Slate: Does Smoking Make COVID-19 Worse? Better? Here’s What We Actually Know.

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LoveVanilla

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Does Smoking Make COVID-19 Worse? Better? Here’s What We Actually Know.
Are smokers and vapers more likely to die of COVID-19? To judge by news coverage of the topic, the answer is an unequivocal yes. The New York Times, Wired, CNN, Bloomberg, and numerous other publications have run stories warning that smokers and vapers are at higher risk. Anti-tobacco groups are using the pandemic as an opportunity to push for new restrictions on nicotine, ranging from bans on vapor products to the complete prohibition of cigarettes... Amid all this alarm, one complication has received relatively little notice: Emerging evidence on the risk factors for COVID-19 is ambiguous with regard to smoking and virtually nonexistent for its relationship to vaping.
The question of whether vaping increases the risks of COVID-19 has received nearly as much attention as the effects of smoking but has not, in fact, been specifically studied. Nonetheless, warnings that vaping will worsen the pandemic have been given substantial press and are lending further motivation to political efforts to ban e-cigarettes. These fears are highly speculative.
In a letter to the FDA signed by 13 experts in the field of tobacco harm reduction, the authors urge that any advice on vaping and COVID-19 should be “based on recognition of the pronounced difference in risk between smoking and vaping, the difficulty that many face in quitting nicotine use completely, the risks of harmful unintended consequences, and the strong association of smoking with poverty and various forms of disadvantage.” In other words, they worry that the promotion of unfounded fears in relation to COVID-19 may drive vapers back to smoking, with destructive consequences for their health.

Recent experience suggests that this concern is well founded. In a different outbreak, the mysterious lung illnesses that began last year and hospitalized nearly 3,000 Americans, statements by the CDC, campaigns by anti-smoking advocacy groups, and reports by mainstream press all blamed nicotine e-cigarettes for the disease. It was later established that contaminants in primarily black-market cannabis products were overwhelmingly behind the outbreak, but the damage was done: Public opinion turned decisively against e-cigarettes, flavor bans proliferated, and misperceptions about the risks of vaping have persisted in spite of the newer information.
Less than a year later, both the media and anti-smoking groups seem poised to repeat the mistake. It’s possible that vaping may marginally increase the risks of COVID-19; it’s also possible that exaggerating fears will harden public attitudes against vaping, discourage smokers from switching, and lead to even more restrictions on e-cigarette products. These possibilities highlight the danger of politicizing science and taking advantage of a frightening illness to promote a preexisting agenda.
 

mcduffy

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  • Jul 9, 2017
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    Editorial: Nicotine and SARS-CoV-2: COVID-19 may be a disease of the nicotinic cholinergic system
    ...
    SARS-CoV-2 is known to use the
    angiotensin converting enzyme 2
    (ACE2) as a receptor for cell entry [ 47].
    ACE2 has well-established
    vasodilatory, anti-inflammatory and
    antioxidant properties. Studies on
    smoking and ACE2 have reported
    contradictory findings. Studies
    published before the COVID-19
    pandemic reported that smoking and
    nicotine down-regulate ACE2 [ 48, 49].
    However, more recent studies suggest
    that they up-regulate ACE2 [ [50] , [51] ,
    [52] ]. There is currently no evidence to
    suggest that up-regulation of ACE2 is
    associated with increased COVID-19
    susceptibility or severity. In fact, up-
    regulation of ACE2 appears to be
    protective against tissue damage
    caused by SARS-CoV-2. ACE2 has been
    found to protect mice from developing
    ARDS [ [53] , [54] , [55] ]. Data from SARS
    experimental studies suggest that
    continuous SARS-CoV-2 infection and
    replication induces immediate down-
    regulation of ACE2 that may be
    implicated in organ damage and
    disease severity [ 56]. Further support
    for the beneficial role of ACE2 comes
    from data that estrogens appear to up-
    regulate ACE2 while children and
    younger adults have higher ACE2
    levels compared to older people
    [ 57, 58]. At the same time, women,
    children and young people have milder
    COVID-19 symptoms. If accurate and
    verified, the recently-observed ACE2
    up-regulation in smokers is probably
    induced as a defence mechanism to
    counteract the effects of angiotensin II...
     
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