I think they are freaking out because the Chinese freaked out. I conjecture that when more data rolls in, the world will conclude it is a run of the mill virus, and wonder why the Chinese freaked out.
Well, that, and all the people dying
You don’t need a comorbid vaping disease to explain the lethality of SARS-CoV2, because it’s well enough explained by the its high affinity for ACE-2 receptor sites, which are present in both the cilial cells and type-2 pneumocytes deep in the lungs. In attacking those cells, the virus makes it harder for the lungs to clear fluid as well as making the smaller alveoli harder to inflate.
I wonder, only semi-facetiously, whether the reason it’s killing older folks is related to the fact that older people are more likely to be using ACE-inhibitors.
LOL, wouldn’t ACE-I use thus block the sites and reduce infections? And how would ARBs affect things? 
Maybe it protects! On the other hand, maybe it upregulates them. I have no idea and actually took a superficial look through Pubmed when I first heard that ACE2 is the receptor for the virus. There wasn’t much out there that I could find. I’m not even sure that the ACE we know and love is controlled/regulated in the same way as the virus receptor. But ICES makes Ontario a great place to get relevant population data and possibly answer questions like this.
Since you seem to have an issue with connecting evidence and argument, how about approaching this in a different way?
What level of mortality or other measure(s) would you set as convincing evidence that indicated it was not ‘run of the mill’ or an over-hyped reaction?
I think that is a reasonable question to ask you since you’re the one making the claim. It would distinguish between someone who is genuinely offering a critical / sceptical perspective from a denialist, against which no level of deaths among non-vaping humans would be sufficiently convincing.
The extant ACE-inhibitors don’t inhibit ACE-2 receptors, and if they did I‘d think it would be protective. Having said that, use of ACE inhibitors have been associated with a decreased pneumonia risk.
I think you want this linked to vaping as some sort of magic shield, so you can say “hey, I don’t vape - I’m safe!”.
Sorry, that is not congruent with reality.
Maybe the “freaking out” has something to do with the thousands of real, actual deaths that are occurring. More than 7,500 people have died of this in Italy, and Spain just passed 4,000 deaths. In Italy, those 7,500 deaths from COVID-19 have happened in less than a month, and Spain had lost 4,000 people in less than three weeks.
There are reasonable arguments to be made about what the proper response might be to this outbreak. Some people are arguing that the current lockdown policies are too broad, and that we would be better to adopt a more targeted set of policies. But no-one with any credibility whatsoever is denying that the virus itself, and the illness it causes, are serious and present a clear danger to the global community.
There might be some “freaking out” going on, but it’s in response to an actual threat that is actually killing actual people. For you to keep suggesting otherwise, based on what you admit is nothing but conjecture, is, quite frankly, idiotic and irresponsible.
I just read that scientists noticed in animals on some med (heart?) that inhibited ACE receptors, there was an increase in ACE2. They were thinking it may apply to humans and something worth looking into regarding why underlying heart probs seem to be a weakness when it comes to covid-19.
How does this conjecture fit with what is happening in the rest of the world, right now?