On 2017 Mar 29, Zvi Herzig commented:

Despite the fact that this study relates to e-cigarette (EC) vapor dissolved in a liquid medium, the authors surprisingly attribute outcomes to fine particulate matter:

… our findings suggest it is not nicotine or toxic combustion product that activates the hemostatic system, but instead the hemostatic system is most responsive to fine particulate matter

This conclusion is puzzling because particulate matter of EC aerosol are in fact liquid droplets. When these are merged with the liquid medium, their former particle sizes become irrelevant. (Solid particles emitted from EC hardware are at quantities below safety limits Farsalinos KE, 2015 and thus unlikely to be of significance).

It is also unclear what the causes or the relevance of these in vitro platelet effects are. For example, propylene glycol and glycerol are not rapidly metabolized here as they are in vivo. Indeed, Hom et al write:

There are some important limitations to the work presented here, including the use of an ex vivo static system, without negative hemostatic regulators (such as endothelial cells), to evaluate the effects of e-vapor on platelet functions.

In contrast, a recent clinical study of smokers switching to Tobacco Heating System 2.2 (whose emissions also include the limited cigarette smoke toxicants present in EC vapor Schaller JP, 2016) shows a level of reduction in platelet activation among switchers approaching those of quitters Lüdicke F, 2018:

Reductions in 8-epi-prostaglandin F2α (biomarker of oxidative stress), 11-dehydro-thromboxane B2 (biomarker of platelet activation)… occurred in the menthol tobacco heating (mTHS) system group compared with the menthol conventional cigarette group. The changes in the mTHS group approached those in the smoking abstinence group.

This would indicate that the outcomes of Hom et al are not manifested in real use. While it can be countered that perhaps EC flavorants not emitted by heated tobacco have induced the platelet effects, this is unlikely considering that outcomes were similar for two disparate EC products tested.

It would also be interesting to consider the effects of air bubbles present from bubbling the aerosol through the extraction buffer. It's well-known that air bubbles induce platelet activation Sandgren P, 2011 and this might help explain the strange outcome.

On 2017 Mar 29, Zvi Herzig commented:

Despite the fact that this study relates to e-cigarette (EC) vapor dissolved in a liquid medium, the authors surprisingly attribute outcomes to fine particulate matter:

… our findings suggest it is not nicotine or toxic combustion product that activates the hemostatic system, but instead the hemostatic system is most responsive to fine particulate matter

This conclusion is puzzling because particulate matter of EC aerosol are in fact liquid droplets. When these are merged with the liquid medium, their former particle sizes become irrelevant. (Solid particles emitted from EC hardware are at quantities below safety limits Farsalinos KE, 2015 and thus unlikely to be of significance).

It is also unclear what the causes or the relevance of these in vitro platelet effects are. For example, propylene glycol and glycerol are not rapidly metabolized here as they are in vivo. Indeed, Hom et al write:

There are some important limitations to the work presented here, including the use of an ex vivo static system, without negative hemostatic regulators (such as endothelial cells), to evaluate the effects of e-vapor on platelet functions.

In contrast, a recent clinical study of smokers switching to Tobacco Heating System 2.2 (whose emissions also include the limited cigarette smoke toxicants present in EC vapor Schaller JP, 2016) shows a level of reduction in platelet activation among switchers approaching those of quitters Lüdicke F, 2018:

Reductions in 8-epi-prostaglandin F2α (biomarker of oxidative stress), 11-dehydro-thromboxane B2 (biomarker of platelet activation)… occurred in the menthol tobacco heating (mTHS) system group compared with the menthol conventional cigarette group. The changes in the mTHS group approached those in the smoking abstinence group.

This would indicate that the outcomes of Hom et al are not manifested in real use. While it can be countered that perhaps EC flavorants not emitted by heated tobacco have induced the platelet effects, this is unlikely considering that outcomes were similar for two disparate EC products tested.

It would also be interesting to consider the effects of air bubbles present from bubbling the aerosol through the extraction buffer. It's well-known that air bubbles induce platelet activation Sandgren P, 2011 and this might help explain the strange outcome.