes into account additive effects from the nitrosamines involved. The carcinogenic effect from formaldehyde, if it occurs at all, proceeds via a different mechanism of action than carcinogenicity from nitrosamines. Additivity (i.e. cumulative effects of different chemicals) is not warranted here. 11

Assessment for second-hand exposure

Visser et al. (2016 and 2019) evaluated two specific second-hand exposure scenarios. The first scenario concerns a daily car trip of one hour in a small unventilated car of 2 m3 with two electronic cigarette users (puffing frequency 0.5 per minute, 1 hour of use). The exposed person is a child, sitting in the same car. This exposure scenario approximates the highest levels of exposure that may be expected in everyday situations. The second scenario concerns a daily exposure of four hours in an office-sized space (30 m3) with one electronic cigarette user (puffing frequency 2 per minute, 4 h of use). Based on the exposure levels of table 6 the concentrations for the assessment of local effects and the systemic dose were calculated for propylene glycol, nicotine, TSNAs and copper. The air concentration (final concentration (mg/m3) reached at the end of the use period) and internal systemic exposure (expressed as mg/kg bw), were used. For each chemical, the exposure concentrations were calculated from the highest amounts exhaled by the volunteers (see table 6), taking into account pulmonary retention (0% for local effects, 50% for systemic effects), that exhalation of the chemical may not have been complete in the first exhalation but may continue with subsequent exhalations, and taking into account ventilation. The estimated air concentrations for the individual chemicals were compared with human limit values with respect to chronic exposure for the general population. Air concentrations of chemicals below their (WHO Air Quality Guideline) limit value are considered not to result in adverse health effects. In cases where appropriate human health-based limit values were lacking, the risk assessment was based on a Margin of Exposure (MOE) approach.

It was concluded (by Visser et al., 2016 and 2019) that:
The risk for local effects on the respiratory tract of propylene glycol cannot be excluded for scenario 1 (MoEs 17-18) and is low for scenario 2 (MoE 74-81). There is no risk for systemic effects (MoEs 535-1475).
Glycerol was not detected in exhaled air and therefore the risk for second-hand exposed persons is considered low.
Local effects from nicotine exposure are not expected (MoEs 170-750. The MoE for systemic cardiovascular effects is 2.1 for scenario 1: adverse systemic effects are expected. For scenario 2 systemic cardiovascular effects cannot be excluded either (MoE 6). 45
Aldehydes are not detected in exhaled air allowing the conclusion that there is no risk for adverse effects for second-hand exposed persons.
For TSNAs MoEs are 521 and 2297 for scenario 1 and 2, respectively. A carcinogenic risk cannot be excluded for scenario 1 and is uncertain for scenario 2.

6.5.5.4 Other risk assessments

Assessment for electronic cigarette users
Several reviews are available that predominantly compare exposure levels of substances in aerosol from electronic cigarettes with health based guidance values (e.g., Farsalinos et al., 2015; Zulkifli et al., 2016; McNeill et al., 2018; US-NAS, 2018). As argued in Section 2.1, such values are based on more continuous exposure scenarios that are completely different from electronic cigarette exposure scenarios that are characterised by multiple peak exposures with irregular time intervals of zero or background exposure only. Therefore such risk assessment are not applicable for the purpose of this Opinion, unless they show that the puff concentrations measured are below these standards and therefore clearly point at the absence of any risk with a wide margin. This is the case for the review by Farsalinos et al. (2015d) in which metal levels in aerosol, found in two studies, were compared to 3 different health based guidance values: the Permissible Daily Exposure (PDE) from inhalational medications, defined by the United States Pharmacopeia, the Minimal Risk Level (MRL), defined by the US Agency for Toxic Substances and Disease Registry (ATSDR), and the Recommended Exposure Limit (REL), defined by the US National Institute of Occupational Safety and Health (NIOSH). In spite of the assumption of a very high puff frequency of 1200/day to estimate daily exposure, none of the levels detected were above these limits except for a 10% increase for cadmium above the PDE for one of the products investigated. This study was re-evaluated by Zulkifli et al. (2016) who calculated hazard quotients based on a comparison of the metal concentrations measured with reference concentrations and cancer slope factors/minimal risk levels from US-EPA/ ATSDR. In this assessment hazard quotients higher than 1 were not only found for cadmium (28.5) but also for nickel (1.6), aluminium (9.4) and titanium (2.4). Lifetime cancer risks for cadmium, chromium, lead and nickel were all below 1.10-6. Note these quotients are based under the assumption of continuous exposure and therefore likely to be overestimated.

In a recent review Stephens et al. (2018) calculated an aggregated lifetime cancer risk for different first- and second-generation electronic cigarettes based on concentration-weighted inhalation potencies and concentrations of IARC-classified carcinogenic substances in undiluted aerosol. Exposure data came from the published literature. The daily use volume was estimated at 30 l/day. The substances were: acetaldehyde, formaldehyde, NNN, NNK, cadmium, lead and nickel. Although the absolute unit risk estimates used may not be applicable to this specific exposure scenario, the relative contribution to the aggregate cancer potency suggest that the carcinogenic risk was determined mainly by carbonyls and, if present, cadmium, but is highly variable. Nitrosamines appeared to be minor contributors. Scungio et al., (2018) also evaluated the overall carcinogenic risk of substances condensed on particulate matter from electronic cigarettes. The excess lifetime cancer risk (ELCR) was estimated based on inhalation slope factors of IARC Group 1 pollutants, their mass concentration condensed on the aerosol particles, the measured doses of deposited particles and electronic cigarette use characteristics. The pollutants were arsenic, cadmium, nickel, NNN and NNK. The ELCR values for mainstream aerosol with and without nicotine were found to be below 10−5. It is noted that slope factors were used for continuous exposure over a lifetime, but that the ELCR was averaged for the number of years of using electronic cigarettes to better match the actual exposure scenario.

Hahn et al. (2014) assessed the risk of measured constituents of electronic cigarettes by a MoE estimation based on the use levels found (see section 1.1) and toxicological PoDs. However, this assessment was exclusively based on oral data and therefore the SCHEER considers the conclusions not applicable to electronic cigarette exposure scenarios.

Risk assessments for fragrances were not found. The SCHEER agrees with McNeill et al. (2018) in concluding that ‘To date, there is no clear evidence that specific flavourings pose health risks but there are suggestions that inhalation of some could be a source of preventable risks’. However, as noted earlier, inhalation toxicology data are scarce for flavourings which are mainly being assessed for oral exposure through food.

Tierney et al. (2016) analysed flavour chemicals in 2 brands of electronic cigarettes. Many of the products contained the same flavour chemicals (vanillin and ethyl vanillin, maltol and ethyl maltol, benzaldehyde and benzyl alcohol, and ethyl butyrate and ethyl acetate), a significant number of which (6/24) were aldehydes, recognised toxicologically to be ‘primary irritants’ of the mucosa of the respiratory tract. Based on a rough comparison with the occupational exposure limits for vanillin and benzaldehyde it was concluded that aerosol exposure may be close to or even exceed these limits. It was also shown (Erythropel et al., 2 2019) that reactions are occurring between flavouring and solvent components such as propylene glycol, resulting in compounds, e.g. aldehyde–propylene glycol acetals, having toxicological properties that differ from either the flavourings or solvent components with hitherto unknown consequences for the risk assessment.

Assessment for second-hand exposure
Hess et al. (2016) reviewed 16 studies, with varying designs and of different quality, investigating potential adverse health effects of passive exposure to electronic cigarette aerosols. The conclusion of this qualitative meta risk assessment was that the majority of studies concluded that passive exposure to electronic cigarette aerosol may pose a health risk to second-hand exposed persons. Only 4 studies were negative, but these studies were reported to have been undertaken by tobacco employees or funded by the National Vapers Club. None of the studies looked at potential long-term impacts from exposure to electronic cigarette aerosol. Scungio et al. (2018) evaluated the excess lifetime carcinogenic risk (ELCR) of substances on particulate matter in second-hand smoke from electronic cigarettes and found about two orders of magnitude of difference between ELCR associated to mainstream aerosol (that were below 1.10-5) and second-hand aerosol.

6.5.5.5 Risk estimates from epidemiology

In a Cochrane systematic review of epidemiological studies into adverse events with a follow-up of 6-24 months, 3 random clinical trials (RCT) and 9 cohort studies were found eligible for further analysis. The quality of the evidence was judged to be weak (GRADE- system: further research is very likely to have an important impact on the confidence in the estimate of effect and is likely to change the estimate). No studies reported serious adverse effects considered related to electronic cigarette use. One RCT provided data on the proportion of participants experiencing any adverse events with a relative risk of 0.99 29 (electronic cigarette versus nicotine patch, n=456) and 0.97 (electronic cigarette versus placebo, n=298). Cohort studies found mouth and throat irritation, dissipating over time, to be the most frequently reported adverse effect in electronic cigarette users (Hartmann- Boyce, et al., 2016; update of Hajek, 2014).

6.5.5.6 Conclusions

On risks for electronic cigarette users
In its report on "Electronic Nicotine Delivery Systems and Electronic Non-Nicotine Delivery Systems (ENDS/ENNDS)" published in August 2016 the WHO (WHO, 2016) stated: "Based mostly on the levels and number of toxicants produced during the typical use of unadulterated ENDS/ENNDS made with pharmaceutical-grade ingredients, it is very likely that ENDS/ENNDS are less toxic than cigarette smoke. However, ENDS/ENNDS are unlikely to be harmless, and long-term use is expected to increase the risk of chronic obstructive pulmonary disease, lung cancer, and possibly cardiovascular disease as well as some other diseases also associated with smoking. The magnitude of these risks is likely to be smaller than from tobacco smoke although there is not enough research to quantify the relative risk of ENDS/ENNDS over combustible products".

Based on the exposure assessment (Section 6.5.2), the hazard identification (Section 6.5.3), the human health impacts (Section 6.5.4) and the risk assessment (Section 6.5.5), and taking into account the moderate to strong weight of evidence for the exposure assessment for users of electronic cigarettes, the SCHEER concludes for exposure of electronic cigarette users that:

- The overall weight of evidence is moderate for risk of local irritative damage to the respiratory tract of electronic cigarette users due to the cumulative exposure to polyols, aldehydes and nicotine. The lines of evidence are the following These substances are all identified as irritants.
In cohort studies, mouth and throat irritation, dissipating over time, was the most frequently reported adverse effect in electronic cigarette users. The overall reported incidence was low.
The model studies revealed low MoEs for irritative effects for individual chemicals and these will be even lower in an additive approach.
The alveolar concentrations of nicotine calculated are higher than or comparable to effect concentrations in studies with human volunteers exposed repeatedly to nicotine vapour.
With regard to the risk calculation on aldehydes: formaldehyde, acrolein and diacetyl were present in concentrations sufficient for potential damage to the respiratory tract for heavy users, while the risk was considered not to be excluded or uncertain for average and light users.
The overall weight of evidence for risk of long-term systemic effects on the cardiovascular system is strong. The lines of evidence are the following:
Heart rate and blood pressure effects were identified as hazards for nicotine (and lead).
The level of evidence regarding the cardiovascular effects of nicotine contained in electronic cigarettes and the related pathophysiological mechanisms is considered from moderate to strong.
Based on human evidence, there is a moderate and growing evidence for harmful health effects for electronic cigarette users, especially, for cardiovascular disease.
The alveolar concentrations of nicotine calculated in the model studies are higher than effect concentrations in studies with human volunteers exposed repeatedly to nicotine vapour.
The overall weight of evidence for risk of respiratory tract carcinogenicity due to long-term, cumulative exposure to nitrosamines and due to exposure to acetaldehyde and formaldehyde is weak to moderate. The lines of evidence are the following:
Nitrosamines, formaldehyde and acetaldehyde have been identified as genotoxic and carcinogenic.
The human evidence is very limited and does not allow a conclusion.
In the model calculations, exposure to the nitrosamines increased the calculated risk of tumour development in the respiratory tract, especially, in heavy users. It is assumed that this risk will increase due to cumulative exposure to these chemicals.
The formaldehyde-induced damage to the respiratory epithelium can be a precursor to tumour formation and in a few cases, the formaldehyde concentrations were sufficient to create a risk of tumour development in the respiratory tract, maybe exacerbated by the presence of acetaldehyde, acrolein and diacetyl.
The weight of evidence for risk of adverse effects from the metals in aerosols, specifically carcinogenicity, is weak. This conclusion is mainly based on the comparison between measured exposure levels in aerosols and health-based guidance values.
The overall weight of evidence for risk of other long-term adverse health effects, such as pulmonary disease and CNS- and reprotoxic effects, plausible based on the hazard identification and limited human evidence, cannot be established due to lack of consistent data.
To date, there is no specific data that specific flavourings used in the EU pose health risks for electronic cigarette users following repeated exposure. The concentrations of aldehyde flavourings are considered too low to add substantially to the already apparent cumulative risk to the respiratory tract from the aldehydes generated in the electronic cigarette and from polyols and nicotine. The weight of evidence is weak due to the absence of inhalation toxicological data and specific risk assessments.
The overall weight of evidence for poisoning and injuries due to burns and explosion, is strong. However, the incidence is low. Therefore, the risk is expected to be low.

On risks for second-hand exposure
Based on the exposure assessment (Section 6.5.2), the hazard identification (Section 6.5.3), the hazard assessment (Section 6.5.4) and the risk assessment (Section 6.5.5), and taking into account the weak to moderate weight of evidence for the second-hand exposed persons, the SCHEER concludes that:

- The overall weight of evidence is moderate for risk of local irritative damage to the respiratory tract. The lines of evidence are the following:
This irritation is mainly due to exposure to glycols. Glycols are identified as irritants.
The model studies revealed low MoEs for irritative effects from propylene glycol.
MoEs for nicotine do not point at a risk for respiratory irritation.
Exposure of bystanders to glycerol or aldehydes is negligible or orders of magnitude lower than for electronic cigarette users.
- The overall weight of evidence for risk of systemic cardiovascular effects in second-hand exposed persons due to exposure to nicotine is weak to moderate. The lines of evidence are the following:
Heart rate and blood pressure effects were identified as hazards for nicotine
In the model calculations, the MoEs for cardiovascular effects are low
There exists a complete paucity of human evidence regarding the acute and long-term effects on cardiovascular and other health outcomes in children and adolescents.
- The overall weight of evidence for a carcinogenic risk due to cumulative exposure to TSNAs is weak to moderate. The lines of evidence are the following:

Nitrosamines have been identified as genotoxic and carcinogenic.
The MoEs calculated for the carcinogenic risk from TSNAs are low.
Human evidence is lacking.
Further research is needed whether children and adolescents have higher risk than adults when regularly second-hand exposed within their home environments.

Ja ich weiss. Wieder mal verdammmt viel Text den wir hier heute bearbeiten. Aber in diesem Text steckt auch wieder verdammt viel Zündstoff.

As a pragmatic alternative, the Margin of Exposure (MoE) approach may be applied. A MoE is the ratio of a reference point (the Point of Departure or PoD), often taken from an animal experiment and corresponding to an exposure that causes a low but measurable response, and the exposure estimate in humans (EFSA, 2005). This approach offers the possibility to take the specific exposure characteristics into account. The minimal value required for the MoE to come to a conclusion of no or low concern depends on the hazard information available and on the exposure characteristics and thus will be different for different scenarios. In general, only interspecies and inter-individual differences in susceptibility need to be taken into account in the evaluation of the MoE if no adverse effects are observed at the PoD. Typically, a MOE of minimally a factor of 100 is then considered to be required for non-carcinogenic effects. If the exposure scenario from which the PoD is derived significantly differs from the human exposure scenario under consideration, these differences need to be bridged by taking them into account in the evaluation of whether a MoE is sufficient to reach a conclusion of low concern....Exposure to nicotine may induce effects on the respiratory tract since the alveolar concentrations calculated are higher than (effects likely) or comparable to (effects cannot be excluded) effect concentrations in human volunteer studies. Systemic effects on the cardiovascular system are considered possible since the alveolar concentrations calculated are higher than effect concentrations in human volunteer studies. There may be a risk for adverse effects on the foetus for heavy users since the absorbed doses calculated were slightly lower than effect concentrations in a study with monkeys. Nicotine dependence and addiction will be discussed in Section 6.6.

Uff, hier muss ich doch noch mal was wiederholen. Der Mensch ist kein Zellhaufen, der Mensch ist keine Maus, der Mensch ist kein Pottwal. Und noch was, der Mensch hat zwar mit dem Affen gemeinsame Vorfahren, aber die meisten Menschen sind keine Affen. (Na gut vielleicht bis auf die Ausnahmen Corona-Leugner, Reichsbürger, und alles andere was sich radikalisiert.) Merkt Ihr da was bei SCHEER? Werte zu benutzen die nicht auf den Menschen geeicht sind ist ziemlich sinnfrei.

6.5.5.3 Risk assessment based on modelled topography of electronic cigarette consumption and second-hand exposure scenarios

.....
Light user: fifteen inhalations per day, 1 puff per 4 minutes, with a total daily use duration of sixty minutes.
Average user: sixty inhalations per day, 1 puff per 2 minutes, with a total daily use duration of 120 minutes.
Heavy user: five hundred inhalations per day, 2 puffs per minute with a total daily use duration of 240 minutes.

Ernsthaft? Ihr unterteilt die Dampfer in quantitative Gruppen. Schon mal was davon gehört das man unter Stress mehr dampft. Oder wenn man auf einer Party ist. Gut Party ist coronabedingt für viele ein Fremdwort. Aber Leute ernsthaft eine solche Unterteilung ist so unlogisch wie das Leben fair ist. Zum Beispiel steigt mein Kaffee- und Liquidverbrauch bei dem was ich hier aufarbeite gerade nahe zu exponentiell an. (Den Grund dafür lass ich mal offen).

It was concluded for the e-liquid samples considered that:
Exposure to the polyols brings a high risk of irritative damage to the respiratory tract in heavy smokers of electronic cigarettes (MoEs 0.27 – 16, no MoE for diethylene-glycol) and that this risk cannot be excluded in light and average users (MoEs 0.6- 36). It was considered likely that the mechanism by which the various polyols damage the respiratory epithelium is the same in all cases and therefore that cumulative effects are likely. The possibility of heavy users experiencing systemic effects (reduced lymphocyte count) as a result of exposure to propylene glycol cannot be excluded (MoEs 6.7-30). There was no risk for systemic effects from polyols for other scenarios for use of electronic cigarettes.
Exposure to nicotine may induce effects on the respiratory tract since the alveolar concentrations calculated are higher than (effects likely) or comparable to (effects cannot be excluded) effect concentrations in human volunteer studies. Systemic effects on the cardiovascular system are considered possible since the alveolar concentrations calculated are higher than effect concentrations in human volunteer studies. There may be a risk for adverse effects on the foetus for heavy users since the absorbed doses calculated were slightly lower than effect concentrations in a study with monkeys. Nicotine dependence and addiction will be discussed in Section 6.6.
Exposure to the tobacco-specific nitrosamines (e.g. NNK) will increase the risk of tumour development in the respiratory tract in heavy users (MoEs 24-766); in light and average users, the additional tumour risk may vary between negligible (typical MoE 1685) and increased (typical MoE 54) depending on the type of liquid
With regard to aldehydes: formaldehyde, acrolein and diacetyl were present in concentrations sufficient for potential damage to the respiratory tract for heavy users (MoEs 0.11-34), while the risk was considered not to be excluded (MoEs 0.24 – 0.9) or uncertain for average and light users (MoEs 5 -75). It was noted that formaldehyde-induced damage to the respiratory epithelium can be a precursor to tumour formation and that in a few cases, the formaldehyde concentrations were 54 sufficient to create a risk of tumour development in the respiratory tract, maybe exacerbated by the presence of acetaldehyde, acrolein and diacetyl. No definite conclusion was drawn. Other systemic risks were considered low for these substances.

So hier muss ich dann doch noch mal in altbekanntes reingrätschen(hoffe es tut den Richtigen auch weh). "Cannot be excluded" also auf deutsch -kann nicht ausgeschlossen werden. Sorrry aber das ist echt..ein Scheinargument. denn wirklich ausschliessen lässt sich in diesem Leben wirklich nichts. "There may be a risk for...." Natürlich könnte überall ein Risiko sein. Wenn ich das Haus verlasse könnte das Risiko auftreten, das mich ein Auto erwischt und ich überfahren werde. Verbietet Ihr darauf hin die Autos? Sorry reine Phrasendrescherei kombiniert mit Panikmache.

Zu Nitrosaminen sag ich schon gar nichts mehr. Oft genug erwähnt, das es eine mögliche Verunreinigung durch die diese in den Produkten sein könnten nicht existiert.

Für "not to be excluded" gilt das gleiche wie für "Cannot be excluded"

The overall weight of evidence for risk of other long-term adverse health effects, such as pulmonary disease and CNS- and reprotoxic effects, plausible based on the hazard identification and limited human evidence, cannot be established due to lack of consistent data.
To date, there is no specific data that specific flavourings used in the EU pose health risks for electronic cigarette users following repeated exposure. The concentrations of aldehyde flavourings are considered too low to add substantially to the already apparent cumulative risk to the respiratory tract from the aldehydes generated in the electronic cigarette and from polyols and nicotine. The weight of evidence is weak due to the absence of inhalation toxicological data and specific risk assessments.
The overall weight of evidence for poisoning and injuries due to burns and explosion, is strong. However, the incidence is low. Therefore, the risk is expected to be low.

What the Fuck! Warum gibt es denn diesen ganzen #ScheerReport. Warum tue ich mir dann das ganze an und schreibe eine Kritik/Stellungnahme zu Euren geistigen Ergüssen. Wenn es eh kein oder bis minimale Risiken gibt. Sorry da fehlen mir echt die Worte.

6.5.5.4 Other risk assessments

Assessment for electronic cigarette users
Several reviews are available that predominantly compare exposure levels of substances in aerosol from electronic cigarettes with health based guidance values (e.g., Farsalinos et al., 2015; Zulkifli et al., 2016; McNeill et al., 2018; US-NAS, 2018). As argued in Section 2.1, such values are based on more continuous exposure scenarios that are completely different from electronic cigarette exposure scenarios that are characterised by multiple peak exposures with irregular time intervals of zero or background exposure only. Therefore such risk assessment are not applicable for the purpose of this Opinion, unless they show that the puff concentrations measured are below these standards and therefore clearly point at the absence of any risk with a wide margin.

Wie bitte? Lese ich da richtig? Reicht mein Englisch dafür um das richtig zu übersetzen? Studien von Fachleuten die sich weitaus länger mit dem Thema beschäftigen, als Ihr es in Euren "Studien" tut, werden nicht berücksichtigt? Na das nenn ich mal eine Hybris die ihres gleichen sucht. Sorry aber damit zeigt sich nur die Voreingenommenheit und die Dummheit die hinter diesem Machwerk steht.

Risk assessments for fragrances were not found. The SCHEER agrees with McNeill et al. (2018) in concluding that ‘To date, there is no clear evidence that specific flavourings pose health risks but there are suggestions that inhalation of some could be a source of preventable risks’. However, as noted earlier, inhalation toxicology data are scarce for flavourings which are mainly being assessed for oral exposure through food.

Damit ist eine Diskussion über einen Aroma-Bann durch eure eigenen Worte widerlegt. Merkt Ihr selber eigentlich wie widersprüchlich und hanebüchen das ~~teilweise~~ ist, was Ihr da schreibt?

6.5.5.6 Conclusions

On risks for electronic cigarette users
In its report on "Electronic Nicotine Delivery Systems and Electronic Non-Nicotine Delivery Systems (ENDS/ENNDS)" published in August 2016 the WHO (WHO, 2016) stated: "Based mostly on the levels and number of toxicants produced during the typical use of unadulterated ENDS/ENNDS made with pharmaceutical-grade ingredients, it is very likely that ENDS/ENNDS are less toxic than cigarette smoke. However, ENDS/ENNDS are unlikely to be harmless, and long-term use is expected to increase the risk of chronic obstructive pulmonary disease, lung cancer, and possibly cardiovascular disease as well as some other diseases also associated with smoking. The magnitude of these risks is likely to be smaller than from tobacco smoke although there is not enough research to quantify the relative risk of ENDS/ENNDS over combustible products".

Wie zum Geier kommt es denn, das ausser in Euren "Bewertungen" noch in keiner Studie krebserregende Stoffe nachgewiesen wurden, welche nicht auf ein fehlerhaftes Benutzen einer E-Zigarette zurück zu führen sind? Ernsthaft, irgendwo ist da ein Logikfehler, wie Spass beim Suchen.

6.5.5.6 Conclusions

On risks for electronic cigarette users
In its report on "Electronic Nicotine Delivery Systems and Electronic Non-Nicotine Delivery Systems (ENDS/ENNDS)" published in August 2016 the WHO (WHO, 2016) stated: "Based mostly on the levels and number of toxicants produced during the typical use of unadulterated ENDS/ENNDS made with pharmaceutical-grade ingredients, it is very likely that ENDS/ENNDS are less toxic than cigarette smoke. However, ENDS/ENNDS are unlikely to be harmless, and long-term use is expected to increase the risk of chronic obstructive pulmonary disease, lung cancer, and possibly cardiovascular disease as well as some other diseases also associated with smoking. The magnitude of these risks is likely to be smaller than from tobacco smoke although there is not enough research to quantify the relative risk of ENDS/ENNDS over combustible products"....

Wie bitte? Was? Wow ihr habt es geschafft alle Argumente der Gegner der E-Zigarette und der Harm-Reduction in einen Absatz zu quetschen, Respekt. Auf Jugendschutz und dergleichen gehe ich schon gar nicht mehr ein. Das habe ich oft genug getan. So so es ist also sehr unwahrscheinlich wenn die ganzen als Carcinogen erkannten Stoffe des Tabakrauches in einem Ersatzprodukt für Raucher fehlen, das diese dann eben nicht krebserregend sind. Leute, hackt es bei Euch? Schon mal mit gesundem Menschenverstand probiert? Oder reicht das Schmiermittel der Harm-Reduction und E-Zigaretten-Gegner vom Rektum bis ins Gehirn. Sorry, aber anders kann ich mir einen solchen Schwachsinn an Hand der Vielzahl von Ex-Rauchern die jetzt nur noch dampfen nicht vorstellen. Die weitere Zusammenfassung und erneute Zitierung der Zusammenfassung erspare ich mir hier, denn im Grunde stellt Ihr ja nur fest, das die Risiken gering sind. Selbst für Stoffe die nachweislich nicht enthalten sind. Diesbezügliche Widersprüche wurden von mir schon in den vorigen Abschnitten und Artikeln angesprochen. Sorry das entbehrt jedweder Logik. Aber wie gesagt:"Findet den Logikfehler."

Fazit

Ja was soll ich dazu noch für ein Fazit verfassen? Ernsthaft! Ich bezweifel wirklich das sich hier an moralische, ethische Standards gehalten wurde. Ich bewundere aber die Kreativität um etwas zu beweisen, das es schlichtweg nicht gibt. Ich bewundere wie mit künstlichen Situationen Schlussfolgerungen getroffen wurden, welche nicht der Realität entsprechen. Ich bin echt fasziniert wie tief die WHO und die Gegner der Harm-Reduction ihre Hand im Rektum der Kommission hatten/haben. Ansonsten gilt für heute wieder mal der Satz vom heiligen Trappatoni "Ich habe fertig!"

in diesem Sinne

Seid Achtsam